Vol. 11 No. 03 (May - June) (2021): Innovative Journal of Medical and Health Science
Pattern of left ventricular abnormalities in people with pre-diabetes
Dr Mohd abass Bhat, Dr Nazir A Pala, Dr Syed Manzoor Anderabi, Dr Shahnawaz HassanOnline First: May 5, 2021
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Pattern of left ventricular abnormalities in people with pre-diabetes
Purpose of study: Left ventricular dysfunction in people with diabetes mellitus has been demonstrated by various studies in past. However, there is little and conflicting data with regard to Left Ventricular abnormalities in people with Pre-diabetes. In view of Scarcity of data, we designed a study to investigate the early abnormalities in left ventricular function in normotensive people with prediabetes compared to healthy controls, using Doppler Echocardiography
Methods: Prospective hospital based case-control study, conducted at a tertiary care hospital in north India. 100 people with prediabetes without known cardiovascular disease, with equal number of matched controls were enrolled in the study. A detailed medical history, clinical examination, biochemical profile and echocardiographic studies were performed in all study subjects.
Results: Early diastolic wave (E;0.693±0.092m/s), Early diastolic wave (E)/late diastolic wave (A) ratio (E/A;0.887±0.095), left ventricular end systolic diameter (LVESD; 24.78±1.640mm) were significantly lower in people with prediabetes, whereas isovolumetric relaxation time (IVRT;87.45±8.148ms), sphericity index (0.595±0.028) and left atrial diameter (35.50±1.693mm) were significantly higher in people with pre-diabetes compared to matched controls. However, no correlation was observed with regard to anthropometric variables (body-mass index (BMI), waist circumference) and lipid profile
Conclusion: Prediabetes is associated with subclinical left Ventricular systolic and diastolic abnormalities as evaluated on conventional and pulse-wave echocardiography.
Pattern of left ventricular abnormalities in people with pre-diabetes
Purpose of study: Left ventricular dysfunction in people with diabetes mellitus has been demonstrated by various studies in past. However, there is little and conflicting data with regard to Left Ventricular abnormalities in people with Pre-diabetes. In view of Scarcity of data, we designed a study to investigate the early abnormalities in left ventricular function in normotensive people with prediabetes compared to healthy controls, using Doppler Echocardiography
Methods: Prospective hospital based case-control study, conducted at a tertiary care hospital in north India. 100 people with prediabetes without known cardiovascular disease, with equal number of matched controls were enrolled in the study. A detailed medical history, clinical examination, biochemical profile and echocardiographic studies were performed in all study subjects.
Results: Early diastolic wave (E;0.693±0.092m/s), Early diastolic wave (E)/late diastolic wave (A) ratio (E/A;0.887±0.095), left ventricular end systolic diameter (LVESD; 24.78±1.640mm) were significantly lower in people with prediabetes, whereas isovolumetric relaxation time (IVRT;87.45±8.148ms), sphericity index (0.595±0.028) and left atrial diameter (35.50±1.693mm) were significantly higher in people with pre-diabetes compared to matched controls. However, no correlation was observed with regard to anthropometric variables (body-mass index (BMI), waist circumference) and lipid profile
Conclusion: Prediabetes is associated with subclinical left Ventricular systolic and diastolic abnormalities as evaluated on conventional and pulse-wave echocardiography.
Pattern of left ventricular abnormalities in people with pre-diabetes
Purpose of study: Left ventricular dysfunction in people with diabetes mellitus has been demonstrated by various studies in past. However, there is little and conflicting data with regard to Left Ventricular abnormalities in people with Pre-diabetes. In view of Scarcity of data, we designed a study to investigate the early abnormalities in left ventricular function in normotensive people with prediabetes compared to healthy controls, using Doppler Echocardiography
Methods: Prospective hospital based case-control study, conducted at a tertiary care hospital in north India. 100 people with prediabetes without known cardiovascular disease, with equal number of matched controls were enrolled in the study. A detailed medical history, clinical examination, biochemical profile and echocardiographic studies were performed in all study subjects.
Results: Early diastolic wave (E;0.693±0.092m/s), Early diastolic wave (E)/late diastolic wave (A) ratio (E/A;0.887±0.095), left ventricular end systolic diameter (LVESD; 24.78±1.640mm) were significantly lower in people with prediabetes, whereas isovolumetric relaxation time (IVRT;87.45±8.148ms), sphericity index (0.595±0.028) and left atrial diameter (35.50±1.693mm) were significantly higher in people with pre-diabetes compared to matched controls. However, no correlation was observed with regard to anthropometric variables (body-mass index (BMI), waist circumference) and lipid profile
Conclusion: Prediabetes is associated with subclinical left Ventricular systolic and diastolic abnormalities as evaluated on conventional and pulse-wave echocardiography.
Pattern of left ventricular abnormalities in people with pre-diabetes
Purpose of study: Left ventricular dysfunction in people with diabetes mellitus has been demonstrated by various studies in past. However, there is little and conflicting data with regard to Left Ventricular abnormalities in people with Pre-diabetes. In view of Scarcity of data, we designed a study to investigate the early abnormalities in left ventricular function in normotensive people with prediabetes compared to healthy controls, using Doppler Echocardiography
Methods: Prospective hospital based case-control study, conducted at a tertiary care hospital in north India. 100 people with prediabetes without known cardiovascular disease, with equal number of matched controls were enrolled in the study. A detailed medical history, clinical examination, biochemical profile and echocardiographic studies were performed in all study subjects.
Results: Early diastolic wave (E;0.693±0.092m/s), Early diastolic wave (E)/late diastolic wave (A) ratio (E/A;0.887±0.095), left ventricular end systolic diameter (LVESD; 24.78±1.640mm) were significantly lower in people with prediabetes, whereas isovolumetric relaxation time (IVRT;87.45±8.148ms), sphericity index (0.595±0.028) and left atrial diameter (35.50±1.693mm) were significantly higher in people with pre-diabetes compared to matched controls. However, no correlation was observed with regard to anthropometric variables (body-mass index (BMI), waist circumference) and lipid profile
Conclusion: Prediabetes is associated with subclinical left Ventricular systolic and diastolic abnormalities as evaluated on conventional and pulse-wave echocardiography.
Pattern of left ventricular abnormalities in people with pre-diabetes
Purpose of study: Left ventricular dysfunction in people with diabetes mellitus has been demonstrated by various studies in past. However, there is little and conflicting data with regard to Left Ventricular abnormalities in people with Pre-diabetes. In view of Scarcity of data, we designed a study to investigate the early abnormalities in left ventricular function in normotensive people with prediabetes compared to healthy controls, using Doppler Echocardiography
Methods: Prospective hospital based case-control study, conducted at a tertiary care hospital in north India. 100 people with prediabetes without known cardiovascular disease, with equal number of matched controls were enrolled in the study. A detailed medical history, clinical examination, biochemical profile and echocardiographic studies were performed in all study subjects.
Results: Early diastolic wave (E;0.693±0.092m/s), Early diastolic wave (E)/late diastolic wave (A) ratio (E/A;0.887±0.095), left ventricular end systolic diameter (LVESD; 24.78±1.640mm) were significantly lower in people with prediabetes, whereas isovolumetric relaxation time (IVRT;87.45±8.148ms), sphericity index (0.595±0.028) and left atrial diameter (35.50±1.693mm) were significantly higher in people with pre-diabetes compared to matched controls. However, no correlation was observed with regard to anthropometric variables (body-mass index (BMI), waist circumference) and lipid profile
Conclusion: Prediabetes is associated with subclinical left Ventricular systolic and diastolic abnormalities as evaluated on conventional and pulse-wave echocardiography.
USE OF AYURVEDIC FORMULATION FOR INFLUENZA LIKE ILLNESS: A PILOT STUDY
Pravesh Agarwal, Shuchi Mahajan, Manju SharmaOnline First: May 5, 2021
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USE OF AYURVEDIC FORMULATION FOR INFLUENZA LIKE ILLNESS: A PILOT STUDY
Background: Ayurvedic medicines (Kadhas) has become the best-selling remedies for influenza-like illness (ILI) these days, yet much is not known about the efficacy of the these drugs in reducing the symptoms of ILI. The aim of the study is to assess the efficacy of these medicines in alleviation of symptoms of ILI in the adults. We conducted a pilot study to assess whether these formulations help in alleviation of symptoms of ILI.
Methods: A observational study was designed and patients having symptoms of ILI were screened and enrolled by trained authors during an encounter for acute respiratory illness with symptoms of fever, cough, running nose, wheeze, headache, muscle aches, sore throat and fatigue. A total of 51 subjects were recruited from the general population. The 27 were instructed to take Ayurvedic formulation provide by research coordinator along with standard treatment. Rest 24 were provided with standard treatment. The primary outcome included the time to alleviation of symptoms and the incidence of complications.
Results: In this study, no significant differences were found in the time to alleviation of symptoms, incidence of complications, time until becoming afebrile, or rate of severe illness among the combination treatment group and standard treatment group. No adverse drug reactions and drug intolerance was observed to Ayurvedic formulation or to standard treatment during the follow-up periods.
Conclusions: Although limited in terms of number of patients, our results suggested that, Ayurvedic formulation has yet to show a clear advantage over conventional treatments in the treatment of influenza like illness. The results support the feasibility of a large-scale randomized controlled trial to confirm these findings.
Keywords: Ayurvedic kadhas, Influenza like illness, Combination group, Standard treatment group.
USE OF AYURVEDIC FORMULATION FOR INFLUENZA LIKE ILLNESS: A PILOT STUDY
Background: Ayurvedic medicines (Kadhas) has become the best-selling remedies for influenza-like illness (ILI) these days, yet much is not known about the efficacy of the these drugs in reducing the symptoms of ILI. The aim of the study is to assess the efficacy of these medicines in alleviation of symptoms of ILI in the adults. We conducted a pilot study to assess whether these formulations help in alleviation of symptoms of ILI.
Methods: A observational study was designed and patients having symptoms of ILI were screened and enrolled by trained authors during an encounter for acute respiratory illness with symptoms of fever, cough, running nose, wheeze, headache, muscle aches, sore throat and fatigue. A total of 51 subjects were recruited from the general population. The 27 were instructed to take Ayurvedic formulation provide by research coordinator along with standard treatment. Rest 24 were provided with standard treatment. The primary outcome included the time to alleviation of symptoms and the incidence of complications.
Results: In this study, no significant differences were found in the time to alleviation of symptoms, incidence of complications, time until becoming afebrile, or rate of severe illness among the combination treatment group and standard treatment group. No adverse drug reactions and drug intolerance was observed to Ayurvedic formulation or to standard treatment during the follow-up periods.
Conclusions: Although limited in terms of number of patients, our results suggested that, Ayurvedic formulation has yet to show a clear advantage over conventional treatments in the treatment of influenza like illness. The results support the feasibility of a large-scale randomized controlled trial to confirm these findings.
Keywords: Ayurvedic kadhas, Influenza like illness, Combination group, Standard treatment group.
USE OF AYURVEDIC FORMULATION FOR INFLUENZA LIKE ILLNESS: A PILOT STUDY
Background: Ayurvedic medicines (Kadhas) has become the best-selling remedies for influenza-like illness (ILI) these days, yet much is not known about the efficacy of the these drugs in reducing the symptoms of ILI. The aim of the study is to assess the efficacy of these medicines in alleviation of symptoms of ILI in the adults. We conducted a pilot study to assess whether these formulations help in alleviation of symptoms of ILI.
Methods: A observational study was designed and patients having symptoms of ILI were screened and enrolled by trained authors during an encounter for acute respiratory illness with symptoms of fever, cough, running nose, wheeze, headache, muscle aches, sore throat and fatigue. A total of 51 subjects were recruited from the general population. The 27 were instructed to take Ayurvedic formulation provide by research coordinator along with standard treatment. Rest 24 were provided with standard treatment. The primary outcome included the time to alleviation of symptoms and the incidence of complications.
Results: In this study, no significant differences were found in the time to alleviation of symptoms, incidence of complications, time until becoming afebrile, or rate of severe illness among the combination treatment group and standard treatment group. No adverse drug reactions and drug intolerance was observed to Ayurvedic formulation or to standard treatment during the follow-up periods.
Conclusions: Although limited in terms of number of patients, our results suggested that, Ayurvedic formulation has yet to show a clear advantage over conventional treatments in the treatment of influenza like illness. The results support the feasibility of a large-scale randomized controlled trial to confirm these findings.
