Serum-ascites albumin gradients in nonalcoholic liver disease

Several studies performed in alcoholics with advanced liver disease have demonstrated a positive correlation between the serum-ascites albumin gradient (SAAG) and measured portal venous pressure. A single study performed in 15 patients with exudative malignant ascites and 29 patients with alcoholic liver disease demonstrated that a SAAG of <1.1 was essentially diagnostic of a malignant origin of the ascites. In an effort to confirm and extend these observations to individuals with nonalcoholic liver disease, 24 patients with nonalcoholic liver disease and 11 with alcoholic liver disease undergoing orthotopic liver transplantation (OTLx) were studied. At the time of liver transplantation, each had their serum and ascitic fluid albumin levels determined, the gradient calculated, and their portal venous pressure (PVP) as well as the corrected portal venous pressure (PPc) measured directly. A significant correlation (r=0.624) between the PPc and the SAAG was found in the 11 alcoholics (P<0.05). No such correlation existed for those with nonalcoholic liver disease (r=0.398). Moreover, a SAAG <1.1 was found in three of nonalcoholics with cirrhosis in the absence of an abdominal malignancy. We conclude that (1) the SAAG and PPc are statistically related to each other in individuals with alcoholic liver disease but not in those with a nonalcoholic cause for cirrhosis, and (2) SAAG <1.1 is not diagnostic of abdominal malignancy but can occur in those with advanced nonmalignant hepatic disease.This work was supported by grants NIAAA AA04425-07, AA06772-03, and NIDDK DK32556-05.     

Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis

Hepatic venous catheterization is widely used to assess portal pressure. However, it remains unclear whether wedged hepatic venous pressure is a close indicator of portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. To address this issue, we analyzed the data from our previous published studies. Forty patients with nonalcoholic cirrhosis (HBV infection in five, HCV infection in 28, and cryptogenic in seven) were available in this analysis. A vasoconstrictor (N=14), vasodilator (N=10), or combination (N=16) was administered. The agreement of the changes between portal and wedged hepatic venous pressures during pharmacological manipulation was assessed by an intraclass correlation coefficient. The intraclass correlation coefficient in each subgroup was more than 0.60 (0.62 in vasoconstrictor group, 0.87 in vasodilator group, and 0.73 in combination group). When the analysis was performed according to the cause of liver disease, the values were 0.67 in HBV infection, 0.73 in HCV infection, and 0.74 in cryptogenic cirrhosis. These results suggest that wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in patients with nonalcoholic cirrhosis.     

Wedged hepatic venous pressure adequately reflects portal pressure in hepatitis C virus-related cirrhosis

Wedged hepatic venous pressure (WHVP) is equivalent to portal venous pressure in patients with alcoholic liver diseases. However, it may underestimate portal pressure in nonalcoholics, which is important because hepatitis C virus (HCV) infection is a frequent cause of chronic liver disease. We investigated the agreement between directly measured portal pressure and WHVP in alcoholic and HCV-related liver diseases. Seventy-one patients with liver disease resulting from HCV infection (n = 32), alcohol (n = 25), or both (n = 14) underwent simultaneous measurements of WHVP (by hepatic vein catheterization) and portal pressure (by direct puncture). In 9 patients, measurements were repeated 20 minutes after acute iv propranolol administration. WHVP showed an excellent agreement with portal pressure in patients with cirrhosis resulting from either HCV, alcohol or both (intraclass correlation coefficient: 0.94, 0.93, and 0.97, respectively; P <.001). A discrepancy of >/=5 mm Hg was observed in 7 cases. WHVP underestimated portal pressure in only 1 case and exceeded portal pressure by >/=5 mm Hg in 6 patients. The WHVP response to propranolol closely and significantly correlated with changes in portal pressure (intraclass correlation coefficient: 0.87; P <.004). The simple and safe measurement of WHVP accurately reflects portal pressure in alcoholic and HCV-related liver disease. This technique also allows us to accurately assess the portal pressure response to propranolol in both alcoholic and HCV-related cirrhosis.     

