Cell-mediated immunity to acetaldehyde in alcoholic liver disease demonstrated by leukocyte migration test.

To determine whether a sensitization to ethanol metabolites occurs in alcoholic liver disease, reactivity of lymphocytes to nontoxic amounts of acetaldehyde was studied by direct elaboration of migration inhibitory factor (MIF) production. Eighteen alcoholics with various degrees of biopsy-proven liver damage showed increased MIF production in response to acetaldehyde; the mean value of the group differed significantly from 15 healthy controls, 15 subjects with nonalcoholic liver disease, and 15 alcoholics without liver involvement (P less than 0.001, P less than 0.001, P less than 0.02, respectively). Among the alcoholics with liver disease, none individuals (50%) with histological signs of advanced alcoholic hepatitis showed the highest percentage of inhibition of migration; the value differed significantly from the remaining patients with lesser degrees of hyaline necrosis in liver biopsies (P less than 0.005). These results indicate that acetaldehyde is involved in the pathogenesis of alcoholic hepatitis. Clinically, this test might facilitate the selection of patients with alcoholic hyaline necrosis.     

Plasma fibronectin concentrations in patients with liver diseases

Plasma, obtained just prior to diagnostic liver biopsy in 71 patients with various liver diseases, was examined by electroimmunoassay using immunoglobulin against human fibronectin and purified plasma fibronectin as standard. The plasma fibronectin concentration was not significantly different from age- and sex-matched healthy controls in patients with chronic persistent or chronic active hepatitis (n = 7), primary biliary cirrhosis (n = 8), alcoholic fatty liver (n = 9), alcoholic hepatitis (n = 10), and alcoholic cirrhosis (n = 16). Patients with acute viral hepatitis (type A (n = 2); type B (n = 7); type non A, non B (n = 1] had significantly (P less than 0.01) raised plasma fibronectin concentrations (median 506 mg/l (range 339-804] compared to controls (median 399 mg/l (range 304-462]. Morbidly obese patients with fatty liver (n = 11) had significantly (P less than 0.001) raised plasma fibronectin concentrations (median 610 mg/l (range 429-862] compared to controls (median 361 mg/l (range 303-419].     

Localization of T and B cells and alpha fetoprotein in hepatic biopsies from patients with liver disease.

Peripheral blood and hepatic tissue T- and B-lymphocyte distributions, serum alpha fetoprotein (AFP) concentrations, and hepatic AFP were studied in 46 patients undergoing diagnostic percutaneous liver biopsy. The patients included 26 with alcoholic liver disease, 13 with nonalcoholic hepatitis or cirrhosis, and 7 with either normal histology or minor nonspecific changes. Serum AFP was determined by radioimmunoassay and hepatic tissue AFP by indirect immunofluorescence. Peripheral blood T lymphocytes were identified by the sheep red-cell rosette technique; and B lymphocytes by fluoresceinated anti-immunoglobulin antisera and IgG aggregates. Tissue identification of T lymphocytes was accomplished using an extensively absorbed rabbit antihuman thymocyte antiserum and indirect immunofluorescence; tissue B lymphocytes were identified using pepsin F (ab')2 fragments of rabbit IgG antibodies to human immunoglobulins. T lymphocytes predominanted in hepatic lymphoid infiltrates from patients with alcoholic liver disease (91+/-4%), whereas in patients with chronic active or chronic persistant hepatitis, viral hepatitis, or cryoptogenic cirrhosis proportions of T and B lymphocytic infiltrates were similar (50+/-15%). Hepatic tissue AFP was detected in 9 of 18 patients with alcoholic hepatitis; serum AFP concentration was increased in only 1 of these 9 patients. Tissue AFP was not observed in the remaining biopsy material nor were serum AFP concentrations increased. Peripheral blood T-cell numbers were significantly decreased in patients with alcoholic liver disease (P less than 0.01) and in nonalcoholic hepatitis or cirrhosis (P less than 0.025). A close relationship between peripheral blood T-lymphocytopenia and hepatic T-cell infiltrates was observed in patients with alcoholic liver disease; this relationship was less apparent in patients with nonalcoholic hepatitis or cirrhosis.     

