Thalidomide combined with short-term low-dose glucocorticoid therapy for the treatment of severe COVID-19: A case-series study.

• Thalidomide significantly accelerated the negative conversion of SARS-CoV-2 and shortened the hospital stay length of affected patients. • Thalidomide reduced the requirement for mechanical ventilation in patients with critical COVID-19. • Combination therapy of thalidomide plus low dose glucocorticoid was effective in improving the prognosis of patients with critical COVID-19. • The mechanism of action is most likely inhibition of inflammatory cytokine production. The aim was to evaluate the safety and effectiveness of thalidomide, an immunomodulatory agent, in combination with glucocorticoid, for the treatment of COVID-19 patients with life-threatening symptoms. A nonrandomized comparative case series study was performed. Six patients received thalidomide 100 mg per day (with therapy lasting for ≥7 days) plus low-dose short-term dexamethasone, and 6 control patients matched with patients in the thalidomide group, received low-dose short-term treatment with dexamethasone alone. The main outcomes were: the duration of SARS-CoV-2 negative conversion from admission; length of hospital stay; and changes in inflammatory cytokine concentrations and lymphocyte subsets. The median thalidomide treatment time was 12.0 days. The median duration of SARS-CoV-2 negative conversion from admission and hospital stay length were briefer in the thalidomide group compared to the control group (respectively, 11.0 vs 23.0 days, P = 0.043; 18.5 vs 30.0 days, P = 0.043). The mean reduction rates at 7–10 days after treatment for serum interleukin-6 and interferon-γ concentrations were greater in the thalidomide group compared to the control group. Alterations in lymphocyte numbers in the subsets between the 2 groups were similar. Thalidomide plus short-term glucocorticoid therapy is an effective and safe regimen for the treatment of severely ill COVID-19 patients. The mechanism of action is most likely inhibition of inflammatory cytokine production. [ABSTRACT FROM AUTHOR]