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initial prolongation. Further investigation into the autonomic dysfunctionassociated with end-stage liver disease and the effects that OLT has on thisphenomenon are warranted to better understand the underlying etiology ofthis disease process.
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The role of triple therapy (interferon, ribavirin and amantidine) inthe treatment of chronic hepatitis CMunira Charania, M.D., K. Iswara, M.D., FACG, Jane Vlodov, M.D.,Seth Lapin, M.D., Sima Terebelo, P.A., Michael Bernstein, M.D., ScottTenner, M.D., M.P.H. Division of Gastroenterology, Department ofMedicine, Maimonides Medical Center, State University of New York,Health Sciences Center, Brooklyn, NY.
Chronic Hepatitis C is a major cause of chronic liver disease in the UnitedStates. Dual Therapy with interferon alfa-2b and ribavirin (Rebetron) hasbecome a standard of treatment for patients with Chronic Hepatitis C.Unfortunately, almost half of the patients treated with Rebetron will notclear the virus. There may be a role for amantadine in the treatment ofChronic Hepatitis C. Either ribavirin or amantadine has no value in viraleradication, when used alone. However, ribavirin has shown to be effica-cious when used in combination with interferon. Several investigators havesuggested that amantadine may have a synergistic effect when used inconjunction with Rebetron—Triple Therapy. The goal of this ongoingstudy is to evaluate the role of Triple Therapy (interferon alfa-2b, ribavirinand amantadine) with Chronic Hepatitis C patients. Two-hundred consec-utive patients with Chronic Hepatitis C were invited to participate. Patientswere included in the study if transaminases were elevated. HCV RNA waspositive and/or a liver biopsy was consistent with Chronic Hepatitis C.Patients were stratified into three groups, (1) patients not having beentreated previously, (2) patients who had failed to respond or relapsed toprior therapy with interferon, and (3) patients who had failed to respond orrelapsed to prior Dual Therapy. Patients not previously treated with DualTherapy were randomized to either Dual Therapy (Rebetron) or TripleTherapy (Rebetron and amantadine). All patients who failed to respond orrelapsed on Dual Therapy were placed on an open label protocol of TripleTherapy. The mean age of enrolled patients was 45.16 9.8. Fifty-fivepercent were men. Seventy percent had Genotype 1a, 1b. Fifty percent hadbeen previously treated with interferon or Rebetron and had not responded.The mean pre-treatment ALT of 1206 119 had significantly decreased atweek 12 to 42.86 33 (p 5 0.005). However, patients who had beenpreviously treated and who had failed to respond, did not have a significantdecrease in their ALT; pre-treatment 1156 88 and post-treatment 986 71.At present, none of the patients who failed to clear the virus on priorRebetron, had cleared the virus on Triple Therapy (Rebetron and amanta-dine). We conclude that amantadine has a limited role in the treatment ofpersons with Chronic Hepatitis C.
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Hypothyroidism presenting as liver test abnormalitiesAyaz Chaudhary, MD, Robert R. Schade, MD, FACG. Medical Collegeof Georgia, Augusta, GA.
It is unusual to find abnormal liver enzyme tests due to hypothyroidism. Incontrast, it is well known that hypothyroidism may develop in patients withliver disease, especially in those treated for Hepatitis C. We present 2 casesreferred for abnormal liver enzymes who were discovered to be hypothy-roid and who’s liver tests normalized following hormone replacementtherapy.
Case I: A 40 year old male with severe gout was being treated withallopurinol and indomethcin. He was referred for abnormal liver tests. Alt105 mu/ml, Ast 156 mu/ml. Liver tests one year earlier while on allopurinalhad been normal. There had been no alcohol in the previous 2 years.Serologic tests were negative for HBV, HCV, and autoimmune hepatitis.Iron studies were normal. The CPK however, was elevated at 4947 mu/mland the TSH 713.41 uiu/ml. The patient was started on hormone replace-
ment therapy. Within 3 months liver enzymes were normal although heremained on allopurinal and NSAIDS.
