ABSTRACT
Background: Many central and peripheral nervous system complications, following COVID-19 vaccination, have been described. We report an unusual case of central demyelinating disorder, following the administration of the ChAdOx1 nCoV-19 SARS-CoV-2 (COVISHIELDTM) vaccine. Case-report: The 28-year female developed sudden onset headache followed by weakness of the left upper and lower limbs, and gait ataxia. Neurological symptoms developed two weeks after administration of the first dose of the ChAdOx1 nCoV-19 SARS-CoV-2 (COVISHIELDTM) vaccine. Magnetic resonance imaging brain revealed T2/FLAIR hyperintense lesions involving bilateral subcortical white matter, splenium of the corpus callosum, and both cerebellar hemispheres. Few lesions showed blooming on gradient echo sequence suggestive of a hemorrhagic component. Post-contrast T1 images showed mild enhancement of demyelinating lesions. The patient was treated intravenously with methylprednisolone. After 12 weeks of follow-up, there was a substantial improvement in her symptoms. She became independent in all her activities of daily living. Conclusion(s): In conclusion, this is an unusual case of acute hemorrhagic leukoencephalitis following ChAdOx1 nCoV-19 SARS-CoV-2 (COVISHIELDTM) vaccination.Copyright © 2022 The Author(s)
ABSTRACT
Introduction: Severe COVID-19 infection in a subset of patients is associated with hyperinflammation similar to hemophagocytic lymphohistiocytosis (HLH) however it may not fulfill the required diagnostic criteria (HLH 2004 criteria or H score). We compared clinical, laboratory parameters, bone marrow findings and disease outcome of severe COVID-19 infection related HLH with HLH secondary to causes other than severe COVID-19 to describe features specific to severe COVID-19 associated HLH and limitations of currently available diagnostic criteria of HLH in context to severe COVID -19 infection induced hyperinflammation. Method(s): We analyzed 69 patients diagnosed as HLH of which 47 had severe COVID-19 and 22 had HLH secondary to causes other than COVID-19. Clinical, hematological and biochemical parameters were compared using Mann-Whitney U test. Bone marrow examination (BME) was done in all for presence of hemophagocytosis. Immunohistochemical staining for CD68 and CD163 were done for identification of histiocytes. Occurrence of COVID-19 related HLH was taken as the dependent variable to determine predictors of COVID-19 HLH. Result(s): Organomegaly was seen in only 4.3% (2/47) cases with COVID-19 related HLH as compared to 54.5% (12/22) with non-COVID HLH (p< 0.001). Amongst the quantitative variables, a significant difference in COVID-19 related and non-COVID-19 related HLH was found in the following parameters: Age (p< 0.001), Triglyceride (p=0.009), Fibrinogen (p< 0.001), Ferritin (p< 0.001), Hemoglobin (p< 0.001), Total leukocyte count (p=0.003), Absolute neutrophil count (p< 0.001), Neutrophil lymphocyte ratio (p< 0.001) and H score (p< 0.001). BME of all patients showed presence of hemophagocytes. Only 6.4% (3/47) cases with COVID related HLH had 5/8 HLH 2004 criteria as compared to 63.6% (14/22) cases with non-COVID related HLH (p< 0.001). H-Score >=169 was also significantly less common in COVID HLH as compared to non-COVID HLH (40.42% vs 86.36%, p=0.001). Conclusion(s): Organomegaly, cytopenias, hypofibrinogenemia and hypertriglyceridemia which are part of HLH diagnostic criteria are rare in severe COVID-19 making it difficult to diagnose. Demonstration of hemophagocytes in bone marrow should be recommended in suspicious cases for initiation of early immunosuppressive therapy. (Figure Presented).
ABSTRACT
Introduction: The second wave of COVID-19 in India was followed by large number of mucormycosis cases. Indiscriminate use of immunosuppressive drugs, underlying diseases like diabetes cancers, or autoimmune diseases was thought to be the cause. However, the mortality was not as high as that seen in non-COVID mucormycosis. Aims & Objectives: To study the detailed characteristics of T-cells for evaluating the underlying differences in the T-cell immune dysfunction in post-COVID and non-COVID mucor patients. Material(s) and Method(s): The study included histopathologically confirmed cases of mucor (13 post-COVID, 13 non-COVID) and 15 healthy individuals (HI). Expression of T-cell activation (CD44, HLADR, CD69, CD38) and exhaustion (CTLA, PD-1, LAG-3 and TIM-3) markers was evaluated by flow cytometry. Result(s): All cases showed significant depletion of T-cells compared to HI. Both post-COVID and non-COVID groups showed increased activation and exhaustion as compared to HI. Non-COVID mucor group showed significant activation of CD4 + T cells for HLADR and CD38 ((P = 0.025, P = 0.054) and marked T-cell exhaustion in form of co-expression of PD-1 and LAG-3 on both CD4 + and CD8 + T cells in comparison to post-COVID patients (P = 0.002, P = 0.001). Additionally, co-expression of PD-1 & CTLA and LAG-3 & TIM-3 on CD8 + T cells was statistically significant in non- COVID mucor patients ((P = 0.031, P = 0.003). Conclusion(s): Immunosuppression in non-COVID mucor showed pronounced exhaustion of T-cells in comparison to post-COVID mucor cases implicating T-cell immune dysfunction is much more severe in non-COVID mucor which are in a state of continuous activation followed by extreme exhaustion leading to poorer outcome.