1764 CORRESPONDENCE HEPATOLOGYJune 1995 ful rereview of the biopsy specimens used in this study is therefore warranted to determine if a relationship between the degree of hepatic steatosis and MEG-X formation truly exists. However, we believe that inherent genetic variability in P450 activity between patients, not steatosis, is a more likely explanation for this observation. Studies by Watkins ~ have clearly shown that the activity of P4503A4 varies widely among normal individuals. In addition, Oellerich et al s have demonstrated that MEG-X formation in normal individuals without any history of liver disease ranges between 15 and 130 ng/mL. As such, a single "low" value for MEG-X in the absence of clinically apparent liver disease may simply reflect genetically low P4503A4 activity. Based on these and our observations, we currently believe that every patient has their own unique maxim u m MEG-X value that is slowly reduced as chronic liver disease progresses and hepatic histology worsens over time. In theory, progression of chronic liver disease could be monitored via serial determinations of MEG-X, and therein lies the benefit of such a test. Studies to investigate whether this hypothesis is correct and to determine the sensitivity, specificity, and predictive value of a decrease in MEG-X values over time in relation to changes in hepatic histology and Child's class are currently underway at our center. If these studies show that MEG-X is useful in this regard, then this test has the ability to become a useful adjuvant in the care of patients with chronic hepatitis and cirrhosis in the future. MITCHELL L. SHIFFMAN,MD, FACP Hepatology Section Liver Transplant Program Medical College of Virginia Richmond, VA REFERENCES 1. Schroeder TJ, Gremse DA, Mansour ME, Theuerling AW, Brunson ME, Ryckman FC, Suchy FJ, Penn I, et al. Lidocaine metabolite formation as an index of liver function in hepatic transplant donors and recipients. Transplant Proc 1989;21:2299-2301. 2. Shiffman ML, Fisher RA, Sanyal AJ, Edinboro LE, Luketic VA, Purdum PP, et al. Hepatic lidocaine metabolism and complications of cirrhosis. Implications for assessing patient priority for hepatic transplantation. Transplantation 1992;55:830-835. 3. Lautz HU, Oellerich M, Burdelski M, Burger M, Engelmayer V, Pirlich M, Knoke A, et al. Assessment of short-term prognosis in liver transplant candidates with postnecrotic or biliary cirrhosis. Transplant Proc 1991;23:1572-1574. 4. Oellerich M, Burdelski M, Lautz HU, Schultz M, Schmidt FW, Herrmann H. Lidocaine metabolite formation as a measure of liver function in patients with cirrhosis. Ther Drug Monit 1990; 12:219-226. 5. Oellerich M, Burdelski M, Lautz HU, Binder L, Pichlmayer R. Predictors of one-year pretransplant survival in patients with cirrhosis~ HEPATOLOGY1991; 14:1029-1034. 6. Shiffman ML, Luketic VA, Sanyal AJ, Duckworth PF, Purdum PP, Contos MJ, Mills AS, et al. Hepatic lidocaine metabolism and liver histology in patients with chronic hepatitis and cirrhosis. HEPATOLOGY1994; 19:933-940. 7. Watkins PB. The role of cytochromes P450 in drug metabolism and hepatotoxicity. Semin Liver Dis 1990;10:235-250. 8. Oellerich M, Burdelski M, Schulz M, Schmidt FW, Ringe B, Lamesch P, Pichlmayr R, et al. Monoethylglycinexylodide formation kinetics: a novel approach to assessment of liver lidocaine. J Clin Chem Clin Biochem 1987;25:845-853. Lichen Planus, Chronic Hepatitis C, and Interferon To the Editor: We read with interest the report by Pawlotsky et al. 1 The investigators found that except for cryoglobulinemia associated vasculitis, the most frequent symptomatic immunologically mediated disease observed in their series was lichen planus (5%). One of their conclusions is that "history of lichen planus in patients with chronic hepatitis C may represent a contraindication to interferon therapy." There have been some reports suggesting that there m a y be liver abnormalities in patients with lichen planus. However, these have either been anecdotal reports or retrospective studies. Prospective studies have failed to establish any significant evidence of liver disease in patients with oral or cutaneous lichen planus. 