Efficacy of rituximab in refractory and relapsing myositis with anti-JO1 antibodies: a report of two cases.

SIR, We write in response to an editorial in Rheumatology defining what is known and what remains to be learned about fatigue in RA [1]. Repping-Wuts et al. [1] recognize fatigue as a common and severe complaint, having a major impact on the quality of life in patients with RA. They emphasize that doctors often underestimate this effect and also that the issue is usually raised by patients rather than by health care professionals. We agree with this and welcome the suggestion that a more proactive approach to the identification and management of fatigue in RA is necessary. However, it is important that fatigue is not assumed to be secondary to RA in isolation. Other potentially treatable contributory conditions should be actively sought. Anaemia is frequently associated with RA and often presents with fatigue. Hypothyroidism is also common in patients with RA, usually as a result of autoimmune disease, and symptoms may include fatigue. Most rheumatologists would recognize these associations and check a full blood count and thyroid stimulating hormone in an RA patient with such symptoms. We recently investigated fatigue in our RA population by checking random cortisol levels in 50 patients who complained of excessive fatigue, and in whom anaemia and hypothyroidism had already been excluded. We performed a Synacthen test in the eight patients whose results were low (<200 nmol). This was normal, excluding hypoadrenalism, in four. Two further patients had a blunted response as a result of previous long-term oral steroid therapy producing inhibition of adrenal response. The two remaining patients had little response to ACTH, with high circulating ACTH levels and anti-adrenal antibodies. Baseline cortisol levels were 26 and 51 nmol, rising 30min after ACTH to just 112 and 120 nmol, respectively. These two patients had primary adrenal failure (Addison’s disease) of autoimmune aetiology. They subsequently responded well to physiological doses of hydrocortisone. Ethical approval for the study was provided by the Northern Regional Ethical Committee. Clearly our data do not allow any firm conclusions to be drawn about the prevalence of Addisons disease in RA. However, it is feasible that autoimmune adrenalitis may be more common in RA than in the population at large [2]. Certainly an association between Addisons disease and other chronic disorders has been demonstrated, with the authors postulating links through autoimmunity [3]. We suggest that fatigue in patients with RA, in addition to being a feature of that disease, might represent coexisting physical disorders relating to other autoimmune processes. Before assigning such symptoms to RA itself, clinicians may be well advised to check thyroid function and cortisol levels. Such a strategy should sensibly preface the introduction of oral steroids.