Hormone and metabolite profiles in alcoholic liver disease

Abstract. Circulating hormone and metabolite profiles have been studied in ten patients with alcoholic cirrhosis, five patients with alcoholic hepatitis and/or fatty liver, and nine normal controls over a 12-h period of meals and activity. Blood glucose was elevated throughout the day in both cirrhotic and non-cirrhotic alcoholics (mean 12-h glucose; controls 5.38 ± 0.16 (SEM) mmol/l; cirrhotics 6.98 ± 0.30 mmol/l, P < 0.001; non-cirrhotics 7.18 ± 0.26 mmol/l, P < 0.001). Non-cirrhotic alcoholics had an exaggerated insulin response to meals, whereas cirrhotic patients had hyperinsulinaemia throughout the day (mean 12-h insulin; controls 16.3 ± 2.3 mU/l; cirrhotics 35.8 ± 6.6 mU/l, P < 0.02). Growth hormone levels were elevated only in patients with cirrhosis (mean 12-h growth hormone, 7.06 ± 1.35 v. 0.85 ± 0.17 μg/l, P < 0.001). Serum Cortisol was persistently elevated in cirrhotics but only in the evening in non-cirrhotic alcoholics. Lactate and pyruvate responses to meals were exaggerated in non-cirrhotic patients whereas in cirrhotics, levels were persistently raised. Blood glycerol was elevated in all alcoholic patients whereas ketone body levels were normal. Hypertriglyceridae-mia was observed only in non-cirrhotic patients. No relationship between the endocrine and metabolic state was observed in either cirrhotic or non-cirrhotic patients.     

Serum ferritin in the assessment of liver iron overload and iron removal therapy in porphyria cutanea tarda

Serum ferritin, an index of iron stores, was studied in 60 patients with porphyria cutanea tarda (PCT), in 21 patients who had other liver diseases without siderosis (cirrhosis [LC] and chronic active hepatitis [CAH]), and in 32 patients with associated liver siderosis (alcoholic LC, LC and CAH in minor thalassemia). Ferritin levels were higher in patients with porphyria than in healthy controls and patients without liver siderosis (P less than 0.001), whereas no statistical difference was observed between patients with porphyria and those with liver siderosis. Because iron removal is considered the treatment of choice for PCT, some patients with PCT underwent phlebotomy and others received chelating therapy with subcutaneous infusion of deferoxamine. Follow-up of the patients showed a correlation between serum ferritin level and urinary porphyrin excretion; when the clinical and biochemical syndrome became normal, serum iron and ferritin had fallen to normal values (t test pair data analysis before and after: P less than 0.001 in each group). No appreciable difference was found between controls and patients with PCT whose conditions had been normalized, irrespective of the chronic liver damage always present in PCT. Our results suggest that serum ferritin increase in PCT is related more to liver iron overload than to liver damage, and ferritin follow-up is recommended to indicate the exhaustion of hepatic iron stores during iron depletion therapy, as well as to detect an early replenishment after remission.     

Plasma prolidase and prolinase activity in alcoholic liver disease

Prolidase (EC 3.4.13.9) and prolinase (EC 3.4.13.8) activity was measured in the plasma of 53 patients with alcoholic liver disease. Plasma prolinase activity was not correlated with histological characteristics in liver biopsies. In contrast, prolidase activity rose significantly (p less than 0.02) in cirrhotic patients with alcoholic hepatitis in comparison with those without alcoholic hepatitis. It also showed a significant positive correlation with ASAT activity (r = 0.505, p less than 0.001) and with the ASAT/ALAT ratio (r = 0.452, p less than 0.001). Plasma prolidase activity did not allow the differentiation of patients with reversible fibrosis from those with cirrhosis. The interest of this new marker is discussed.     

Autoantibodies, sheep cell agglutinins and anti-albumin antibodies in alcoholic liver disease

The frequency of serum autoantibodies including anti-albumin antibodies was investigated for patients with various categories of alcoholic liver disease (ALD). The 95 patients were grouped into 3 categories: fatty liver (25 cases), alcoholic hepatitis (29 cases), and alcoholic cirrhosis (41 cases), and each group was matched with healthy controls by age, sex, ethnic origin and socio-economic status. For all patients with ALD, there was a 5-fold greater frequency over the controls of positive tests for antinuclear antibody (ANA), but titres were low; the pattern of ANA reactions was speckled in 50% of the cases. For patients with alcoholic cirrhosis, there was an 8-fold increase in frequency over the controls in anti-smooth muscle antibody (ASMA), but titres were low, pointing to a possibility that autoimmunity might be one of several determinants of progression of alcoholic hepatitis to cirrhosis. For none of the groups was there an increase over the controls in the mean titre of sheep red cell agglutinins, nor were there increased haemagglutinin titres of antibody to bovine serum albumin or to human albumin, arguing against a general increase in antibody production in ALD. Greater knowledge of the frequency, significance and pathogenicity of reactive autoantibodies which occur in response to various types of tissue damage is required for interpretation of the increase in ANA and ASMA in alcoholic liver disease.     

