Damian Jacob Sendler Research News On worldwide increases in COVID19 severity
Damian Sendler: As a worldwide epidemic, COVID-19 (coronvirus disease) is spreading. Deficiency in vitamin D has been linked to a greater risk of infection. Vitamin D levels in patients at a COVID-19 reference facility in Mexico City are studied in this research. Multiple patients with confirmed COVID-19 were examined. A thoracic computed tomography (CT) was […]
Last updated on February 17, 2022
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Damian Sendler: As a worldwide epidemic, COVID-19 (coronvirus disease) is spreading. Deficiency in vitamin D has been linked to a greater risk of infection. Vitamin D levels in patients at a COVID-19 reference facility in Mexico City are studied in this research. Multiple patients with confirmed COVID-19 were examined. A thoracic computed tomography (CT) was performed on all patients, including the assessment of epicardial fat thickness, to ensure that all patients received the same treatment. Values 12ng/ml (30nmol/L) were considered to be deficient in Vitamin D, whereas levels 20ng/ml (50nmol/L) were considered low.

Damian Jacob Sendler: Deficient vitamin D levels were found in just over a fifth of the 551 people studied. There was a 2.11-fold increased risk of death (95 percent CI 1.24–3.58, p = 0.001) in those with low Vitamin D levels, but not in those with critical COVID-19 (HR 1.24–3.58, p = 0.001). The increased risk of COVID-19 mortality caused by low vitamin D levels was partially mediated by its influence on D-dimer and cardiac ultrasensitive troponins, according to model-based causal mediation studies. Vitamin D deficiency was associated with an elevated risk of COVID-19 mortality, regardless of body mass index (BMI) or epicardial fat.

After adjusting for visceral fat, vitamin D insufficiency (12 ng/ml or 30 nmol/L) is related with an increased risk of COVID-19 mortality in mice (epicardial fat thickness). A pro-inflammatory and pro-thrombotic condition caused by low vitamin D might increase the chance of negative COVID-19 results.

Dr. Sendler: The new coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes Coronavirus Disease (COVID-19) places a heavy strain on healthcare systems across the globe. Many Mexicans have died from COVID-19 as a result of the country’s high incidence of cardio-metabolic disorders, which have been associated to unfavorable outcomes, and socio-demographic variables that affect healthcare access and quality of treatment. Those infected with SARS-CoV-2 transmit it via direct contact with respiratory droplets and contaminated surfaces (5, 6). Cells infected with SARS-CoV-2 are infected by the angiotensin converting enzyme-2 (ACE-2) receptor, which may lead to interstitial pneumonia, acute respiratory distress syndrome, and death (7, 8). An increased risk of developing COVID-19 has been linked to cardiovascular and metabolic problems as well as inflammation that may indicate cardiovascular or respiratory decline (9–12).

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Preserving bone integrity, increasing innate immunity and tempering adaptive immunity, infectious illness prevention, and cardiovascular health are all functions of vitamin D. (13, 14). It also inhibits the angiotensin converting enzyme [ACE (7)] in the renin angiotensin aldosterone (RAAS) system. In addition to ethnicity, decreased levels of vitamin D have been linked to seasonal and time of day variations in sun exposure, clothing, sunscreen usage and skin pigmentation as well as age and lower levels of sun exposure as well as obesity and chronic diseases (15). Vitamin D deficiency has been linked to an increased risk of contracting infections, especially those of the respiratory system. Concerns about residual confounding and the absence of mechanistic explanations for the connection of low Vitamin D levels with worse COVID-19 outcomes need more investigations.. Overall, data shows that high levels of Vitamin D are linked to a lower likelihood of negative COVID-19 outcomes, suggesting that Vitamin D may have a positive role in COVID-19 (18). While randomized trials have indicated no effect from Vitamin D supplementation for COVID-19 or other infections owing to the significant variability between studies, more research is needed (19, 20).