Keywords: Ayurvedic kadhas, Influenza like illness, Combination group, Standard treatment group.
USE OF AYURVEDIC FORMULATION FOR INFLUENZA LIKE ILLNESS: A PILOT STUDY
Background: Ayurvedic medicines (Kadhas) has become the best-selling remedies for influenza-like illness (ILI) these days, yet much is not known about the efficacy of the these drugs in reducing the symptoms of ILI. The aim of the study is to assess the efficacy of these medicines in alleviation of symptoms of ILI in the adults. We conducted a pilot study to assess whether these formulations help in alleviation of symptoms of ILI.
Methods: A observational study was designed and patients having symptoms of ILI were screened and enrolled by trained authors during an encounter for acute respiratory illness with symptoms of fever, cough, running nose, wheeze, headache, muscle aches, sore throat and fatigue. A total of 51 subjects were recruited from the general population. The 27 were instructed to take Ayurvedic formulation provide by research coordinator along with standard treatment. Rest 24 were provided with standard treatment. The primary outcome included the time to alleviation of symptoms and the incidence of complications.
Results: In this study, no significant differences were found in the time to alleviation of symptoms, incidence of complications, time until becoming afebrile, or rate of severe illness among the combination treatment group and standard treatment group. No adverse drug reactions and drug intolerance was observed to Ayurvedic formulation or to standard treatment during the follow-up periods.
Conclusions: Although limited in terms of number of patients, our results suggested that, Ayurvedic formulation has yet to show a clear advantage over conventional treatments in the treatment of influenza like illness. The results support the feasibility of a large-scale randomized controlled trial to confirm these findings.
Keywords: Ayurvedic kadhas, Influenza like illness, Combination group, Standard treatment group.
A CLINICAL EVALUATION OF PROPOFOL IN SHORT SURGICAL PROCEDURES AND COMPARISON WITH THIOPENTONE SODIUM AS INDUCTION AGENT IN IMMUNOCOMPROMISED HIV PATIENTS
Lalit Kumar Garg, Anjana, Deepak Berry, Tanveer Singh KundraOnline First: May 19, 2021
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A CLINICAL EVALUATION OF PROPOFOL IN SHORT SURGICAL PROCEDURES AND COMPARISON WITH THIOPENTONE SODIUM AS INDUCTION AGENT IN IMMUNOCOMPROMISED HIV PATIENTS
BACKGROUND: Numerous attempts have been made in the past for the selection of an ideal intravenous anaesthetic agent for outpatient short surgical procedures in immunocompromised patients. The present study compared the effect of two drugs namely propofol and thiopentone sodium as an induction agent in short surgical procedures in immunocompromised HIV patients.
Materials and Methods: This was a randomized study evaluating two drugs- propofol and thiopentone sodium in short surgical procedures. It was carried out on 100 immunocompromised HIV patients in age group of 18-45 yrs of ASA grade 1/2 undergoing short surgical procedures .
These patients were randomly divided into 2 groups 1 and 2 which were further subdivided into 1a and 1b , 2a and 2b respectively, each consisiting of 25 pts.
Group 1a and 2 a were given inj pentazocine 30mg and inj promethazine 25mg
Group 1b and 2b were administered 2 ml of saline .
Group 1a and 1b received inj propofol 1%i/v dose 2.5mg/kg wt and group 2a and 2b were given inj thiopentone 2.5% i/v at dose of 5mg/kg wt.
RESULT: Propofol showed a greater decrease in diastolic and systolic BP at induction, respiratory rate with more incidence of apnea.
CONCLUSION: Propofol produces rapid, pleasant and safe anaesthesia, with smooth recovery while thiopentone is associated with poor psychomotor recovery in immunocompromised HIV patients.
KEY WORDS: Propofol, Thiopentone sodium, Short surgical procedures, immunocompromised, HIV
A CLINICAL EVALUATION OF PROPOFOL IN SHORT SURGICAL PROCEDURES AND COMPARISON WITH THIOPENTONE SODIUM AS INDUCTION AGENT IN IMMUNOCOMPROMISED HIV PATIENTS
BACKGROUND: Numerous attempts have been made in the past for the selection of an ideal intravenous anaesthetic agent for outpatient short surgical procedures in immunocompromised patients. The present study compared the effect of two drugs namely propofol and thiopentone sodium as an induction agent in short surgical procedures in immunocompromised HIV patients.
Materials and Methods: This was a randomized study evaluating two drugs- propofol and thiopentone sodium in short surgical procedures. It was carried out on 100 immunocompromised HIV patients in age group of 18-45 yrs of ASA grade 1/2 undergoing short surgical procedures .
These patients were randomly divided into 2 groups 1 and 2 which were further subdivided into 1a and 1b , 2a and 2b respectively, each consisiting of 25 pts.
Group 1a and 2 a were given inj pentazocine 30mg and inj promethazine 25mg
Group 1b and 2b were administered 2 ml of saline .
Group 1a and 1b received inj propofol 1%i/v dose 2.5mg/kg wt and group 2a and 2b were given inj thiopentone 2.5% i/v at dose of 5mg/kg wt.
RESULT: Propofol showed a greater decrease in diastolic and systolic BP at induction, respiratory rate with more incidence of apnea.
CONCLUSION: Propofol produces rapid, pleasant and safe anaesthesia, with smooth recovery while thiopentone is associated with poor psychomotor recovery in immunocompromised HIV patients.
KEY WORDS: Propofol, Thiopentone sodium, Short surgical procedures, immunocompromised, HIV
A CLINICAL EVALUATION OF PROPOFOL IN SHORT SURGICAL PROCEDURES AND COMPARISON WITH THIOPENTONE SODIUM AS INDUCTION AGENT IN IMMUNOCOMPROMISED HIV PATIENTS
BACKGROUND: Numerous attempts have been made in the past for the selection of an ideal intravenous anaesthetic agent for outpatient short surgical procedures in immunocompromised patients. The present study compared the effect of two drugs namely propofol and thiopentone sodium as an induction agent in short surgical procedures in immunocompromised HIV patients.
Materials and Methods: This was a randomized study evaluating two drugs- propofol and thiopentone sodium in short surgical procedures. It was carried out on 100 immunocompromised HIV patients in age group of 18-45 yrs of ASA grade 1/2 undergoing short surgical procedures .
These patients were randomly divided into 2 groups 1 and 2 which were further subdivided into 1a and 1b , 2a and 2b respectively, each consisiting of 25 pts.
Group 1a and 2 a were given inj pentazocine 30mg and inj promethazine 25mg
Group 1b and 2b were administered 2 ml of saline .
Group 1a and 1b received inj propofol 1%i/v dose 2.5mg/kg wt and group 2a and 2b were given inj thiopentone 2.5% i/v at dose of 5mg/kg wt.
RESULT: Propofol showed a greater decrease in diastolic and systolic BP at induction, respiratory rate with more incidence of apnea.
CONCLUSION: Propofol produces rapid, pleasant and safe anaesthesia, with smooth recovery while thiopentone is associated with poor psychomotor recovery in immunocompromised HIV patients.
KEY WORDS: Propofol, Thiopentone sodium, Short surgical procedures, immunocompromised, HIV
A CLINICAL EVALUATION OF PROPOFOL IN SHORT SURGICAL PROCEDURES AND COMPARISON WITH THIOPENTONE SODIUM AS INDUCTION AGENT IN IMMUNOCOMPROMISED HIV PATIENTS
BACKGROUND: Numerous attempts have been made in the past for the selection of an ideal intravenous anaesthetic agent for outpatient short surgical procedures in immunocompromised patients. The present study compared the effect of two drugs namely propofol and thiopentone sodium as an induction agent in short surgical procedures in immunocompromised HIV patients.
Materials and Methods: This was a randomized study evaluating two drugs- propofol and thiopentone sodium in short surgical procedures. It was carried out on 100 immunocompromised HIV patients in age group of 18-45 yrs of ASA grade 1/2 undergoing short surgical procedures .
These patients were randomly divided into 2 groups 1 and 2 which were further subdivided into 1a and 1b , 2a and 2b respectively, each consisiting of 25 pts.
Group 1a and 2 a were given inj pentazocine 30mg and inj promethazine 25mg
Group 1b and 2b were administered 2 ml of saline .
Group 1a and 1b received inj propofol 1%i/v dose 2.5mg/kg wt and group 2a and 2b were given inj thiopentone 2.5% i/v at dose of 5mg/kg wt.
RESULT: Propofol showed a greater decrease in diastolic and systolic BP at induction, respiratory rate with more incidence of apnea.
CONCLUSION: Propofol produces rapid, pleasant and safe anaesthesia, with smooth recovery while thiopentone is associated with poor psychomotor recovery in immunocompromised HIV patients.
KEY WORDS: Propofol, Thiopentone sodium, Short surgical procedures, immunocompromised, HIV
The Accuracy of Documented Nursing Care Plan among Registered Nurses
Muneerah Mahmood AlhawsawiOnline First: May 24, 2021
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The Accuracy of Documented Nursing Care Plan among Registered Nurses
Background: Nursing documentation is a record of care planned and provided by qualified nurses under the guidance of a competent nurse for each patient as well as the clients.
Objective: to provide published studies about accuracy of nursing documentation.
Methods: Searches were conducted using the following electronic databases: PUBMED, MEDLIN, CINAHAL, SAUDI DIGETAL LIBRALY and GOOGLE SCOLAR as gray data base. Search was limited to English-Language publication. And include study over 10year period.
Result: nursing documentations is inaccurate, lacking precision, and low in quality. Factors that influence nursing documentation differ but are also interrelated with each other. Shortage of employees, insufficient knowledge about the significance of documentation, patient load, lack of hospital education, and lack of support from nurse leaders are the reported challenges to documentation.
Conclusion: Most of the lecture revel the necessary need of nursing documentation practice. Affected factor and with several recommendations for improvement noted.
Keywords: ''nursing care plan," "nursing documentation,'' "accuracy of documentation" and ''nursing report.''
The Accuracy of Documented Nursing Care Plan among Registered Nurses
Background: Nursing documentation is a record of care planned and provided by qualified nurses under the guidance of a competent nurse for each patient as well as the clients.
Objective: to provide published studies about accuracy of nursing documentation.
Methods: Searches were conducted using the following electronic databases: PUBMED, MEDLIN, CINAHAL, SAUDI DIGETAL LIBRALY and GOOGLE SCOLAR as gray data base. Search was limited to English-Language publication. And include study over 10year period.
Result: nursing documentations is inaccurate, lacking precision, and low in quality. Factors that influence nursing documentation differ but are also interrelated with each other. Shortage of employees, insufficient knowledge about the significance of documentation, patient load, lack of hospital education, and lack of support from nurse leaders are the reported challenges to documentation.
Conclusion: Most of the lecture revel the necessary need of nursing documentation practice. Affected factor and with several recommendations for improvement noted.
Keywords: ''nursing care plan," "nursing documentation,'' "accuracy of documentation" and ''nursing report.''
The Accuracy of Documented Nursing Care Plan among Registered Nurses
Background: Nursing documentation is a record of care planned and provided by qualified nurses under the guidance of a competent nurse for each patient as well as the clients.
Objective: to provide published studies about accuracy of nursing documentation.
Methods: Searches were conducted using the following electronic databases: PUBMED, MEDLIN, CINAHAL, SAUDI DIGETAL LIBRALY and GOOGLE SCOLAR as gray data base. Search was limited to English-Language publication. And include study over 10year period.
Result: nursing documentations is inaccurate, lacking precision, and low in quality. Factors that influence nursing documentation differ but are also interrelated with each other. Shortage of employees, insufficient knowledge about the significance of documentation, patient load, lack of hospital education, and lack of support from nurse leaders are the reported challenges to documentation.
Conclusion: Most of the lecture revel the necessary need of nursing documentation practice. Affected factor and with several recommendations for improvement noted.
Keywords: ''nursing care plan," "nursing documentation,'' "accuracy of documentation" and ''nursing report.''
The Accuracy of Documented Nursing Care Plan among Registered Nurses
Background: Nursing documentation is a record of care planned and provided by qualified nurses under the guidance of a competent nurse for each patient as well as the clients.
Objective: to provide published studies about accuracy of nursing documentation.
