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Purpose Vitamin D deficiency has emerged as another potential risk factor for coronavirus disease (COVID‐19) due to the immunomodulatory effects of 25 hydroxyvitamin D [25 (OH)D]. Vitamin D receptor (VDR) gene polymorphisms such as Fok I, Bsm I, Apa I, and Taq I are also associated with different courses of viral infections. This study aimed to evaluate the association between the VDR gene polymorphism at Fok I, Taq I, Bsm I, and Apa I genotypes and the prognosis of COVID‐19 in respect to vitamin D deficiency. Methods Two‐hundred ninety‐seven patients with COVID‐19 were enrolled. Serum 25 (OH)D levels were measured. Four variant regions of the VDR gene, FokI, BsmI, ApaI, and TaqI were determined. Results Eighty‐three percent of subjects had vitamin D deficiency, and 40.7% of the whole group had severe deficiency. Median 25 (OH)D level was 11.97 ng/ml. Vitamin D levels were not related to inflammatory markers, disease severity, admission to intensive care unit (ICU), and mortality. While disease severity was related to Fok I Ff genotype, it was Taq TT genotype for ICU admission. Moreover, the ApaI aa genotype was common among the patients who were died. None of the deceased subjects had the Fok I FF genotype. Conclusion 25 (OH)D levels were not related to the severity and mortality of COVID‐19. VDR gene polymorphisms are independently associated with the severity of COVID‐19 and the survival of patients.

Background Angiotensin‐converting enzyme 2 and transmembrane protease serine 2 are critical factors of virus transmission. Expression of angiotensin‐converting enzyme 2 is highest in testes, and testicular function and testosterone levels were affected by coronavirus disease 2019. Low testosterone levels are related to infections, especially respiratory tract infections, and could worsen clinical conditions by exacerbating cytokine storms and increasing pro‐inflammatory cytokines. Objectives We aimed to evaluate the acute and chronic effects of coronavirus disease 2019 on gonadal functions. Our second aim was to detect the relationship between free testosterone levels and disease prognosis and determine the impact of low‐free testosterone on admission to the intensive care unit. Methods Eighty‐one patients with reverse‐transcription polymerase chain reaction‐confirmed coronavirus disease 2019 were enrolled. Twenty‐nine patients were assessed again for 6 months post‐coronavirus disease 2019 follow‐up, and seven of them had a semen analysis. Serum follicle‐stimulating hormone, luteinizing hormone, sex hormone‐binding globulin, and total testosterone levels were measured. Results In this observational study, 71.6% (n = 58) of patients had low free testosterone levels at baseline, in which 69% were considered secondary hypogonadism. A longer length of hospitalization and increased inflammatory markers (d‐dimer, high‐sensitive C‐reactive protein, and procalcitonin) were detected in the low‐free testosterone group. Follicle‐stimulating hormone, total, free, and bioavailable testosterone levels were lower in patients who required admission to the intensive care unit. Free testosterone levels were inversely correlated with the length of hospitalization and prognostic disease factors. Oligozoospermia and impaired progressive motility were present in 42.8% (3/7) of the patients. In 6 months post‐coronavirus disease 2019 follow‐up, out of 29 patients, 48.2% still had low testosterone levels. Conclusion A high rate of hypogonadism (71.6%) was found, especially secondary hypogonadism, and about half of the patients had hypogonadism in the sixth months' follow‐up. Low free testosterone levels were correlated with inflammatory parameters, and it is related to the intensive care unit admission. Studies with long‐term follow‐up data in larger groups are needed to determine persistent hypogonadism and impaired spermatogenesis.

Lack of response to SRLs does not necessarily increase the risk of harboring AIP mutations. The finding of decreased AIP, SSTR2A, and SSTR2B immunostaining in patients with poor response to SRLs and decreased SSTR2A and SSTR3 level in those with low AIP immunostaining suggests a possible interaction between AIP and some SSTR subtypes that might alter SRL sensitivity.

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Although there were subtle differences, clinical practice guidelines were usually followed among Turkish endocrinologists.

Background. COVID-19 infection may have multiorgan effects in addition to effects on the lungs and immune system. Recently, studies have found thyroid function abnormalities in COVID-19 cases which were interpreted as euthyroid sick syndrome (ESS) or destructive thyroiditis. Therefore, in this study, we aimed to evaluate the thyroid function status and thyroid autoimmunity in COVID-19 patients. Material and Method. 205 patients were included. The medical history and laboratory parameters at admission were collected from medical records. Serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), thyroid peroxidase antibody, and thyroglobulin antibody were measured, and patients were classified according to thyroid function status. Results. 34.1% of the patients were euthyroid. Length of hospitalization ( p < 0.001 ), rate of oxygen demand ( p < 0.001 ), and intensive care unit (ICU) admission ( p = 0.022 ) were lower, and none of the euthyroid patients died. 108 (52.6%) patients were classified to have ESS, 57 were classified as mild, and 51 were moderate. The inflammatory parameters were higher in patients with moderate ESS. In cluster analysis, a high-risk group with a lower median FT3 value (median = 2.34 ng/L; IQR = 0.86), a higher median FT4 value (median = 1.04 ng/dL; IQR = 0.33), and a lower median TSH value (median = 0.62 mIU/L; IQR = 0.59) included 8 of 9 died patients and 25 of the 31 patients that were admitted to ICU. Discussion. Length of hospitalization, oxygen demand, ICU admission, and mortality were lower in euthyroid patients. Moreover, none of the euthyroid patients died. In conclusion, evaluation of thyroid function tests during COVID-19 infection may give information about the prognosis of disease.