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1.
Clin Chim Acta ; 511: 342-345, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33159954

RESUMO

COVID-19 is a disease caused by a coronavirus named as SARS-CoV-2. It has become pandemic due to its contagious nature. Majority of the patients are asymptomatic or having mild flu like symptoms. Few need hospitalisation due to severe acute respiratory infection (SARI). Co-morbidity like diabetes, hypertension, renal failure etc. are associated with severe COVID-19 that often causes death. There have been only two published case reports of monoclonal gammopathy of unknown significance (MGUS) in patients with COVID-19 disease. Cytokine storm is often observed in severe COVID-19 and various cytokines including IL-6 that activates plasma cells are increased in blood in this condition. Here we present a case of severe COVID-19 patient with bioclonal gammopathy. He was known diabetic and hypertensive on treatment. He developed SARI, cytokines storm and septicaemia, treated with antibiotics, enoxaparin, hydroxychloroquine, insulin, anti-hypertensives, put on ventilator, subsequently developed septicaemia, multi-organ failure and died. Two M-bands on serum capillary electrophoresis with presence IgG-κ on both the M-bands indicates a biclonal gammopathy of unknown significance in this patient. We conclude that like MGUS, early stage biclonal gammopathy, although rare, gets manifested with M-bands on plasma protein electrophoresis. It is probably due to high level of IL-6 associated with cytokine storm in severe COVID-19 that stimulate early stage dyscratic plasma cells. Such biclonal gammopathy might be a risk factor for severe COVID-19 and associated mortality.


Assuntos
COVID-19/sangue , COVID-19/diagnóstico , Gamopatia Monoclonal de Significância Indeterminada/sangue , Gamopatia Monoclonal de Significância Indeterminada/diagnóstico , SARS-CoV-2 , Índice de Gravidade de Doença , COVID-19/complicações , Síndrome da Liberação de Citocina/sangue , Síndrome da Liberação de Citocina/complicações , Síndrome da Liberação de Citocina/diagnóstico , Evolução Fatal , Humanos , Masculino , Pessoa de Meia-Idade , Gamopatia Monoclonal de Significância Indeterminada/complicações
2.
J Clin Diagn Res ; 10(2): BC08-10, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27042444

RESUMO

INTRODUCTION: Oxidative damage induces alteration in the status of pro-inflammatory markers like IL-6 and TNF-α in meningocele. The study was performed with estimation of the levels of MDA (Malonyldialdehyde), SOD (Superoxide dismutase) taken as oxidative damage markers and IL-6 (interleukin 6) and TNF-α (Tumour necrosis factor alpha) taken as inflammatory markers, in the serum of meningocele patients and age, sex matched normal neonates. Correlation among the different serum levels of MDA, SOD, IL-6 and TNF-α was determined. MATERIALS AND METHODS: It is a case-control study, comprising of 153 participants: 101 newborns with meningocele and 52 healthy newborns. The study was conducted in the Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, in collaboration with the Department of Paediatric Surgery and Department of Obstetrics and Gynecology, Sir Sunderlal Hospital, Banaras Hindu University, Varanasi. The study was conducted during the period of 2012 to 2014. Serum was extracted from blood collected from both groups i.e. meningocele patient group and healthy neonatal control group. The levels of MDA and SOD were determined by spectrophotometric method. IL-6 was determined by the Human IL-6 High Sensitivity ELISA Kit and TNF-α was determined by the Human TNF-α ELISA KIT. RESULTS: The levels of MDA, TNF-α and IL-6 were found to be much higher and level of SOD was found lower in the patients with meningocele as compared to the normal healthy neonates. CONCLUSION: Increased MDA (oxidative damage product), IL-6, and TNF-α (inflammatory marker) and low level of SOD shows an increased inflammatory response in Meningocele. Our study shows Negative Correlation between MDA and SOD in case & control groups, while a Positive Correlation between TNF alpha and IL-6 in control & case groups.

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