Background and aims: it is unclear whether male hypogonadism is ascribable to the diabetic state per se, or because of other factors, such as obesity or age. We aimed to investigate the prevalence and identify the predictors for testosterone deficiency among non-obese type 2 diabetic males. Methods: This cross-sectional study was conducted on 95 nonobese type 2 diabetic males with BMI below 30. We evaluated the total testosterone (TT) levels to determine prevalence and risk factors of testosterone deficiency. Serum TT ≤ 300 ng/dl defined testosterone deficiency. Results: The prevalence of testosterone deficiency was 29.1%. Testosterone deficient patients had statistically significantly higher visceral adiposity index (VAI), waist, and triglyceride in comparison with normal testosterone patients. TT level correlated with VAI, waist, BMI, LH, and age. VAI was the only significant predictor of TT levels even after adjustment for age and BMI in regression analysis. Furthermore, VAI was a statistically significant risk factor for testosterone deficiency in binary logistic analysis. Conclusions: testosterone deficient non-obese type 2 diabetic male patients had elevated VAI, waist, and triglyceride. Moreover, elevated VAI was a risk factor for testosterone deficiency. VAI could be an easily applicable and reliable index for the evaluation and prediction in type 2 non-obese diabetic males.

Objective: Although multiple studies have addressed the clinical outcomes of coronavirus disease, little data exist regarding the definition of immune and inflammatory profiles associated with this infection. Its clinical manifestations often worsen in association with hypercytokinemia (elevated interleukin 8 and interleukin 17). We conducted this research to elucidate the effect of interleukin 17 levels and interleukin 17F gene polymorphism on the severity and outcomes of coronavirus disease. Material and Methods: Ninety patients with confirmed coronavirus disease and 30 healthy controls were enrolled. Coronavirus disease cases were classified into nonsevere, severe, and critical according to the World Health Organization definition. Approximately 10 mL peripheral blood sample was collected from all patients and controls by venipuncture in-plane and ethylenediaminetetraacetic acid tube. Enzyme-linked immunosorbent assay kits were used for calculating serum interleukin 17 levels, whereas real-time polymerase chain reaction was used for genotyping using the 5'-nuclease allelic discrimination assay for single nucleotide polymorphisms genotyping. Results: As regards interleukin 17 levels, there was a significant elevation of interleukin 17 in coronavirus disease cases compared to control healthy persons ( P < .001). Moreover, serum interleukin 17 levels tended to be significantly higher with increased disease severity ( P = .004). Patients with critical diseases expressed a significant rise of interleukin 17 compared to severe ( P = .03) and nonsevere cases ( P = .02). We noted no significant difference between the critical, severe, and nonsevere cases regarding different interleukin 17F genotypes. Conclusion: Coronavirus disease is associated with elevated levels of interleukin 17, which tended to be considerably higher with disease severity. However, different interleukin 17F genotypes do not affect either the predisposition or the severity of coronavirus disease.

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