Case II: A 53 year old white female who had had a prior history of breastcancer, chemotherapy and autologous bone marrow transplant was referredfor abnormal liver tests. Alt 108 mu/ml, Ast 149 mu/ml. Serologic tests forliver disease were negative. The cholesterol was 420 mg/dl, CPK 1853mu/ml and the TSH was 16.9 uiu/ml. Following hormone therapy all valuesreturned to normal.
Hypoththroidism is an unusual cause of hepatic enzyme elevation. Bothpatients were referred by other internists and were not overtly hypothroid.Hypothyroidism should be considered in the differential diagnosis of ab-normal liver enzymes.
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Combination therapy with interferon and ribavirin in naive patientsof chronic hepatitis C in India: Role of genotype and stage of liverdiseaseG Choudhuri MD, FACG, Anshu Srivastava MD, Sundeep LakhtakiaMD, Kamal Chetri MD, Sameer Mohindra MD, TS Negi M Sc, SR NaikMD, Vijay Sharma*. Department of Gastroenterology, Sanjay GandhiPostgraduate Institute of Medical Sciences, Lucknow, India andSpeciality Ranbaxy Limited, Mumbai, India*.
Background: The reported efficacy of anti-viral therapy for patients withchronic hepatitis C (CHC) has ranged from 7%–70%.Aims: (1) assess the rate of sustained virological clearance in patients fromIndia, and (2) correlate our results with the stage of liver disease andprevalence of Hepatitis C virus genotypes.Patients and methods:Forty patients (M 26, age 17 to 76, mean 38.12 yr)with compensated liver disease (chronic hepatitis 17, mean age 38.12 yr;compensated cirrhosis with evidence of portal hypertension 15, mean age49.07 yr) who were anti-HCV (ELISA) and HCV RNA (RT-PCR) positivereceived combination therapy with Interferon Alpha 2B and ribavirin for 6months.Results: 28 patients completed 6 mo follow-up after completion of anti-viral treatment in whom sustained response (SR) could be assessed (4dropped out due to side effects of therapy); 22 (78.5%) had end of treatmentresponse (ETR) while 18 of 26 (69%) had SR. The results in the twoclinical groups were as follows:
ParameterChronic Hepatitis
(n 5 17)Liver Cirrhosis
(n 5 15) P
ALT (baseline) 331.68 U/L 142.69 U/LETR 16 of 17 (94%) 6 of 11 (55%) ,0.02SR 14 of 16 (88%) 4 of 10 (40%) ,0.02Genotype 2A–1, 2C–1, 3A–2, 3C–1 2B–2, 3A–1, 3C–1
Conclusion: 1–Chrome Hepatitis C responds very well to antiviral treat-ment in our population due probably to the high prevalence of genotypes2 and 3. 2–Compensated cirrhosis in India may benefit from antiviraltherapy.
Financial support for genotyping was provided by Fulford India Ltd.
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Lack of difference in response to Rebetron by race in priorinterferon non-responders (NRs) with chronic hepatitis CJH Lewis, KP Collier, GA Marino, MS Epstein, CD Howell, PThuluvath, N Ravendhran, M Cox, A Schulman, S Dellon, R Finkel, ILobis, M Koch, N Julie, T Sato, R Gelfand, L Korman, R Chasen, RMusselman, A Diamond, M Golding, D Doman, S Hunt, J Laurin, HFromm. Georgetown Univ Med Ctr, Univ of Maryland Med Ctr, JohnsHopkins Med Ctr, George Washington Med Ctr, Washington, DC,Baltimore and Annapolis.
Response rates among AA pts have been noted to be less than those in Caucin some studies. The Wash, DC metropolitan area HCV investigators study
2508 Abstracts AJG – Vol. 95, No. 9, 2000