Methods: Searches were conducted using the following electronic databases: PUBMED, MEDLIN, CINAHAL, SAUDI DIGETAL LIBRALY and GOOGLE SCOLAR as gray data base. Search was limited to English-Language publication. And include study over 10year period.
Result: nursing documentations is inaccurate, lacking precision, and low in quality. Factors that influence nursing documentation differ but are also interrelated with each other. Shortage of employees, insufficient knowledge about the significance of documentation, patient load, lack of hospital education, and lack of support from nurse leaders are the reported challenges to documentation.
Conclusion: Most of the lecture revel the necessary need of nursing documentation practice. Affected factor and with several recommendations for improvement noted.
Keywords: ''nursing care plan," "nursing documentation,'' "accuracy of documentation" and ''nursing report.''
EVALUATION OF MATERNAL AND FETAL OUTCOME AND COMPLICATIONS IN MULTIPLE REPEAT CAESAREAN SECTIONS
Samar Mukhtar, Asma Mufti , Shazia AshrafOnline First: May 26, 2020
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EVALUATION OF MATERNAL AND FETAL OUTCOME AND COMPLICATIONS IN MULTIPLE REPEAT CAESAREAN SECTIONS
Objective: To study maternal and fetal outcome and to determine the complications and difficulties faced by the operating surgeon in women who undergo multiple repeat caesarean sections.
Methodology: A prospective study was carried in government Lalla Ded Hospital over a period of one and a half year in which patients undergoing repeat caesarean sections were divided in 2 groups. The study group included those women undergoing fourth or higher order caesarean sections and the control group included those having previous one or two caesarean sections. The demographic criteria, neonatal outcome and the incidence of maternal complications like adhesions, scar dehiscence or rupture, placenta previa and accreta were noted and compared.
Results: Maternal age and parity was higher in the study group. Gestation at cesarean section was less in the study group. Birth weight, along with 1- and 5- minute Apgar scores were lower in the study group, but the difference was not statistically significant. There were no significant differences in preterm birth rates, NICU admission and postpartum neonatal follow-up with related morbidity conditions. Duration of surgery, was longer in study group (55+18.4 mins) than control groups (44+16.6mins). Adhesions were encountered in higher number of cases in study group as compared to control group; 67 cases (47.86%) versus 54 (27%) cases, the difference being statistically significant. Uterine scar dehiscence was found in 10.7% patients in study group as against 4.5% patients in control group, the difference being statistically significant. Abnormal placentation, placenta praevia and accreta were almost of equal occurrence in both the groups
Conclusion: This study demonstrated that as compared to previous one and two caesarean sections, higher order repeat caesarean sections have increased complication rates and more difficulties encountered during surgery.
EVALUATION OF MATERNAL AND FETAL OUTCOME AND COMPLICATIONS IN MULTIPLE REPEAT CAESAREAN SECTIONS
Objective: To study maternal and fetal outcome and to determine the complications and difficulties faced by the operating surgeon in women who undergo multiple repeat caesarean sections.
Methodology: A prospective study was carried in government Lalla Ded Hospital over a period of one and a half year in which patients undergoing repeat caesarean sections were divided in 2 groups. The study group included those women undergoing fourth or higher order caesarean sections and the control group included those having previous one or two caesarean sections. The demographic criteria, neonatal outcome and the incidence of maternal complications like adhesions, scar dehiscence or rupture, placenta previa and accreta were noted and compared.
Results: Maternal age and parity was higher in the study group. Gestation at cesarean section was less in the study group. Birth weight, along with 1- and 5- minute Apgar scores were lower in the study group, but the difference was not statistically significant. There were no significant differences in preterm birth rates, NICU admission and postpartum neonatal follow-up with related morbidity conditions. Duration of surgery, was longer in study group (55+18.4 mins) than control groups (44+16.6mins). Adhesions were encountered in higher number of cases in study group as compared to control group; 67 cases (47.86%) versus 54 (27%) cases, the difference being statistically significant. Uterine scar dehiscence was found in 10.7% patients in study group as against 4.5% patients in control group, the difference being statistically significant. Abnormal placentation, placenta praevia and accreta were almost of equal occurrence in both the groups
Conclusion: This study demonstrated that as compared to previous one and two caesarean sections, higher order repeat caesarean sections have increased complication rates and more difficulties encountered during surgery.
EVALUATION OF MATERNAL AND FETAL OUTCOME AND COMPLICATIONS IN MULTIPLE REPEAT CAESAREAN SECTIONS
Objective: To study maternal and fetal outcome and to determine the complications and difficulties faced by the operating surgeon in women who undergo multiple repeat caesarean sections.
Methodology: A prospective study was carried in government Lalla Ded Hospital over a period of one and a half year in which patients undergoing repeat caesarean sections were divided in 2 groups. The study group included those women undergoing fourth or higher order caesarean sections and the control group included those having previous one or two caesarean sections. The demographic criteria, neonatal outcome and the incidence of maternal complications like adhesions, scar dehiscence or rupture, placenta previa and accreta were noted and compared.
Results: Maternal age and parity was higher in the study group. Gestation at cesarean section was less in the study group. Birth weight, along with 1- and 5- minute Apgar scores were lower in the study group, but the difference was not statistically significant. There were no significant differences in preterm birth rates, NICU admission and postpartum neonatal follow-up with related morbidity conditions. Duration of surgery, was longer in study group (55+18.4 mins) than control groups (44+16.6mins). Adhesions were encountered in higher number of cases in study group as compared to control group; 67 cases (47.86%) versus 54 (27%) cases, the difference being statistically significant. Uterine scar dehiscence was found in 10.7% patients in study group as against 4.5% patients in control group, the difference being statistically significant. Abnormal placentation, placenta praevia and accreta were almost of equal occurrence in both the groups
Conclusion: This study demonstrated that as compared to previous one and two caesarean sections, higher order repeat caesarean sections have increased complication rates and more difficulties encountered during surgery.
EVALUATION OF MATERNAL AND FETAL OUTCOME AND COMPLICATIONS IN MULTIPLE REPEAT CAESAREAN SECTIONS
Objective: To study maternal and fetal outcome and to determine the complications and difficulties faced by the operating surgeon in women who undergo multiple repeat caesarean sections.
Methodology: A prospective study was carried in government Lalla Ded Hospital over a period of one and a half year in which patients undergoing repeat caesarean sections were divided in 2 groups. The study group included those women undergoing fourth or higher order caesarean sections and the control group included those having previous one or two caesarean sections. The demographic criteria, neonatal outcome and the incidence of maternal complications like adhesions, scar dehiscence or rupture, placenta previa and accreta were noted and compared.
Results: Maternal age and parity was higher in the study group. Gestation at cesarean section was less in the study group. Birth weight, along with 1- and 5- minute Apgar scores were lower in the study group, but the difference was not statistically significant. There were no significant differences in preterm birth rates, NICU admission and postpartum neonatal follow-up with related morbidity conditions. Duration of surgery, was longer in study group (55+18.4 mins) than control groups (44+16.6mins). Adhesions were encountered in higher number of cases in study group as compared to control group; 67 cases (47.86%) versus 54 (27%) cases, the difference being statistically significant. Uterine scar dehiscence was found in 10.7% patients in study group as against 4.5% patients in control group, the difference being statistically significant. Abnormal placentation, placenta praevia and accreta were almost of equal occurrence in both the groups
Conclusion: This study demonstrated that as compared to previous one and two caesarean sections, higher order repeat caesarean sections have increased complication rates and more difficulties encountered during surgery.
Association of lichen planus with metabolic syndrome – a case control study in a tertiary care centre
Nishant Saurabh Saxena, , Nimisha Saxena, Harsh SharmaOnline First: May 29, 2021
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Association of lichen planus with metabolic syndrome – a case control study in a tertiary care centre
Background: Lichen planus is an inflammatory papulosquamous disease
which affects skin and mucous membrane and cause metabolic
derangements.
Methods: This is an hospital based case control study during a span of 2
year (Jan2018-Dec 2019) which includes 60 cases of lichen planus and
60 age and sex matched controls. Relevant clinical history and physical
examination was done and collaborated with blood investigations.
Diagnosis was made based on IDF criteria.
Results: No significant association can be established between lichen
planus and metabolic syndrome ( p=0.278) Although prevalence of
hypertension was higher in cases as compared to controls (36% vs. 26%,
p=0.027) , TG levels (12% vs. 6%, p=0.030 and low HDLC levels (47%
vs. 33%, p=0.039). No significant association was established between
FBS and waist circumference with lichen planus.
Conclusions: Although no significant association can be established
between lichen planus and metabolic syndrome but its components such
as hypertension ,TG and HDLC were found to be associated with LP as
per the study .Therefore screening of these parameters in LP patients is
necessary to avoid future complications in these patients.
Keywords: Lichen planus, Metabolic syndrome, Hypertension, Triglyceride
Association of lichen planus with metabolic syndrome – a case control study in a tertiary care centre
Background: Lichen planus is an inflammatory papulosquamous disease
which affects skin and mucous membrane and cause metabolic
derangements.
Methods: This is an hospital based case control study during a span of 2
year (Jan2018-Dec 2019) which includes 60 cases of lichen planus and
60 age and sex matched controls. Relevant clinical history and physical
examination was done and collaborated with blood investigations.
Diagnosis was made based on IDF criteria.
Results: No significant association can be established between lichen
planus and metabolic syndrome ( p=0.278) Although prevalence of
hypertension was higher in cases as compared to controls (36% vs. 26%,
p=0.027) , TG levels (12% vs. 6%, p=0.030 and low HDLC levels (47%
vs. 33%, p=0.039). No significant association was established between
FBS and waist circumference with lichen planus.
Conclusions: Although no significant association can be established
between lichen planus and metabolic syndrome but its components such
as hypertension ,TG and HDLC were found to be associated with LP as
per the study .Therefore screening of these parameters in LP patients is
necessary to avoid future complications in these patients.
Keywords: Lichen planus, Metabolic syndrome, Hypertension, Triglyceride
Association of lichen planus with metabolic syndrome – a case control study in a tertiary care centre
Background: Lichen planus is an inflammatory papulosquamous disease
which affects skin and mucous membrane and cause metabolic
derangements.
Methods: This is an hospital based case control study during a span of 2
year (Jan2018-Dec 2019) which includes 60 cases of lichen planus and
60 age and sex matched controls. Relevant clinical history and physical
examination was done and collaborated with blood investigations.
Diagnosis was made based on IDF criteria.
Results: No significant association can be established between lichen
planus and metabolic syndrome ( p=0.278) Although prevalence of
hypertension was higher in cases as compared to controls (36% vs. 26%,
p=0.027) , TG levels (12% vs. 6%, p=0.030 and low HDLC levels (47%
vs. 33%, p=0.039). No significant association was established between
FBS and waist circumference with lichen planus.
Conclusions: Although no significant association can be established
between lichen planus and metabolic syndrome but its components such
as hypertension ,TG and HDLC were found to be associated with LP as
per the study .Therefore screening of these parameters in LP patients is
necessary to avoid future complications in these patients.
Keywords: Lichen planus, Metabolic syndrome, Hypertension, Triglyceride
DISEASE SEVERITY IN RELATION TO NUTRITIONAL STATUS AMONG 2-5-YEAR OLD CHILDREN WITH WHEEZE
K Rugmini , K Divya , KE Elizabeth , Sanjay MasaraddiOnline First: May 30, 2021
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DISEASE SEVERITY IN RELATION TO NUTRITIONAL STATUS AMONG 2-5-YEAR OLD CHILDREN WITH WHEEZE
Introduction: Effect of nutritional status on under-five wheezers is less studied. Undernutrition which is prevalent in this age group may have an impact on the severity of asthma.
Objective: To determine the association of nutritional status as measured by anthropometric parameters Weight for Age (WFA), Height for Age (HFA) and Body Mass Index (BMI) on severity of asthma.
Materials and Methods: A study was undertaken on 40 consecutive children in the age group of 2-5-years with a clinical diagnosis of asthma (> 3 episodes of wheezing) which included children on controller therapy and those on intermittent treatment. These children were categorized into Well-controlled, Poorly-controlled and Uncontrolled asthma as per GINA Guidelines, 2018. Weight, Height and BMI were recorded.
Statistical-Analysis: Data analyzed by SPSS software version 16.0, Chi-square test and One-way ANOVA test.
