Mycophenolate mofetil reduces disease activity and steroid dosage in Takayasu arteritis.

Mycophenolate mofetil (MMF) has recently been reported as a useful alternative immunosuppressive drug in autoimmune diseases including in Takayasu arteritis (TA). The aim of this study was to verify the efficacy and tolerability of MMF administration in controlling TA disease activity and allowing glucocorticosteroid reduction. Ten consecutive active TA patients followed at the Vasculitis Clinic were enrolled from January 2003 to 2006 and received oral MMF (2 g/day) for an average of 23.3 months. Disease activity assessed using the National Institutes of Health criteria, clinical features, and inflammatory laboratory findings were evaluated. Five patients had received at least one immunosuppressive drug before administration of MMF (four methotrexate, two azathioprine, and one chlorambucil) but had not achieved clinical and laboratory remission. The other five patients received MMF as their first immunosuppressive drug because of an important disease flare during steroid dose reduction. Clinical activity disappeared in all patients with MMF therapy, except in one patient who abandoned the study because of an important headache, attributed to the drug. Moreover, the MMF therapy allowed significant tapering of the prednisone dose in the rest of the nine patients (24.5 +/- 17.1 vs 5.8 +/- 7.8 mg/day; p = 0.0019). Reinforcing this finding, a significant reduction in inflammatory laboratory parameters, erythrocyte sedimentation rate (24.7 +/- 15.5 vs 12.8 +/- 10.8 mm/h; p = 0.036) and C-reactive protein (24.0 +/- 14.9 vs 11.2 +/- 10.7 mg/l; p = 0.0167), was observed. In summary, MMF therapy reduced clinical and laboratory parameters of TA disease activity, suggesting that this drug is a promising immunosuppressive drug, particularly in refractory cases and as a steroid-sparing agent.

Chloroquine-induced bull's eye maculopathy in rheumatoid arthritis: related to disease duration?

Chloroquine diphosphate has been used in the treatment of various rheumatic diseases, including rheumatoid arthritis. The most important of its side effects is retinopathy. If not diagnosed early, this lesion can evolve into irreversible bull's eye maculopathy and visual loss. The aim of this study was to define the outcome of chloroquine-induced maculopathy after cessation of chloroquine therapy and also to identify the risk factors involved in case of retinopathy evolution. The design of this cohort study was longitudinal and retrospective. Over the period spanning 2000 to 2005, out of 607 medical records of patients with rheumatoid arthritis followed in our Division of Rheumatology, 27 had been diagnosed with chloroquine-induced maculopathy through clinical funduscopy with pupil dilation. In all cases, there was immediate chloroquine intake cessation. After a mean time of 5 years, 16 of these patients were available for follow-up and underwent a new ophthalmologic evaluation by funduscopy, using biomicroscopy and angiofluorescein when necessary. Sequelae maculopathy were reconfirmed in all 16 cases, but progression to advanced stage (bull's eye maculopathy) was found in half of the cohort, even though chloroquine had been suspended. All patients complained of visual alterations, but without progression. Comparison between patient groups with and without bull's eye maculopathy revealed a statistically significant longer rheumatoid arthritis disease history in the former group. Also, the bull's eye group had higher dose intakes of chloroquine and over a longer period compared to the other group, but not statistically significant. This study corroborates the progression of maculopathy even after cessation of chloroquine intake, pointing out the need for careful screening in the high-risk patients. Furthermore, it indicates that duration of rheumatoid arthritis disease could be a possible factor linked to worse prognosis of chloroquine-induced maculopathy.