Fatal streptococcal toxic shock syndrome in a patient with rheumatoid arthritis treated with etanercept.

beclomethasone inhaler with no return of symptoms. PFT 3 months after stopping all medication had returned to normal (Table 1). Eosinophils also returned to normal within 3 weeks of stopping the drug. Adalimumab is a fully human recombinant monoclonal anti-tumour necrosis factor-(anti-TNF-) antibody recently licensed for the treatment of moderate to severely active RA. Like all anti-TNF-drugs, adalimumab has recognized side-effects, increased susceptibility to infection being the most worrying. This is the only Committee on Safety of Medicines (CSM)-reported adverse event of asthma with adalimumab to date in the UK. Further information from Abbott Laboratories revealed that in the pivotal trials of adalimumab asthma has been reported as an adverse event in 0.3% of adalimumab-treated patients compared with 0.1% of placebo-treated patients. Neither treatment nor the pre-existence of asthma was recorded; however, no patient had to stop adalimumab. A possible explanation of the new onset of asthma in these patients lies in the contrasting inflammatory responses in RA compared with asthma and other allergic diseases. Among T-helper cells (Th), two opposite poles of immune responses can be distinguished based on secretion of cytokines: the Th1 cytokine pattern, with predominant secretion of interferon (IFN-BLOCKIN) and TNF-, and induction of a cellular immune response. In contrast, the Th2 cytokine pattern has predominant secretion of interleukin (IL)-4, IL-5 and IL-13 and induction of the humoral immune response. Atopic disorders show a raised level of IgE and a Th2 cytokine response [1], whilst RA is considered to be a Th1-polarized disease [1–5]. The generation of a Th2 immune response is inhibited in the presence of Th1 cytokines and vice versa [6]. Based on reciprocal inhibition of the development of Th1 and Th2 responses, it has been suggested that Th1-and Th2-polarized diseases mutually exclude one another. We hypothesize that active RA in this case produced a Th1 cytokine response, which suppressed the clinical expression of asthma. However, once the TNF-blocking drug was introduced, the Th1 response was suppressed, allowing the Th2-activated pathway to express itself clinically as asthma. This hypothesis would suggest a class effect. Indeed, asthma has been reported as an adverse event to the CSM for both infliximab and etanercept. There have been two reported cases of new onset asthma with etanercept and two exacerbations of asthma, one with each of etanercept and infliximab. Additionally, there have been another 25 cases of reported bronchospasm or wheezing, although most of these have been related …