Hepatic collagen synthesis in patients with alcoholic and nonalcoholic liver disease

To examine the synthesis of hepatic collagen in patients with alcoholic and nonalcoholic liver disease, liver biopsy specimens were incubated in vitro with 14C-proline, and the radioactivity of the newly synthesized protein-bound 14C-hydroxyproline was measured. Mean hepatic collagen synthesis was 0.82 +/- 0.19 pmole of 14C-hydroxyproline/g liver/2 h in control subjects without histological liver fibrosis. Hepatic collagen synthesis was increased in patients with alcoholic and nonalcoholic liver diseases, especially in those with alcoholic fibrosis, alcoholic cirrhosis and chronic active hepatitis. The raised collagen synthesis in alcoholic liver disease rapidly decreased after withdrawal of alcohol. When alcoholic liver disease were compared with nonalcoholic liver disease, there was no significant difference in hepatic collagen synthesis.     

Different hemodynamic patterns of alcoholic and viral endstage cirrhosis: analysis of explanted liver weight, degree of fibrosis and splanchnic Doppler parameters

OBJECTIVE: In cirrhosis, portal hemodynamics is usually considered independently of the disease etiology. The objective of this study was to investigate the role of the etiology of liver disease on the relationship between liver blood flow and liver pathology in endstage cirrhosis. MATERIAL AND METHODS: Portal blood velocity and volume, congestion index of the portal vein, and hepatic and splenic pulsatility indices were evaluated with echo-Doppler in cirrhotic patients immediately before liver transplantation. When a patent paraumbilical vein was present, its blood flow was measured and effective portal liver perfusion was calculated as portal blood flow minus paraumbilical blood flow. The hemodynamic parameters were correlated with liver weight and the pattern of the liver fibrosis morphometrically assessed in explanted livers. A total of 131 patients with alcoholic or viral cirrhosis were included in the study. RESULTS: In alcoholic cirrhosis, liver weight was higher than that in viral disease (1246+/-295 g versus 1070+/-254 g, p=0.001), portal liver perfusion per gram of liver tissue was lower (0.49+/-0.36 ml g(-1) min(-1) versus 0.85+/-0.56 ml g(-1) min(-1), p=0.004) and hepatic pulsatility indices were higher (1.45+/-0.31 versus 1.26+/-0.30, p=0.018). The degree of liver fibrosis was similar in alcoholic and viral cirrhosis (11.7+/-5.5% versus 11.0+/-4.4%, p=NS). An inverse relationship between liver weight and Child-Pugh score was disclosed in viral (p<0.001) but not in alcoholic disease. CONCLUSIONS: A different hemodynamic pattern characterizes the advanced stage of cirrhosis of alcoholic and viral origin. A more severe alteration of intrahepatic portal perfusion, probably coexisting with a more severe hepatocyte dysfunction, and a higher liver weight can be detected in alcoholic cirrhosis.     

Serum laminin and portal pressure in alcoholic cirrhosis. A study of 39 patients

A correlation between serum laminin, a glycoprotein found in basement membranes, and hepatic wedge pressure has previously been reported in a small number of patients with various liver diseases. To study this relationship in patients with alcoholic cirrhosis, we measured the wedge hepatic pressure and venous gradient, in comparison with serum concentrations of laminin and collagen metabolism products: N-terminal peptide of type III procollagen, collagen type I, and collagen type III in 39 patients. A statistically significant correlation was observed between serum laminin and wedged hepatic pressure (r = 0.529; p less than 10(-3] or hepatic venous gradient (r = 0.482; p = 0.002). By contrast, no statistically significant correlation was found between hemodynamic parameters and serum concentrations of N-terminal peptide of type III procollagen, collagen type I or collagen type III. These results suggest that, in patients with alcoholic cirrhosis, portal pressure may be estimated by serum concentration of laminin, and that perisinusoidal fibrosis, especially basement membrane thickening, may play an important role in the pathogenesis of portal hypertension in these patients.     

