The present study aimed to identify useful biomarkers to predict deterioration in patients with coronavirus disease 2019 . A total of 201 COVID-19 patients were classified according to their disease severity into non-severe (n=125) and severe (n=76) groups, and the behavior of laboratory biomarkers was examined according to the prognosis. Neutrophil count, aspartate aminotransferase (AST), alanine aminotransferase, lactate dehydrogenase (LDH), C-reactive protein (CRP), sialylated carbohydrate antigen KL-6 (KL-6), procalcitonin (PCT), presepsin (PSP) and D-dimer levels were significantly higher, and lymphocyte count and platelet count were significantly lower in the non-severe group compared with the severe group. In the non-severe group, ROC analysis demonstrated that only four biomarkers, CRP, PSP, AST and LDH were useful for differentiating the prognosis between improvement and deterioration subgroups. No strong correlation was revealed for any of the markers. Multivariate analysis identified CRP as a significant prognostic factor in non-severe cases (odds ratio, 41.45; 95% confidence interval, 4.91-349.24; P<0.001). However, there were no blood biomarkers that could predict the outcome of patients in the severe group. Overall, several blood markers changed significantly according to disease severity in the course of COVID-19 infection. Among them, CRP, PSP, LDH and AST were the most reliable markers for predicting the patient's prognosis in non-severe COVID-19 cases.
A 70-year-old man was admitted due to SARS-CoV-19. Computed tomography (CT) revealed severe ground-glass opacity and fibrosis in both lung fields (PictureA). Three weeks after a positive COVID-19 polymerase chain reaction test, his platelet counts gradually dropped to a minimum of 3×10 9 /L, while other blood cell counts were normal. Immune thrombocytopenia (ITP) associated with COVID-19 was diagnosed by exclusion of other potential entities, such as drug-induced thrombocytopenia. High dose intravenous γ globulin (HDIVG) and glucocorticoids at 1 mg/kg/day were started (1), which led to an improvement in the platelet count to 100×10 9 /L within 1 week. However, his awareness declined further, and follow-up CT revealed multiple cerebral hemorrhaging on day 15 (PictureB, arrowhead).We considered ITP in this patient to be a complication of COVID-19, especially since he was an elderly patient with severe disease (1). Furthermore, late-occurring severe throm-bocytopenia that might lead to life-threatening bleeding and cerebral hemorrhaging has been previously reported (2).The authors state that they have no Conflict of Interest (COI).
Arthritis has been reported as an acute pattern, generally evanescent with oligoarthritis, mostly affecting knees and ankles in childhood systemic polyarteritis nodosa. However, chronic polyarthritis with morning stiffness mimicking juvenile idiopathic arthritis has not been reported. We describe the case of a 4-year old girl who had additive and chronic polyarthritis with edema, tenderness, pain on motion and morning stiffness for 2 months. After 45 days, she also presented painful subcutaneous nodules and erythematous-violaceous lesions in the extensor region of upper and lower limbs. She was admitted to university hospital due to high fever, malaise, myalgia, anorexia, loss of weight (1kg), painful skin lesions and severe functional disability. She was bedridden by chronic polyarthritis with limitation on motion. Systolic and diastolic blood pressures were greater than 95th percentile for height. Urine protein/creatinine ratio was 0.39g/day, and immunological tests were negative. Anti-streptolysin O was 1,687UI/mL. Skin biopsy revealed necrotizing vasculitis in medium- and small-sized vessels compatible with polyarteritis nodosa. Therefore, we had the diagnosis of systemic polyarteritis nodosa. Prednisone 2mg/kg/day was administered with complete resolution of skin lesions and arthritis, and improvement of proteinuria (0.26g/day) after 15 days. The diagnosis of childhood systemic polyarteritis nodosa should be considered for patients with chronic polyarthritis associated to cutaneous vasculitis triggered by streptococcal infection.
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