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Effects of alcoholism and liver injury on hepatic alcohol and acetaldehyde metabolizing enzymes
EFFECTS OF ALCOHOLISM AND LIVER INJURY ON HEPATIC ALCOHOL AND ACETALDEHYDE METABOLIZING ENZYMES. A. Par~s, X. Soler, J. Pan~s, J. Farr~s, J. Caballer~a, X. Par~s and J. Rod,s. 245 Liver Unit. Hospital Clfnic i Provincial. Faoultat de Medicina. Universitat de Barcelona. Department of Biochemistry. Facultat de Ci~ncies. U.A.B. Bellaterra. To investigate the influence of hepatic lesion on the a c t i v i t i e s of enzymes involved in ethanol metabolism we have studied the alcohol dehydrogenase (ADH) and the low-Km and high-Km aldehyde dehydrogenase (ALDH) activities in liver biopsies from 44 chronic alcoholics (3 normal liver, 17 fibrosteatosis, 13 alcoholic hepatitis and ii cirrhosis) and 17 patients with non-alcoholic liver disease (i0 chronic hepatitis and 7 cirrhosis). Results of enzyme activities (Mean + SDM) are expressed as mU/mg protein in tissue. ADH activity at pH 10.5 was significantly lower in alcoholics than in non-alcoholics (23.2 + 15.9 vs 41.4 + 18.7, p
ZERUM PROTEASE-INHIBITORS
246
IN ACUTE VIRAL HEPATITIS
(AUH): RELATION TO AETIOLOGY
AND CLINICAL COURSE. O.Parracin%
R.Meliconi t G . R u ~ e r i ~
G.Verucchi~
F.Chiod%
M.L.Schiattone,
G.Gasbarrini. III Patologia Medica and Istituto Malattie Infettive, Universit~ Patologia Clinica, Ospedale Maggiore, Bologna, Italy.
F.Miglio,
di Bologna, Lab.
Alphal-antitrypsin (gl AT) and 2-macroglobulin (/2 M) may exert immunosuppressive activity. It has been suggested that they represent a feed-back mechanism involved in the termination of the immune reacting during the late phase of acute hepatitis. To verify this hypothesis we tested serum I I A T and 1 2 M by immunonephelometry, in 17 patients with AVH-A, 16 patients with AVH-B and 12 with AVH-NANB. in addition we tested 8 patients with fulminant hepatitis due to HBV. In AVH-A 6 patients had elevated IAT levels at admission (range mg/d 170-300; normal range 70-275) while ~2 M levels were normal throughout the follow-up. In AVR-B, 5 patients had eleveted ~IAT levels at admission (range mg/dl 170-355) while at week 3-4, 40% of the patients presented elevated 2M levels (range mg/dl 200-550; normal range 75-350). No elevations of protease-inhibitors were observed in AVH-NANB. Fulminant hepatitis cases presented significantly lower levels of I I A T and 12 M compared to AVHB at admission. In conclusion: increases of protease-inhibitors are produced in AVH-B and in lesser extent in AVH-A, whereas NANB viruses, which arc probably directly cytopathic, do not cause this acute phase reaction. In fulminant hepatitis the lower levels of IIAT and ~2 M can probably be due to the synthetic failure of damaged liver and, in turns, can contribute to the massive liver cell necrosis via the decreased immunosuppression activity.
$301
ZERUM PROTEASE-INHIBITORS
246
IN ACUTE VIRAL HEPATITIS
(AUH): RELATION TO AETIOLOGY
AND CLINICAL COURSE. O.Parracin%
R.Meliconi t G . R u ~ e r i ~
G.Verucchi~
F.Chiod%
M.L.Schiattone,
G.Gasbarrini. III Patologia Medica and Istituto Malattie Infettive, Universit~ Patologia Clinica, Ospedale Maggiore, Bologna, Italy.
F.Miglio,
di Bologna, Lab.
Alphal-antitrypsin (gl AT) and 2-macroglobulin (/2 M) may exert immunosuppressive activity. It has been suggested that they represent a feed-back mechanism involved in the termination of the immune reacting during the late phase of acute hepatitis. To verify this hypothesis we tested serum I I A T and 1 2 M by immunonephelometry, in 17 patients with AVH-A, 16 patients with AVH-B and 12 with AVH-NANB. in addition we tested 8 patients with fulminant hepatitis due to HBV. In AVH-A 6 patients had elevated IAT levels at admission (range mg/d 170-300; normal range 70-275) while ~2 M levels were normal throughout the follow-up. In AVR-B, 5 patients had eleveted ~IAT levels at admission (range mg/dl 170-355) while at week 3-4, 40% of the patients presented elevated 2M levels (range mg/dl 200-550; normal range 75-350). No elevations of protease-inhibitors were observed in AVH-NANB. Fulminant hepatitis cases presented significantly lower levels of I I A T and 12 M compared to AVHB at admission. In conclusion: increases of protease-inhibitors are produced in AVH-B and in lesser extent in AVH-A, whereas NANB viruses, which arc probably directly cytopathic, do not cause this acute phase reaction. In fulminant hepatitis the lower levels of IIAT and ~2 M can probably be due to the synthetic failure of damaged liver and, in turns, can contribute to the massive liver cell necrosis via the decreased immunosuppression activity.
$301