Characteristics of serum IgA and liver IgA deposits in alcoholic liver disease

Patients with alcoholic liver disease frequently reveal an increase in IgA serum concentration and IgA deposits in a continuous pattern along hepatic sinusoids. We investigated whether the hepatic IgA deposits are a passive reflection of changes in concentration or composition of IgA in the circulation, or represent a distinct effect of alcohol on the liver. Forty-one patients with alcoholic liver disease (daily alcohol intake at least 50 gm for more than five consecutive years) were compared with 41 patients with nonalcoholic liver disease. Patients in both groups were matched for serum IgA and histopathological changes in the liver biopsy. IgA deposits in the liver were found in 78% of the alcoholic patients and in 12% of the nonalcoholic patients. The presence of deposits was not related to histopathological changes in the liver or to the serum IgA concentration. In serum IgA subclass distribution, alcoholic patients differed from nonalcoholic patients by a slight but significant shift to IgA2; in contrast, the hepatic IgA deposits in alcoholic patients were almost of the IgA1 subclass. Serum secretory component (which is an equivalent of serum secretory IgA) was elevated in both alcoholic and nonalcoholic patients; patients with a liver biopsy revealing hepatitis showed the highest level. In contrast, the hepatic deposits did not contain secretory component. We conclude that the continuous deposits of IgA along liver sinusoids are not a passive reflection of changes in concentration or composition of circulating IgA, but may represent a distinct effect of alcohol on the liver related to the role of this organ in IgA metabolism.     

Splanchnic and renal extraction of circulating hyaluronan in patients with alcoholic liver disease

Splanchnic and renal extraction of hyaluronan was determined in patients with alcoholic cirrhosis (n = 9), non-cirrhotic alcoholic liver disease (n = 5), and controls without liver disease (n = 19) in the supine fasting condition. Arterial plasma concentration of hyaluronan was significantly increased in patients with cirrhosis (mean 480 micrograms/l) as compared to non-cirrhotic patients (29 micrograms/l, P less than 0.001) and controls (25 micrograms/l, P less than 0.001), whereas no difference was present between the two last-mentioned groups. In patients with liver disease, circulating hyaluronan was inversely correlated to indocyanine green clearance (r = -0.85, P less than 0.001) and to galactose elimination capacity (r = -0.62, P less than 0.02), but positively correlated to portal pressure (determined as wedged-to-free hepatic vein pressure) (r = 0.92, P less than 0.001). Splanchnic extraction ratio (arterio-hepatic venous extraction ratio) had a mean value of 0.14 in patients with cirrhosis as compared to 0.36 in non-cirrhotic patients (P less than 0.05) and 0.34 in controls (P less than 0.025). Splanchnic hyaluronan extraction was not correlated to liver function tests or portal pressure. In patients with alcoholic liver disease no significant renal hyaluronan extraction was found as compared to an extraction ratio of 0.17 in controls (P less than 0.05). Our results suggest that the increased level of circulating endogenous hyaluronan found in patients with cirrhosis is caused by a combination of increased supply to and decreased extraction from plasma.     

Portal cirrhosis in alcoholic and nonalcoholic women

Summary 1. During a 10-year period 59 women with portal cirrhosis were hospitalized at the University of Oklahoma Hospital. Approximately half of the patients were alcoholic. Twenty-one of the nonalcoholic and 12 of the alcoholic women and diagnoses of portal cirrhosis supported by examination of hepatic tissue. These 33 patients with tissue diagnosis are compared in detail.2. The alcoholic women were younger at the onset of their symptoms and were commonly from urban areas. The initial clinical diagnosis on these patients was usually cirrhosis, since they frequently had the symptoms, physical findings, and abnormal hepatic function tests associated with this disease.3. The nonalcholic women were on the average older at the onset of their symptoms. Since they usually had abdominal pain and ascites without many of the expected physical findings of cirrhosis, their initial clinical diagnoses were frequently incorrect. Arterial hypertension or other extrahepatic disease occurred in the majority.A high index of suspicion and a liver biopsy are needed to make the diagnosis in these patients.4. The possible etiologic factors leading to cryptogenic portal cirrhosis in the nonalcoholic women are discussed briefly.Research Fellow, National Institute of Arthritis and Metabolic Diseases.     

