Tânia Santiago

Safety of low- to medium-dose glucocorticoid treatment in rheumatoid arthritis: myths and reality over the years

Low‐ to medium‐dose glucocorticoids have been shown to have not only anti‐inflammatory but also disease‐modifying properties in rheumatoid arthritis. The evidence for the benefit of its early use in combination with disease‐modifying antirheumatic drugs underlines the need for a close evaluation of their risk–benefit ratio. Over time, numerous myths and fears about glucocorticoid toxicity in rheumatoid arthritis have arisen from observational studies, and many concerns have been unduly extrapolated from observations with higher‐dose treatment. Furthermore, we cannot exclude the possibility of a powerful effect of bias by indication in these studies. Low‐ to medium‐dose glucocorticoid regimens continued to be evaluated in randomized clinical trials, particularly in early disease, but these studies also have relevant methodological limitations in assessing safety, particularly due to small size and/or short duration. At present, the evidence on which to support clear recommendations about glucocorticoid toxicity remains remarkably weak. A large prospective pragmatic trial dedicated to the toxicity of low‐dose glucocorticoids is dearly needed. Meanwhile, adherence to recommendations on standardized methodologies for registration and report of glucocorticoid adverse events is essential for improving our knowledge and competence in the best management of these important medications.

Safety of Glucocorticoids in Rheumatoid Arthritis: Evidence from Recent Clinical Trials

Glucocorticoids are one of the most effective treatments for rheumatoid arthritis, with well-established efficacy in controlling the disease symptoms and structural progression. Fears regarding their toxicity are reflected in common recommendations for the use of the lowest possible dose for the shortest possible time. We herein review toxicity data obtained in randomized clinical trials of low-dose glucocorticoid in rheumatoid arthritis, given that observational studies cannot guarantee the avoidance of bias by indication. Seven eligible randomized controlled trials were identified. These publications do not identify any strong signal of relevant toxicity of glucocorticoid in doses of up to 10 mg of prednisone equivalent/day for up to 2 years. However, the quantity (1,100 patient years of exposure) and especially the quality of evidence are too limited to establish conclusions. A large prospective trial dedicated to the toxicity of low-dose glucocorticoid is dearly needed. Meanwhile, adherence to recommendations on standardized methodologies for the registration and report of glucocorticoid adverse events is essential to improve our knowledge and competence in the best management of these important medications.

A case of infliximab-induced lupus in a patient with ankylosing spondylitis: is it safe switch to another anti-TNF-α agent?

Anti-TNF-α therapies are the latest class of medications found to be associated with drug-induced lupus, a distinctive entity known as anti-TNF-α-induced lupus (ATIL) (Williams et al., Rheumatology (Oxford) 48:716–20, 2009; De Rycke et al., Lupus 14:931–7, 2005; De Bandt et al., Clin Rheumatol 22:56–61, 2003). With the widespread use of these agents, it is likely that the incidence of ATIL will increase. The onset of ATIL in patients with rheumatoid arthritis and Crohns disease has been described, but the literature regarding the occurrence of this entity in patients with ankylosing spondylitis (AS) is scarce (De Bandt et al., Clin Rheumatol 22:56–61, 2003; Ramos-Casals et al., Autoimmun Rev 9:188–93, 2010; Perez-Garcia et al., Rheumatology 45:114–116, 2006). To our knowledge, few reports of switching anti-TNF-α therapy after ATIL in AS have been reported (Akgül et al., Rheumatol Int, 2012). Therefore, it is not clear whether the development of ATIL should prohibit switch to another therapy, since patients may respond to another anti-TNF-α agent (Akgül et al., Rheumatol Int, 2012; Bodur et al., Rheumatol Int 29:451–454, 2009; Mounach et al., Clin Exp Rheumatol 26:1116–8, 2008; Williams and Cohen, Int J Dermatol 50:619–625, 2011; Ye et al., J Rheumatol 38:1216, 2011; Wetter and Davis, Mayo Clin Proc 84:979–984, 2009; Cush, Clin Exp Rheumatol 22:S141–147, 2004; Kocharla and Mongey, Lupus 18:169–7, 2009). A lack of published experience of successful anti-TNF-α switching is a cause of concern for rheumatologists faced with this challenging clinical scenario. We report the case of a 69-year-old woman with AS who developed infliximab-induced lupus, which did not recur despite the subsequent institution of etanercept. The authors review and discuss ATIL and the possible implications for subsequent treatment with alternative anti-TNF-α agents.

The many faces of IgG4-related disease: report of a case with inaugural recurrent aortic aneurism ruptures and literature review

Vascular involvement in IgG4-related disease (IgG4-RD), is a well-recognized feature and large vessel commitment, especially the aorta, can be the only manifestation of the disease. Being a newly recognized disease, its diagnosis and workup still represents a challenge in clinical practice. A 47-year-old-man with two aortic aneurysms ruptures, one at abdominal and the other at thoracic level, was referred to our rheumatology department. The initial analysis of the surgical specimen obtained 3xa0years earlier revealed a nonspecific aortitis. Re-evaluation of the biopsy with immunohistology now demonstrated the presence of IgG4 deposits. Evidence-based recommendations regarding diagnosis, treatment and follow-up of IgG4-related large-vessel involvement are lacking. In this particular case, histopathology were crucial. The authors review and discuss vascular involvement in IgG4-RD and respective treatment options.

Milwaukee shoulder (and knee) syndrome

An 80-year-old woman presented with a 1-month history of bilateral shoulder pain and swelling (figure 1). There was no history of any trauma. Physical examination showed limited and painful active and passive range of motion of the shoulders and a valgus deformity of the knees. Anteroposterior X-rays of the shoulders and knees were performed (figure 2). Shoulder ultrasound revealed exuberant subacromial bursitis (figure 3) associated with complete rotator cuff tear bilaterally. Bursa aspiration yielded a haemorrhagic non-inflammatory fluid and hydroxyapatite crystals were identified with alizarin red staining (figure 4). Synovial fluid culture was …