Background Identifying the non-survived patients' characteristics compared to survived subjects and introducing the critical risk factors of COVID-19 mortality would help enhance patients' prognosis and treatment. Methods In the current case-control study, medical records of 103 non-survived COVID-19 patients (cases) and 147 sexmatched survivors (controls) who admitted to Razi University Hospital in Rasht, Guilan, Northern Iran from April 21 to August 21, 2020, were explored. Data on demographic, anthropometric, clinical, and laboratory assessment was extracted from the electronic medical records. To estimate the association between variables of interest and mortality odds due to COVID-19 logistic regression was carried out. Results The patients who died (mean age = 62.87 years) were older than the discharged patients (57.33 years; P value = 0.009). According to the results of multivariable regression adjusted for potential confounders, elevated BMI (OR = 2.49; 95% CI = 1.15-5.41), higher CRP levels (OR = 2.28; 95% CI = 1.08-4.78), increased FBS levels (OR = 2.88; 95% CI = 1.35-6.17), higher levels of total cholestrol (OR = 2.55; 95% CI = 1.19-5.45) and LDL (OR = 2.27; 95% CI = 1.07-4.79), elevated triglyceride (OR = 5.14; 95% CI = 2.28-11.56), and raised levels of D-dimer (OR = 5.68; 95% CI = 2.22-14.49) were identified as independent risk factors of COVID-19 mortality. No significant association was detected regarding HDL level, QTc interval or heart size, and COVID-19 fatality odds. Conclusion The present findings demonstrated that obesity, higher levels of CRP, blood sugar, D-dimer, and lipid markers were likely to be predictive factors of COVID-19-related mortality odds.

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Interleukin (IL)-35 and IL-37 are two anti-inflammatory cytokines. IL-35 inhibits the development of T-effector cells such as Th1, and Th17; while increasing regulatory T cells (Tregs). IL-37 causes the suppression of inflammatory cytokines. Regarding the positive impact of Helicobacter pylori (H. pylori) infection on inflammation and considering the anti-inflammatory effects of IL-35 and IL-37, this study aimed to evaluate the expression of these two cytokines in H. pylori-infected patients with gastrointestinal problems. The case group consisted of H. pylori-infected individuals with gastric ulcer and/or gastritis (n=50) and the control group consisted of cases with gastric ulcer and/or gastritis non-H. pylori-infected (n=50). Sampling and classification of patients were based on pathology findings. A real-time polymerase chain reaction was performed for evaluating the IL-35 and IL-37 expression levels. h.pylori-infected gastritis patients showed lower expression of IL-35 and IL-37 than the non-infected group. There was a significant difference between the expression levels of IL-35 and IL-37 in patients with gastric ulcers and/or gastritis who were infected and non-infected by H. pylori. There were no significant differences in the expression level of IL-35 and IL-37 in H. pylori-infected patients with gastric ulcer or gastritis. Interleukins 37 and 35 were less expressed in patients with H. pylori-infection. In differentiation between patients with gastrointestinal symptoms who have H. pylori infection or with similar symptoms who do not have H. pylori-infection, mentioned interleukins can be used as diagnostic markers.