Feelings of guilt and shame in patients with rheumatoid arthritis.

This study aims to determine whether patients with rheumatoid arthritis (RA) experience more general feelings of guilt and shame than their peers without RA and to examine possible correlates of guilt and shame in RA. In a cross-sectional survey study, 85 out-patients with RA (77 % female; median disease duration, 11 years) and 59 peer controls completed the Experience of Shame Scale (ESS) and the Test of Self-Conscious Affect (TOSCA). Patients additionally completed measures of health status, self-efficacy, cognitive emotion regulation, and numerical rating scales for life satisfaction and happiness. Patients and peer controls were well matched for sociodemographic characteristics. No significant differences between patients and controls were found for guilt or different types of shame as measured with the TOSCA or ESS. In multivariate analyses, female patients reported more feelings of bodily shame and higher guilt proneness, while younger patients reported more character and bodily shame. Worse social functioning and more self-blaming coping strategies were the strongest independent correlates of shame. Shame proneness was only independently associated with more self-blame, whereas guilt proneness was only associated with female sex. None of the physical aspects of the disease, including pain and physical functioning, correlated with feelings of guilt and shame. Patients with longstanding RA do not experience more general feelings of shame or guilt than their peers without RA. Shame and guilt in RA is primarily associated with demographic and psychosocial characteristics and not with physical severity of the disease.

Prevalence of methotrexate intolerance in rheumatoid arthritis and psoriatic arthritis.

INTRODUCTION: The aim of this study was to determine the prevalence of gastrointestinal and behavioural symptoms occurring before (anticipatory/associative) and after methotrexate (MTX) administration, termed MTX intolerance, in rheumatoid (RA) and psoriatic arthritis (PsA). METHODS: Methotrexate Intolerance Severity Score (MISS), previously validated in juvenile idiopathic arthritis patients, was used to determine MTX intolerance prevalence in 291 RA/PsA patients. The MISS consisted of four domains: abdominal pain, nausea, vomiting and behavioural symptoms, occurring upon, prior to (anticipatory) and when thinking of MTX (associative). MTX intolerance was defined as ≥6 on the MISS with ≥1 point on anticipatory and/or associative and/or behavioural items. RESULTS: A total of 123 patients (42.3%) experienced at least one gastrointestinal adverse effect. The prevalence of MTX intolerance was 11%. MTX intolerance prevalence was higher in patients on parenteral (20.6%) than on oral MTX (6.2%) (p < 0.001). CONCLUSION: Besides well-known gastrointestinal symptoms after MTX, RA and PsA patients experienced these symptoms also before MTX intake. RA and PsA patients on MTX should be closely monitored with the MISS for early detection of MTX intolerance, in order to intervene timely and avoid discontinuation of an effective treatment.

Clinical efficacy of leflunomide in primary Sjogren's syndrome is associated with regulation of T-cell activity and upregulation of IL-7 receptor α expression.

OBJECTIVES: To investigate whether the immunomodulatory capacities of leflunomide are associated with clinical efficacy in the treatment of primary Sjögren's syndrome (SS) in a phase II pilot study. METHODS: Peripheral blood mononuclear cells from 13 primary SS patients were obtained at baseline and after 24 weeks of leflunomide treatment. Ex-vivo production of interleukin (IL) 1ß and tumour necrosis factor α (TNFα) and of interferon (IFN), IL-4, as well as TNFα ELISA measured production on T-cell and monocyte stimulation. In addition, the authors investigated the ability of leflunomide to influence systemic levels of inflammatory cytokines, as well as T-cell activation markers and the expression of IL-7 receptor α by flow cytometry. Correlations between changes in cytokine levels and changes in clinical response parameters were studied. RESULTS: Ex-vivo production of IL-1ß and TNFα was decreased at 24 weeks in the whole patient group, whereas IFN and IL-4 production were not significantly changed. However, a significant decrease in T-cell-stimulated IFN and TNFα production was observed in clinical responders, but not in non-responders. Moreover, significant correlations were found between increased sialometry values and decreased IFN and TNFα production. In addition, leflunomide reduced levels of inflammatory serum cytokines and CD40L expression, whereas it upregulated IL-7Rα expression on CD4 T cells with persistent serum IL-7 concentrations. CONCLUSIONS: Leflunomide treatment suppressed cytokine release from circulating immune cells. Inhibition of T-helper 1 cell cytokine production was related to clinical efficacy. This suggests that selective T-cell targeting might be a relevant therapeutic strategy in primary SS, possibly enhancing clinical efficacy and safety.