Zinc absorption in patients with compensated alcoholic cirrhosis

Zinc absorption was measured by whole-body counting in 10 patients with compensated alcoholic cirrhosis without steatorrhoea and in 8 healthy subjects. After oral administration of 65Zn the absorption was measured at regular intervals until a straight time/activity retention curve was obtained in a semilogarithmic system, whereafter it was calculated by extrapolation to time zero. Cirrhotic patients had a median absorption of 69% (27-90%), compared with 42% (25-67%) in healthy subjects (P less than 0.01). Median T1/2 of 65Zn as calculated from the retention curve was 156 days (83-280 days) in cirrhotic patients and 103 days (72-132 days) in healthy subjects (P less than 0.05). Median serum zinc value was 11 mumol/l (9-17 mumol/l) in cirrhotic patients and 16 mumol/l (12-17 mumol/l) in healthy subjects (P less than 0.01). Median erythrocyte zinc value was 224 mumol/l (205-281 mumol/l) in cirrhotics and 223 mumol/l (188-275 mumol/l) in healthy subjects (P less than 0.1). Six cirrhotic patients, of whom four took diuretics, had increased urinary zinc excretion (greater than 15 mumol/24 h). Zinc absorption seems intact in compensated alcoholic cirrhosis. The increased absorption and prolonged T1/2 of 65Zn might be compensatory to a moderate zinc depletion.     

Significance of blood taurine levels in patients with first time acute ischaemic cardiac pain

We studied blood taurine levels of 91 consecutive patients admitted with first time cardiac pain suggestive of myocardial ischaemia. Blood taurine levels of patients with coronary arterial disease, but without a recent myocardial infarction (n = 36), at rest and after a maximal treadmill stress testing were also determined. The blood taurine level at the time of admission was significantly elevated (P less than 0.001) in patients with an acute myocardial infarction (n = 63) (271 +/- 98 mumol/l) and those with unstable angina (n = 22) [214 +/- 81 mumol/l] compared to that of normal subjects (n = 75) at rest (140 +/- 40 mumol/l). Patients with a myocardial infarction had a higher level than those with unstable angina (P less than 0.01) and non-ischaemic chest pain (n = 6) [P less than 0.05]. The levels peaked after 12-48 hours only in patients with infarction [367 +/- 140 mumol/l] (P less than 0.001) and unstable angina (273 +/- 82 mumol/l) (P less than 0.02). The levels of creatine kinase within the serum at the time of admission did not correlate well with those of blood taurine, but the peak levels of the former did correlate with the latter (P less than 0.02). Patients with known coronary arterial disease had a higher resting [236 +/- 69 mumol/l] level of blood taurine than normal subjects (P less than 0.001), which was further elevated [269 +/- 80 mumol/l] following exercise (P less than 0.001). Thus, an elevated level of taurine in whole blood at the time of admission of patients with an acute cardiac pain suggested the diagnosis of either a myocardial infarction or unstable angina. The level of taurine may be utilised to differentiate the two conditions.     

Computerized measurement of iron in liver biopsies: a comparison with biochemical iron measurement

The measurement of stainable hepatic iron using a microcomputer image analysis system was compared with standard biochemical measurements of liver iron content in 103 liver biopsy specimens--29 of idiopathic hemochromatosis, 51 of alcoholic liver disease and 23 of various nonalcoholic liver diseases. Sections were stained using Perls' method for iron; the mean area staining positively for iron was measured and expressed as a percentage of the area of biopsy measured. Biochemical (biochemical hepatic iron [mumol/gm dry wt]/age) and morphometrical (morphometrical hepatic iron [%]/age x 100) hepatic iron indices were calculated. Patients in the idiopathic hemochromatosis group had significantly higher biochemical hepatic iron concentrations (p less than 0.001) compared with the alcoholic liver disease and nonalcoholic liver disease groups: 284 (range = 119 to 631), 21 (range = 2 to 65) and 15 (range = 3 to 31) mumol/gm dry wt, respectively. The biochemical hepatic iron index was also significantly higher (p less than 0.001) in the hemochromatosis group compared with the alcoholic liver disease and nonalcoholic liver disease groups: 5.8 (range = 2.1 to 13.7), 0.4 (range = 0 to 1.6) and 0.4 (range = 0 to 1.1), respectively. Computerized measurements were significantly higher in the hemochromatosis group (p less than 0.001) compared with the alcoholic liver disease and nonalcoholic liver disease groups: 9.72% (range = 1.50% to 29.26%), 0.13% (range = 0% to 1.20%) and 0.03% (range = 0% to 0.40%), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sinusoidal caliber in alcoholic and nonalcoholic liver disease: diagnostic and pathogenic implications

