ABSTRACT
Background: Coronavirus disease 2019 (COVID-19) infection is linked to high levels of inflammatory cytokines and prolonged immobilization;furthermore, corticosteroid treatment leads to increased bone loss and resorption. We aimed to study the change in bone mineral density (BMD) after COVID-19 infection in osteoporotic and osteopenic patients. One hundred osteoporotic or osteopenic patients were selected in this single-center retrospective study;the patients were divided into two groups. Group 1 included 56 patients who got COVID-19 infection. Group 2 included 44 patients who did not get COVID-19 infection. BMD was assessed at baseline, after 9 months of COVID infection, and then after 1 year follow-up using dual energy x-ray absorptiometry (DXA) scan. Results: There was no significant difference between two groups regarding demographic data (p > 0.05);there was a significant decrease in BMD of the lumbar region and femur at 9 months as compared to baseline in group1 (p < 0.001), while there was a significant increase in the lumbar BMD of osteoporotic patients who did not get COVID infection after 21 months. Concerning activity of COVID infection, there was a significant difference between the three subgroups of COVID patients regarding percentage of change in BMD after 9 months, the severe group having the highest decrease in BMD (p < 0.001). Conclusions: COVID-19 may have deleterious effect on BMD in osteoporotic patients. It is recommended to assess BMD in osteoporotic/osteopenic patients who got COVID infection to detect if there is an increased risk of fracture which may necessitate post-COVID change in the therapeutic intervention plan. Supplementary Information: The online version contains supplementary material available at 10.1186/s43166-022-00165-7.
ABSTRACT
Background Thrombotic consequences have been reported in COVID-19-infected patients, especially those who are critically ill. Multiple studies have tested antiphospholipid antibodies (aPLs) among COVID-19 patients, but to date, the actual frequency of aPLs is still uncharted. In this cohort study, we analyzed the outcomes of 173 consecutive patients with confirmed COVID-19 infection. Anti-phospholipid antibodies, which include anti-cardiolipin antibodies [aCL (IgM), aCL (IgG)], and B2-glycoprotein I antibodies [a beta 2GPI (IgM), a beta 2GPI (IgG)] were detected by using immunoassays. In contrast, lupus anti-coagulant (LAC) antibodies are identified through a coagulation-based assay. Results The study demonstrated a high incidence of thrombotic consequences in severe COVID pneumonia cases and supported an increased risk of developing aPLs following COVID-19 infection. Pulmonary embolism had the most common prevalence of all thrombotic events. Among the various aPLs tested in thrombotic patients, lupus anti-coagulant (LAC) had the highest positivity (46.2%). Most patients with arterial thromboembolism (stroke, myocardial infarction, limb ischemia, bowel ischemia, and renal artery thrombosis) had triple positivity of anti-phospholipid antibodies. Testing aPLs antibodies after 12 weeks of recovery for survived patients only 2 out of 23 patients had aPLs positivity compared to 35 out of 65 tested during hospital admission. Furthermore, we found no significant changes in aPLs positivity between survived and non-survived patients with thrombotic event. Conclusions aPLs increased transiently as an inflammatory-mediated condition. Individuals with aPLs triple positivity (positive LAC, aCL, and aB2GPI) had a considerable risk of arterial thromboembolism (ATE).