Rheumatoid Arthritis: Balblanc JC

Wendling D, Balblanc JC, Briançon D, Brousse A, Lohse A, Deprez P, Humbert P, Aubin F. · Rheumatology Department, CHU Jean Minjoz, Minjoz Teaching Hospital, Franche-Comté University, Boulevard Fleming, 25030 Besançon Cedex, France. · Joint Bone Spine. · Pubmed #18329935 No free full text.

Abstract: The widespread use of TNFalpha antagonists in recent years has led to the recognition of paradoxical adverse effects, defined as the onset or exacerbation of disorders that are usually improved by TNFalpha antagonists. Cutaneous psoriasis is an example, of which several cases have been reported. OBJECTIVE: To identify cases of psoriasis onset or exacerbation during TNFalpha antagonist therapy and to look for potential predictive factors. METHODS: We retrospectively reviewed cases of psoriasis onset or exacerbation during TNFalpha antagonist therapy. For each case we recorded the following data: age, sex, underlying disease, nature of the TNFalpha antagonist, effectiveness in improving the underlying disease, history of psoriasis in the patient or family, time to psoriasis development, type of psoriasis (confirmed by an experienced dermatologist), concomitant treatments, whether the TNFalpha antagonist was stopped or continued, and the outcome of the psoriasis. These data were compared to those in the literature. RESULTS: We identified 12 patients, six men and six women, with a mean age of 45.5 years. The TNFalpha antagonist was adalimumab in four patients, etanercept in six patients, and infliximab in two patients. The underlying disease was ankylosing spondylitis in six cases, rheumatoid arthritis in four, and psoriatic arthritis in two. Mean time from treatment initiation to psoriasis was 4.1 months (range, 1-15 months). A previous history of psoriasis in the patient was noted in six cases, including four of the six patients taking etanercept. TNFalpha antagonist therapy was effective on the underlying disease in 11 of the 12 patients. The drug was discontinued in five patients, of whom four experienced resolution of their psoriasis. In the remaining seven patients, the drug was continued and the skin lesions remained unchanged. Most of the patients had psoriasis vulgaris (plaque psoriasis); palmoplantar pustulosis was a feature in five patients. DISCUSSION: Over 40 cases of psoriasis onset or exacerbation during TNFalpha antagonist therapy have been reported in the literature. The prevalence of this adverse effect has been estimated at 1.5-5% of patients taking TNFalpha antagonists. The findings from our case series are consistent with data in the literature. Psoriasis is a class effect that has been reported with all the currently available TNFalpha antagonists. The skin lesions develop within the first few months of therapy. Patients with a wide range of underlying diseases can be affected. Palmoplantar pustulosis is a common feature. A previous history of psoriasis seems more common in patients who experience psoriasis onset or exacerbation during etanercept therapy (four of six patients in our study and 55% in the literature); thus, previous psoriasis may be a risk factor for psoriasis exacerbation during etanercept therapy.

Wendling D, Balblanc JC, Brousse A, Lohse A, Lehuede G, Garbuio P, Toussirot E, Auge B, Jacques D. · No affiliation provided · Ann Rheum Dis. · Pubmed #16100348 links to  free full text

This publication has no abstract.

Toussirot E, Le Huédé G, Mougin C, Balblanc JC, Bettinger D, Wendling D. · Department of Rheumatology, University Hospital Jean Minjoz, Besançon, France. · J Rheumatol. · Pubmed #12415596 No free full text.

Abstract: OBJECTIVE: To determine whether hepatitis C virus (HCV) RNA could be detected in the salivary glands of patients with both a diagnosis of Sjögren's syndrome (SS) and HCV infection. METHODS: Five patients with primary SS (European criteria) and chronically infected by HCV and 3 controls (one with primary SS without HCV infection, another with HCV infection without sicca syndrome, and a third without SS and HCV infection) were tested for the presence of HCV-RNA (using reverse transcriptase-polymerase chain reaction) in their saliva, serum, and salivary glands. RESULTS: In the patient group, HCV-RNA was detected in the serum and saliva of all cases and RNA extracted from salivary gland specimens tested positive in 3 cases. In the control group, HCV-RNA was not detected in the serum, saliva, or salivary glands from subjects without HCV infection. Only the control subject with HCV but without sicca syndrome tested positive for the presence of HCV-RNA in the serum, saliva, and salivary gland tissue. CONCLUSION: Our results showed that HCV may propagate and reside within salivary gland tissue, leading to HCV associated sialadenitis or Sjögren's-like syndrome in some cases, a phenomenon that does not seem specific. However, a direct role for HCV in the physiopathology of certain cases of primary SS is suggested.