Recent studies showed that a low 25-hydroxyvitamin D (25(OH)D) level was associated with a higher risk of morbidity and severe course of COVID-19. Our study aimed to evaluate the effects of cholecalciferol supplementation on the clinical features and inflammatory markers in patients with COVID-19. A serum 25(OH)D level was determined in 311 COVID-19 patients. Among them, 129 patients were then randomized into two groups with similar concomitant medication. Group I (n = 56) received a bolus of cholecalciferol at a dose of 50,000 IU on the first and the eighth days of hospitalization. Patients from Group II (n = 54) did not receive the supplementation. We found significant differences between groups with the preferential increase in serum 25(OH)D level and Δ 25(OH)D in Group I on the ninth day of hospitalization (p < 0.001). The serum 25(OH)D level on the ninth day was negatively associated with the number of bed days (r = −0.23, p = 0.006); we did not observe other clinical benefits in patients receiving an oral bolus of cholecalciferol. Moreover, in Group I, neutrophil and lymphocyte counts were significantly higher (p = 0.04; p = 0.02), while the C-reactive protein level was significantly lower on the ninth day of hospitalization (p = 0.02). Patients with supplementation of 100,000 IU of cholecalciferol, compared to those without supplementation, showed a decrease in the frequencies of CD38++CD27 transitional and CD27−CD38+ mature naive B cells (p = 0.006 and p = 0.02) and an increase in the level of CD27−CD38− DN B cells (p = 0.02). Thus, the rise in serum 25(OH)D level caused by vitamin D supplementation in vitamin D insufficient and deficient patients may positively affect immune status and hence the course of COVID-19.

In the last 2 years, observational studies have shown that a low 25-hydroxyvitamin D (25(OH)D) level affected the severity of infection with the novel coronavirus (COVID-19). This study aimed to analyze the potential effect of vitamin D supplementation in reducing SARS-CoV-2 infection morbidity and severity in health care workers. Of 128 health care workers, 91 (consisting of 38 medical doctors (42%), 38 nurses (42%), and 15 medical attendants (16%)) were randomized into two groups receiving vitamin D supplementation. Participants of group I (n = 45) received water-soluble cholecalciferol at a dose of 50,000 IU/week for 2 consecutive weeks, followed by 5000 IU/day for the rest of the study. Participants of group II (n = 46) received water-soluble cholecalciferol at a dose of 2000 IU/day. For both groups, treatment lasted 3 months. Baseline serum 25(OH)D level in health care workers varied from 3.0 to 65.1 ng/mL (median, 17.7 (interquartile range, 12.2; 24.7) ng/mL). Vitamin D deficiency, insufficiency, and normal vitamin D status were diagnosed in 60%, 30%, and 10%, respectively. Only 78 subjects completed the study. Vitamin D supplementation was associated with an increase in serum 25(OH)D level, but only intake of 5000 IU/day was accompanied by normalization of serum 25(OH)D level, which occurred in 53% of cases. Neither vitamin D intake nor vitamin D deficiency/insufficiency were associated with a decrease in SARS-CoV-2 morbidity (odds ratio = 2.27; 95% confidence interval, 0.72 to 7.12). However, subjects receiving high-dose vitamin D had only asymptomatic SARS-CoV-2 in 10 (26%) cases; at the same time, participants who received 2000 IU/day showed twice as many SARS-CoV-2 cases, with mild clinical features in half of them.

We evaluated associations between serum 25-hydroxyvitamin D [25(OH)D] level and severity of new coronavirus infection (COVID-19) in hospitalized patients. We assessed serum 25(OH)D level in 133 patients aged 21–93 years. Twenty-five (19%) patients had severe disease, 108 patients (81%) had moderate disease, and 18 (14%) patients died. 25(OH)D level ranged from 3.0 to 97.0 ng/mL (median, 13.5 [25%; 75%, 9.6; 23.3] ng/mL). Vitamin D deficiency was diagnosed in 90 patients, including 37 with severe deficiency. In patients with severe course of disease, 25(OH)D level was lower (median, 9.7 [25%; 75%, 6.0; 14.9] ng/mL), and vitamin D deficiency was more common than in patients with moderate course (median, 14.6 [25%; 75%, 10.6; 24.4] ng/mL, p = 0.003). In patients who died, 25(OH)D was 9.6 [25%; 75%, 6.0; 11.5] ng/mL, compared with 14.8 [25%; 75%, 10.1; 24.3] ng/mL in discharged patients (p = 0.001). Severe vitamin D deficiency was associated with increased risk of COVID-19 severity and fatal outcome. The threshold for 25(OH)D level associated with increased risk of severe course was 11.7 ng/mL. Approximately the same 25(OH)D level, 10.9 ng/mL, was associated with increased risk of mortality. Thus, most COVID-19 patients have vitamin D deficiency; severe vitamin D deficiency is associated with increased risk of COVID-19 severity and fatal outcome.

