Indeed, the 2013 update of EULAR recommendations for management of RA emphasized the role of conventional DMARDs and stated a number of key issues to favourable outcomes including early commencement of MTX after RA is diagnosed, close monitoring of disease activity every 1–3 month and adjustment of treatment regimen if no improvement selleck compound is observed at 3 months or if failure to meet a target of low disease activity or remission in 6 months of methotrexate based conventional DMARD regimen. This is followed by the use of any biologic agent (first
line rituximab in special conditions) with MTX as the anchor drug in the treatment algorithm for patients who have poor prognostic factors like high disease load, positive rheumatoid factor or anti-citrullinated peptide antibody and early erosive disease.[6] In this issue of IJRD, Alten R and van den Bosch F conducted a literature review to evaluate the effect of dose optimization on clinical response in infliximab-treated RA patients and
observed a trend of improvement after dose increase among small number of studies of different study design. While increase in dose or reduction in infusion interval may benefit some patients who have inadequate response and those who subsequently lose response to this TNF inhibitor, a balance between efficacy and risk of high dose biologics and the heterogeneity of pathophysiology of RA are find more important issues to be considered in the management of RA patients on biologic based regimen. Up to this point in time, a few recent studies
have suggested a potential role of biologics as induction therapy to achieve clinical remission in patients with early RA. This finding has not been confirmed in other studies which found high relapse rates upon withdrawal of biologics. Before clear evidences are there, RA patients with active disease are likely to benefit as much from early aggressive treatment with combinational conventional DMARD based regimen targeting tight disease control Megestrol Acetate as biologic therapy. “
“Primary Sjögren syndrome (SS) is a connective tissue disease which may involve the musculoskeletal system in addition to autoimmune epithelitis in the exocrine glands.[1] Peyronie’s disease is a localized fibrotic disease of the penis which involves the outer part of corpus cavernosum.[2] Although its etiology is not clear, it takes place among localized fibrotic diseases. Coexistance of Peyronie’s disease with certain connective tissue diseases (i.e., systemic sclerosis) has been reported.[3] Attempts have been made to explained this by local collagen accumulation. The present report introduces primary Sjögren’s syndrome coexisting with Peyronie’s disease.