Polyarteritis nodosa related to hepatitis B virus. A prospective study with long-term observation of 41 patients.

Extrahepatic manifestations of chronic hepatitis B.

Scleritis: Immunopathogenesis and molecular basis for therapy.

Resume Des virus, causes de vascularites Si la plupart des vascularites systemiques sont de cause inconnue, la responsabilite d’une infection virale a ete demontree de facon formelle pour certaines d’entre elles, un traitement specifique pouvant les guerir definitivement. Chaque virus incrimine rend compte d’un type particulier de vascularite. Infection par le virus de l’hepatite B (VHB) Elle est la cause de la periarterite noueuse dans 36 a 50 % des cas. La symptomatologie apparait de facon aigue, en general dans les mois suivant l’infection; elle est comparable a celle observee en l’absence d’infection par VHB. Cryoglobulinemies liees au virus de l’hepatite C (VHC) Les manifestations cliniques sont celles d’une vascularite systemique avec un tropisme plus particulier pour la peau (atteinte le plus souvent inaugurale et presque constante), les nerfs peripheriques, les glomerules. Elles surviennent assez tardivement au decours de l’infection. Vascularites associees a l’infection par le VIH (virus de l’immunodeficience humaine) Il existe un fort tropisme pour le systeme nerveux peripherique (multinevrites) et central. Au cours de l’infection aigue par le Parvovirus B19 Des lesions de vascularite ont ete parfois signalees apres la phase viremique, se limitant generalement a une ou plusieurs poussees de pupura vasculaire predominant aux membres inferieurs. Apres infection par le virus varicelle-zona Une vascularite se developpe parfois, sous la forme d’un deficit neurologique central (deficit moteur avec ou sans aphasie environ un mois apres un zona ophtalmologique), d’une atteinte de la retine, plus rarement de la peau ou des reins. Vascularites associees a l’infection par le cytomegalovirus (CMV) Survenant essentiellement chez le sujet immunodeprime, les vascularites apres infection par le CMV sont diffuses interessant surtout le tube digestif, en particulier le colon, le systeme nerveux central et la peau. Une complication rare de l’infection a HTLV1 (Human T-cell Lymphoma Virus) Une vascularite retinienne prenant volontiers la forme d’une retinite necrosante est souvent associee a une paraparesie spasmodique. Strategie therapeutique Pour de nombreuses vascularites d’origine virale, les traitements corticoides et immunosuppresseurs ne sont indiques qu’en seconde intention en cas d’echec des antiviraux et de l’association d’antiviraux et d’echanges plasmatiques.

Vascularites associées aux infections virales

OBJECTIVE: To examine polyarteritis nodosa (PAN) reports to the Vaccine Adverse Event Reporting System (VAERS) as the initial stage in investigating the hypothesis that vaccination can very rarely cause PAN. METHODS: We reviewed PAN reports submitted from 1990 through 2001 using a causal inference framework to evaluate the consistency of the reports9 clinical details with this hypothesis. We also reviewed published literature relating to the hypothesized association9s biological plausibility. RESULTS: VAERS received 25 PAN reports. Ten met our case definition for definite or possible PAN and had no alternative etiology for PAN identified. Nine of these 10 followed hepatitis B vaccine with a modal peak (4 definite cases) in time to symptom onset 2 weeks after vaccination. However, all potential triggering infections were not excluded, and identification of vaccine antigens in clinical specimens was not attempted. Also, 14 of 25 reports were European, with 11 from France. All 9 French reports with a known diagnosis date began during 1994-97, when autoimmune and rheumatologic events following hepatitis B vaccine were a focus of public concern in France. CONCLUSION: While we identified some supportive evidence, overall, current adverse event reports do not support a causal link between vaccination and PAN. Appropriate prospective evaluation of future post-vaccination PAN cases could add to current knowledge with rigorous confirmation of diagnosis, appropriate testing for possible triggering infections including polymerase chain reaction testing for latent hepatitis B infection, and an attempt to link the vaccine antigen to pathology such as by immunohistochemical staining or immune complex identification.

https://www.jrheum.org/content/jrheum/31/11/2181.full.pdf

Polyarteritis nodosa reports to the vaccine adverse event reporting system (VAERS): implications for assessment of suspected vaccine-provoked vasculitis.

We have investigated hepatitis B virus (HBV) infection in systemic necrotizing vasculitis (SNV). Our approach included the detection of the viral surface antigen (HBsAg) with a radioimmunoassay employing monoclonal anti-HBs (m-RIA); in addition, HBV DNA was looked for in serum and peripheral mononuclear blood cells. Among 28 subjects with SNV, 12 were found to be positive for HBsAg with the conventional test (p-RIA) and 7 additional subjects had anti-HBc and/or anti-HBs. From the 16 HBsAg negative individuals, 9 had HBsAg epitopes identified in serum with the m-RIA test and 1 had a low amount of circulating viral DNA. In contrast, only 1 among 6 subjects with other systemic vasculitis showed a positive test for m-RIA and HBV DNA assays; this individual had acquired HIV infection through transfusions which were also probably the source of his HBV infection. HBV DNA sequences were identified in peripheral mononuclear blood cells of 9 from the 37 tested, including 2 individuals who were HBsAg positive only with m-RIA. Therefore, our study indicates a much higher rate of HBV infection in patients with polyarteritis nodosa than previously suspected.

Latent hepatitis B virus (HBV) infection in systemic necrotizing vasculitis.

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Latent hepatitis B virus (HBV) infection in systemic necrotizing vasculitis.