Portal hypertension in alcoholic liver disease has been attributed to an increased resistance to blood flow either of sinusoidal or of postsinusoidal origin. The former should be accompanied by sinusoidal compression while the latter is expected to result in an increased or a normal sinusoidal diameter. Patients with alcoholic liver disease showed a marked reduction (p less than 0.001) in relative sinusoidal area (995 +/- 135 micron 2; n = 19) when compared to nonalcoholic patients with normal liver histology (5,100 +/- 389 micron 2; n = 6), or to patients with nonalcoholic liver disease (6,242 +/- 467 micron 2; n = 19). Hepatocyte surface area was significantly increased in patients with alcoholic liver disease when compared to hepatocytes from normal biopsies (563 +/- 32 micron 2 vs. 301 +/- 26 micron 2; p less than 0.001). Patients with nonalcoholic liver disease had hepatocyte surface areas within the normal range (327 +/- 14 micron 2). There was a significant inverse correlation between hepatocyte size and sinusoidal area (r = -0.63; p less than 10(-6); n = 44), indicating that larger hepatocytes were associated with sinusoidal compression. In the alcoholic patients, portal pressure correlated inversely (r = -0.77; p less than 0.01) with sinusoidal area only after the sinusoidal area was markedly reduced to areas below 20% of normal. Such a threshold was not reached in patients with nonalcoholic liver disease, in whom no correlation between sinusoidal area and portal pressure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

The importance of AST / ALT rate in nonalcoholic steatohepatitis diagnosis

BACKGROUND/AIMS: There is a histologic similarity between nonalcoholic steatohepatitis and alcoholic liver disease and in some cases differential diagnosis may be difficult, since some patients do not report abusive alcohol consumption. OBJECTIVE: Evaluating the usefulness of setting the rate AST/ALT for the differential diagnosis of nonalcoholic steatohepatitis and alcoholic liver disease. PATIENTS AND METHODS: Twenty nine obese patients with nonalcoholic steatohepatitis were compared with 28 patients with alcoholic liver disease. The diagnosis of nonalcoholic steatohepatitis was made after exclusion of other causes of liver disease and by histologic findings of, at least, macrovesicular steatosis and hepatocellular necrosis. RESULTS: In patients with nonalcoholic steatohepatitis the medium AST value was 52.3 +/- 21.2 U/L and ALT of 90.1 +/- 37.9 U/L, being the AST/ALT rate lower than 1 in all patients. In patients with alcoholic liver disease the medium AST value was 140 +/- 82.5 U/L and ALT was 50.6 +/- 40.3 U/L. The rate was higher than 1 in all cases and higher than 2 in 24 (85.7%), being statistically significant when compared with patients with nonalcoholic steatohepatitis. CONCLUSION: The AST/ALT rate seems to be useful in the differential diagnosis of liver diseases, while lower than 1 is highly suggestive of nonalcoholic steatohepatitis.     

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.     

Higher levels of serum aminoterminal type III procollagen peptide, and laminin in alcoholic than in nonalcoholic cirrhosis of equal severity.

In vitro models have shown that metabolites of ethanol (acetaldehyde and lactate) stimulate collagen synthesis, thereby, suggesting that they may be important as fibrogenic mediators. The relevance of these findings for fibrogenesis in the human liver in vivo, however, has not as yet been demonstrated. Serum markers for collagen (PIIINP, using radioimmunoassays employing polyclonal antibodies and Fab-fragments (PIIINP-Fab), respectively) and basement membrane (laminin) metabolism were therefore investigated in 25 alcoholic cirrhotics (Pugh-Score: 6.7 +/- 1.9 S.D.) and in 19 comparable nonalcoholic cirrhotics (Pugh-Score: 6.3 +/- 1.5, n.s.) with only slight evidence for inflammation: GOT 28 +/- 22 vs. 24 +/- 21 U/l; GPT 24 +/- 23 vs. 31 +/- 28 U/l; gamma-globulins 24 +/- 8 vs. 22 +/- 5%, respectively (all n.s.). Severity of the disease was assessed by quantitative liver function tests. Levels of PIIINP, PIIINP-Fab and laminin measured by RIA were 21 +/- 19 micrograms/l, 90 +/- 42 micrograms/l and 2.5 +/- 0.8 U/ml in alcoholic cirrhosis and 10 +/- 6 micrograms/l, 61 +/- 10 micrograms/l and 1.9 +/- 0.4 U/ml in nonalcoholic cirrhosis, respectively (all p less than 0.01). Differences on PIIINP and PIIINP-Fab remained significant even after accurate matching for galactose elimination capacity, aminopyrine breath test and hepatic sorbitol clearance. Laminin levels were higher in alcoholic cirrhosis only after matching for the hepatic sorbitol clearance (p less than 0.01). The higher levels of serum markers for collagen and basement membrane metabolism in alcoholic vs. nonalcoholic patients with cirrhosis at equal severity of the disease and with only minimal signs of inflammation may be the clinical reflection of a specific fibrogenic effect of ethanol metabolites.     