Serum beta 2-microglobulin levels in chronic post-transfusion non A non B liver disease

Serum beta 2-microglobulin (beta 2 mu), a reliable marker of T-cell activation, was measured in 25 patients with chronic post-transfusion non A non B (NANB) liver disease and in 21 patients with HBsAg positive chronic liver disease. beta 2 mu levels were elevated in NANB patients when compared with controls but not in comparison with the HBsAg carriers. In NANB patients, beta 2 mu concentrations were significantly correlated with serum IgG (P less than 0.001) and with circulating immune complex activity, assessed by the 125IClq binding test (P less than 0.01). These findings suggest that, in addition to T-cells, the B-cells contributed also to the beta 2 mu production. Patients with "active disease" (chronic active hepatitis and active cirrhosis) had significantly higher beta 2 mu levels (P less than 0.001) than did those with "inactive disease" (chronic persistent hepatitis and inactive cirrhosis). This relation of serum beta 2 mu concentrations and histological activity was also observed in the HBsAg carriers and suggests that the course of post-transfusion NANB chronic hepatitis could be determined by host's immune response rather than by a direct effect of the virus.     

Are increases in thyroxin-binding globulin in patients with acute hepatitis ascribable to synthesis by regenerating hepatocytes?

We describe a case of liver cirrhosis lacking the expected increase in serum thyroxin (T4)-binding globulin (TBG) despite abrupt, severe increases in aspartate and alanine aminotransferases (ASAT and ALAT) in serum. Sequential change in serum T4, triiodothyronine (T3), and TBG concentrations were also measured retrospectively in serum of 10 hospitalized patients with acute viral hepatitis. Although their mean T4 and TBG concentrations significantly exceeded those in 40 normal subjects (P less than 0.002 and P less than 0.001, respectively), these values were within the normal reference intervals in five patients. ASAT and ALAT concentrations were not significantly different in patients with increased TBG and patients with normal TBG, whereas mean concentrations of serum albumin and cholinesterase and mean prothrombin times (in percent) in the former group were significantly higher than those in the latter group (P less than 0.05, P less than 0.05, and P less than 0.001, respectively). For 60 samples with increased ASAT and ALAT, TBG and albumin or cholinesterase correlated significantly (r = 0.49, P less than 0.001 and r = 0.50, P less than 0.001, respectively), but not TBG and ASAT or ALAT. Collectively, these results suggest that the increase in serum TBG in acute hepatitis may reflect its synthesis in regenerating hepatocytes rather than a simple leakage from damaged hepatocytes.     

A study of the microheterogeneity of transferrin in cirrhotic patients

In order to assess the specificity of transferrin molecular changes, we compared concentrations of subfractions and total transferrin in cirrhotic patients, in patients having non-alcoholic hepatitis, in patients with liver cancer, and in controls. The study was carried out in 79 patients divided into four groups: 20 patients with biopsy-proven cirrhosis of alcoholic origin, 20 patients with non-alcoholic hepatitis, 19 patients with liver cancer and 20 controls. Subfractions of serum transferrin were separated by isoelectric focusing followed by direct immunofixation. Fractions pI 5.7 percentages (expressed as percentages of one fraction over total transferrin) were significantly higher in the cirrhotic group than in the control group (p less than 0.01). Fraction pI 5.9 percentages were significantly higher in the cirrhotic group than in the hepatitis or control groups (p less than 0.05), or liver cancer group (p less than 0.01). A quantitative increase of fraction pI 5.7 was found in the cirrhotic patients. However, in this study, this parameter did not discriminate between patients with parenchymal liver diseases of alcoholic or other origin. Therefore, the value of determining fraction pI 5.7 as a marker of chronic alcohol consumption seems questionable. The elevation of fraction pI 5.9 constantly found in the cirrhotic patients could not be explained and needs further investigations.     

Reduced peripheral conversion of thyroxine to triiodothyronine in patients with hepatic cirrhosis.

