Cutaneous Manifestations of Hepatitis C 

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 4, 2011
 

Background

The hepatitis C virus (HCV) is an RNA virus. HCV is a major cause of both acute and chronic hepatitis. Persons become infected mainly through parenteral exposure to infected material by blood transfusions or injections with nonsterile needles. Persons who inject illegal drugs, people who snort cocaine with shared straws, and health care workers who are at risk for needlestick and other exposures are at highest risk for HCV infection. Another major risk factor for HCV is high-risk sexual behavior. The incidence of acute HCV infection has sharply decreased in the United States during the past decade, but its prevalence remains high (approximately 2.7 million Americans) because chronic hepatitis C (CHC) infection develops in approximately 75% of patients acutely infected.

Most patients with acute and chronic infection are asymptomatic. Patients and health care providers may detect no indications of the conditions for long periods; however, chronic hepatitis C infection and chronic active hepatitis are slowly progressive diseases and result in severe morbidity in 20-30% of infected persons. Astute observation and integration of findings of extrahepatic symptoms, signs, and disease are often the first clues to underlying HCV infection.

Cutaneous symptoms or findings relevant to HCV infection manifest in 20-40% of patients presenting to dermatologists and in a significant percentage (15-20%) of general patients. HCV is suggested and must appear in the differential diagnosis of these patients to avoid missing this important but occult factor in clinical disease in the appropriate setting.

Extrahepatic manifestations of hepatitis C virus are numerous.[1] The most prevalent and most closely linked with HCV is essential mixed cryoglobulins with dermatologic, neurologic, renal, and rheumatologic complications. A less definite relationship to HCV is observed with systemic vasculitis, porphyria cutanea tarda, and the sicca syndromes.

HCV is a major public health problem because it causes chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). HCV also induces extrahepatic manifestations such as mixed cryoglobulinemia, porphyria cutanea tarda, leukocytoclastic vasculitis, lichen planus (LP), and sicca syndrome, all of which should be regarded as early markers of a potentially fatal chronic liver disease.[2]

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Pathophysiology

Chronic hepatitis C infection is associated with many extrahepatic manifestations in joints, muscles, neural and gastrointestinal tissues, and skin. In this article, the many dermatologic manifestations of hepatitis C virus (HCV) are classified according to diseases with proven or suspected etiology or causation.

Primary causation results from direct infection of HCV in the skin, lymphocytes, dendric antigen-presenting cells, and blood vessels. An example of this type of disorder is the recent finding of epidermal cells with HCV-RNA particles.

Secondary causation occurs when HCV infection manifests in the skin due to epiphenomena resulting from the disruption of immune responses. Leukocytoclastic vasculitis due to cryoglobulinemia is a good example of a specific skin manifestation resulting from the production of immunoglobulins, with rheumatoid characteristics causing an immune complex–mediated vasculitis.

Tertiary causation of dermatologic manifestations results when the disruption of another organ infected or affected by HCV causes skin manifestations that are nonspecific and typical of skin responses to that organ; these responses result from a wide range of causes, including flushing and other findings of thyroid hormone release in early HCV-linked autoimmune thyroiditis. Chronic active hepatitis leading to fibrotic liver disease in chronic hepatitis C infection can also cause cutaneous vascular changes, such as spider nevus and palmar erythema. Arteriovenous hemangioma, a benign acquired cutaneous vascular lesion, has also been reported to be associated with chronic liver disease, including chronic active hepatitis associated with HCV infection.

Another category of dermatologic manifestations in HCV infections in a causative schema includes those diseases in which an association has been identified, but the details of causation have not yet been clarified. Porphyria cutanea tarda (PCT) is a good example of this type of HCV-related disease in which causation is unexplained but undeniable. In patients with PCT, 70% are HCV positive.

Neoplastic dermatologic manifestations are another category of extrahepatic findings.

Dermatologic manifestations are associated with treatments of HCV infection, especially interferon.