Results: Out of 40 children, 24 children were on controller therapy and the rest were on intermittent therapy. They were categorized as Well-controlled(45%), Poorly-controlled(20%) and Uncontrolled asthma(35%). 16(40%) were under-weight, 2(5%) overweight and 2(5%) were obese. 14(35%) were stunted and 18(45%) had BMI<5th percentile. Significant negative association (p value < 0.05) was noted between all the three anthropometric parameters (WFA, HFA and BMI) and severity of asthma.
Conclusion: There was a significant negative association between severity of asthma and poor nutritional status. This highlights the need for periodic growth monitoring and appropriate nutritional intervention to achieve optimal growth and control of asthma.
KEYWORDS: BMI, Nutritional status, Severity of asthma.
DISEASE SEVERITY IN RELATION TO NUTRITIONAL STATUS AMONG 2-5-YEAR OLD CHILDREN WITH WHEEZE
Introduction: Effect of nutritional status on under-five wheezers is less studied. Undernutrition which is prevalent in this age group may have an impact on the severity of asthma.
Objective: To determine the association of nutritional status as measured by anthropometric parameters Weight for Age (WFA), Height for Age (HFA) and Body Mass Index (BMI) on severity of asthma.
Materials and Methods: A study was undertaken on 40 consecutive children in the age group of 2-5-years with a clinical diagnosis of asthma (> 3 episodes of wheezing) which included children on controller therapy and those on intermittent treatment. These children were categorized into Well-controlled, Poorly-controlled and Uncontrolled asthma as per GINA Guidelines, 2018. Weight, Height and BMI were recorded.
Statistical-Analysis: Data analyzed by SPSS software version 16.0, Chi-square test and One-way ANOVA test.
Results: Out of 40 children, 24 children were on controller therapy and the rest were on intermittent therapy. They were categorized as Well-controlled(45%), Poorly-controlled(20%) and Uncontrolled asthma(35%). 16(40%) were under-weight, 2(5%) overweight and 2(5%) were obese. 14(35%) were stunted and 18(45%) had BMI<5th percentile. Significant negative association (p value < 0.05) was noted between all the three anthropometric parameters (WFA, HFA and BMI) and severity of asthma.
Conclusion: There was a significant negative association between severity of asthma and poor nutritional status. This highlights the need for periodic growth monitoring and appropriate nutritional intervention to achieve optimal growth and control of asthma.
KEYWORDS: BMI, Nutritional status, Severity of asthma.
DISEASE SEVERITY IN RELATION TO NUTRITIONAL STATUS AMONG 2-5-YEAR OLD CHILDREN WITH WHEEZE
Introduction: Effect of nutritional status on under-five wheezers is less studied. Undernutrition which is prevalent in this age group may have an impact on the severity of asthma.
Objective: To determine the association of nutritional status as measured by anthropometric parameters Weight for Age (WFA), Height for Age (HFA) and Body Mass Index (BMI) on severity of asthma.
Materials and Methods: A study was undertaken on 40 consecutive children in the age group of 2-5-years with a clinical diagnosis of asthma (> 3 episodes of wheezing) which included children on controller therapy and those on intermittent treatment. These children were categorized into Well-controlled, Poorly-controlled and Uncontrolled asthma as per GINA Guidelines, 2018. Weight, Height and BMI were recorded.
Statistical-Analysis: Data analyzed by SPSS software version 16.0, Chi-square test and One-way ANOVA test.
Results: Out of 40 children, 24 children were on controller therapy and the rest were on intermittent therapy. They were categorized as Well-controlled(45%), Poorly-controlled(20%) and Uncontrolled asthma(35%). 16(40%) were under-weight, 2(5%) overweight and 2(5%) were obese. 14(35%) were stunted and 18(45%) had BMI<5th percentile. Significant negative association (p value < 0.05) was noted between all the three anthropometric parameters (WFA, HFA and BMI) and severity of asthma.
Conclusion: There was a significant negative association between severity of asthma and poor nutritional status. This highlights the need for periodic growth monitoring and appropriate nutritional intervention to achieve optimal growth and control of asthma.
KEYWORDS: BMI, Nutritional status, Severity of asthma.
DISEASE SEVERITY IN RELATION TO NUTRITIONAL STATUS AMONG 2-5-YEAR OLD CHILDREN WITH WHEEZE
Introduction: Effect of nutritional status on under-five wheezers is less studied. Undernutrition which is prevalent in this age group may have an impact on the severity of asthma.
Objective: To determine the association of nutritional status as measured by anthropometric parameters Weight for Age (WFA), Height for Age (HFA) and Body Mass Index (BMI) on severity of asthma.
Materials and Methods: A study was undertaken on 40 consecutive children in the age group of 2-5-years with a clinical diagnosis of asthma (> 3 episodes of wheezing) which included children on controller therapy and those on intermittent treatment. These children were categorized into Well-controlled, Poorly-controlled and Uncontrolled asthma as per GINA Guidelines, 2018. Weight, Height and BMI were recorded.
Statistical-Analysis: Data analyzed by SPSS software version 16.0, Chi-square test and One-way ANOVA test.
Results: Out of 40 children, 24 children were on controller therapy and the rest were on intermittent therapy. They were categorized as Well-controlled(45%), Poorly-controlled(20%) and Uncontrolled asthma(35%). 16(40%) were under-weight, 2(5%) overweight and 2(5%) were obese. 14(35%) were stunted and 18(45%) had BMI<5th percentile. Significant negative association (p value < 0.05) was noted between all the three anthropometric parameters (WFA, HFA and BMI) and severity of asthma.
Conclusion: There was a significant negative association between severity of asthma and poor nutritional status. This highlights the need for periodic growth monitoring and appropriate nutritional intervention to achieve optimal growth and control of asthma.
KEYWORDS: BMI, Nutritional status, Severity of asthma.
CONTRADICTION TO CLINICAL IMMUNOLOGY. SUPPRESSION AND STIMULATION OF IMMUNE REACTIVITY IN PATHOLOGICAL PROCESSES
Vladimir M Zemskov, Andrey M Zemskov, Victoria Neymann, Konstantin N Pronko, Aliexander A Barsukov, Veronica A Zemskova, Maria N Kozlova, Nadezhda S Shishkina, Valentina S Demidova, Alekseev Andrey A.Online First: May 6, 2021
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CONTRADICTION TO CLINICAL IMMUNOLOGY. SUPPRESSION AND STIMULATION OF IMMUNE REACTIVITY IN PATHOLOGICAL PROCESSES
The analysis of literature data and our published results of examination of patients with a wide range of pathological processes was carried out. It has been established that polar changes in reactivity provoke the development of immune-dependent ones, which include primary and secondary immunodeficiencies, auto-aggressive and immunocomplex diseases, or immunoassociated purulent-inflammatory, nonspecific inflammatory lung diseases, cerebrovascular diseases, in which suppression and stimulation of reactivity is a pathogenetic mechanism for normalizing homeostasis, depending on the links of the immune system, doses of antigens, the initial state of protective functions, phases of the immune response, etc.
Keywords: Stimulation. Suppression. Immunodeficiency
CONTRADICTION TO CLINICAL IMMUNOLOGY. SUPPRESSION AND STIMULATION OF IMMUNE REACTIVITY IN PATHOLOGICAL PROCESSES
The analysis of literature data and our published results of examination of patients with a wide range of pathological processes was carried out. It has been established that polar changes in reactivity provoke the development of immune-dependent ones, which include primary and secondary immunodeficiencies, auto-aggressive and immunocomplex diseases, or immunoassociated purulent-inflammatory, nonspecific inflammatory lung diseases, cerebrovascular diseases, in which suppression and stimulation of reactivity is a pathogenetic mechanism for normalizing homeostasis, depending on the links of the immune system, doses of antigens, the initial state of protective functions, phases of the immune response, etc.
Keywords: Stimulation. Suppression. Immunodeficiency
CONTRADICTION TO CLINICAL IMMUNOLOGY. SUPPRESSION AND STIMULATION OF IMMUNE REACTIVITY IN PATHOLOGICAL PROCESSES
The analysis of literature data and our published results of examination of patients with a wide range of pathological processes was carried out. It has been established that polar changes in reactivity provoke the development of immune-dependent ones, which include primary and secondary immunodeficiencies, auto-aggressive and immunocomplex diseases, or immunoassociated purulent-inflammatory, nonspecific inflammatory lung diseases, cerebrovascular diseases, in which suppression and stimulation of reactivity is a pathogenetic mechanism for normalizing homeostasis, depending on the links of the immune system, doses of antigens, the initial state of protective functions, phases of the immune response, etc.
Keywords: Stimulation. Suppression. Immunodeficiency
CONTRADICTION TO CLINICAL IMMUNOLOGY. SUPPRESSION AND STIMULATION OF IMMUNE REACTIVITY IN PATHOLOGICAL PROCESSES
The analysis of literature data and our published results of examination of patients with a wide range of pathological processes was carried out. It has been established that polar changes in reactivity provoke the development of immune-dependent ones, which include primary and secondary immunodeficiencies, auto-aggressive and immunocomplex diseases, or immunoassociated purulent-inflammatory, nonspecific inflammatory lung diseases, cerebrovascular diseases, in which suppression and stimulation of reactivity is a pathogenetic mechanism for normalizing homeostasis, depending on the links of the immune system, doses of antigens, the initial state of protective functions, phases of the immune response, etc.
Keywords: Stimulation. Suppression. Immunodeficiency
Linezolid Induced Thrombocytopenia: A Case Report
Harsh H. Patel, Harsha D. Makwana, Supriya D. MalhotraOnline First: May 28, 2021
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Linezolid Induced Thrombocytopenia: A Case Report
Linezolid (LZD) is an antimicrobial agent with a broad spectrum of activity against virtually all clinically important Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase-negative staphylococci (MRCoNS) and vancomycin-resistant enterococci (VRE). Thrombocytopenia (TP) is a common adverse effect of Linezolid (LZD). Prolonged treatment duration, renal insufficiency, chronic liver disease, malignancy, previous vancomycin use, baseline platelet count, and lower body weight have been reported as possible risk factors for LZD-associated TP. Here, we illustrate a case of a 51-year-old male patient diagnosed with pancreatitis and urinary tract infection and was prescribed several antibiotics including Linezolid. In this case, platelets count which were initially normal started declining from day 7 of initiating Linezolid. Linezolid was withdrawn from treatment from day 9. Platelet count gradually came back to normal on day 16. This suggests reversible type of thrombocytopenia by Linezolid. This case illustrates need for careful observation of platelet count during the treatment with Linezolid.
Keywords:
Linezolid, Thrombocytopenia, Dechallenge
Linezolid Induced Thrombocytopenia: A Case Report
Linezolid (LZD) is an antimicrobial agent with a broad spectrum of activity against virtually all clinically important Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase-negative staphylococci (MRCoNS) and vancomycin-resistant enterococci (VRE). Thrombocytopenia (TP) is a common adverse effect of Linezolid (LZD). Prolonged treatment duration, renal insufficiency, chronic liver disease, malignancy, previous vancomycin use, baseline platelet count, and lower body weight have been reported as possible risk factors for LZD-associated TP. Here, we illustrate a case of a 51-year-old male patient diagnosed with pancreatitis and urinary tract infection and was prescribed several antibiotics including Linezolid. In this case, platelets count which were initially normal started declining from day 7 of initiating Linezolid. Linezolid was withdrawn from treatment from day 9. Platelet count gradually came back to normal on day 16. This suggests reversible type of thrombocytopenia by Linezolid. This case illustrates need for careful observation of platelet count during the treatment with Linezolid.
Keywords:
Linezolid, Thrombocytopenia, Dechallenge
Linezolid Induced Thrombocytopenia: A Case Report
Linezolid (LZD) is an antimicrobial agent with a broad spectrum of activity against virtually all clinically important Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase-negative staphylococci (MRCoNS) and vancomycin-resistant enterococci (VRE). Thrombocytopenia (TP) is a common adverse effect of Linezolid (LZD). Prolonged treatment duration, renal insufficiency, chronic liver disease, malignancy, previous vancomycin use, baseline platelet count, and lower body weight have been reported as possible risk factors for LZD-associated TP. Here, we illustrate a case of a 51-year-old male patient diagnosed with pancreatitis and urinary tract infection and was prescribed several antibiotics including Linezolid. In this case, platelets count which were initially normal started declining from day 7 of initiating Linezolid. Linezolid was withdrawn from treatment from day 9. Platelet count gradually came back to normal on day 16. This suggests reversible type of thrombocytopenia by Linezolid. This case illustrates need for careful observation of platelet count during the treatment with Linezolid.
