No abstract

These results suggest that physical disability, helplessness and passive coping have a significant impact on the levels of pain and depression experienced by RA patients.

Tumour necrosis factor‐alpha (TNF‐α) antagonists have advanced the treatment of inflammatory arthropathies, and are even considered for use in refractory sarcoidosis with some success. Paradoxically, cases of new onset sarcoidosis‐like diseases are increasingly reported in patients receiving TNF‐α antagonists. Here, we report three cases of sarcoid‐like granulomatosis that developed during treatment with TNF‐α antagonists. Review of the Biologics clinic data base at Westmead, Sydney, Australia identified three patients whom, during anti‐TNF therapy, developed non‐caseating granulomas consistent with sarcoidosis. These three cases are described with review of the literature from 2000 to 2009 using PubMed. One hundred and sixty‐nine patients within our data base were reviewed for the period 2003–2009. Sarcoidosis‐like granulomas developed in three patients within a period of 3 to 36 months of treatment with etanercept and/or adalimumab. All cases demonstrated non‐infective, non‐caseating granulomas on renal or lymph node biopsy. Improvement was seen in two cases upon cessation of TNF‐α antagonist and steroid therapy. Interestingly, clinical deterioration was noted upon re‐challenge with the same TNF‐α antagonist in one patient. To date, a total of 37 cases of sarcoid‐like granuloma development after anti‐TNF therapy have been reported in the literature. Development of sarcoidosis‐like granulomatosis in patients treated with TNF‐α antagonists is a phenomenon previously under‐recognised. All three anti‐TNF agents have been observed to cause this phenomenon, suggesting a ‘class effect’ rather than being drug specific.

Objectives To quantify circulating fibroblast activation protein (cFAP) and dipeptidyl peptidase 4 (cDPP4) protease activities in patients with rheumatoid arthritis (RA), systemic sclerosis (SSc), and a control group with mechanical back pain and to correlate plasma levels with disease characteristics. Methods Plasma was collected from patients with RA (n=73), SSc (n=37) and control subjects (n=26). DPP4 and FAP were quantified using specific enzyme activity assays. Results Median cDPP4 was significantly lower in the RA group (p=0.02), and SSc group (p=0.002) compared with controls. There were no significant differences in median cFAP between the three groups. DPP4 and FAP demonstrated a negative correlation with inflammatory markers and duration of disease. There were no associations with disease subtypes in RA, including seropositive and erosive disease. Decreased cDPP4 was found in SSc patients with myositis. Plasma FAP was lower in RA patients receiving prednisone (p=0.001) or leflunomide (p=0.04), but higher with biologic agents (p=0.01). RA patients receiving leflunomide also had decreased cDPP4 (p=0.014). SSc patients receiving prednisone (p=0.02) had lower cDPP4 but there was no association with cFAP. Conclusions No association was found between cFAP and RA or SSc. Plasma DPP4 was decreased in RA and SSc when compared with controls. cDPP4 and cFAP correlated negatively with inflammatory markers and there were no significant correlations with disease characteristics in this RA cohort.

Secondary screening and treatment of osteoporosis in patients following minimal-trauma fracture are low. The implementation of a clinical pathway for osteoporosis management in these patients may be useful.