Relationship between degree of portal hypertension and liver histologic lesions in patients with alcoholic cirrhosis

The relationship between the degree of portal hypertension and histologic liver lesions was studied in a group of 84 patients with histologically proven alcoholic cirrhosis. The degree of portal hypertension was evaluated by the gradient between wedged and free hepatic venous pressures. Five histologic lesions were quantified: liver cell necrosis, Mallory bodies, neutrophilic infiltrate, fibrosis, and fatty infiltration. The gradient between wedged and free hepatic venous pressures was significantly correlated with the degree of liver cell necrosis and the degree of neutrophilic infiltrate. The stepwise regression analysis showed that only liver cell necrosis has a significant and independent correlation for the degree of portal hypertension. The value for the gradient between wedged and free hepatic venous pressures was significantly higher in patients with (N=48) than in those without (N=36) acute alcoholic hepatitis (19.4±0.8 and 16.5±0.7 mmHg, respectively). Thus, histologic liver lesions observed in acute alcoholic hepatitis may play a role in the risk of complications of portal hypertension in patients with alcoholic cirrhosis.     

Evaluation of Quantitative Portal Venous, Hepatic Arterial, and Total Hepatic Tissue Blood Flow Using Xenon CT in Alcoholic Liver Cirrhosis: Comparison With Liver Cirrhosis C

Background/Aims: Xenon computed tomography (Xe-CT) is a noninvasive method of quantifying and visualizing tissue blood flow (TBF). For the liver, Xe-CT allows separate measurement of hepatic arterial and portal venous TBF. The present study evaluated the usefulness of Xe-CT as a noninvasive diagnostic procedure for measuring hepatic TBF in alcoholic liver cirrhosis (AL-LC), compared with liver cirrhosis C (C-LC).
Methods: Xenon computed tomography was performed on 12 patients with AL-LC and 17 patients with C-LC. The severity of LC was classified according to Child–Pugh classification. Correlations between hepatic TBF and Child–Pugh classification were examined. Correlations of hepatic TBF in Child–Pugh class A to C-LC and AL-LC were also examined.
Results: The mean portal venous TBF (PVTBF) was significantly lower in AL-LC than in C-LC ( p =0.0316). Similarly, the mean total hepatic TBF (THTBF) was significantly lower in AL-LC than in C-LC ( p =0.0390). PVTBF displayed a significant negative correlation with Child–Pugh score ( r =−0.396, p =0.0368).
Conclusions: Measurement of hepatic TBF using Xe-CT is useful as a noninvasive, objective method of assessing the state of the liver in chronic liver disease.     

Serum Carbohydrate-Deficient Transferrin as a Marker of Alcohol Consumption in Patients with Chronic Liver Diseases

We meesured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employses, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcohotic liver cirrhosls, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 ± 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 ± 5.1 and 13.7 ± 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and γ-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics     

Relative Versus Absolute Carbohydrate-Deficient Transferrin as a Marker of Alcohol Consumption in Patients With Acute Alcoholic Hepatitis

BACKGROUND: Carbohydrate-deficient transferrin has been described as a sensitive and specific marker for alcohol consumption. This study investigated the usefulness of carbohydrate-deficient transferrin as a marker of alcohol consumption in acute alcoholic hepatitis. METHODS: Absolute concentrations (U/I) and relative values (%) of carbohydrate-deficient transferrin determined in serum with commercial assays, as well as conventional markers for alcohol consumption, were compared with the alcohol consumption (as estimated by a questionnaire) in patients with acute alcoholic hepatitis (n = 19), alcoholic liver cirrhosis (n = 37), and nonalcoholic liver diseases (n = 16). RESULTS: The concentration of carbohydrate-deficient transferrin was increased (p < 0.001) in nonabstaining patients (median intake 80 g alcohol/day) with alcoholic liver cirrhosis (45.7 +/- 30 U/l), but not in patients with acute alcoholic hepatitis (20.0 +/- 7.8 U/l) despite higher alcohol consumption (median 130 g/d), nor in abstainers with alcoholic liver cirrhosis (19.4 +/- 6.0 U/l) or nonalcoholic liver disease (18.5 +/- 6.7 U/l). However, the relative values of carbohydrate-deficient transferrin were increased both in acute alcoholic hepatitis (7.9 +/- 2.1%) and nonabstainers with alcoholic liver cirrhosis (7.4 +/- 2.8%), but not in abstainers with alcoholic liver cirrhosis (4.6 +/- 3.5%) or nonalcoholic liver disease (3.8 +/- 0.9%) (p < 0.001). In acute alcoholic hepatitis, the sensitivity and specificity were only 32% and 87% for absolute concentrations, respectively, but 79% and 97% for relative values of carbohydrate-deficient transferrin. The concentrations of carbohydrate-deficient and total transferrin in serum were strongly correlated (r = 0.60; p = 0.008). CONCLUSIONS: The relative value (% of total), but not the absolute concentration, of carbohydrate-deficient transferrin in serum is a useful marker of alcohol consumption in acute alcoholic hepatitis.     

