Mooren-type hepatitis C virus-associated corneal ulceration

S. E. Wilson, W. M. Lee, C. Murakami, J. Weng, G. A. Moninger

Research output: Contribution to journalArticle

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Abstract

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 hidradentitis 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.

Original languageEnglish (US)
Pages (from-to)736-745
Number of pages10
JournalOphthalmology
Volume101
Issue number4
StatePublished - 1994

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interferon alfa-2b
Hepacivirus
Corneal Diseases
Serum
Liver
Virus Diseases
Hepatitis C Antibodies
Conjunctiva
Chronic Hepatitis C
RNA
Chronic Hepatitis
Therapeutics
Ulcer
Corneal Ulcer
Biopsy
Dermatitis
Reverse Transcriptase Polymerase Chain Reaction
Hepatitis
Reference Values
Referral and Consultation

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Wilson, S. E., Lee, W. M., Murakami, C., Weng, J., & Moninger, G. A. (1994). Mooren-type hepatitis C virus-associated corneal ulceration. Ophthalmology, 101(4), 736-745.

Mooren-type hepatitis C virus-associated corneal ulceration. / Wilson, S. E.; Lee, W. M.; Murakami, C.; Weng, J.; Moninger, G. A.

In: Ophthalmology, Vol. 101, No. 4, 1994, p. 736-745.

Research output: Contribution to journalArticle

Wilson, SE, Lee, WM, Murakami, C, Weng, J & Moninger, GA 1994, 'Mooren-type hepatitis C virus-associated corneal ulceration', Ophthalmology, vol. 101, no. 4, pp. 736-745.
Wilson SE, Lee WM, Murakami C, Weng J, Moninger GA. Mooren-type hepatitis C virus-associated corneal ulceration. Ophthalmology. 1994;101(4):736-745.
Wilson, S. E. ; Lee, W. M. ; Murakami, C. ; Weng, J. ; Moninger, G. A. / Mooren-type hepatitis C virus-associated corneal ulceration. In: Ophthalmology. 1994 ; Vol. 101, No. 4. pp. 736-745.
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abstract = "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 hidradentitis 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.",
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N2 - 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 hidradentitis 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.

AB - 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 hidradentitis 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.

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