Hepatitis C virus–associated polyarteritis nodosa

Saadoun, David; Terrier, Benjamin; Semoun, Oudy; Sène, Damien; Maisonobe, Thierry; Musset, Lucile; Amoura, Zahir; Resche-Rigon, Matthieu; Cacoub, Patrice

doi:10.1002/acr.20381

Cited by 88 publications

(40 citation statements)

References 31 publications

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“…The frequency of liver cirrhosis in HCV patients with MC in this study was 36.66 %. This figure is comparable to those observed in several other studies, which reported advanced fibrosis/cirrhosis in 25-44 % of their patients with HCV vasculitis [34][35][36][37][38]. This study showed a statistically significant increase in the TT genotype in HCV patients compared with the control group (40 versus 13.3 %; P = 0.036).…”

Section: Discussionsupporting

confidence: 94%

Association of BAFF −871C/T Promoter Polymorphism with Hepatitis C-Related Mixed Cryoglobulinemia in a Cohort of Egyptian Patients

et al. 2015

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Section: Discussionsupporting

confidence: 94%

Association of BAFF −871C/T Promoter Polymorphism with Hepatitis C-Related Mixed Cryoglobulinemia in a Cohort of Egyptian Patients

et al. 2015

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“…Association with HCV infection has been suggested for cutaneous polyarteris nodosa [17], and for a variety of other dermatological conditions including psoriasis, urticaria, and erythema multiforme (EM) [6]. However, most reported associations lacked sufficient evidence to establish a strong causal link with HCV.…”

Section: Pruritus and Other Skin Conditionsmentioning

confidence: 97%

Dermatological side effects of hepatitis C and its treatment: Patient management in the era of direct-acting antivirals

Cacoub¹,

Bourlière²,

Lübbe³

et al. 2012

Journal of Hepatology

133

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Dermatological adverse events (AEs) are an existing concern during hepatitis C virus (HCV) infection and peginterferon/ribavirin treatment. HCV infection leads to dermatological and muco-cutaneous manifestations including small-vessel vasculitis as part of the mixed cryoglobulinemic syndrome. Peginterferon/ribavirin treatment is associated with well-characterized dermatological AEs tending towards a uniform entity of dermatitis. New direct-acting antivirals have led to significant improvements in sustained virologic response rates, but several have led to an increase in dermatological AEs versus peginterferon/ribavirin alone. In telaprevir trials, approximately half of treated patients had rash. More than 90% of these events were Grade 1 or 2 (mild/moderate) and in the majority (92%) of cases, progression to a more severe grade did not occur. In a small number of cases (6%), rash led to telaprevir discontinuation, whereupon symptoms commonly resolved. Dermatological AEs with telaprevir-based triple therapy were generally similar to those observed with peginterferon/ribavirin (xerosis, pruritus, and eczema). A few cases were classified as severe cutaneous adverse reaction (SCAR), also referred to as serious skin reactions, a group of rare conditions that are potentially life-threatening. It is therefore important to distinguish between telaprevir-related dermatitis and SCAR. The telaprevir prescribing information does not require telaprevir discontinuation for Grade 1 or 2 (mild/moderate) rash, which can be treated using emollients/moisturizers and topical corticosteroids. For Grade 3 rash, the prescribing information mandates immediate telaprevir discontinuation, with ribavirin interruption (with or without peginterferon) within 7 days of stopping telaprevir if there is no improvement, or sooner if it worsens. In case of suspicion or confirmed diagnosis of SCAR, all study medication must be discontinued.

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“…Subacute bacterial endocarditis (including mycotic aneurysms with distal embolization), as well as HBV, HCV, and HIV, are among the infectious diseases that can mimic vasculitis or cause vascular inflammation. 3,20,[35][36][37] Atherosclerosis, embolic disease from atrial myxomas or cholesterol deposits, segmental arteriolysis medial, calciphylaxis lesions, thrombotic disorders (antiphospholipid syndrome), fibromuscular dysplasia, and ergot use can mimic vasculitis of medium-sized arteries. 41,42 If disease affects the central nervous system, Moyamoya disease, MELAS (mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes), CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy), and granulomatous angiitis of the central nervous system are considerations.…”

Section: Differential Diagnosismentioning

confidence: 99%

Polyarteritis Nodosa

Forbess¹,

Bannykh²

2015

Rheumatic Disease Clinics of North America

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Polyarteritis nodosa (PAN) is a systemic disease, but variants are cutaneous PAN and single-organ disease. Histologic confirmation of vasculitis in medium-sized arteries is desirable, and biopsies should be obtained from the symptomatic and least invasive sites. Angiography can show multiple microaneurysms in the viscera. Treatment includes high-dose corticosteroids, which are combined with immunosuppressive agents when internal organs are involved and with life-threatening disease. Once remission is achieved, maintenance agents are initiated. PAN is becoming a rare disease. International collaborative efforts are under way to establish better diagnostic and classification for all vasculitides, including PAN.

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Hepatitis C virus–associated polyarteritis nodosa

Cited by 88 publications

References 31 publications

Association of BAFF −871C/T Promoter Polymorphism with Hepatitis C-Related Mixed Cryoglobulinemia in a Cohort of Egyptian Patients

Association of BAFF −871C/T Promoter Polymorphism with Hepatitis C-Related Mixed Cryoglobulinemia in a Cohort of Egyptian Patients

Dermatological side effects of hepatitis C and its treatment: Patient management in the era of direct-acting antivirals

Polyarteritis Nodosa

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