2 We have treated a patient with this rather uncommon association (concomitant chronic active hepatitis C and lichen planus) who received 3 megaunits of interferon alfa-2b three times weekly. Alanine transaminase levels became normal and lichen planus lesions improved during the first 5 months of treatment. Thereafter, exacerbation of lichen planus was observed concomitantly with increases in alanine transaminase levels. However, despite increasing interferon dose to 6 megaunits to treat this breakthrough, a marked improvement was observed in lichen planus and disappearance of the lesions occurred 60 days after dose increase. At follow-up 12 months later, there was no evidence of skin lesions. 3 In agreement with other investigators, 4 we feel that interferon therapy is hardly an absolute contraindication to treat patients who present with lichen planus associated with chronic hepatitis C. 5 F u r t h e r patients with cases of lichen planus associated with chronic hepatitis C and who receive interferon therapy should be closely monitored, despite the widely divergent response of skin or oral lesions, before valid conclusions m a y be drawn. BERNARDO FRIDER, M D SILVIA SOOKOIAN, M D GUSTAVO CASTAI~O, M D Division of Internal Medicine/Hepatology G. GIAVINO, MD EDGARDO CHOUELA, M D Dermatology Unit Argerich Hospital Buenos Aires, Argentina HEPATOLOGYVol. 21, No. 6, 1995 REFERENCES 1. Pawlotsky JM, Yahia MB, Andre C, Voisin MC, Intrator L, Thoraval FR, Deforges L, et al. Immunological disorders in C virus chronic active hepatitis: a prospective case-control study. HEPATOLOGY1994; 19:841-848. 2. Graham-Brown RA, Sarkany I. In: McIntyre N, Benhamou J-P, Bircher J, Rizzetto M, Redes J, eds. Oxford Textbook of Clinical Hepatology. Vol II. New York: Oxford University Press, 1991:1176. 3. Frider B, Sookoian S, Castafio G, Giavino G, Chouela E. Liquen plane asociado a hepatitis crSnica C. Respuesta al interferon alfa 2b [Abstract]. Rev Gastroenterol Mex 1994;54(Suppl):118. 4. Boccia S, Gamberini S, Dalla Libera M, Strumia R, Venturini D. Lichen planus and interferon therapy for hepatitis C [corresondence]. Gastroenterology 1993; 105:1921-1922. 5. Doutre HS, Beylot C, Couzigon P, Lung P, Royer P, Beylot J. Lichen planus and virus C hepatitis: disappearance of the lichen planus under interferon alfa therapy. Dermatology 1992,184:229. Reply: Converging data recently suggested that hepatitis C virus (HCV) infections and lichen planus might be significantly associated. Indeed, several studies have reported a high prevalence of chronic hepatitis in patients with lichen planus, 1'2 and it has been shown that HCV was the main agent of liver disease in these pat i e n t s Y However, the prevalence of HCV infections in patients with lichen planus varies from 4% to 38% according to the study area 6-s (13% in our experience; H. Benchiki et al, manuscript submitted), so that the real nature of the relationship between these two diseases remains unknown. HCV could be one of the causal agents of lichen planus, b u t conversely, lichen planus and HCV could be associated, without causal link, because of unknown epidemiological factors. In this context, the observation reported by Frider et al might argue for HCV being the cause of lichen planus in their patient, because under interferon therapy, recovery of lichen planus lesions was parallel to response