The role of liver in the peripheral conversion of thyroxine (T4) to triiodothyronine (T3) was studied in normal subjects and patients with alcoholic liver disease by measurement of thyrotrophin (TSH) and total and free T4 and T3 in randomand serial serum samples. Also, T4 to T3 conversion rates and T3 disposal rates were compared by noncompartmental analysis. While the mean total serum T4 values were similar for the two groups, 8.6 and 8.1 mug/kl, the mean free T4 value was significantly higher in the cirrhotic patients (3.3 ng/dl) than in the normal subjects (2.1 ng/dl, P less than 0.001). The mean serum T3 value, 85 ng/dl, was significantly reduced in the hepatic patients as compared to a mean serum T3 value of 126 ng/dl in the normal subjects (P less than 0.001), while the free T3 value was 0.28 ng/dl in both groups. The reduction of the serum total and free T3 values were closely correlated with the degree of liver damage, as indicated by elevation of serum bilirubin (r equal -0.547) and reduction of serum albumin (r equal 0.471). The mean serum TSH level was 3.1 muU/ml in the normals and 7.1 muU/ml in the cirrhotic aptients ( less than 0.001). 15% of the hepatic patients had serum TSH values above 10 muU/ml, which, however, did not correlate with any of the four liver function tests studied. Serial blood sampling from two convalescing patients with alcoholic hepatitis showed a gradual normalization of serum TSH and T3 levels as the liver function improved. After oral T4 administration, 0.25 mg/day for 10 days, three of four cirrhotic patients studied failed to raise their serum T3 values. The mean T4 to T3 conversion rate of seven normal subjects was 35.7%. The mean T4 to T3 conversion rate of four cirrhotic patients studied was significantly reduced to 15.6% (P less than 0.001). The mean disposal rates of T4 and T3 of the normal subjects were 114 and 34 mug/day, respectively. The ratio of T4 disposal to T3 disposal was 3.5. In contrast, the mean T4 disposal rate, 82 mug/day, and the mean T3 disposal rate, 10 mug/day, were both reduced in the cirrhotic patients. Their ratio of T4 disposal to T3 disposal was 7.9. These findings suggest that impairment of T4 conversion in patients with advanced hepatic cirrhosis may lead to reduced T3 production and lowered serum T3 level. Therefore, the liver is one of the major sites of T4 conversion to T3.     

Desialylated transferrin and mitochondrial aspartate aminotransferase compared as laboratory markers of excessive alcohol consumption

Concentrations of both desialylated transferrin (dTf) and the mitochondrial isoenzyme of aspartate aminotransferase (EC 2.6.1.1, mAST) have been claimed to be increased in sera of alcoholic subjects. To investigate the diagnostic usefulness of these new biochemical markers of alcoholism and to compare them with more conventional markers, we measured dTf and mAST in the sera of controls, alcoholic subjects, and patients with nonalcoholic liver diseases (NALD). Alcoholic subjects had significantly (P less than 0.001) higher ratios of dTf to total transferrin than did either healthy controls or patients with NALD (sensitivity 81%, specificity 97%). The mAST was increased in 92% of alcoholic subjects but also in 48% of patients with NALD. The mAST/total AST ratio differentiated the alcoholic subjects from those with NALD (P less than 0.001) with a sensitivity of 92%, but the specificity was only 70%. In contrast, the conventional markers were less sensitive and less specific. We conclude that the best available single laboratory marker for current heavy alcohol consumption is the ratio dTf/total transferrin.     

酒精性肝病患者健康相关生存质量研究

目的研究酒精性肝病患者健康相关生存质量及其与疾病严重程度的关系以及对比酒精性肝病与慢性乙型肝炎患者健康相关生存质量的差别。方法 2010年12月至2011年10月收治的70例男性酒精性肝病患者(非肝硬化组45例,肝硬化组25例),56例男性慢性乙型肝炎患者(非肝硬化组24例,肝硬化组32例)以及42例男性健康对照组受试者参与试验。所有受试者回答SF-36V2(中文版)量表,通过SF-36V2软件计算出:生理功能、生理职能、躯体疼痛、总体健康、活力、社会功能、情感职能、精神健康共8个维度,以及躯体健康总评和精神健康总评。使用协方差分析对比健康对照组,酒精性肝病非肝硬化组,以及酒精性肝病肝硬化组健康相关生存质量;对比酒精性肝病与慢性乙型肝炎患者健康相关生存质量。结果和健康对照组相比,酒精性肝病患者随着疾病的加重,SF-36V2各维度评分明显降低(P<0.05)。酒精性肝病非肝硬化组患者较慢性乙型肝炎非肝硬化组患者仅生理功能、生理职能、活力、躯体健康总评四项评分轻度受损(P<0.05)。酒精性肝病肝硬化组与慢性乙型肝炎肝硬化组患者SF-36V2各维度评分相似(P>0.05)。结论酒精性肝病患者健康相关生存质量降低,且病情越重,健康相关生存质量越差。酒精性肝病患者健康相关生存质量与慢性乙型肝炎患者相似。     

