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Mooren-type hepatitis C virus-associated corneal ulceration
S E Wilson1, W M Lee, C Murakami
1Department of Ophthalmology, University of Texas Southwestern Medical Center at Dallas 75235.
Insights
Chronic hepatitis C virus (HCV) infection is linked to Mooren-type ulcers. Treatment with interferon alfa-2b can improve corneal disease, but ongoing monitoring is crucial due to potential relapses.
Area of Science:
- Ophthalmology
- Hepatology
- Virology
Background:
- Mooren-type ulcers are a rare, progressive peripheral ulcerative keratitis.
- Chronic hepatitis C virus (HCV) infection was identified in two patients presenting with bilateral Mooren-type ulcers.
- Both patients also exhibited chronic, pruritic dermatitis, with one diagnosed with hidradenitis suppurativa.
Observation:
- Hepatitis C virus genomic RNA was detected in the serum of both patients.
- Liver biopsy revealed severe hepatitis in one patient and normal liver tissue in the other.
- HCV RNA was detected in serum but not in conjunctiva or liver tissue of the second patient.
Findings:
- Interferon alfa-2b treatment led to corneal disease improvement in both patients.
- In one patient, corneal improvement paralleled normalized liver enzyme levels during HCV treatment.
- Relapse of corneal disease occurred upon discontinuation of interferon therapy in the second patient, improving with reinstitution.
Implications:
- Chronic HCV infection is associated with Mooren-type peripheral ulcerative keratitis.
- Testing for HCV infection is recommended for all patients with Mooren-type ulcers.
- Continued follow-up is essential for patients treated with interferon alfa-2b due to the risk of relapse.
Background:
Two patients with bilateral Mooren-type ulcers had underlying chronic hepatitis C virus (HCV) infection. Both patients also had chronic, pruritic dermatitis, which in one patient was diagnosed as hidradenitis suppurativa.
Methods:
Serum from the first patient and serum, conjunctiva, and liver from the second patient were analyzed for HCV genomic RNA using the reverse transcriptase-polymerase chain reaction. Serum anti-HCV antibodies were monitored with a commercially available second-generation test. Liver and conjunctival biopsies were evaluated histopathologically.
Results:
Liver biopsy showed severe hepatitis in the first patient, but normal liver tissue in the second. Hepatitis C virus genomic RNA was detected in the serum of both patients. In the first patient, the virus was detected 4 months after completion of interferon alfa-2b treatment for chronic active hepatitis. In the second patient, HCV genomic RNA was detected in serum, but not in conjunctiva or liver tissue. Hepatitis C virus could not be detected in the serum of the second patient after 2 weeks of interferon alfa-2b treatment. Both patients had serum anti-HCV antibodies. In case 1, there was a marked improvement in the corneal disease during and after 6 months of interferon alfa-2b treatment for chronic active hepatitis that paralleled a return of serum liver enzyme levels to the normal range. In the second patient, the corneal disease improved after 6 weeks of interferon alfa-2b treatment, but abruptly worsened when the patient discontinued therapy. The corneal disease improved again after interferon alfa-2b was reinstituted.
Conclusions:
Chronic HCV virus infection is associated with Mooren-type peripheral ulcerative keratitis. All patients with Mooren-type ulcers should be tested for evidence of HCV infection in consultation with a liver specialist. Even when improvement is obtained with interferon alfa-2b treatment, however, continued follow-up is important because relapse is common and repeat treatment may be effective.