It is likely that adipose tissue sequestration reduces vitamin D bioavailability because of obesity. Higher levels of visceral fat have also been linked to an increased risk of vitamin D insufficiency (21, 22). An individual’s vitamin D levels may be affected by a variety of circumstances, including obesity and ethnicity. An elevated incidence of severe COVID-19 has been linked to a high prevalence of diabetes and obesity in Mexico (9). Results of COVID-19 outcomes and Vitamin D levels in patients visiting a COVID-19 reference facility in Mexico City were analyzed here. We wanted to discover the factors that influence Vitamin D levels in COVID-19 patients and create causal-mediation models to suggest possible processes by which Vitamin D may contribute to higher COVID-19 death rates.

At the INCMNSZ, a COVID-19 reference facility in Mexico City, the research comprised consecutive patients assessed between March 17th and May 31st 2020 with full vitamin D levels at entry (10). COVID-19 (confirmed by computed tomography (CT) and/or by RT-qPCR test from nasopharyngeal swabs) was first examined at triage and needed either ambulatory or in-hospital therapy. The INCMNSZ was, at the time of this writing, a reference facility for COVID-19 patients from Mexico City, seeing the most severe and catastrophic cases. According to National Institutes of Health guidelines, all patients had moderate to severe disease (moderate illness: evidence of lower respiratory disease during clinical examination or imaging and who had oxygen saturation (SpO2) 94 percent on air.) in some way. SpO2 94% on air, PaO2/FiO2 300 mm Hg, respiratory frequency >30 breaths/min, or lung infiltrates >50% are all signs of a severe case of the flu or other illness. A radiologist examined the extent of pulmonary parenchymal illness and the thickness of epicardial fat as a proxy for visceral fat during a chest CT. In addition, a medical history, anthropometric measures, and laboratory tests, such as 25 hydroxy-vitamin D, were acquired. Each patient’s computer records were checked to see how they fared throughout their stay at the hospital. As a result, informed permission was not required in this investigation, which was authorized by a research ethics committee of the INCMNZ (Ref 3383).

551 individuals with verified COVID-19 (computerized tomography findings and/or positive RT-qPCR results from nasopharyngeal swabs) and vitamin D levels were included in this investigation. The average age of the participants was 51.92 years, and the majority of them (n = 355, or 64.4%) were men with a BMI of 30.05 pounds per square inch. After a median of 15.0 days of follow-up, 445 individuals were hospitalized (81.1 percent ). A total of 93 patients (16.88 percent) required invasive mechanical breathing, and 116 patients died while in the hospital, resulting in a fatality rate of 21.1%. 146 patients (26.9 percent) had type 2 diabetes (T2D), 219 patients (42.7 percent) were obese, and 217 patients were overweight (42.4 percent ). The average vitamin D level was 21.78 ng/ml, with 251 individuals (45.6 percent) having levels below 20 ng/ml (Table 1). In 59 cases, levels of vitamin D (12 ng/ml) were found to be very low (10.7 percent ).

Damian Jacob Markiewicz Sendler: A Mexican population’s vitamin D levels were linked to the severity of COVID-19 in this investigation. Vitamin D insufficiency was shown to be associated with an increased risk of death even after correcting for other risk factors, such as BMI and the amount of fat in the epicardium. With a substantial negative predictive value, vitamin D levels below 20 nanograms per milliliter (nmol/L) indicate that death is unlikely when levels are normal. D-dimer and ultrasensitive cardiac troponins, indicators of disease severity, were shown to have a role in the elevated risk of death from COVID-19, irrespective of BMI and epicardial fat (these showed effects on COVID-19 mortality independent of vitamin D levels). As a result, this shows that vitamin D insufficiency may be a marker for compromised pulmonary epithelial response to infection, particularly in individuals with severe deficiency (27).