1-14C]Ethanol breath test in alcoholic liver disease

The activity of ethanol metabolising enzymes was assessed in 51 patients with alcoholic and non-alcoholic liver disease using tracer doses of [1-14C]ethanol and measuring 14CO2 excretion in the breath. Alcoholic patients with only fatty infiltration of the liver showed significantly increased activity compared with controls. Comparing alcoholic patients with cirrhosis and a serum albumin greater than 28 g/l, activity in those with a recent history of continued heavy drinking was significantly greater than in patients who had abstained from alcohol. In addition, both groups of alcoholic cirrhosis showed significantly more activity than patients with non-alcoholic cirrhosis. The activities of patients with acute alcoholic or viral hepatitis were normal when their prothrombin times were less than 7 sec prolonged, but were reduced when prolongation exceeded 7 sec. These results demonstrate that in chronic alcoholic liver disease, even with cirrhosis, alcohol can still increase the activity of ethanol oxidising enzymes provided hepatic function remains adequate. However, this response is lost in acute liver damage and in chronic alcoholic disease with severe hepatic dysfunction.     

Pharmacokinetic study of the interaction between rifampicin and ketoconazole

This study assessed the potential pharmacokinetic interaction between rifampicin and ketoconazole, two drugs used to treat the increasingly common combination of Mycobacterium tuberculosis and Candida albicans infection in AIDS patients. The peak plasma rifampicin concentrations in six healthy male subjects were not altered when taken in conjunction with ketoconazole. However, the peak plasma ketoconazole levels were significantly diminished when taken in conjunction with rifampicin, compared to when taken alone (P less than 0.015). The mean area under the curve (AUC) for ketoconazole was significantly diminished when taken with oral or intravenous rifampicin (P less than 0.001).     

Basement membrane-related and type III procollagen-related antigens in serum of patients with chronic viral liver disease

To assess the significance of serum basement membrane- and type III procollagen-related antigens in reflecting the degree of liver fibrosis, we measured radioimmunologically the concentrations of 7S collagen, laminin fragment P1, and the aminoterminal propeptide of type III procollagen (P-III-P) in serum from 48 patients with chronic viral liver disease: chronic persistent hepatitis (9), chronic active hepatitis (13), chronic active hepatitis with lobular disorganization (17), and liver cirrhosis (9). Concentrations of 7S collagen, laminin P1, and P-III-P in serum were increased in respectively 92%, 69%, and 77% of the patients with both chronic active hepatitis with lobular disorganization and liver cirrhosis. Concentrations of 7S collagen and laminin P1 in serum correlated well (r = 0.65, P less than 0.001, and r = 0.55, P less than 0.001, respectively) with the histological grade of liver fibrosis, whereas P-III-P correlated only weakly (r = 0.33, P less than 0.05). Evidently, measurement of serum 7S collagen is a reliable noninvasive test for detection of fibrosis in chronic viral liver disease.     

Three serum markers of collagen biosynthesis in Nigerians with cirrhosis and various infectious diseases

Serum immunoreactive prolyl hydroxylase protein, galactosylhydroxylysyl glucosyltransferase activity, and the aminoterminal propeptide of type III procollagen (S-Pro(III)-N-P) were measured in twenty patients with cirrhosis and ninety with various infectious diseases, and the values were compared with those in sixty apparently healthy Nigerians. The means for all three markers were elevated significantly in the patients with cirrhosis (P less than 0.001), acute viral hepatitis (P less than 0.001), amoebic liver abscess (P less than 0.001) and the early stages of Schistosoma mansoni infection (P less than 0.001 for S-Pro(III)-N-P, P less than 0.005 for the two other markers). The mean S-Pro(III)-N-P was also distinctly elevated during the early stages of Schistosoma haematobium infection (P less than 0.01) and filariasis (P less than 0.001), whereas none of the three markers was elevated during an acute attack of malaria. Significant correlations were found between the values for the three markers within the groups of patients with cirrhosis, amoebic liver abscess and schistosomiasis, the correlations for the pooled group of all patients being highly significant (P less than 0.001). The data suggest that elevated hepatic collagen formation is found not only in cirrhosis but also in several infectious diseases. The three serum markers may be useful for showing the stages of active collagen formation in various liver diseases and for predicting the development of fibrosis in acute cases if the values remain elevated.     