The last category is suspected associations of the disorder in a causative schema. HCV genomic analysis by means of arduous gene sequencing of many viruses has led to the division of HCV into genotypes based on homology. Arabic numerals denote the genotype, and a letter denotes the subtype for lesser homology within each genotype.[3] Note the following:

  • Genotype 1a occurs in 50-60% of patients in the United States. This type is difficult to eradicate using current medications.
  • Genotype 1b occurs in 15-20% of patients in the United States. Subtype 1b is difficult to eradicate using current medications. This type is most prevalent in Europe, Turkey, and Japan.
  • Genotype 1c occurs in less than 1% of patients in the United States.
  • Genotypes 2a, 2b, and 2c occur in 10-15% of patients in the United States. These subtypes are widely distributed and are most responsive to medication.
  • Genotypes 3a and 3b occur in 4-6% of patients in the United States. These subtypes are most prevalent in India, Pakistan, Australia, and Scotland.
  • Genotype 4 occurs in less than 5% of patients in the United States. It is most prevalent in the Middle East and Africa.
  • Genotype 5 occurs in less than 5% of patients in the United States. It is most prevalent in South Africa.
  • Genotype 6 occurs in less than 5% of patients in the United States. It is most prevalent in Hong Kong and Macao.
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Epidemiology

Frequency

United States

The prevalence of hepatitis C virus (HCV) seropositivity in the United States was 3.9 million persons.[4] In persons who were seropositive, 65% were aged 30-49 years, and 74% of patients demonstrating positive results were positive for HCV RNA, meaning active viral replication continued to occur. An estimated 2.7 million persons have chronic hepatitis C infection. Genotype 1a occurs in 57% of patients; genotype 1b occurs in 17%. From 1989-1993, the occurrence of HCV decreased 80%, from 50 cases per 100,000 to approximately 28,000 new cases per year. Decreased transfusion-associated disease and a dramatic decrease in intravenous drug use account for this change.

International

Worldwide, 170 million persons have hepatitis C virus (HCV) infection, which represents 3% of the world population.[5] The prevalence of HCV antibody is less than 3% in developed nations. The prevalences are as high as 70% in highly endemic countries, such as Egypt; the high prevalences relate to specific practices that transmit the disease at specific times in the population.

Mortality/Morbidity

Although acute hepatitis C virus (HCV) infection is usually mild, chronic hepatitis results in at least 75% of patients.[3] While liver enzyme levels may be in the reference range, the presence of persistent HCV-RNA levels discloses chronic infection. Biopsy samples of the liver also reveal chronic liver disease in patients. Cirrhosis develops in 20-50% of patients with chronic hepatitis C infection. Liver failure and hepatocellular carcinoma can eventually result. Hepatocellular carcinoma occurred in 11-19% of patients. The risk of cirrhosis and hepatocellular carcinoma doubles in patients who have undergone transfusion.[6]

Two studies of compensated cirrhosis in the United States and Europe showed that decompensation occurred in 20% of patients and that hepatocellular carcinoma occurred in approximately 10% of patients.[7, 8] The survival rate at 5 and 10 years was 89% and 79%, respectively. The onset of chronic hepatitis C infection early in life often leads to less serious consequences.[9, 10] Hepatitis B virus (HBV) infection, iron overload, and alpha 1-antitrypsin deficiency may play a role in the progression of chronic hepatitis C infection to HCV-related cirrhosis.[11, 12]

Chronic hepatitis C infection and its major sequelae (cirrhosis and hepatoma) are responsible for 8,000-10,000 deaths a year.

Race

Race and ethnicity do not relate to hepatitis C virus (HCV). HCV infection is associated with lower economic status, less education, and groups other than whites.

Sex

No sex preponderance occurs with hepatitis C virus (HCV) infection. Sex differences were not significant.[4]

Age

Of individuals positive for hepatitis C virus (HCV) antibodies, 65% are aged 30-49 years. Younger age at infection often relates to lesser consequences of the infection. Infection is uncommon in persons aged 20 years and younger and is more prevalent in persons older than 40 years.[13, 14] Data suggest the presence of age-related methods of infection, such as nonsterile medical procedures, including vaccination and parenteral drug treatment.[15]

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Arthur P Birnkrant, MD  Clinical Instructor, Department of Dermatology, University of Medicine and Dentistry of New Jersey

Arthur P Birnkrant, MD is a member of the following medical societies: American Academy of Dermatology and American Society for MOHS Surgery

Disclosure: Nothing to disclose.