A low 25-hydroxyvitamin D (25(OH)D) level is considered as an independent risk factor for COVID-19 severity. However, the association between vitamin D status and outcomes in COVID-19 is controversial. In the present study we investigate the association between the serum 25(OH)D level, immune response, and clinical disease course in patients with COVID-19. A total of 311 patients hospitalized with COVID-19 were enrolled. For patients with a vitamin D deficiency/insufficiency, the prevalence of severe COVID-19 was higher than in those with a normal 25(OH)D level (p < 0.001). The threshold of 25(OH)D level associated with mortality was 11.4 ng/mL (p = 0.003, ROC analysis). The frequency of CD3+CD4+ T helper (Th) cells was decreased in patients with 25(OH)D level ≤ 11.4 ng/mL, compared to healthy controls (HCs). There were no differences in the frequency of naive, central memory (CM), effector memory (EM), and terminally differentiated effector memory Th cells in patients with COVID-19 compared to HCs. The frequency of T-follicular helpers was decreased both in patients with 25(OH)D level > 11.4 ng/mL (p < 0.001) and 25(OH)D level ≤ 11.4 ng/mL (p = 0.003) compared to HCs. Patients with 25(OH)D level > 11.4 ng/mL had an increased frequency of Th2 CM (p = 0.010) and decreased Th17 CM (p < 0.001). While the frequency of Th2 EM was significantly increased, the frequency of Th17 EM was significantly decreased in both groups compared to HCs. Thus, 25(OH)D level is an independent risk factor for the disease severity and mortality in patients with COVID-19. We demonstrate that the serum 25(OH)D level ≤ 11.4 ng/mL is associated with the stimulation of Th2 and the downregulation of Th17 cell polarization of the adaptive immunity in patients with COVID-19.

During the COVID-19 pandemic, the efforts of many researchers around the world are aimed at finding preventive and prophylactic measures as well as therapeutic agents against SARS-CoV-2. Recent studies have showed that vitamin D deficiency could be one of many factors associated with the development and severity of acute respiratory infections, and vitamin D could be used for prevention and treatment of these patients. This review summarizes data about the role of vitamin D in the pathogenesis and prevention of respiratory viral infections, including new coronavirus infection as well as mechanisms for reducing the risk of infection with vitamin D therapy. Probably, this review will be of interest for endocrinologists and other specialists.

Background. Hypokalemia is a common electrolyte complication among hospitalized patients with pneumonia caused by a new coronavirus SARS-CoV-2. Hyperactivation of the renin-angiotensin-aldosterone system (RAAS) is suggested as a possible cause of hypokalemia in patients with COVID-19.Objective. To investigate the RAAS activity in COVID-19 patients with and without hypokalemia and its possible association with treatment outcomes.Design and methods. The cross-sectional cohort study included 172 patients with COVID-19 pneumonia. Potassium, aldosterone and venous renin were measured in 77 patients. The differences in the levels of acute phase proteins, the degree of lung damage and the severity of COVID-19 were compared between patients with and without hypokalemia.Results. Hypokalemia was found in 19 of 77 patients (25%): the median potassium level in hypokalemia and eukalemia group was 3,1 [2,8–3,3] and 4,1 [3,9–4,5] mmol/L, respectively (p = 0,001). Plasma aldosterone and renin levels in patients with and without hypokalemia did not differ significantly: aldosterone 76,0 [57,7–121,5] and 70,9 [26,3–113,8] pg/ml (p = 0,23), renin 17,0 [8,5–47,2] and 11,0 [6,5–38,1] pg/ml (p = 0,35), respectively. Differences in the degree of lung tissue damage, acute phase proteins, severity of COVID-19, length of hospitalization and mortality in patients with and without identified electrolyte disturbances were also not significant.Conclusions. Our results showed that there were no laboratory signs of RAAS hyperactivation in COVID-19 patients with registered hypokalemia. Identification of the cause and clinical significance of hypokalemia among patients with COVID-19 needs to be specified.

Objective: to measure the serum TSH level in hospitalized patients with moderate-to-severe COVID-19.Material and methods: this was a retrospective study at Almazov National Medical Research Centre enrolled 133 hospitalized COVID-19 patients without known thyroid disorders. Clinical data, biochemical parameters (TSH, 25(OH)D, C-reactive protein, Lactate dehydrogenase and Ferritin), fi ndings of chest computed tomography (CT) imaging as well as obtained corticosteroids therapy were analyzed.Results: the median TSH level at the 1st-2nd day of hospitalization and at the 9-10th day was 1,15 mIU/L [0, 76; 1, 8] and 1,04 mIU/L [0,7; 1,78] respectively. Th e initial level of TSH <0,4 mIU/L was found in four patients, while by the 9-10th day of hospitalization their number doubled and reached 9 (11,7%). Furthermore, by the 9-10th day of hospitalization the TSH level more than 4,5 mIU/L was detected in four patients (4,2%). Th us, 13 out of 77 patients had the serum TSH level outside the reference range by the 9-10th day of hospitalization.Conclusions: in case of alteration in the serum TSH level it is necessary to take into account the personal history of thyroid disorders. Th e level of thyroid hormones and autoimmune markers as well as thyroid ultrasound results may be useful in clinical interpretation of thyroidal insults during and aft er COVID-19. Th e hypothalamic-pituitary-thyroid axis may also be aff ected by drugs used to treat COVID-19.

The year 2022 marks the 100th anniversary of the vitamin D discovery, however, vitamin D insufficiency and deficiency is globally widespread both in Russia and around the world. At the same time, the COVID-19 pandemic poses a serious challenge to global health. To date, more and more evidence is emerging to consider vitamin D deficiency as a modifiable COVID-19 severe course risk factor. Current review presents possible mechanisms behind the immunomodulatory effects of vitamin D, as well as shows the relationship between the vitamin D level and the course of COVID-19. In addition, the therapeutic potential of cholecalciferol supplementation to standard therapy for COVID-19 is being discussed.