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Introduction The quest to understand the pathophysiology behind the deleterious effects of the coronavirus disease 2019 (COVID-19) outbreak took a turn when involvement of the angiotensin converting enzyme (ACE) receptors in different organs, especially the lungs, could explain all the clinical manifestations and adverse events in patients. The I/D polymorphism in the ACE gene, having been attributed in various studies, was also seen to have an effect in this pandemic. Present study aimed to analyze the effect of this I/D mutation in COVID-19 patients and in their healthy contacts. Methods Patients with past history of COVID-19 infection and their healthy contacts were enrolled in the study after obtaining ethical clearance and informed consent. The polymorphism was studied by real-time polymerase chain reaction (PCR). Data was analyzed in SPSS version 20 (IBM Corp., Armonk, NY, USA). p value less than 0.05 was taken as significant. Results The allelic distribution followed the Hardy-Weinberg equilibrium, with the wild 'D' allele being dominant in the population. Between the case and controls, the mutant 'I' allele was observed more in the controls, and the association was statistically significant. Conclusion From the results of the present study, it could be concluded that while the wild 'D' allele led to higher chances of being affected with COVID-19, the polymorphism to 'I' allele was relatively protective in nature.
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Background and Objective: This study explored the role of various laboratory biomarkers on inflammatory indices for predicting disease progression toward severity in COVID-19 patients. Methods: This retrospective study was conducted on 1233 adults confirmed for COVID-19. The participants were grouped undermild, moderate, and severe grade disease. Serum bio-inflammatory index (SBII) and systemic inflammatory index (SII) were calculated and correlated with disease severity. The study variables, including clinical details and laboratory variables, were analyzed for impact on the inflammatory indices and severity status using a sequential multiple regression model to determine the predictors for mortality. Receiver operating characteristics defined the cut-off values for severity. Results: Among the study population, 56.2%, 20.7%, and 23.1% were categorized as mild, moderate, and severe COVID-19 cases. Diabetes with hypertension was the most prevalent comorbid condition. The odds for males to have the severe form of the disease was 1.6 times (95% CI = 1.18-2.18, P = 0.002). The median (inter-quartile-range) of SBII was 549 (387.84-741.34) and SII was 2097.6 (1113.9-4153.73) in severe cases. Serum urea, electrolytes, gamma-glutamyl transferase, red-cell distribution width-to-hematocrit ratio, monocytopenia, and eosinopenia exhibited a significant influence on the SpO2, SBII, and SII. Both SBII (r = -0.582, P < 0.001) and SII (r = -0.52, P < 0.001) strongly correlated inversely with SpO2 values [Figures 3a and 3b]. More than 80% of individuals admitted with severe grade COVID-19 had values of more than 50th percentile of SBII and SII. The sensitivity and specificity of SBII at 343.67 for severity were 81.4% and 70.1%, respectively. SII exhibited 77.2% sensitivity and 70.8% specificity at 998.72. Conclusion: Serial monitoring of the routinely available biomarkers would provide considerable input regarding inflammatory status and severity progression in COVID-19.
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Introduction An array of routinely accessible serum biomarkers was assessed to explore their overall impact on severity and mortality in coronavirus disease 2019. Materials and Methods A retrospective analysis of 1,233 adults was conducted. The study groups comprised 127 nonsurvivors and 1,106 survivors. Data for demographic details, clinical presentations, and laboratory reports were recorded from the medical record section. The predictors were analyzed for their influence on mortality. Results The mean (+ standard deviation) age of the patients in the nonsurvivor group was 58.8 (13.8) years. The mean age (56.4 years) was highest in severe grade patients. The odds ratio for death was 2.72 times for patients above the age of 40 years. About 46% of nonsurvivors died within 5 days of admission. Males were found to be more prone to death than females by a factor of 1.36. Serum urea depicted highest sensitivity (85%) for nonsurvival at 52.5 mg/dL. Serum albumin (3.23 g/dL), albumin-to-globulin ratio (0.97), and C-reactive protein-to albumin ratio (CAR) (2.08) showed a sensitivity of more than 70% for mortality outcomes. The high hazard ratio (HR) for deceased patients with hyperkalemia was 2.419 (95% confidence interval [CI] = 1.96-2.99; p < 0.001). The risk for nonsurvival was increased with elevated serum creatinine by 15.6% and uric acid by 21.7% ( p < 0.001). The HR for hypoalbuminemia was 0.254 (95% CI: 0.196-0.33; p < 0.001) and CAR was 1.319 (95% CI: 1.246-1.397; p < 0.001). Saturation of oxygen ( p < 0.001), lactate dehydrogenase ( p = 0.006), ferritin ( p = 0.004), hyperuricemia ( p = 0.027), hyperkalemia ( p < 0.001), hypoalbuminemia ( p = 0.002), and high CAR values (0.031) served as potential predictors for mortality. Conclusion Adjusting for all the predictor variables, serum uric acid, potassium, albumin, and CAR values at the time of admission were affirmed as the potential biomarkers for mortality.
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Cutaneous manifestation of COVID 19 in children has not yet been reviewed systematically. Hence, this review gives the clinicians a future direction to be vigilant for skin presentations during pandemics. The Pubmed database used for literature search with keywords COVID 19, children, and skin in different combinations. Articles published in English with cases of age one month to 18 years were eligible. The outcome included varied aspects of cutaneous and COVID 19 infection. The authors did not register review protocol. Of 51 publications identified, 13 studies containing 149 children met the eligibility criteria. Acrally located erythematous maculopapular lesion was the most common finding in 138 children. The researcher reported Erythema multiforme, varicella like exanthem, and Kawasaki disease like presentations in the rest of the cases. The duration of the skin lesion was 1 2 weeks in 43%. Skin biopsy done in 18 patients revealed superficial and deep perivascular and peri eccrine lymphocytic infiltrate and lymphocytic vasculitis. RT PCR was positive13.8% cases. Serological markers for HSV, parvovirus B19 analyzed across various studies, were negative, except positive mycoplasma pneumonia in 2 of 20 cases tested. Clinicopathologic analysis established chilblains like lesion in 43% cases with no confirmed etiology like cold exposure, autoimmune dysfunction, drug reaction, or viral infection. The usual cephalo caudal spread of a viral exanthem was also missing. However, a low number of discussed cases was a limitation of the study. The absence of any confirmed etiology for such cutaneous manifestations, the possibility of COVID 19, should be explored and thoroughly evaluated and isolated during such a pandemic.