of liver disease. It has to be stressed, however, that the effect of interferon therapy on lichen planus in patients with chronic hepatitis C differs markedly from one case to the next. Indeed, interferon has been reported to have no influence (personal data), to improve, 9 to trigger (personal data), or to worsen 1°~2 lichen planus lesions. In the last two settings, mucosal involvement was usually so severe that it led to t r e a t m e n t withdrawal. Taken together, these data suggest that a history of lichen planus should be sought for in patients with chronic hepa- Granulomatous CORRESPONDENCE 1765 titis C who are candidates to interferon therapy. Although we agree that lichen planus cannot be considered an absolute contraindication to interferon, it should be viewed as a possible side effect. In patients with both chronic hepatitis C and lichen planus, interferon therapy calls for careful monitoring, and patients should be informed of the possible aggravation, as well as improvement, of skin lesions. JEAN-MICHEL PAWLOTSKY, M D DANIEL DHUMEAUX, M D Department of Bacteriology and Virology Department of Hepatology and Gastroenterology Hdpital Henri Mender, Universitd Paris XII Crdteil, France REFERENCES 1. Rebora A, Rongioletti F. Lichen p]anus and chronic active hepatitis: a retrospective survey. Acta Derm Venereol (Stockh) 1984;64:52-56. 2. Korkij W, Chuang TY, Soltani K. Liver abnormalities in patients with lichen planus: a retrospective case-control study. J Am Acad Dermatol 1984; 11:609-615. 3. Agner T, Fogh H, Weismann K. The relation between lichen planus and hepatitis C: a case report. Acta Derm Venereel (Stockh) 1992;72:380. 4. Divano MC, Parodi A, Rebora A. Lichen planus, liver kidney microsemal (LKM1) antibodies and hepatitis C virus antibodies. Dermatology 1992; 185:132-133. 5. Jubert C, Pawlotsky JM, Pouget F, Andr~ C, Deforges L, Bretagne S, Mavier JP, et al. Lichen planus and hepatitis C virusrelated chronic active hepatitis. Arch Dermatol 1994; 130:73-76. 6. Rebora A, Robert F, Rongioletti F. Clinical and laboratory presentation of lichen planus patients with chronic liver disease. J Dermatol Sci 1992;4:38-41. 7. Cribier B, Gamier C, Laustriat D, Heid E. Lichen planus and hepatitis C virus infection: an epidemiologic study. J Am Acad Dermatol 1994;31:1070-1072. 8. Santander C, De Castro M, Garcia-Monzo C, Garcia-Buey I, Sanchez J, Herrera JF, Borque MJ, et al. Prevalence of hepatitis C virus (HCV) infection and liver damage in patients with lichen planus (LP) [Abstract]. HEPATOLOGY1994;20:238A. 9. Doutre MS, Beylot C, Couzigou P, Long P, Royer P, Beylot J. Lichen planus and C virus hepatitis: disappearance of the lichen under interferon therapy. Dermatology 1992; 184:229. 10. Protzer U, Ochsendorf FR, Leopolder-Ochsendorf A, Holtermuller KH. Exacerbation of lichen planus during interferon alpha-2a therapy for chronic active hepatitis C. Gastroenterology 1993; 104:903-905. 11. Boccia S, Gamberini S, Dalla Libera M, Strumia R, Venturini D. Lichen planus and interferon therapy for hepatitis C [Correspondence]. Gastroenterology 1993; 105:1921-1922. 12. d'Aguay-AbensourL, et al. [Correspondence]. Gastroenterol Clin Biol 1992; 16:610-611. Destruction of Bile Ducts After Liver Transplantation: Primary Bi]iary Cirrhosis Recurrence or Hepatitis C Virus Infection? To the Editor: Transplantation." In this study, the investigators were able to identify within the grafts of 5 of 60 (8%) patients We read with interest the study of Balan et al 1 from who underwent transplantation for primary biliary cirthe Mayo Clinic entitled "Histological Evidence for Re- rhosis (PBC), a granulomatous destruction of the bile currence of Primary Biliary Cirrhosis After Liver duct, the so-called "florid duct lesion" considered as the