Keywords:
Linezolid, Thrombocytopenia, Dechallenge
Linezolid Induced Thrombocytopenia: A Case Report
Linezolid (LZD) is an antimicrobial agent with a broad spectrum of activity against virtually all clinically important Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase-negative staphylococci (MRCoNS) and vancomycin-resistant enterococci (VRE). Thrombocytopenia (TP) is a common adverse effect of Linezolid (LZD). Prolonged treatment duration, renal insufficiency, chronic liver disease, malignancy, previous vancomycin use, baseline platelet count, and lower body weight have been reported as possible risk factors for LZD-associated TP. Here, we illustrate a case of a 51-year-old male patient diagnosed with pancreatitis and urinary tract infection and was prescribed several antibiotics including Linezolid. In this case, platelets count which were initially normal started declining from day 7 of initiating Linezolid. Linezolid was withdrawn from treatment from day 9. Platelet count gradually came back to normal on day 16. This suggests reversible type of thrombocytopenia by Linezolid. This case illustrates need for careful observation of platelet count during the treatment with Linezolid.
Keywords:
Linezolid, Thrombocytopenia, Dechallenge
Prospective studies are required to assess the prevalence/incidence of neuro-COVID
Josef Finsterer, Fulvio A ScorzaOnline First: May 13, 2021
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Prospective studies are required to assess the prevalence/incidence of neuro-COVID
With interest we read the article by Khedr et al. about a retrospective cohort study of 117 patients with neuro-COVID collected during a three months period in Upper Egypt [1]. It was found that stroke was the most frequent central nervous system (CNS) manifestation of neuro-COVID in this cohort and that anosmia/ageusia was the most frequent peripheral nervous system (PNS) manifestation of neuro-COVID [1]. The study is appealing but raises the following comments and concerns.
The main shortcoming of the study is its retrospective design [1]. Since not all 447 COVID-19 patients admitted during the observational period were systematically seen by a neurologist [1], the frequency of neuro-COVID manifestations cannot be reliable assessed. We should know how many of the 117 patients were truly seen by a neurologist and how many had an MRI, nerve conduction studies, electromyography, electroencephalography, and cerebro-spinal fluid (CSF) investigations. According to the method section, supplementary investigations were carried out only “if indicated” [1]. Thus, a number of abnormalities may have been missed, particularly in patients with “non-specific neuropsychiatric symptoms”.
A further shortcoming is that among the 117 patients with neuro-COVID only in 55 patients the SARS-CoV-2 infection was confirmed by PCR testing. The remaining 62 patients were classified as probable COVID-19 patients, which is why the evaluation should be carried out for both groups separately.
Another shortcoming is that the term “convulsions” was not defined in the method section. Thus, we should know if exclusively seizures, myoclonic jerks, or all hyperkinesias were included or not.
Furthermore, an explanation should be provided why 47 patients with headache were assigned to the group with non-specific neuropsychiatric symptoms and why 36 patients with headache were included in the neuro-COVID group. Patients with headache require thorough neurological work-up to exclude meningitis/encephalitis, venous sinus thrombosis, dissection, bleeding, or tumour. Thus, we should be informed if all 47 patients with non-specific headache were truly seen by a neurologist.
Interestingly, two patients with myasthenia were found. We should be told if myasthenia was newly diagnosed after onset of COVID-19 or if these patients had myasthenia already before becoming infected. In the majority of the patients with COVID-19 and myasthenia so far reported, myasthenia was already present before onset of COVID-19 [2]. Only in few patients was myasthenia probably triggered by SARS-CoV-2 as per the end of February 2021 [3].
The title is misleading as not 439 patients had neuro-COVID but only 117.
Overall, this interesting study has several limitations which should be addressed before drawing final conclusions. To assess the prevalence of neuro-COVID prospective studies are inevitable. Such a study should include only COVID-19 patients in whom the infection has been confirmed by PCR.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Prospective studies are required to assess the prevalence/incidence of neuro-COVID
With interest we read the article by Khedr et al. about a retrospective cohort study of 117 patients with neuro-COVID collected during a three months period in Upper Egypt [1]. It was found that stroke was the most frequent central nervous system (CNS) manifestation of neuro-COVID in this cohort and that anosmia/ageusia was the most frequent peripheral nervous system (PNS) manifestation of neuro-COVID [1]. The study is appealing but raises the following comments and concerns.
The main shortcoming of the study is its retrospective design [1]. Since not all 447 COVID-19 patients admitted during the observational period were systematically seen by a neurologist [1], the frequency of neuro-COVID manifestations cannot be reliable assessed. We should know how many of the 117 patients were truly seen by a neurologist and how many had an MRI, nerve conduction studies, electromyography, electroencephalography, and cerebro-spinal fluid (CSF) investigations. According to the method section, supplementary investigations were carried out only “if indicated” [1]. Thus, a number of abnormalities may have been missed, particularly in patients with “non-specific neuropsychiatric symptoms”.
A further shortcoming is that among the 117 patients with neuro-COVID only in 55 patients the SARS-CoV-2 infection was confirmed by PCR testing. The remaining 62 patients were classified as probable COVID-19 patients, which is why the evaluation should be carried out for both groups separately.
Another shortcoming is that the term “convulsions” was not defined in the method section. Thus, we should know if exclusively seizures, myoclonic jerks, or all hyperkinesias were included or not.
Furthermore, an explanation should be provided why 47 patients with headache were assigned to the group with non-specific neuropsychiatric symptoms and why 36 patients with headache were included in the neuro-COVID group. Patients with headache require thorough neurological work-up to exclude meningitis/encephalitis, venous sinus thrombosis, dissection, bleeding, or tumour. Thus, we should be informed if all 47 patients with non-specific headache were truly seen by a neurologist.
Interestingly, two patients with myasthenia were found. We should be told if myasthenia was newly diagnosed after onset of COVID-19 or if these patients had myasthenia already before becoming infected. In the majority of the patients with COVID-19 and myasthenia so far reported, myasthenia was already present before onset of COVID-19 [2]. Only in few patients was myasthenia probably triggered by SARS-CoV-2 as per the end of February 2021 [3].
The title is misleading as not 439 patients had neuro-COVID but only 117.
Overall, this interesting study has several limitations which should be addressed before drawing final conclusions. To assess the prevalence of neuro-COVID prospective studies are inevitable. Such a study should include only COVID-19 patients in whom the infection has been confirmed by PCR.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Prospective studies are required to assess the prevalence/incidence of neuro-COVID
With interest we read the article by Khedr et al. about a retrospective cohort study of 117 patients with neuro-COVID collected during a three months period in Upper Egypt [1]. It was found that stroke was the most frequent central nervous system (CNS) manifestation of neuro-COVID in this cohort and that anosmia/ageusia was the most frequent peripheral nervous system (PNS) manifestation of neuro-COVID [1]. The study is appealing but raises the following comments and concerns.
The main shortcoming of the study is its retrospective design [1]. Since not all 447 COVID-19 patients admitted during the observational period were systematically seen by a neurologist [1], the frequency of neuro-COVID manifestations cannot be reliable assessed. We should know how many of the 117 patients were truly seen by a neurologist and how many had an MRI, nerve conduction studies, electromyography, electroencephalography, and cerebro-spinal fluid (CSF) investigations. According to the method section, supplementary investigations were carried out only “if indicated” [1]. Thus, a number of abnormalities may have been missed, particularly in patients with “non-specific neuropsychiatric symptoms”.
A further shortcoming is that among the 117 patients with neuro-COVID only in 55 patients the SARS-CoV-2 infection was confirmed by PCR testing. The remaining 62 patients were classified as probable COVID-19 patients, which is why the evaluation should be carried out for both groups separately.
Another shortcoming is that the term “convulsions” was not defined in the method section. Thus, we should know if exclusively seizures, myoclonic jerks, or all hyperkinesias were included or not.
Furthermore, an explanation should be provided why 47 patients with headache were assigned to the group with non-specific neuropsychiatric symptoms and why 36 patients with headache were included in the neuro-COVID group. Patients with headache require thorough neurological work-up to exclude meningitis/encephalitis, venous sinus thrombosis, dissection, bleeding, or tumour. Thus, we should be informed if all 47 patients with non-specific headache were truly seen by a neurologist.
Interestingly, two patients with myasthenia were found. We should be told if myasthenia was newly diagnosed after onset of COVID-19 or if these patients had myasthenia already before becoming infected. In the majority of the patients with COVID-19 and myasthenia so far reported, myasthenia was already present before onset of COVID-19 [2]. Only in few patients was myasthenia probably triggered by SARS-CoV-2 as per the end of February 2021 [3].
The title is misleading as not 439 patients had neuro-COVID but only 117.
Overall, this interesting study has several limitations which should be addressed before drawing final conclusions. To assess the prevalence of neuro-COVID prospective studies are inevitable. Such a study should include only COVID-19 patients in whom the infection has been confirmed by PCR.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Prospective studies are required to assess the prevalence/incidence of neuro-COVID
With interest we read the article by Khedr et al. about a retrospective cohort study of 117 patients with neuro-COVID collected during a three months period in Upper Egypt [1]. It was found that stroke was the most frequent central nervous system (CNS) manifestation of neuro-COVID in this cohort and that anosmia/ageusia was the most frequent peripheral nervous system (PNS) manifestation of neuro-COVID [1]. The study is appealing but raises the following comments and concerns.
The main shortcoming of the study is its retrospective design [1]. Since not all 447 COVID-19 patients admitted during the observational period were systematically seen by a neurologist [1], the frequency of neuro-COVID manifestations cannot be reliable assessed. We should know how many of the 117 patients were truly seen by a neurologist and how many had an MRI, nerve conduction studies, electromyography, electroencephalography, and cerebro-spinal fluid (CSF) investigations. According to the method section, supplementary investigations were carried out only “if indicated” [1]. Thus, a number of abnormalities may have been missed, particularly in patients with “non-specific neuropsychiatric symptoms”.
A further shortcoming is that among the 117 patients with neuro-COVID only in 55 patients the SARS-CoV-2 infection was confirmed by PCR testing. The remaining 62 patients were classified as probable COVID-19 patients, which is why the evaluation should be carried out for both groups separately.
Another shortcoming is that the term “convulsions” was not defined in the method section. Thus, we should know if exclusively seizures, myoclonic jerks, or all hyperkinesias were included or not.
Furthermore, an explanation should be provided why 47 patients with headache were assigned to the group with non-specific neuropsychiatric symptoms and why 36 patients with headache were included in the neuro-COVID group. Patients with headache require thorough neurological work-up to exclude meningitis/encephalitis, venous sinus thrombosis, dissection, bleeding, or tumour. Thus, we should be informed if all 47 patients with non-specific headache were truly seen by a neurologist.
Interestingly, two patients with myasthenia were found. We should be told if myasthenia was newly diagnosed after onset of COVID-19 or if these patients had myasthenia already before becoming infected. In the majority of the patients with COVID-19 and myasthenia so far reported, myasthenia was already present before onset of COVID-19 [2]. Only in few patients was myasthenia probably triggered by SARS-CoV-2 as per the end of February 2021 [3].
The title is misleading as not 439 patients had neuro-COVID but only 117.
Overall, this interesting study has several limitations which should be addressed before drawing final conclusions. To assess the prevalence of neuro-COVID prospective studies are inevitable. Such a study should include only COVID-19 patients in whom the infection has been confirmed by PCR.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Genotype/phenotype correlations are crucial for establishing pathogenicity of mtDNA variants
Josef FinstererOnline First: May 13, 2021
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Genotype/phenotype correlations are crucial for establishing pathogenicity of mtDNA variants
With interest we read the article by Loos et al. about 27 patients with mtDNA-associated mitochondrial disorders (MID) from Argentina [1]. MELAS was the most common phenotype and the variants m.13513G>A in MT-ND5 and m.9185T>C in ATP6, phenotypically manifesting as Leigh syndrome, occurred sporadically [1]. The report is interesting but raises the following comments and concerns.
Concerning the pathogenicity of the variant m.13513G>A, the heteroplasmy rate of 20% in lymphocytes argues against causality. If clinically more severely affected tissues did not carry higher heteroplasmy rates, the patient should be investigated for mutations in alternative genes associated with MELAS. Using quantitative real-time PCR and hair follicles or urinary epithelial cells might be more efficient in this respect [2].