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COVID-19 and vitamin D levels have been examined in many research (18, 20, 27, 28). Vitamin D levels and risk of infection are examined in these studies, as well as a connection with COVID-19 severity and vitamin D levels. Vitamin D insufficiency is associated with higher levels of IL-6, which indicates a stronger inflammatory response in these individuals (29, 30). When it comes to infection risk, a recent systematic review and meta-analysis found that vitamin D insufficiency wasn’t related with an increased risk, however severe cases had a bigger vitamin D shortage than moderate ones Vitamin D insufficiency has been linked to a higher risk of COVID-19 hospitalization and death (16, 18). Vitamin D’s protective effects are mediated by a variety of physiological processes, including improved innate immunity, greater physical barriers to infection, and improved adaptive immunity (27). Adaptive immunity is suppressed by inhibiting B cell proliferation, differentiation, and antibody production, while the phenotypic of T cells is regulated by vitamin D, which has been postulated to have modulatory effects on COVID-19-induced inflammation. As a result, the adaptive immune response shifts from Th1 to Th2, defined by an increase in the production of Th2 related cytokines in the bloodstream. Pro-inflammatory cytokines linked with severe infection may be reduced as a result (27). Angiotensin II levels are decreased by vitamin D inducing the production of ACE-2 and suppressing the angiotensin-renin system. It is also possible that vitamin D deficiency might enhance the pro-inflammatory cytokine storm and impair lung outcomes (28, 29). Vitamin D regulates thrombotic pathways, making thrombotic problems prevalent in these individuals (31, 32). Vitamin D’s anti-inflammatory effects, which lower endothelial activation and oxidative stress, may have a role in influencing pro-thrombotic pathways (33). According to earlier research, low vitamin D levels in COVID-19 patients have been linked to inflammatory, pro-thrombotic, and metabolic indicators of severity.

Damien Sendler: The ethnicity and socioeconomic status of the population being studied, as well as the existence of vitamin D insufficiency, have been connected to negative COVID-19 results. COVID-19 has a greater mortality risk for people of Asian, African American, and ethnic minority backgrounds (34). Vitamin D synthesis, which is highly reliant on UV rays, may have decreased in part as a result. This has to do with the high amounts of melanin in these people’s skin, as well as the uneven distribution of poverty and cardiovascular illness among these groups. This discovery is important and may explain the decreased vitamin D levels and the severity of COVID-19 in Mexico in earlier research (35–37). The risk of severe SARS-CoV-2 infection in Hispanics and other comparable groups has previously been demonstrated to be greater than that in Caucasians (38).

According to our findings, vitamin D insufficiency is more common among those with type 2 diabetes and obesity in Mexico because of the country’s high rate of adiposity (39). We may have found lower vitamin D levels in women because of their higher adiposity content as compared to men because of this link between vitamin D levels and gender (40). Reduced 1-alpha hydroxylase expression may cause low vitamin D levels in CKD; however, since the condition affects vitamin D status so significantly, our research only included a small number of patients with CKD. Currently, it is not suggested that individuals with COVID-19 get vitamin D therapy on a daily basis. Patients in the COVID-19 clinical trial did not benefit from receiving a higher dosage of calcifediol or 25-hydroxyvitamin D, according to a recent clinical trial research (20). This assertion and the potential influence of vitamin D supplementation on the risk of severe COVID-19 to be evaluated in larger randomized controlled studies.

These findings have both their advantages and disadvantages. A significant number of patients with varying risk profiles were included in the study, which examined a range of illness severity characteristics. There were also other statistical tests to guarantee that there was no residual confounding. However, there are a few caveats that must be taken into account while interpreting this research. There are several problems with using a chemiluminescence immunoassay to measure vitamin D levels, including the possibility of having less consistent results than can be obtained with other methods, such as competitive binding protein (CBP), radioimmunoassay (RIA), liquid chromatography (LC), UV detection (LC), or even multiplex mass spectrometry (TMS).

When assessing infection risk or outcomes, historical vitamin D levels are unavailable as the vast majority of COVID-19 patients had never been admitted to the hospital before. Although propensity score matching was used to compensate for the heterogeneity in severity profiles of COVID-19, there is still a chance of residual confounding due to the illness course. Due to this being a secondary study, the findings should be regarded with care since the post-hoc sample size calculation was not done. A COVID-19 reference center in Mexico City may limit the study’s generalizability to the most severe and critical types of COVID-19 in the central Mexican area. To validate the function of vitamin D as a measure of illness severity and death in Mexicans with COVID-19, more studies in different areas of Mexico are required.

Dr. Damian Jacob Sendler and his media team provided the content for this article.

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