Combined Upper and Lower Gastrointestinal Endoscopy: A Prospective Study in Alcoholic and Nonalcoholic Cirrhosis

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis. Most of the available data regarding the prevalence of upper and lower gastrointestinal sites of bleeding in cirrhotic patients have been obtained in individuals with alcoholic cirrhosis evaluated in the course of an acute gastrointestinal bleeding episode. Few data exist, however, as to the prevalence of either potential bleeding sites or of normal endoscopic findings in hemodynamically stable individuals with cirrhosis of any etiology. Five hundred ten cirrhotic subjects, who were evaluated for possible liver transplantation (OLTx) between January 1985 and June 1987, were included in this study. Seventy-five had alcoholic cirrhosis and 435 had nonalcoholic cirrhosis of various etiologies. Of these 510 patients, 412 underwent combined upper and lower gastrointestinal endoscopy and 98 underwent upper gastrointestinal endoscopy alone. Gastritis, gastric and duodenal ulcer disease were found significantly (each at least p less than 0.025) more often in patients with alcoholic liver disease than in those with nonalcoholic liver disease. The prevalence of the various lower gastrointestinal lesions in both groups was similar. Of particular interest is the fact that in alcoholic cirrhotics, the prevalence of gastritis, gastric ulcer and duodenal ulcer disease was unrelated to the degree of portal hypertension, whereas in the nonalcoholic cirrhotics the prevalence of gastritis and duodenal ulcer disease but not gastric ulcer disease was associated significantly with the degree of portal hypertension as assessed by the presence or absence of large esophageal varices, ascites, and hepatic encephalopathy.     

酒精性肝病患者血清瘦素及其受体基因Gln223Arg多态性变化

目的 观察酒精性肝病患者血清瘦素（Lep）水平及其受体（LEPR）基因Gln223Arg多态性变化,并探讨其意义.方法 选择酒精性肝病患者106例,其中酒精性脂肪性肝炎45例（AH组）,酒精性肝硬化61例（AC组）,同期健康体检者65例作为对照组.采用ELISA法检测血清Lep,葡萄糖氧化酶—过氧化物酶法检测空腹血糖（FPG）,化学发光免疫分析法检测空腹血清胰岛素（FINS）,PCR-RFLP法检测LEPR基因Gln223Arg多态性,并计算HOMA-IR.结果 AH组血清Lep、HOMA-IR分别为（8.95±1.81） ng/mL、2.44±0.25,AC组分别为（10.57±2.00） ng/mL、3.21 ±0.17,对照组分别为（4.44±0.81） ng/mL、1.77 ±0.18;AH组、AC组与对照组比较,P均＜0.05.AH组、AC组血清Lep与HOMA-IR均呈正相关（r=0.45、0.38,P均＜0.01）.AH组AA、A/G、GG的例数分别为3、11、31例,AC组分别为0、25、36例,对照组分别为1、12、52例;AC组与对照组比较,P＜0.05.结论 酒精性肝病患者血清Lep、HOMA-IR水平升高,AC组患者LEPR基因Gln223 Arg杂合基因频率高于健康人群,可能通过胰岛素—瘦素轴促进胰岛素抵抗,影响体内脂肪代谢,参与酒精性肝病的发病机制.     

