AbstractThe coronavirus disease 2019 (COVID‐19) has various presentations, of which immune dysregulation or the so‐called cytokine storm syndrome (COVID‐CSS) is prominent. Even though cytokines are vital regulators of body immunoinflammatory responses, their exaggerated release can be harmful. This hyperinflammatory response is more commonly observed during severe COVID‐19 infections, caused by the excessive release of pro‐inflammatory cytokines, such as interleukin‐1 (IL‐1), IL‐6, IL‐8, tumour necrosis factor, granulocyte‐macrophage colony‐stimulating factor, and interferon‐gamma, making their blockers and antagonists of great interest as therapeutic options in this condition. Thus, the pathophysiology of excessive cytokine secretion is outlined, and their most important blockers and antagonists are discussed, mainly focussing on tocilizumab, an interleukin‐6 receptor blocker approved to treat severe COVID‐19 infections.
Coronavirus disease 2019 (Covid‐19) vaccination recommendations in special populations and patients with existing comorbidities
SummaryVaccination against severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is a crucial step in ending the current worldwide pandemic. However, several particularly vulnerable groups in the population were not included in sufficient numbers in coronavirus disease 2019 (Covid‐19) vaccine trials. Therefore, as science advances, the advice for vaccinating these special populations against Covid‐19 will continue to evolve. This focused review provides the latest recommendations and considerations for these special populations (i.e., patients with rheumatologic and autoimmune disorders, cancer, transplant recipients, chronic liver diseases, end‐stage renal disease, neurologic disorders, psychiatric disorders, diabetes mellitus, obesity, cardiovascular diseases, chronic obstructive pulmonary disease, human immunodeficiency virus, current smokers, pregnant and breastfeeding women, the elderly, children, and patients with allergic reactions) using the currently available research evidence.