COVID-19: Type O blood linked to lower risk, taking Vitamin D unlikely to help

A large study adds to evidence that people with type O or Rh−negative blood may be at slightly lower risk from the new coronavirus.

Among 225,556 Canadians who were tested for the virus, the risk for a COVID-19 diagnosis was 12% lower and the risk for severe COVID-19 or death was 13% lower in people with blood group O versus those with A, AB, or B, researchers reported on Tuesday in Annals of Internal Medicine.

People in any blood group who were Rh-negative were also somewhat protected, especially if they had O-negative blood.

People in these blood type groups may have developed antibodies that can recognize some aspect of the new virus, coauthor Dr. Joel Ray of St. Michael's Hospital in Toronto told Reuters.

"Our next study will specifically look at such antibodies, and whether they explain the protective effect," Ray said. Whether or how this information might influence COVID-19 prevention or treatment is still unclear.

Low levels of vitamin D have been linked to higher risk for severe COVID-19, but high vitamin D levels do not fix the problem. Increasing vitamin D levels in critically ill patients did not shorten their hospital stay or lower their odds of being moved to intensive care, needing mechanical ventilation, or dying, doctors in Brazil found.

They randomly gave 240 patients hospitalized with severe COVID-19 either a single high dose of vitamin D3 or a placebo.

Only 6.7% of patients in the vitamin D group had "deficient" levels of the nutrient, compared to 51.5% of patients in the placebo group, but there was no difference in the outcomes, according to a paper posted on medRxiv ahead of peer review.

The same was true when the researchers focused on the 116 patients with vitamin D deficiency before the treatment.

The authors say theirs is the first randomized trial of its kind to show that vitamin D supplementation "is ineffective to improve hospital length of stay or any other clinical outcomes among hospitalized patients with severe COVID-19."

A form of inflammatory cell death called panoptosis triggers the storm of cytokines, or inflammatory proteins, that causes critical illness in COVID-19, researchers say.

During panoptosis, "cells spew out their contents instead of neatly packaging them away" as happens during routine cell death, Thirumala-Devi Kanneganti of St. Jude Children's Research Hospital told Reuters.

Neighboring cells see the debris, including cytokines, as a sign of danger, and respond by secreting more cytokines, allowing the cytokine storm to build, said Kanneganti.

Her team identified a synergy between two cytokines, TNF-alpha and IFN-gamma, as the cause of panoptosis in COVID-19. Mice given TNF-alpha and IFN-gamma developed the symptoms and organ damage of COVID-19 and died rapidly, Kanneganti said.

Treatment with antibodies that neutralize these two cytokines protected the mice from death, not just from COVID-19 but also from other life-threatening illnesses involving cytokine storms, such as sepsis, her team reported in Cell.

Trials are needed to test these treatments in humans, Kanneganti said.

COVID-19 survivors benefit from home health care after being discharged from hospital, new data show. Researchers from the Visiting Nurse Service of New York, the University of Pennsylvania, and Villanova University studied 1,409 patients who received home health care, nearly half of whom were under age 65.

When they were discharged, 80% were still short of breath, most reported anxiety or confusion, and more than 80% needed help walking, dressing, and bathing.

After an average of 32 days of home health care, 94% no longer needed the service. The vast majority were not completely recovered, but most symptoms were significantly improved, as was the patients' ability to perform daily activities. Only 10% needed to be rehospitalised, the researchers reported on Tuesday in Annals of Internal Medicine.