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.

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.

Background The renin-angiotensin-aldosterone system was shown to be activated in severe COVID-19 infection. We aimed to investigate the relationship between angiotensin converting enzyme (ACE) levels, ACE gene polymorphism, type 2 diabetes (T2DM), and hypertension (HT) and the prognosis of COVID-19 infection. Methods This cross-sectional study analyzed the clinical features of adult patients with SARS-CoV-2 infection. ACE gene analysis and ACE level measurements were performed. The patients were grouped according to ACE gene polymorphism (DD, ID or II), disease severity (mild, moderate, or severe), and the use of dipeptidyl peptidase-4 enzyme inhibitor (DPP4i), ACE-inhibitor (ACEi) or angiotensin receptor blocker (ARB). Intensive care unit (ICU) admissions and mortality were also recorded. Results A total of 266 patients were enrolled. Gene analysis detected DD polymorphism in the ACE 1 gene in 32.7% (n = 87), ID in 51.5% (n = 137), and II in 15.8% (n = 42) of the patients. ACE gene polymorphisms were not associated with disease severity, ICU admission, or mortality. ACE levels were higher in patients who died (p = 0.004) or were admitted to the ICU (p<0.001) and in those with severe disease compared to cases with mild (p = 0.023) or moderate (p<0.001) disease. HT, T2DM, and ACEi/ARB or DPP4i use were not associated with mortality or ICU admission. ACE levels were similar in patients with or without HT (p = 0.374) and with HT using or not using ACEi/ARB (p = 0.999). They were also similar in patients with and without T2DM (p = 0.062) and in those with and without DPP4i treatment (p = 0.427). ACE level was a weak predictor of mortality but an important predictor of ICU admission. It predicted ICU admission in total (cutoff value >37.092 ng/mL, AUC: 0.775, p<0.001). Conclusion Our findings suggest that higher ACE levels, but not ACE gene polymorphism, ACEi/ARB or DPP4i use, were associated with the prognosis of COVID-19 infection. The presence of HT and T2DM and ACEi/ARB or DPP4i use were not associated with mortality or ICU admission.

Introduction Tumoral calcinosis (TC) is a rare disease characterized by soft tissue calcification as a result of repetitive trauma and prolonged pressure in periarticular areas of large joints; such as hip, knee, shoulder and elbow. There are three different forms; sporadic, familial and secondary TC due to chronic renal diseases, vitamin D hypervitaminosis. Familial hyperphosphatemic TC, which will be presented in this case, causes by relative deficiency or resistance of FGF-23, which is the critical regulatory hormone in the phosphorus metabolism. Clinical Case A 38-year-old male patient was referred from the nephrology department for hyperphosphatemia. He underwent 14 operations mass lesions, which were painful, progressively enlarging, in the different regions. His first operation at the age of 11 for a lesion in the right knee. Pathologic diagnoses of surgical specimens were reported as tumoral calcinosis. The patient was followed up by different orthopedic clinics from the age of 11, and was operated as new masses appeared. He does not have any complaints other than the pain in the periods when the lesions appear. He has 4 siblings without any known diseases, and his parents were third degree consanguineous. In physical examination, blood pressure was 115/72 mmHg, pulse was 76/min, and temperature was 36.7°C. Her height was 183 cm, and weight was 82 kg, BMI: 24.5 kg/m2. In laboratory tests, serum calcium 10.1 mg/dl, serum phosphate 6,8 mg/dl, parathormone 25 pg/ml, 25-OH Vitamin D 19 ng/ml, creatinine 0.9 mg/dl, alkaline phosphatase 71 U/l, 24-h urinary calcium 129 mg/day and 24-h urinary phosphate 205 mg/day. Bone mineral density at the femoral neck was 1.258 g/cm2, Z score was -1.6, and BMD at the lumbar spine was 1.081 g/cm2, Z score was -0.9. In bone survey, we detected that mild right-facing rotoscoliosis in the thoracolumbar region, increased calcification of the costosternal cartilages, osteophytic tapering in the thoracic region, intracranial calcification in the parietal region, L3-L4 level syndesmophyte, irregularity and adjacent soft tissue calcification at the distal phalanx level of the first toe of the right and left foot (Fig 1). We recommended the patient to avoid trauma and a low phosphorus diet. Maintenance dose vitamin D replacement and phosphorus-binding treatment (calcium-asetate 700 mg 3×2) with meals were started. When phosphate reduction could not be achieved, sevalemer 800 mg 3×3 was added with gradually increasing, phosphorus level dropped to 5.2 mg/dl. Genetic analysis revealed GALNT3 homozygous mutation. Genetic counseling and eye examination were recommended. Conclusion TC should also be considered in patients with a history of multiple surgery due to soft tissue masses, especially in the presence of hyperphosphatemia. In our case, a mutation was detected at a rather late age, and phosphorus-lowering therapy was started at the age of 38 years and genetic counseling should be offered to these patients at an early age.