J Rheumatol

Temporal arteritis symptoms in a patient with hepatitis C virus associated type II cryoglobulinemia and small vessel vasculitis.

Genereau T. Martin A. Lortholary O. Noel V. Guillevin L.
Department of Internal Medicine, Hopital Avicenne, Paris, France. med.int.genereau@lsol.tm.fr
We describe temporal artery localization of hepatitic C virus related cryoglobulin induced vasculitis in a 66-year-old woman. The patient had features of both cryoglobulin induced vasculitis (palpable purpura, arthralgia, hypocomplementemia, no inflammatory syndrome) and temporal arteritis (recent onset of headaches, jaw claudication). In the temporal artery biopsy, the vasculitis was localized to a small adventitial artery and did not involve the superficial temporal artery. Thus temporal arteritis and jaw claudication can be signs of cryoglobulin induced vasculitis.

High seroprevalence of Helicobacter pylori infection in patients with systemic sclerosis: association with esophageal involvement.

Year 1998
Yazawa N. Fujimoto M. Kikuchi K. Kubo M. Ihn H. Sato S. Tamaki T. Tamaki K.
Department of Dermatology, Faculty of Medicine, Tokyo University, Japan.
OBJECTIVE: To determine the prevalence and clinical relevance of Helicobacter pylori infection in patients with systemic sclerosis (SSc). METHODS: Serum samples were obtained from 124 patients with SSc (67 with limited cutaneous SSc, 57 with diffuse cutaneous SSc). Fifty samples from age and sex matched individuals were used as controls. IgG antibodies to H. pylori infection were measured by ELISA. RESULTS: IgG antibodies to H. pylori were found in 55.6% (69 of 124) of the patients with SSc, significantly more than in the controls. There was a significant correlation of the presence of antibodies to H. pylori with the prevalence of esophageal hypomotility in the patients with SSc (p < 0.02). CONCLUSION: Patients with SSc have H. pylori infection at a higher prevalence than the general population. H. pylori might play a role in the development of esophageal dysfunction in SSc.

A close temporal relationship of liver disease to antiribosomal P0 protein antibodies and central nervous system disease in patients with systemic lupus erythematosus.

Year 1998
Yoshio T. Masuyama JI. Minota S. Kaneko N. Iwamoto M. Okazaki H. Mimori A. Takeda A. Kano S.
Department of Medicine, Jichi Medical School, Japan.
OBJECTIVE: To determine whether there is a close temporal relationship of liver disease to serum IgG and/or IgM antiribosomal P0 protein antibodies (anti-P0) and central nervous system (CNS) lupus in patients with systemic lupus erythematosus (SLE). METHODS: The study included 70 patients with active SLE. Of these, 30 had IgG and/or IgM anti-P0 and 14 had CNS lupus other than psychiatric disease (nonpsychiatric CNS lupus). Of these 14 patients, 11 had anti-P0. Laboratory manifestations of liver disease were retrospectively analyzed. RESULTS: Liver disease not attributed to any cause other than SLE (SLE liver disease) was present in 8 of the 11 patients with anti-P0 with nonpsychiatric CNS lupus (72.7%), in none of the 19 patients with anti-P0 without nonpsychiatric CNS lupus (0%), and in one of the 40 patients without anti-P0 (2.5%). The prevalence of SLE liver disease was significantly greater in patients with anti-P0 with nonpsychiatric CNS lupus than in the other 2 groups (p < 0.0001). Mean levels of liver enzymes (lactate dehydrogenase, glutamic oxaloacetic transaminase, glutamate pyruvate transaminase, gammaglutamyl transpeptidase) were significantly higher in patients with anti-P0 with nonpsychiatric CNS lupus than in the other 2 groups. Serial studies in 3 patients showed that the appearance of anti-P0 and liver dysfunction slightly preceded the onset of nonpsychiatric CNS lupus. CONCLUSION: Anti-P0 may be related to the pathogenesis of CNS lupus and SLE liver disease found simultaneously in SLE. The appearance of anti-P0 and liver dysfunction may predict onset of CNS lupus.

Corticosteroids and systemic lupus erythematosus pancreatitis: a case series.

Year 1998
Saab S. Corr MP. Weisman MH.
Department of Medicine, University of California, San Diego Medical Center, 92103-8418, USA.
OBJECTIVE: To determine whether (1) corticosteroids cause pancreatitis in patients with systemic lupus erythematosus (SLE); (2) SLE pancreatitis occurs in the setting of a generalized SLE flare; and (3) corticosteroids can be used to treat SLE pancreatitis. METHODS: A total of 8 patients over a 10 year period with pancreatitis and SLE were identified retrospectively from a hospital database at the University of California San Diego Medical Center. RESULTS: All 8 patients received therapeutic doses of corticosteroids as part of their treatment for SLE and pancreatitis. All patients manifested both clinical and biochemical resolution of their pancreatitis with the administration of corticosteroids. No patient in our study experienced immediate complications related to corticosteroids. Only 2 of the 8 patients manifested active concurrent systemic disease related to the SLE. CONCLUSION: Corticosteroids do not cause pancreatitis in patients with SLE, and they should be administered during episodes of acute pancreatitis if clinically necessary. Pancreatitis does not tend to occur in the setting of a generalized SLE flare.

Ribavirin in hepatitis C related cryoglobulinemia.

Year 1998
Durand JM. Cacoub P. Lunel-Fabiani F. Cosserat J. Cretel E. Kaplanski G. Frances C. Bletry O. Soubeyrand J. Godeau P.
Department of Internal Medicine, CHU Sainte Marguerite, Marseille, France.
OBJECTIVE: An open, uncontrolled trial of ribavirin, an oral guanosine nucleoside analog for treatment of hepatitis C, in patients with hepatitis C virus (HCV) associated cryoglobulinemia intolerant to interferon. METHODS: Five patients with cryoglobulinemia related to HCV infection unresponsive to interferon therapy received oral ribavirin (100 to 1200 mg daily) for 10 to 36 months. RESULTS: Patients treated with ribavirin had prompt decrease in serum aminotransferase levels and marked improvement of manifestations of cryoglobulinemia within a few weeks. Ribavirin did not eradicate HCV RNA from the sera, but a decrease in viral load was observed in 3 patients, from 232 to 86 x 10(5) copies HCV/ml. Relapse occurred within 3 months once therapy was discontinued. The drug was well tolerated, but mild dose related hemolysis was common. CONCLUSION: Ribavirin monotherapy may be effective in patients with symptomatic cryoglobulinemia related to HCV infection, but this effect is not sustained when ribavirin therapy is discontinued.