非酒精性脂肪性肝病发病时瘦素的变化

目的研究血清瘦素水平在非酒精性脂肪性肝病发病时的变化。方法样本取自2004年10月14日~11月4日在本院体体检中心体检人群,入选标准:BMI25~29.9,无酗酒史,肝炎病毒标志物阴性,无糖尿病者。符合标准的人群共有81例,其中非酒精性脂肪肝患者59例,男40例,女19例;正常对照组22例,男17例,女5例。结果非酒精性脂肪肝病组较对照组BMI更高(26.7 vs 26.15 kg/m2;P=0.02)、WHR(0.9 vs 0.86;P=0.002)及血脂更高(1.99 vs 1.42 mmol/L;P=0.001)、胰岛素敏感指数更低(2.53×10-2vs 3.96×10-2L2*mmoL-1*IU-1;P=0.005),以单因素分析为基础的二值多元lo-gistic回归分析显示:BMI和血脂的影响不存在统计学意义,对非酒精性脂肪肝的发病具有影响的依次是:WHR(P=0.001)和瘦素(P=0.027)。结论在BMI匹配及没有糖尿病的轻度肥胖人群中,瘦素水平在NAFLD组和正常对照之间没有差异,但是多元logistic回归分析显示WHR和瘦素是非酒精性脂肪性肝病发病的独立影响因素。     

Effects of antiretroviral dideoxynucleosides on polymorphonuclear leukocyte function.

Dideoxynucleosides (zidovudine[AZT], dideoxycytidine[ddC], and dideoxyinosine[ddI]) are promising new agents for the management of human immunodeficiency virus type 1 (HIV-1) infections. In light of recent data demonstrating defects in the polymorphonuclear leukocyte (PMN) bactericidal activity of HIV-1-infected patients and since many chemotherapeutic agents affect PMN function, we examined their effects on the function of PMNs from both healthy and HIV-1-infected individuals in vitro. AZT (0.1 to 25 microM), ddC (0.01 to 1 microM), and ddI (0.2 to 50 microM) had no effect on viability, chemotaxis to N-fromylmethionyl leucyl phenylalanine, phagocytosis of Candida albicans or Staphylococcus aureus, or superoxide production following stimulation by N-formylmethionyl leucyl phenylalanine. Killing of C. albicans was not affected by AZT but was enhanced by 0.1 and 1 microM ddc (a 1 microM, killing was 26.0 +/- 2.02% compared with 17.0 +/- 0.73% for controls: P = 0.006) and 0.2 to 50 microM ddI (at 10 microM, killing was 25.0 +/- 0.68% compared with 17.8 +/- 0.91% for controls; P = 0.002). Killing of S. aureus was unchanged by AZT and ddC but was significantly enhanced by ddI at 0.2 to 20 microM (at 2 microM, killing was 71.2 +/- 5.57% compared with 51.4 +/- 6.29% for controls; P = 0.0045). In addition, the preexisting defective bactericidal capacity of PMNs from HIV-1-infected patients was enhanced by ddI (P less than 0.025). Potential enhancement by these dideoxynucleosides of certain PMN functions of HIV-1-infected patients deserves further study.     

Erythrocyte aldehyde dehydrogenase activity in alcoholic subjects and its value as a marker for hepatic aldehyde dehydrogenase in subjects with and without liver disease

Erythrocyte aldehyde dehydrogenase activity was assayed in actively drinking alcoholics, patients with alcoholic liver disease who claimed to be abstaining, patients with non-alcoholic liver disorders and normal controls. Hepatic cytosolic aldehyde dehydrogenase was also assayed in the majority of the subjects. Actively drinking alcoholics had significantly lower erythrocyte aldehyde dehydrogenase activity than controls (P less than 0.01) but abstaining alcoholic liver disease and non-alcoholic liver disorder subjects did not. There was a significant correlation between erythrocyte and hepatic cytosolic aldehyde dehydrogenase activity in the control group (r = 0.94, P less than 0.05) but not in the other study groups.