According to table-1 only 10 of the 11 MELAS patients had a stroke-like episode (SLE) [1]. We should know if the patient without a SLE fulfilled the Hirano or Japanese criteria for diagnosing MELAS [3].
According to table 1 only 2 of 3 patients with Kearns-Sayre syndrome had cardiac involvement. Since cardiac conduction defects are part of the diagnostic criteria [4], we should be told if the patient without cardiac involvement fulfilled the diagnostic criteria.
Most MELAS patients present with lactic acidosis on magnetic resonance spectroscopy (MRS) or investigations of the cerebro-spinal fluid. We should be told why only 2/11 MELAS patients had elevated lactate in the brain.
Since mtDNA variants are inherited via the maternal line in 75% of the cases [5], we should know in how many of the 27 patients the family history was positive for the disease. Furthermore, we should know how many of the 27 mothers carried the mutation of their child. Since most of the MIDs are non-syndromic, it should be explained why no patient with non-syndromic MID was included. Overall, the report is appealing but has several limitations which challenge the results and their interpretation.
Declarations
COI: The authors declare no conflicts of interest
Funding: No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments
Informed consent: was obtained
Ethics approval: The study was approved by the institutional review board
Data availability: not applicable
Consent to participate: not applicable
Consent for publication: not applicable
Genotype/phenotype correlations are crucial for establishing pathogenicity of mtDNA variants
With interest we read the article by Loos et al. about 27 patients with mtDNA-associated mitochondrial disorders (MID) from Argentina [1]. MELAS was the most common phenotype and the variants m.13513G>A in MT-ND5 and m.9185T>C in ATP6, phenotypically manifesting as Leigh syndrome, occurred sporadically [1]. The report is interesting but raises the following comments and concerns.
Concerning the pathogenicity of the variant m.13513G>A, the heteroplasmy rate of 20% in lymphocytes argues against causality. If clinically more severely affected tissues did not carry higher heteroplasmy rates, the patient should be investigated for mutations in alternative genes associated with MELAS. Using quantitative real-time PCR and hair follicles or urinary epithelial cells might be more efficient in this respect [2].
According to table-1 only 10 of the 11 MELAS patients had a stroke-like episode (SLE) [1]. We should know if the patient without a SLE fulfilled the Hirano or Japanese criteria for diagnosing MELAS [3].
According to table 1 only 2 of 3 patients with Kearns-Sayre syndrome had cardiac involvement. Since cardiac conduction defects are part of the diagnostic criteria [4], we should be told if the patient without cardiac involvement fulfilled the diagnostic criteria.
Most MELAS patients present with lactic acidosis on magnetic resonance spectroscopy (MRS) or investigations of the cerebro-spinal fluid. We should be told why only 2/11 MELAS patients had elevated lactate in the brain.
Since mtDNA variants are inherited via the maternal line in 75% of the cases [5], we should know in how many of the 27 patients the family history was positive for the disease. Furthermore, we should know how many of the 27 mothers carried the mutation of their child. Since most of the MIDs are non-syndromic, it should be explained why no patient with non-syndromic MID was included. Overall, the report is appealing but has several limitations which challenge the results and their interpretation.
Declarations
COI: The authors declare no conflicts of interest
Funding: No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments
Informed consent: was obtained
Ethics approval: The study was approved by the institutional review board
Data availability: not applicable
Consent to participate: not applicable
Consent for publication: not applicable
Genotype/phenotype correlations are crucial for establishing pathogenicity of mtDNA variants
With interest we read the article by Loos et al. about 27 patients with mtDNA-associated mitochondrial disorders (MID) from Argentina [1]. MELAS was the most common phenotype and the variants m.13513G>A in MT-ND5 and m.9185T>C in ATP6, phenotypically manifesting as Leigh syndrome, occurred sporadically [1]. The report is interesting but raises the following comments and concerns.
Concerning the pathogenicity of the variant m.13513G>A, the heteroplasmy rate of 20% in lymphocytes argues against causality. If clinically more severely affected tissues did not carry higher heteroplasmy rates, the patient should be investigated for mutations in alternative genes associated with MELAS. Using quantitative real-time PCR and hair follicles or urinary epithelial cells might be more efficient in this respect [2].
According to table-1 only 10 of the 11 MELAS patients had a stroke-like episode (SLE) [1]. We should know if the patient without a SLE fulfilled the Hirano or Japanese criteria for diagnosing MELAS [3].
According to table 1 only 2 of 3 patients with Kearns-Sayre syndrome had cardiac involvement. Since cardiac conduction defects are part of the diagnostic criteria [4], we should be told if the patient without cardiac involvement fulfilled the diagnostic criteria.
Most MELAS patients present with lactic acidosis on magnetic resonance spectroscopy (MRS) or investigations of the cerebro-spinal fluid. We should be told why only 2/11 MELAS patients had elevated lactate in the brain.
Since mtDNA variants are inherited via the maternal line in 75% of the cases [5], we should know in how many of the 27 patients the family history was positive for the disease. Furthermore, we should know how many of the 27 mothers carried the mutation of their child. Since most of the MIDs are non-syndromic, it should be explained why no patient with non-syndromic MID was included. Overall, the report is appealing but has several limitations which challenge the results and their interpretation.
Declarations
COI: The authors declare no conflicts of interest
Funding: No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments
Informed consent: was obtained
Ethics approval: The study was approved by the institutional review board
Data availability: not applicable
Consent to participate: not applicable
Consent for publication: not applicable
Genotype/phenotype correlations are crucial for establishing pathogenicity of mtDNA variants
With interest we read the article by Loos et al. about 27 patients with mtDNA-associated mitochondrial disorders (MID) from Argentina [1]. MELAS was the most common phenotype and the variants m.13513G>A in MT-ND5 and m.9185T>C in ATP6, phenotypically manifesting as Leigh syndrome, occurred sporadically [1]. The report is interesting but raises the following comments and concerns.
Concerning the pathogenicity of the variant m.13513G>A, the heteroplasmy rate of 20% in lymphocytes argues against causality. If clinically more severely affected tissues did not carry higher heteroplasmy rates, the patient should be investigated for mutations in alternative genes associated with MELAS. Using quantitative real-time PCR and hair follicles or urinary epithelial cells might be more efficient in this respect [2].
According to table-1 only 10 of the 11 MELAS patients had a stroke-like episode (SLE) [1]. We should know if the patient without a SLE fulfilled the Hirano or Japanese criteria for diagnosing MELAS [3].
According to table 1 only 2 of 3 patients with Kearns-Sayre syndrome had cardiac involvement. Since cardiac conduction defects are part of the diagnostic criteria [4], we should be told if the patient without cardiac involvement fulfilled the diagnostic criteria.
Most MELAS patients present with lactic acidosis on magnetic resonance spectroscopy (MRS) or investigations of the cerebro-spinal fluid. We should be told why only 2/11 MELAS patients had elevated lactate in the brain.
Since mtDNA variants are inherited via the maternal line in 75% of the cases [5], we should know in how many of the 27 patients the family history was positive for the disease. Furthermore, we should know how many of the 27 mothers carried the mutation of their child. Since most of the MIDs are non-syndromic, it should be explained why no patient with non-syndromic MID was included. Overall, the report is appealing but has several limitations which challenge the results and their interpretation.
Declarations
COI: The authors declare no conflicts of interest
Funding: No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments
Informed consent: was obtained
Ethics approval: The study was approved by the institutional review board
Data availability: not applicable
Consent to participate: not applicable
Consent for publication: not applicable
Neuro-COVID of muscle and nerves
Josef Finsterer, Fulvio A Scorza, Carla A Scorza, Ana C FioriniOnline First: May 13, 2021
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Neuro-COVID of muscle and nerves
Letter to the Editor
With interest we read the review article by Paliwal et al. about the neuromuscular manifestations in SARS-CoV-2 infected patients with COVID-19 [1]. It was concluded that the infection with SARS-CoV-2 also involves the peripheral nervous system (PNS) manifesting as anosmia/hyposmia, ageusia/hypogeusia, cranial nerve palsies, Guillain-Barre syndrome (GBS), polyneuropathy, exacerbation of myasthenia gravis (MG), myositis, myalgia, or rhabdomyolysis [1]. We have the following comments and concerns.
We do not agree with the statement that “there are no reports of de-novo occurrence of myasthenia gravis secondary to COVID-19” [1]. In a recent report by Restivo et al. three patients (2 males, 1 female) were reported in whom newly developing MG was attributed to the infection with SARS-CoV-2 [2]. Myasthenic symptoms occurred 5-7 days after onset of fever [2]. All three patients had elevated antibodies against the acetyl-cholin receptor. Patient-1 recovered upon pyridostigmin and steroids, patient-2 upon intravenous immunoglobulins, and patient-3 upon mechanical ventilation, plasmapheresis, and ritonavir/lopinavir [2]. Occurrence of MG was explained by a cross-reaction of antibodies against the virus and the acetyl-cholin receptor [2].
We do not agree that only 6 patients with MG were reported in whom the infection with SARS-CoV-2 exacerbated clinical manifestations of MG [1]. In a recent mini-review about the association between SARS-CoV-2 and MG it has been shown that among 16 COVID-19 patients with MG exacerbation of myasthenic symptoms occurred in 8 of them [3]. Three of these patients experienced even a myasthenic crisis [3].
The authors identified 44 patients with GBS in association with a SARS-CoV-2 infection [1]. However, in a recent mini-review 62 COVID-19 patients with GBS, as of 12th August, were reported [4]. Among these 62 patients the latency between onset of COVID-19 and GBS ranged between 3 and 33 days. Acute inflammatory demyelinating neuropathy (AIDP) was diagnosed in 42 patients, acute motor and axonal neuropathy (AMAN) in 6 patients, Miller-Fisher syndrome (MFS) in 5 patients, and acute, motor, sensory, axonal neuropathy (AMSAN) in 3 patients [4]. The virus was evidenced in the CSF in none of the 62 patients. Patients were treated with intravenous immunoglobulins (IVIG) (n=50), plasmapheresis (n=8), steroids (n=2), and mechanical ventilation (n=18). Twenty-four patients recovered without sequelae and 23 partially. Two patients died.
Polyneuropathy has not only been reported in the 6 patients presented but also in one further COVID-19 patient as of 17th September [5]. In this patient sensory-motor polyneuropathy was even the presenting manifestation of COVID-19 [5].
Neuromuscular manifestations in COVID-19 patients may not only be explained by the direct attack of the virus or by the immune-response to the virus but also by neuromuscular side effects of the treatment applied to COVID-19 patients. It is well appreciated that steroids, chloroquine, protease-inhibitors (lopinavir/ritonavir), remdesivir, azithromycin, toclizumab, or cromstat may cause neuromuscular adverse reactions. From steroids it is known that they can cause mitochondrial myopathy. Protease-inhibitors carry the risk of triggering sensory neuropathy [6]. Azithromycin has been reported to trigger rhabdomyolysis [7]. Toclizumab has been reported to cause facial palsy and diplopia [8]. Chloroquine may induce toxic myopathy [9] or even a myasthenic syndrome [10].
Overall, the review by Paliwal et al. lacks data about MG, GBS, and polyneuropathy in COVID-19 patients. Additionally, neuromuscular disease as a side effect of the anti-COVID-19 treatment should be addressed.
There are no conflicts of interest
No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, FS, CS, and AF: literature search, discussion, critical comments
All authors have read the journal’s position on issues involved in ethical publication
Neuro-COVID of muscle and nerves
Letter to the Editor
With interest we read the review article by Paliwal et al. about the neuromuscular manifestations in SARS-CoV-2 infected patients with COVID-19 [1]. It was concluded that the infection with SARS-CoV-2 also involves the peripheral nervous system (PNS) manifesting as anosmia/hyposmia, ageusia/hypogeusia, cranial nerve palsies, Guillain-Barre syndrome (GBS), polyneuropathy, exacerbation of myasthenia gravis (MG), myositis, myalgia, or rhabdomyolysis [1]. We have the following comments and concerns.