Retinol and retinyl esters in patients with alcoholic liver disease

Liver retinoid levels and the retinyl esters were examined in liver biopsy specimens from 70 patients with alcoholic and nonalcoholic liver diseases. There was a wide variation in the liver retinoid levels. The liver retinoid level was statistically significantly lower in 15 patients with alcoholic liver disease and a depressed Normotest (NT) value of less than 65% compared with patients with alcoholic liver disease and a normal NT value of greater than 65% (P less than 0.01). The mean serum retinol level in patients with alcoholic cirrhosis was 0.68 +/- 0.38 mumol/l compared with 1.99 +/- 1.14 mumol/l in patients with alcoholic fatty liver (P less than 0.03). The relative amount of retinyl oleate was increased in the alcoholic fatty liver compared with the nonalcoholic fatty liver (P less than 0.001).     

Latent portasystemic encephalopathy

Forty patients with chronic liver disease and portal hypertension but without clinical signs of portasystemic encephalopathy (15 patients with nonalcoholic cirrhosis, 15 patients with alcoholic cirrhosis, and 10 patients with minimal EEG changes) and a control group of 12 patients with chronic alcoholic pancreatitis were studied using an extensive psychometric program, which, in the same form, is used for expert reports on driving capacity. Of the cirrhotic patients, 60% were considered unfit to drive; in 25% driving capacity was questionable, 15% (only nonalcoholic cirrhotics) were considered fit to drive. In contrast 75% of the patients with alcoholic pancreatitis were considered fit to drive. Major defects were found only in three heavy alcoholics. Patients with alcoholic cirrhosis scored lower than patients with nonalcoholic cirrhosis. This was due, to differences in liver function rather than to the effect of alcohol consumption. Patients with minimal EEG changes were practically all considered unfit to drive.     

Hepatic collagen synthesis in patients with alcoholic and nonalcoholic liver disease

To examine the synthesis of hepatic collagen in patients with alcoholic and nonalcoholic liver disease, liver biopsy specimens were incubated in vitro with¹⁴C-proline, and the radioactivity of the newly synthesized protein-bound¹⁴C-hydroxyproline was measured. Mean hepatic collagen synthesis was 0.82±0.19 pmole of¹⁴C-hydroxyproline/g liver/2 h in control subjects without histological liver fibrosis. Hepatic collagen synthesis was increased in patients with alcoholic and nonalcoholic liver diseases, especially in those with alcoholic fibrosis, alcoholic cirrhosis and chronic active hepatitis. The raised collagen synthesis in alcoholic liver disease rapidly decreased after withdrawal of alcohol. When alcoholic liver disease were compared with nonalcoholic liver disease, there was no significant difference in hepatic collagen synthesis. This work was supported in part by a grant-in-aid for EncourageMent of Young Scientists (No.57770489) from the Ministry of Education, Science and Culture of Japan.     

Diagnosis of alcohol-induced liver cirrhosis by indirect portal vein pressure measurement and liver venography]

Indirect measurement of portal pressure and hepatic venography using the balloon catheter technique were investigated to assess the stage of chronic alcoholic liver disease, especially, to diagnose cirrhoses. 80 patients were studied and were categorised in 4 groups according to their liver histology: normal liver (N, n = 6), fibrosis (F, n = 27), incomplete cirrhosis (F/C, n = 11), complete cirrhosis (C, n = 36). Medians of wedged hepatic venous pressure gradient P (= WHVP-FHVP) and of a semiquantitative venographic score S showed increasingly higher values with more severe stages of the disease. Portal pressure (P) and venographic appearance (S) were correlated significantly (r = 0.778, p less than 0.0001). P was most useful to diagnose cirrhosis: Precirrhotic forms were associated with pressure gradients P less than or equal to 5 mm Hg in 97%. Incomplete cirrhoses were distributed in about 50% above and below P = 5 mm Hg, for complete cirrhoses P greater than or equal to 8 mm Hg was found in 97%. Pressure gradients P greater than or equal to 5 mm Hg indicated cirrhotic disease with a specificity of 97%. Sensitivity for complete cirrhoses was also high (97%), for incomplete cirrhoses however low (47%). Venography and measurement of portal pressure as diagnostic tools to predict cirrhoses of alcoholic origin were clearly more useful than biochemical tests (serum bilirubin, quick and cholinesterase). In comparison to laparoscopy the acceptance by patients is higher and the risk is lower if patients with known adverse reactions to contrast materials and risk of thyreotoxicosis induced by iodine are excluded.