Low Plasma Vitamin D, A Risk Factor For COVID-19 Infection, Scientists Say

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A collaborative group of scientists have established associations of low plasma 25(OH)D with the risk of COVID-19 infection and hospitalisation.

They are from the Leumit Health Services (LHS) and the Azrieli Faculty of Medicine of Bar-Ilan University, Israel.

The scientists used the real-world data and Israeli cohort of 782 COVID-19 positive patients and 7,025 COVID-19 negative patients. They have so far identified that low plasma vitamin D level appears to be an independent risk factor for COVID-19 infection and hospitalisation.

The research was just published in The FEBS Journal.

Before now, vitamin D was recognised as an important co-factor in several physiological processes linked with bone and calcium metabolism, and also in diverse non-skeletal outcomes, including autoimmune diseases, cardiovascular diseases, type 2 diabetes, obesity and cognitive decline, and infections.

In particular, the pronounced impact of vitamin D metabolites on the immune system response, and on the development of COVID-19 infection by the novel SARS CoV-2 virus, has been previously described in a few studies worldwide.

Head of the Department of Managed Care and leading researcher of the LHS group, Dr. Eugene Merzon, says “the main finding of our study was the significant association of low plasma vitamin D level with the likelihood of COVID-19 infection among patients who were tested for COVID-19, even after adjustment for age, gender, socio-economic status and chronic, mental and physical disorders.

Head of the LHS Research Institute, Dr. Ilan Green, says “our finding is in agreement with the results of previous studies in the field. Reduced risk of acute respiratory tract infection following vitamin D supplementation has been reported.”

Adding, Merzon said, “furthermore, low vitamin D level was associated with the risk of hospitalization due to COVID-19 infection, although this association wasn’t significant after adjustment for other confounders.”

Leader of the Azrieli Faculty of Medicine research group, Dr. Milana Frenkel-Morgenstern, says “according to our analysis, persons that were COVID-19 positive were older than non-infected persons. Interestingly, the two-peak distributions for age groups were demonstrated to confer increased risk for COVID-19: around ages 25 and 50 years old.

“The first peak may be explained by high social gathering habits at the young age. The peak at age 50 years may be explained by continued social habits, in conjunction with various chronic diseases.”

LHS Chief Medical Officer, Prof. Shlomo Vinker, notes “surprisingly, chronic medical conditions, like dementia, cardiovascular disease, and chronic lung disease that were considered to be very risky in previous studies, were not found as increasing the rate of infection in our study.

“However, this finding is highly biased by the severe social contacts restrictions that were imposed on all the population during the COVID-19 outbreak. Therefore, we assume that following the Israeli Ministry of Health instructions, patients with chronic medical conditions significantly reduced their social contacts. This might indeed minimize the risk of COVID-19 infection in that group of patients.’’

Dr. Dmitry Tworowski, and Dr. Alessandro Gorohovski. from the Frenkel-Morgenstern laboratory at Bar-Ilan University’s Azrieli Faculty of Medicine, suggest that the study will have a very significant impact. “The main strength of our study is its being large, real-world, and population-based”, they explained.

Now researchers are planning to evaluate factors associated with mortality due to COVID-19 in Israel.

“We are willing to find associations to the COVID-19 clinical outcomes (for example, pre-infection glycemic control of COVID-19 patients) to make the assessment of mortality risk due to COVID-19 infection in Israel”, said Dr. Eugene Merzon.

In the meantime, the differing immune system responses of patients with COVID-19 can help predict who will experience moderate and severe consequences of the disease, according to a new study by Yale researchers published July 27 in the journal Nature.

The findings may help identify individuals at high risk of severe illness early in their hospitalization and suggest drugs to treat COVID-19.

Researchers examined 113 patients admitted to Yale-New Haven Hospital, and analyzed the varying immune system responses they exhibited during their hospital stay, from admittance to discharge or death.

They found that all patients shared a common COVID-19 “signature” in immune system activity early in the course of the disease. But those who experienced only moderate symptoms exhibited diminishing immune system responses and viral load over time.

Patients who went on to develop severe cases of the disease showed no decrease in viral load or immune system reaction, and many of the immune signals in these patients accelerated.

But even in the early course of treatment, researchers found indicators that predicted which patients were at greatest risk of developing severe forms of the illness.

“We were able to pull out signatures of disease risk”, said senior author Akiko Iwasaki, the Waldemar Von Zedtwitz Professor of Immunobiology and Molecular, Cellular and Developmental Biology and investigator for the Howard Hughes Medical Institute.

Researchers had known that the immune system unleashed a massive and damaging “cytokine storm” in severe cases of COVID-19. But the specific elements of the immune system response most responsible for the damage were unknown.

The Yale analysis found some intriguing links to poor outcomes. Curiously, researchers said, one risk factor was the presence of alpha interferon, a cytokine mobilized to combat viral pathogens such as the flu virus. However, COVID-19 patients with high levels of alpha interferon fared worse than those with low levels.

“This virus just doesn’t seem to care about alpha-interferon,” Iwasaki said. “The cytokine appears to be hurting, not helping.”

Another early prognosticator of poor outcomes is the activation of the inflammasome, a complex of proteins that detects pathogens and triggers an inflammatory response to infection. Inflammasome activation was linked to poor outcomes and death in several patients.

Researchers found that people who respond better to the infection tend to express high levels of growth factors, a type of cytokine that repairs issue damage to the linings of blood vessels and lungs.

Taken together, the data can help predict patients at high risk of poor outcomes, the authors said.

They also said drugs that target specific causes of inflammation identified in the study could help treat patients at risk of developing severe cases of COVID-19.

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