Specialty Editor Board

Craig A Elmets, MD  Professor and Chair, Department of Dermatology, Director, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine

Craig A Elmets, MD is a member of the following medical societies: American Academy of Dermatology, American Association of Immunologists, American College of Physicians, American Federation for Medical Research, and Society for Investigative Dermatology

Disclosure: Palomar Medical Technologies Stock None; Astellas Consulting fee Review panel membership; Massachusetts Medical Society Salary Employment; Abbott Laboratories Grant/research funds Independent contractor; UpToDate Salary Employment; Biogen Grant/research funds Independent contractor; Clinuvel Independent contractor; Covan Basilea Pharmaceutical Grant/research funds Independent contractor; ISDIN None Consulting; TenX BIopharma Grant/research funds Independent contractor

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD  Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Cold agglutinin disease indistinguishable from cryoglobulinemia. Courtesy of Walter Reed Army Medical Center Dermatology.
Cryoglobulinemia, palpable purpura, dysproteinemic purpura, and leukocytoclastic vasculitis (small vessel vasculitis). Courtesy of Walter Reed Army Medical Center Dermatology.
Cutis marmorata. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme, bull's-eye lesions. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema dyschromicum perstans. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema dyschromicum perstans. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema nodosa. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema nodosa. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme of the oral mucosa. Courtesy of Walter Reed Army Medical Center Dermatology.
Erythema multiforme (Stevens-Johnson syndrome). Courtesy of Walter Reed Army Medical Center Dermatology.
Palmar erythema. Courtesy of Walter Reed Army Medical Center Dermatology.
Granuloma annulare. Courtesy of Walter Reed Army Medical Center Dermatology.
Disseminated superficial (actinic) porokeratosis. Courtesy of Walter Reed Army Medical Center Dermatology.
Disseminated superficial (actinic) porokeratosis. Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus (hypertrophic type). Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus (oral lesions). Courtesy of Walter Reed Army Medical Center Dermatology.
Lichen planus (volar wrist). Courtesy of Walter Reed Army Medical Center Dermatology.
Lymphoma cutis. Courtesy of Walter Reed Army Medical Center Dermatology.
Henoch-Schönlein purpura. Courtesy of Walter Reed Army Medical Center Dermatology.
Palpable purpura. Courtesy of Walter Reed Army Medical Center Dermatology.
Purpura in hemophilia (factor VIII deficiency). All ecchymoses and bland petechiae are in the differential diagnosis of thrombocytopenic purpuras, including thrombocytopenia secondary to hepatitis C virus in which an autoantibody to platelets is present. Courtesy of Walter Reed Army Medical Center Dermatology.
Progressive pigmented purpuric eruption. Courtesy of Walter Reed Army Medical Center Dermatology.
Progressive pigmented purpura (photo rotated 90°). Courtesy of Walter Reed Army Medical Center Dermatology.
Progressive pigmented purpura (Gougerot-Blum disease). Courtesy of Walter Reed Army Medical Center Dermatology.
Progressive pigmented purpura (Schamberg disease). Courtesy of Walter Reed Army Medical Center Dermatology.
Thrombocytopenic purpura. Courtesy of Walter Reed Army Medical Center Dermatology.
Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.
Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.
Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.
Chronic urticaria. Courtesy of Walter Reed Army Medical Center Dermatology.
Urticaria (secondary to penicillin). Courtesy of Walter Reed Army Medical Center Dermatology.
Nodular vasculitis. Courtesy of Walter Reed Army Medical Center Dermatology.
Henoch-Schönlein purpura, palpable purpura, and leukocytoclastic vasculitis. Courtesy of Walter Reed Army Medical Center Dermatology.
Vitiligo. Courtesy of Walter Reed Army Medical Center Dermatology.
Vitiligo. Courtesy of Walter Reed Army Medical Center Dermatology.
Waldenström hypergammaglobulinemic purpura. Courtesy of Walter Reed Army Medical Center Dermatology.
 
 
 
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