Development of active tuberculosis in patients treated with biological disease-modifying antirheumatic drugs
Biological disease-modifying antirheumatic drugs (bDMARDs) have been shown to be highly effective in the treatment of immunemediated inflammatory arthritides such as rheumatoid arthritis (RA), psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA). However, their use has been limited by cost and the risk of opportunistic infections. This type of therapy is therefore reserved for patients who have failed treatment with conventional synthetic disease-modifying antirheumatic drugs (sDMARDs). bDMARDs are classified according to their molecular target. Although the mechanism of action will vary accordingly, a common way of grouping bDMARDs has been to divide them into tumour necrosis factor alpha (TNF-α) inhibitors and non-TNF-α inhibitors. TNF-α is a key inflammatory cytokine in the immunopathogenesis of RA and various other rheumatic conditions. However, it also plays an important role in the containment and elimination of Mycobacterium tuberculosis. Tuberculosis (TB) is therefore of particular concern among patients receiving TNF-α inhibitors, a premise supported by several reports of increased risk of active TB among patients receiving TNF-α inhibitors v. those receiving non-TNF-α-inhibiting bDMARDs. Furthermore, within the class of TNF-α inhibitors, the monoclonal antibodies infliximab, adalimumab and golimumab have been found to carry a slightly higher risk of TB than the dimeric receptor fusion protein, etanercept. Initially, TNF-α inhibitors were the only type of bDMARD available for treatment of PsA and axSpA, whereas bDMARDs for the treatment of RA included both TNF-α-inhibitor and non-TNF-α-inhibitor options.
Prolonged SARS-CoV-2 RNA shedding in a young man recovering from traumatic pneumothorax
RNA shedding and viral load kinetics of SARS-CoV-2, the causative agent of COVID-19, remain incompletely understood. The duration of RNA shedding in respiratory samples has been reported as a median of ~18 days, but shedding is heterogeneous and can occur up to 92 days after symptom onset, in what can be termed prolonged RNA shedding. A concise definition of prolonged SARS-CoV-2 RNA shedding remains lacking in the current literature. Some authors define it as detectable RNA shedding ≥14 days after the onset of symptoms or after the first positive real-time reverse transcription polymerase chain reaction (RT-PCR) result, while others use the median duration of viral RNA shedding in study populations as a cutoff above which shedding is considered prolonged. Although inadequately characterised, prolonged SARS-CoV-2 RNA shedding is not uncommon; there are increasing reports of persistent virus shedding in respiratory samples despite symptom resolution, positive tests after two consecutive negative SARS-CoV-2 molecular tests, and shedding in stool despite respiratory samples testing negative.
COVID-19 constrictive pericarditis
The vast majority of patients infected by the SARS-CoV-2 virus experience upper respiratory symptoms, headache, myalgia and fatigue. However, the virus is able to affect a vast array of organs, and the cardiovascular system is no exception. Several cases of pericarditis have been reported as a result of COVID-19. We report a case of constrictive pericarditis following SARS-CoV-2 infection.
Health Professions Council of South Africa
Attempts allowed: 2
70% pass rate
South African Medical Journal - February 2022 Vol 112 No 2