We do not agree with the statement that “there are no reports of de-novo occurrence of myasthenia gravis secondary to COVID-19” [1]. In a recent report by Restivo et al. three patients (2 males, 1 female) were reported in whom newly developing MG was attributed to the infection with SARS-CoV-2 [2]. Myasthenic symptoms occurred 5-7 days after onset of fever [2]. All three patients had elevated antibodies against the acetyl-cholin receptor. Patient-1 recovered upon pyridostigmin and steroids, patient-2 upon intravenous immunoglobulins, and patient-3 upon mechanical ventilation, plasmapheresis, and ritonavir/lopinavir [2]. Occurrence of MG was explained by a cross-reaction of antibodies against the virus and the acetyl-cholin receptor [2].
We do not agree that only 6 patients with MG were reported in whom the infection with SARS-CoV-2 exacerbated clinical manifestations of MG [1]. In a recent mini-review about the association between SARS-CoV-2 and MG it has been shown that among 16 COVID-19 patients with MG exacerbation of myasthenic symptoms occurred in 8 of them [3]. Three of these patients experienced even a myasthenic crisis [3].
The authors identified 44 patients with GBS in association with a SARS-CoV-2 infection [1]. However, in a recent mini-review 62 COVID-19 patients with GBS, as of 12th August, were reported [4]. Among these 62 patients the latency between onset of COVID-19 and GBS ranged between 3 and 33 days. Acute inflammatory demyelinating neuropathy (AIDP) was diagnosed in 42 patients, acute motor and axonal neuropathy (AMAN) in 6 patients, Miller-Fisher syndrome (MFS) in 5 patients, and acute, motor, sensory, axonal neuropathy (AMSAN) in 3 patients [4]. The virus was evidenced in the CSF in none of the 62 patients. Patients were treated with intravenous immunoglobulins (IVIG) (n=50), plasmapheresis (n=8), steroids (n=2), and mechanical ventilation (n=18). Twenty-four patients recovered without sequelae and 23 partially. Two patients died.
Polyneuropathy has not only been reported in the 6 patients presented but also in one further COVID-19 patient as of 17th September [5]. In this patient sensory-motor polyneuropathy was even the presenting manifestation of COVID-19 [5].
Neuromuscular manifestations in COVID-19 patients may not only be explained by the direct attack of the virus or by the immune-response to the virus but also by neuromuscular side effects of the treatment applied to COVID-19 patients. It is well appreciated that steroids, chloroquine, protease-inhibitors (lopinavir/ritonavir), remdesivir, azithromycin, toclizumab, or cromstat may cause neuromuscular adverse reactions. From steroids it is known that they can cause mitochondrial myopathy. Protease-inhibitors carry the risk of triggering sensory neuropathy [6]. Azithromycin has been reported to trigger rhabdomyolysis [7]. Toclizumab has been reported to cause facial palsy and diplopia [8]. Chloroquine may induce toxic myopathy [9] or even a myasthenic syndrome [10].
Overall, the review by Paliwal et al. lacks data about MG, GBS, and polyneuropathy in COVID-19 patients. Additionally, neuromuscular disease as a side effect of the anti-COVID-19 treatment should be addressed.
There are no conflicts of interest
No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, FS, CS, and AF: literature search, discussion, critical comments
All authors have read the journal’s position on issues involved in ethical publication
Neuro-COVID of muscle and nerves
Letter to the Editor
With interest we read the review article by Paliwal et al. about the neuromuscular manifestations in SARS-CoV-2 infected patients with COVID-19 [1]. It was concluded that the infection with SARS-CoV-2 also involves the peripheral nervous system (PNS) manifesting as anosmia/hyposmia, ageusia/hypogeusia, cranial nerve palsies, Guillain-Barre syndrome (GBS), polyneuropathy, exacerbation of myasthenia gravis (MG), myositis, myalgia, or rhabdomyolysis [1]. We have the following comments and concerns.
We do not agree with the statement that “there are no reports of de-novo occurrence of myasthenia gravis secondary to COVID-19” [1]. In a recent report by Restivo et al. three patients (2 males, 1 female) were reported in whom newly developing MG was attributed to the infection with SARS-CoV-2 [2]. Myasthenic symptoms occurred 5-7 days after onset of fever [2]. All three patients had elevated antibodies against the acetyl-cholin receptor. Patient-1 recovered upon pyridostigmin and steroids, patient-2 upon intravenous immunoglobulins, and patient-3 upon mechanical ventilation, plasmapheresis, and ritonavir/lopinavir [2]. Occurrence of MG was explained by a cross-reaction of antibodies against the virus and the acetyl-cholin receptor [2].
We do not agree that only 6 patients with MG were reported in whom the infection with SARS-CoV-2 exacerbated clinical manifestations of MG [1]. In a recent mini-review about the association between SARS-CoV-2 and MG it has been shown that among 16 COVID-19 patients with MG exacerbation of myasthenic symptoms occurred in 8 of them [3]. Three of these patients experienced even a myasthenic crisis [3].
The authors identified 44 patients with GBS in association with a SARS-CoV-2 infection [1]. However, in a recent mini-review 62 COVID-19 patients with GBS, as of 12th August, were reported [4]. Among these 62 patients the latency between onset of COVID-19 and GBS ranged between 3 and 33 days. Acute inflammatory demyelinating neuropathy (AIDP) was diagnosed in 42 patients, acute motor and axonal neuropathy (AMAN) in 6 patients, Miller-Fisher syndrome (MFS) in 5 patients, and acute, motor, sensory, axonal neuropathy (AMSAN) in 3 patients [4]. The virus was evidenced in the CSF in none of the 62 patients. Patients were treated with intravenous immunoglobulins (IVIG) (n=50), plasmapheresis (n=8), steroids (n=2), and mechanical ventilation (n=18). Twenty-four patients recovered without sequelae and 23 partially. Two patients died.
Polyneuropathy has not only been reported in the 6 patients presented but also in one further COVID-19 patient as of 17th September [5]. In this patient sensory-motor polyneuropathy was even the presenting manifestation of COVID-19 [5].
Neuromuscular manifestations in COVID-19 patients may not only be explained by the direct attack of the virus or by the immune-response to the virus but also by neuromuscular side effects of the treatment applied to COVID-19 patients. It is well appreciated that steroids, chloroquine, protease-inhibitors (lopinavir/ritonavir), remdesivir, azithromycin, toclizumab, or cromstat may cause neuromuscular adverse reactions. From steroids it is known that they can cause mitochondrial myopathy. Protease-inhibitors carry the risk of triggering sensory neuropathy [6]. Azithromycin has been reported to trigger rhabdomyolysis [7]. Toclizumab has been reported to cause facial palsy and diplopia [8]. Chloroquine may induce toxic myopathy [9] or even a myasthenic syndrome [10].
Overall, the review by Paliwal et al. lacks data about MG, GBS, and polyneuropathy in COVID-19 patients. Additionally, neuromuscular disease as a side effect of the anti-COVID-19 treatment should be addressed.
There are no conflicts of interest
No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, FS, CS, and AF: literature search, discussion, critical comments
All authors have read the journal’s position on issues involved in ethical publication
Neuro-COVID of muscle and nerves
Letter to the Editor
With interest we read the review article by Paliwal et al. about the neuromuscular manifestations in SARS-CoV-2 infected patients with COVID-19 [1]. It was concluded that the infection with SARS-CoV-2 also involves the peripheral nervous system (PNS) manifesting as anosmia/hyposmia, ageusia/hypogeusia, cranial nerve palsies, Guillain-Barre syndrome (GBS), polyneuropathy, exacerbation of myasthenia gravis (MG), myositis, myalgia, or rhabdomyolysis [1]. We have the following comments and concerns.
We do not agree with the statement that “there are no reports of de-novo occurrence of myasthenia gravis secondary to COVID-19” [1]. In a recent report by Restivo et al. three patients (2 males, 1 female) were reported in whom newly developing MG was attributed to the infection with SARS-CoV-2 [2]. Myasthenic symptoms occurred 5-7 days after onset of fever [2]. All three patients had elevated antibodies against the acetyl-cholin receptor. Patient-1 recovered upon pyridostigmin and steroids, patient-2 upon intravenous immunoglobulins, and patient-3 upon mechanical ventilation, plasmapheresis, and ritonavir/lopinavir [2]. Occurrence of MG was explained by a cross-reaction of antibodies against the virus and the acetyl-cholin receptor [2].
We do not agree that only 6 patients with MG were reported in whom the infection with SARS-CoV-2 exacerbated clinical manifestations of MG [1]. In a recent mini-review about the association between SARS-CoV-2 and MG it has been shown that among 16 COVID-19 patients with MG exacerbation of myasthenic symptoms occurred in 8 of them [3]. Three of these patients experienced even a myasthenic crisis [3].
The authors identified 44 patients with GBS in association with a SARS-CoV-2 infection [1]. However, in a recent mini-review 62 COVID-19 patients with GBS, as of 12th August, were reported [4]. Among these 62 patients the latency between onset of COVID-19 and GBS ranged between 3 and 33 days. Acute inflammatory demyelinating neuropathy (AIDP) was diagnosed in 42 patients, acute motor and axonal neuropathy (AMAN) in 6 patients, Miller-Fisher syndrome (MFS) in 5 patients, and acute, motor, sensory, axonal neuropathy (AMSAN) in 3 patients [4]. The virus was evidenced in the CSF in none of the 62 patients. Patients were treated with intravenous immunoglobulins (IVIG) (n=50), plasmapheresis (n=8), steroids (n=2), and mechanical ventilation (n=18). Twenty-four patients recovered without sequelae and 23 partially. Two patients died.
Polyneuropathy has not only been reported in the 6 patients presented but also in one further COVID-19 patient as of 17th September [5]. In this patient sensory-motor polyneuropathy was even the presenting manifestation of COVID-19 [5].
Neuromuscular manifestations in COVID-19 patients may not only be explained by the direct attack of the virus or by the immune-response to the virus but also by neuromuscular side effects of the treatment applied to COVID-19 patients. It is well appreciated that steroids, chloroquine, protease-inhibitors (lopinavir/ritonavir), remdesivir, azithromycin, toclizumab, or cromstat may cause neuromuscular adverse reactions. From steroids it is known that they can cause mitochondrial myopathy. Protease-inhibitors carry the risk of triggering sensory neuropathy [6]. Azithromycin has been reported to trigger rhabdomyolysis [7]. Toclizumab has been reported to cause facial palsy and diplopia [8]. Chloroquine may induce toxic myopathy [9] or even a myasthenic syndrome [10].
Overall, the review by Paliwal et al. lacks data about MG, GBS, and polyneuropathy in COVID-19 patients. Additionally, neuromuscular disease as a side effect of the anti-COVID-19 treatment should be addressed.
There are no conflicts of interest
No funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, FS, CS, and AF: literature search, discussion, critical comments
All authors have read the journal’s position on issues involved in ethical publication
Anti-COVID-19 drugs rather than SARS-CoV-2 exacerbate myasthenia
Josef Finsterer, Fulvio A ScorzaOnline First: May 13, 2021
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Anti-COVID-19 drugs rather than SARS-CoV-2 exacerbate myasthenia
Letter to the Editor
With interest we read the article by Zupanic et al. about eight patients with known myasthenia gravis (MG) who experienced an infection with SARS-CoV-2 [1]. Four patients experienced exacerbation of MG during the infection while the remaining four patients did not experience worsening of MG during the infection with SARS-CoV-2. Three patients required mechanical ventilation and two oxygen supplementation. Six responded favourably to intravenous immunoglobulins (IVIG) [1]. One patient died [1]. It was concluded that the outcome of MG patients experiencing exacerbation of MG during an infection with SARS-CoV-2 is fair and that these patients profit from IVIG [1]. The study is appealing but raises the following comment and concerns.
The main shortcoming of the study is that the diagnosis MG was confirmed by elevated acetyl-choline receptor (AchR) antibodies in only half of the patients [1]. In two patients the antibody status was “unknown” and two further patients were negative for AchR antibodies [1]. Since the diagnosis remains unconfirmed in four patients they need to be excluded from the evaluation.
