Hepatitis C and the skin
Section snippets
Etiology
Table 1 lists the major and minor risk factors for HCV infection. The two most common causes are blood or blood product transfusions (particularly before 1989) and illicit intravenous drug use. Since the development of screening techniques for HCV, intravenous drug use is now the most common risk factor accounting for two thirds of new infections [8]. Nosocomial transmission through blood product exposure has been reported in dialysis units, from hollow-bore and solid-bore needlesticks, from
Pathogenesis
The hepatic damage from HCV occurs by viral replication within liver hepatocytes. The mechanism of the extrahepatic effects is uncertain. The virus replicates within lymphoid cells potentially resulting in the extrahepatic manifestations. Another theory suggests that circulating immune complexes composed of HCVag and antibodies deposit in tissues and cause initiation of the inflammatory cascade. Other proposed mechanisms are that viral antigens induce local immune complex formation, or that
Common associations
Many cutaneous findings and diseases are associated with HCV. These may be arbitrarily divided into commonly associated, associated, and uncommonly associated conditions (Table 2). Cryoglobulinemia is commonly seen in patients with HCV. It is an immunologic disorder characterized by the presence of serum immune complexes, which precipitate at cold temperatures. These generally include rheumatoid factor, complement, HCV particles, HCV antibodies, and other immunoglobulins. There are three main
Diagnosis
There are three main laboratory evaluations used in diagnosing hepatitis C infection: (1) ELISA, (2) recombinant immunoblot assay, and (3) HCV proliferation by PCR. The ELISA test is good for general screening but has a high false-positive rate. It detects 95% of all patients with HCV infection.
The recombinant immunoblot assay test is more specific but less sensitive; if a patient has a positive recombinant immunoblot assay it is indicative of active HCV infection. If the recombinant immunoblot
Treatment
The treatment of HCV is difficult and extensive research and studies are underway to develop better therapy for the infection. Currently IFN alfa-2a, ribavirin, or amantadine are the suggested treatments. Viral serotypes are important in determining treatment response, with HCV type I being less responsive.
Hepatitis G virus
The hepatitis G virus is a newly discovered virus seen in some patients with posttransfusion hepatitis. It does not seem to be a major cause of posttransfusion hepatitis, and rarely runs a chronic course. It is seen in 10% to 25% of patients with HCV [93], [94].
Miscellaneous
Co-infection with HCV and HIV is common, occurring in 50% to 80% of people who acquired HIV through parenteral exposure. Antiretroviral with ritonavir therapy has shown to increase the risk of severe hepatotoxicity [95].
Treatment of HCV-infected patients with cyclosporin A at low doses (3 mg/kg) is safe in patients with low viral titers [96]. Corticosteroids have shown a tendency to increase viral load and should be used cautiously in patients with HCV [97].
Occult hepatitis B is commonly seen
Summary
Hepatitis C is an important and common cause of chronic hepatitis and cirrhosis. Cutaneous manifestations are often the first signs of infection. Dermatologists must be aware of these manifestations, because early diagnosis is the best treatment. HCV Ab by ELISA should be ordered in patients with LCV-urticarial vasculitis, cryoglobulinemia, lichen planus, Sjögren's syndrome, unexplained pruritus, PCT, PAN, chronic urticaria, patients starting methotrexate, unexplained pruritus, and any patient
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Cited by (42)
Skin manifestations associated with systemic diseases – Part II
2021, Anais Brasileiros de DermatologiaCitation Excerpt :Hepatitis C is related to pruritus, cryoglobulinemia, porphyria cutanea tarda, vasculitis, livedo reticularis, lichen planus, Sjögren’s syndrome, urticaria, and PAN.24,26 Less commonly associated are EN, erythema multiforme, nevoid telangiectasia, pyoderma gangrenosum, vitiligo, nail dystrophy, psoriasis, Behcet’s syndrome, granuloma annulare, and porokeratosis.26 Acral necrolytic erythema that presents with lichenified plaques and erythematous edges that may show desquamation, pruritus, and pain, is a rare disease and is associated with chronic hepatitis C.24
A study of lichen planus and its association with hepatitis C infection
2015, Journal of Taibah University Medical SciencesCitation Excerpt :LP appears to be related to the pattern of immune dysregulation induced by HCV. The mechanism of HCV induced lichen planus is possibly related to the viral replication in lymphocytes14 and it is well known that one of the characteristic histological features of LP is band like lymphocytic infiltration in the papillary dermis or possibly HCV is related in a way or another to the basal cell layer of the epidermis to which the lymphocytic band like infiltrate seems to be directed and once these cells are destroyed, the infiltrate descends down to the upper dermis. This point needs to be further clarified in more specified studies.
Leukocytoclastic vasculitis and necrolytic acral erythema in patients with hepatitis C infection: Do viral load and viral genotype play a role?
2010, Journal of the American Academy of DermatologyCitation Excerpt :Patients with chronic HCV infection can develop a wide range of cutaneous manifestations. Among the most common skin associations of HCV infection is cutaneous vasculitis.5-7 NAE, although not a commonly reported finding, is the only cutaneous marker of HCV described to date, as 100% of reported NAE cases had HCV infection.8,14,15,18-20
The prevalence of HCV antibodies in skin disease patients in Saudi Arabia
2010, Saudi Pharmaceutical JournalCutaneous Hepatology
2009, Dermatological Signs of Internal DiseaseHair, nail, and pigment changes in major systemic disease
2008, Clinics in DermatologyCitation Excerpt :The deposition of carotinoids and urochromes leads to a yellow shading of the integument.58 The mechanism of hepatitis C–inducing porphyria cutanea tarda is unknown, but there are 4 propositions: (1) decreased intracellular glutathione concentration, (2) decreased uroporphyrinogen decarboxylase activity, (3) elevated hepatocellular iron, and (4) production of an uroporphyrinogen decarboxylase inhibitor.57 Alkaptonuria is a rare metabolic disorder caused by homogentisic acid oxidase deficiency resulting in accumulation of homogentisic acid in collagenous structures.