Hepatitis c skin changes

Hepatitis C is an acute or chronic infection (> 6 months) caused by the hepatitis C virus (HCV), a hepatotropic RNA virus of which 6 gene types (1-6) are known. The infection leaves no lasting immunity. Extrahepatic involvement is multiform and polyetiologic. They involve the lymphatic-immunologic system, thyroid, kidney, skeletal system, and skin. Skin lesions are detected in 20-40% of patients with acute or chronic HCV infection.

Skin lesions that occur in the wake of HCV infection can be divided as follows.

• Early phase of viral infection:
  • Icterus (25%)
  • Non-specific exanthema (rare)
  • Necrolytic acral erythema (possibly in combination with zinc deficiency)
  • Pruritus
• Chronic phase of viral infection (> 6 months)
  • Nonspecific exanthema in childhood: Gianotti-Crosti syndrome
  • HCV-induced autoimmunological diseases with consecutive dermatological manifestations (in about 20% of patients with chronic hepatitis C positive ANA and anti-LMK1 = liver kidney microsome-Ak against cytochrome P 450 - typical for autoimmune hepatitis); 50% of the patients have a positive RF.
    • Essential mixed cryoglobulinemia: type II: mono- and polyclonal mixed cryoglobulinemia with monoclonal IgM rheumatoid factor and polyclonal IgG (monoclonal IgG or IgA rheumatoid factors are less common in the precipitate): this type accounts for about 60% of cases of cryoglobulinemia.
    • Urticariavasculitis
    • Cold urticaria
    • Sjögren's syndrome (13.4% of patients with Sjögren's syndrome have chronic hepatitis C)
    • Lichen planus (?)
    • Oral lichen planus (no close correlation could be proven in a larger Chinese study) see below.Lichen ruber mucosae.
    • Erythema induratum (nodular vasculitis)
    • Erythema elevatum diutinum (described as a double infection with HIV)
    • Purpura Schönlein in the context of hepatitis C induced membranous glomerulonephritis
    • Non-IgA vasculitis
    • pyoderma gangraenosum
    • Antiphospholipid antibody syndrome
    • Necrolytic acral erythema
  • HCV-induced autoimmunological diseases without immediate (but secondary possible) dermatological symptoms:
    • Rheumatoid arthritis
    • Idiopathic thrombocytopenia (purpura).
    • Membranous glomerulonephritis (leukocytoclastic vasculitis).
    • Chronic lymphocytic thyroiditis - Hashimoto's thyroiditis (vitiligo, alopecia areata).
    • HCV-induced insulin resistance with consecutive (insulin-resistant) diabetes mellitus (15% of infected individuals)
    • Positive ANA (20% of HCV-infected individuals)
  • Other secondary skin and systemic changes as a result of persistent HCV infection (chronic hepatitis > 6 months):
    • Increased risk of non-Hodgkin's lymphoma.
    • Activated psoriasis
    • Pityriasis rubra pilaris (especially the circumscribed type 4 of pityriasis rubra pilaris)
    • REM syndrome
    • Increased urinary coproporphyrin excretion (in larger studies, up to 40% of HCV-infected individuals even in early phases of HCV infection; the association has not yet been established). No clinical signs of photosensitivity.
    • Secondary skin changes due to developing or manifest liver cirrhosis with typical liver skin signs (not listed here):
      • Pruritus (especially in cholestatic hepatitis C).
      • Porphyria cutanea tarda
      • Hidradenitis neutrophilic eccrine
• Secondary skin changes due to antiviral therapy
  • erythema multiforme
  • DRESS

About 3% of the world population is chronically infected with HCV. The prevalence in Germany is 0.3% of the population, in Mediterranean countries 2-3%, in some African countries up to 22%. Risk groups are i.v. drug addicts (85% are HCV positive), non-sterile piercings, HIV and/or HBV infected persons.

Acute HC infections are asymptomatic in 75% of cases and symptomatic (icteric) in 25%. Symptomatic HCV infections heal spontaneously in half of the cases. Asymptomatic infections generally lead to a chronic course. 20% of patients with asymptomatic infection develop cirrhosis of the liver. There is an increased rate of liver cell carcinoma. HIV/HCV double infections often progress rapidly and are more often cholestatic.

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