Since myasthenia may not only exacerbate due to an infection but also due addition of myotoxic drugs or increase of the dosage of already used drugs, it is crucial to know the entire medication the eight included patients were taking at the time of admission and the entire medication these patients received during hospitalisation. Several drugs given as an anti-COVID-therapy can potentially exacerbate MG. Furthermore, patients requiring ICU treatment, including mechanical ventilation, are usually exposed to drugs that are potentially myasthenia-toxic. Thus we should know if they received calcium, magnesium, antibiotics, opiates, or chloroquine. From azithromycin, frequently given to COVID-19 patients, it is well-known that it can exacerbate MG [2] or even trigger the development of a myasthenic crisis [3]. There is also evidence that chloroquine, another frequently applied anti-COVID-19 medication, particularly in the first months of the pandemic, can trigger the development of MG [4]. Chloroquine is generally recommended not to be used in MG patients.
A further shortcoming is that exacerbation in four patients was not substantiated by carrying out repetitive nerve stimulation, single-fibre electromyography (SF-EMG), or edrophonium tests. Documentation of exacerbation of myasthenia by means of these tests is crucial as particularly worsening of respiratory function due to myasthenia often cannot be delineated from respiratory insufficiency due to the SARS-CoV-2 infection. It is also crucial that serum titers of causative antibodies against the acetyl-choline receptor (AchR), muscle-specific kinase (MUSK), titin, LRP4, or agrine are determined to substantiate if SARS-CoV-2 increased these serum levels during exacerbation/crisis or not.
Exacerbation of MG in SARS-CoV-2 positive patients may not only be managed by application of intravenous immunoglobulins (IVIG) but also by modification of the established myasthenia treatment or by plasmapheresis, or addition of a new immunosuppressive regimen.
We do not agree with the notion that the case series reported in the index article is the largest of COVID-19 patients with myasthenia. In a recent publication, 380 COVID-19 patients with myasthenia had been reported [5].
Overall, the interesting study has several shortcomings, which should be addressed before drawing final conclusions. It is crucial to delineate if the doctor or the virus is responsible for exacerbation and to avoid that myasthenia patients experiencing a SARS-CoV-2 infection receive medication that potentially worsens myasthenia. In case of respiratory failure, investigations for delineation between respiratory failure due to myasthenia or due to SARS-CoV-2 pneumonia should be carried out.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, first draft, discussion, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Anti-COVID-19 drugs rather than SARS-CoV-2 exacerbate myasthenia
Letter to the Editor
With interest we read the article by Zupanic et al. about eight patients with known myasthenia gravis (MG) who experienced an infection with SARS-CoV-2 [1]. Four patients experienced exacerbation of MG during the infection while the remaining four patients did not experience worsening of MG during the infection with SARS-CoV-2. Three patients required mechanical ventilation and two oxygen supplementation. Six responded favourably to intravenous immunoglobulins (IVIG) [1]. One patient died [1]. It was concluded that the outcome of MG patients experiencing exacerbation of MG during an infection with SARS-CoV-2 is fair and that these patients profit from IVIG [1]. The study is appealing but raises the following comment and concerns.
The main shortcoming of the study is that the diagnosis MG was confirmed by elevated acetyl-choline receptor (AchR) antibodies in only half of the patients [1]. In two patients the antibody status was “unknown” and two further patients were negative for AchR antibodies [1]. Since the diagnosis remains unconfirmed in four patients they need to be excluded from the evaluation.
Since myasthenia may not only exacerbate due to an infection but also due addition of myotoxic drugs or increase of the dosage of already used drugs, it is crucial to know the entire medication the eight included patients were taking at the time of admission and the entire medication these patients received during hospitalisation. Several drugs given as an anti-COVID-therapy can potentially exacerbate MG. Furthermore, patients requiring ICU treatment, including mechanical ventilation, are usually exposed to drugs that are potentially myasthenia-toxic. Thus we should know if they received calcium, magnesium, antibiotics, opiates, or chloroquine. From azithromycin, frequently given to COVID-19 patients, it is well-known that it can exacerbate MG [2] or even trigger the development of a myasthenic crisis [3]. There is also evidence that chloroquine, another frequently applied anti-COVID-19 medication, particularly in the first months of the pandemic, can trigger the development of MG [4]. Chloroquine is generally recommended not to be used in MG patients.
A further shortcoming is that exacerbation in four patients was not substantiated by carrying out repetitive nerve stimulation, single-fibre electromyography (SF-EMG), or edrophonium tests. Documentation of exacerbation of myasthenia by means of these tests is crucial as particularly worsening of respiratory function due to myasthenia often cannot be delineated from respiratory insufficiency due to the SARS-CoV-2 infection. It is also crucial that serum titers of causative antibodies against the acetyl-choline receptor (AchR), muscle-specific kinase (MUSK), titin, LRP4, or agrine are determined to substantiate if SARS-CoV-2 increased these serum levels during exacerbation/crisis or not.
Exacerbation of MG in SARS-CoV-2 positive patients may not only be managed by application of intravenous immunoglobulins (IVIG) but also by modification of the established myasthenia treatment or by plasmapheresis, or addition of a new immunosuppressive regimen.
We do not agree with the notion that the case series reported in the index article is the largest of COVID-19 patients with myasthenia. In a recent publication, 380 COVID-19 patients with myasthenia had been reported [5].
Overall, the interesting study has several shortcomings, which should be addressed before drawing final conclusions. It is crucial to delineate if the doctor or the virus is responsible for exacerbation and to avoid that myasthenia patients experiencing a SARS-CoV-2 infection receive medication that potentially worsens myasthenia. In case of respiratory failure, investigations for delineation between respiratory failure due to myasthenia or due to SARS-CoV-2 pneumonia should be carried out.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, first draft, discussion, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Anti-COVID-19 drugs rather than SARS-CoV-2 exacerbate myasthenia
Letter to the Editor
With interest we read the article by Zupanic et al. about eight patients with known myasthenia gravis (MG) who experienced an infection with SARS-CoV-2 [1]. Four patients experienced exacerbation of MG during the infection while the remaining four patients did not experience worsening of MG during the infection with SARS-CoV-2. Three patients required mechanical ventilation and two oxygen supplementation. Six responded favourably to intravenous immunoglobulins (IVIG) [1]. One patient died [1]. It was concluded that the outcome of MG patients experiencing exacerbation of MG during an infection with SARS-CoV-2 is fair and that these patients profit from IVIG [1]. The study is appealing but raises the following comment and concerns.
The main shortcoming of the study is that the diagnosis MG was confirmed by elevated acetyl-choline receptor (AchR) antibodies in only half of the patients [1]. In two patients the antibody status was “unknown” and two further patients were negative for AchR antibodies [1]. Since the diagnosis remains unconfirmed in four patients they need to be excluded from the evaluation.
Since myasthenia may not only exacerbate due to an infection but also due addition of myotoxic drugs or increase of the dosage of already used drugs, it is crucial to know the entire medication the eight included patients were taking at the time of admission and the entire medication these patients received during hospitalisation. Several drugs given as an anti-COVID-therapy can potentially exacerbate MG. Furthermore, patients requiring ICU treatment, including mechanical ventilation, are usually exposed to drugs that are potentially myasthenia-toxic. Thus we should know if they received calcium, magnesium, antibiotics, opiates, or chloroquine. From azithromycin, frequently given to COVID-19 patients, it is well-known that it can exacerbate MG [2] or even trigger the development of a myasthenic crisis [3]. There is also evidence that chloroquine, another frequently applied anti-COVID-19 medication, particularly in the first months of the pandemic, can trigger the development of MG [4]. Chloroquine is generally recommended not to be used in MG patients.
A further shortcoming is that exacerbation in four patients was not substantiated by carrying out repetitive nerve stimulation, single-fibre electromyography (SF-EMG), or edrophonium tests. Documentation of exacerbation of myasthenia by means of these tests is crucial as particularly worsening of respiratory function due to myasthenia often cannot be delineated from respiratory insufficiency due to the SARS-CoV-2 infection. It is also crucial that serum titers of causative antibodies against the acetyl-choline receptor (AchR), muscle-specific kinase (MUSK), titin, LRP4, or agrine are determined to substantiate if SARS-CoV-2 increased these serum levels during exacerbation/crisis or not.
Exacerbation of MG in SARS-CoV-2 positive patients may not only be managed by application of intravenous immunoglobulins (IVIG) but also by modification of the established myasthenia treatment or by plasmapheresis, or addition of a new immunosuppressive regimen.
We do not agree with the notion that the case series reported in the index article is the largest of COVID-19 patients with myasthenia. In a recent publication, 380 COVID-19 patients with myasthenia had been reported [5].
Overall, the interesting study has several shortcomings, which should be addressed before drawing final conclusions. It is crucial to delineate if the doctor or the virus is responsible for exacerbation and to avoid that myasthenia patients experiencing a SARS-CoV-2 infection receive medication that potentially worsens myasthenia. In case of respiratory failure, investigations for delineation between respiratory failure due to myasthenia or due to SARS-CoV-2 pneumonia should be carried out.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, first draft, discussion, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
Anti-COVID-19 drugs rather than SARS-CoV-2 exacerbate myasthenia
Letter to the Editor
With interest we read the article by Zupanic et al. about eight patients with known myasthenia gravis (MG) who experienced an infection with SARS-CoV-2 [1]. Four patients experienced exacerbation of MG during the infection while the remaining four patients did not experience worsening of MG during the infection with SARS-CoV-2. Three patients required mechanical ventilation and two oxygen supplementation. Six responded favourably to intravenous immunoglobulins (IVIG) [1]. One patient died [1]. It was concluded that the outcome of MG patients experiencing exacerbation of MG during an infection with SARS-CoV-2 is fair and that these patients profit from IVIG [1]. The study is appealing but raises the following comment and concerns.
The main shortcoming of the study is that the diagnosis MG was confirmed by elevated acetyl-choline receptor (AchR) antibodies in only half of the patients [1]. In two patients the antibody status was “unknown” and two further patients were negative for AchR antibodies [1]. Since the diagnosis remains unconfirmed in four patients they need to be excluded from the evaluation.
Since myasthenia may not only exacerbate due to an infection but also due addition of myotoxic drugs or increase of the dosage of already used drugs, it is crucial to know the entire medication the eight included patients were taking at the time of admission and the entire medication these patients received during hospitalisation. Several drugs given as an anti-COVID-therapy can potentially exacerbate MG. Furthermore, patients requiring ICU treatment, including mechanical ventilation, are usually exposed to drugs that are potentially myasthenia-toxic. Thus we should know if they received calcium, magnesium, antibiotics, opiates, or chloroquine. From azithromycin, frequently given to COVID-19 patients, it is well-known that it can exacerbate MG [2] or even trigger the development of a myasthenic crisis [3]. There is also evidence that chloroquine, another frequently applied anti-COVID-19 medication, particularly in the first months of the pandemic, can trigger the development of MG [4]. Chloroquine is generally recommended not to be used in MG patients.
A further shortcoming is that exacerbation in four patients was not substantiated by carrying out repetitive nerve stimulation, single-fibre electromyography (SF-EMG), or edrophonium tests. Documentation of exacerbation of myasthenia by means of these tests is crucial as particularly worsening of respiratory function due to myasthenia often cannot be delineated from respiratory insufficiency due to the SARS-CoV-2 infection. It is also crucial that serum titers of causative antibodies against the acetyl-choline receptor (AchR), muscle-specific kinase (MUSK), titin, LRP4, or agrine are determined to substantiate if SARS-CoV-2 increased these serum levels during exacerbation/crisis or not.
Exacerbation of MG in SARS-CoV-2 positive patients may not only be managed by application of intravenous immunoglobulins (IVIG) but also by modification of the established myasthenia treatment or by plasmapheresis, or addition of a new immunosuppressive regimen.
We do not agree with the notion that the case series reported in the index article is the largest of COVID-19 patients with myasthenia. In a recent publication, 380 COVID-19 patients with myasthenia had been reported [5].
Overall, the interesting study has several shortcomings, which should be addressed before drawing final conclusions. It is crucial to delineate if the doctor or the virus is responsible for exacerbation and to avoid that myasthenia patients experiencing a SARS-CoV-2 infection receive medication that potentially worsens myasthenia. In case of respiratory failure, investigations for delineation between respiratory failure due to myasthenia or due to SARS-CoV-2 pneumonia should be carried out.
Declarations
Acknowledgement: none
Statement of ethics: was in accordance if ethical guidelines
Conflicts of interest: none
Funding sources: no funding was received
Author contribution: JF: design, literature search, discussion, first draft, critical comments, final approval, FS: literature search, first draft, discussion, critical comments, final approval, FS: literature search, discussion, critical comments, final approval
Informed consent: was obtained
The study was approved by the institutional review board