Glycerol clearance in alcoholic liver disease.

Glycerol clearance was studied by a primed dose-constant infusion technique in 14 patients with alcoholic liver disease and six normal control subjects. Fasting blood glycerol concentrations were raised in the alcoholic subjects (0.09 +/- 0.01 vs 0.06 +/- 0.01 mumol/l, p less than 0.05) and glycerol clearance was impaired (24.5 +/- 1.9 vs 37.5 +/- 3.2 ml/kg/min, p less than 0.005). Endogenous production rate of glycerol and distribution space at steady state were similar in alcoholic and control subjects. The metabolic clearance rate of glycerol correlated negatively with basal glycerol concentrations. Thus tissue uptake of glycerol is impaired in liver disease. As glycerol is metabolised primarily in the liver by conversion to glucose, these data suggest a defect of gluconeogenesis in alcoholic 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     

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.     

Serum procollagen III peptide in alcoholic and other chronic liver diseases

Increased levels of serum procollagen III peptide (P-III-P) have been found in patients with alcoholic hepatitis and cirrhosis. Serum P-III-P was increased (greater than 15 micrograms/l) in 38 of 44 (86%) patients with alcoholic liver cirrhosis, in 6 of 20 (30%) with fatty liver, in 1 of 13 (8%) with non-alcoholic fatty liver, and in 3 of 14 (21%) with other chronic liver diseases. Median serum P-III-P was almost three times higher in alcoholic liver cirrhosis than in alcoholic fatty liver (p less than 0.001). Serum P-III-P was increased in three of six patients with alcoholic fatty liver and periportal fibrosis. In the total material (n = 91), a statistically significant negative correlation between serum P-III-P and albumin (r = -0.71, p less than 0.001) and Normotest (r = -0.63, p less than 0.001), respectively, and a positive correlation between serum P-III-P and bilirubin (r = 0.65, p less than 0.001) were found. The serum level of P-III-P had no prognostic value concerning the mortality in patients with alcoholic cirrhosis.     

Predictive value of whole blood chemiluminescence in patients with alcoholic hepatitis

Recent reports suggest that ethanol metabolism leads to reactive oxygen intermediates that may be responsible for the lesions observed in alcoholic hepatitis. This study investigated the production of reactive oxygen intermediates in peripheral blood phagocytes of patients with alcoholic hepatitis and attempts to evaluate its predictive value. Using a luminol-dependent chemiluminescence method, reactive oxygen intermediate production was measured directly within microamounts of whole blood, both in the absence (basal chemiluminescence production) and in the presence of phagocyte-stimulating agents including latex, zymosan, phorbol myristate acetate and N-formyl-methionyl-leucyl-phenylalanine. Thirty patients with well-documented and histologically proven alcoholic hepatitis were studied. Pugh's and Child's classification, Orrego's composite clinical and laboratory index and Maddrey's discriminant function were used to assess the prognosis of the liver disease. Patients were followed up monthly for 6 mo. Results were compared with those obtained in 17 patients with nonalcoholic liver disease and in 78 normal control subjects. Basal chemiluminescence production was significantly higher in patients with alcoholic hepatitis than in those with nonalcoholic liver disease and in normal subjects (p less than 0.001). Chemiluminescence responses to latex, zymosan and phorbol myristate acetate were significantly lower in alcoholic hepatitis patients than in normal subjects (p less than 0.001); however, when compared with nonalcoholic liver disease patients, these responses were significantly decreased only in the presence of zymosan (p less than 0.05). Both basal chemiluminescence production (p less than 0.001) and zymosan-induced chemiluminescence responses (p less than 0.02) were closely related to alcoholic hepatitis prognosis indices (i.e., Pugh's and Child's classification, Orrego's composite clinical and laboratory index and Maddrey's discriminant function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Zinc absorption in alcoholics using zinc-65

Alcoholism is occasionally complicated by zinc deficiency. We have assessed the possibility that malabsorption of zinc may be a potential cause. Using a dual isotope absorption technique the absorption of 65Zn in 18 alcoholic patients was 37% (13 +/- SD) and 56% (10 +/- SD) in a normal control group (p less than 0.001). The mean serum zinc in 55 alcoholic patients was 11.6 mumol/l (3.0 +/- SD) and in 36 normal volunteers the mean serum zinc was 13.6 mumol/l (1.8 +/- SD; p less than 0.001). This study suggests that chronic alcohol abuse will decrease the absorption of zinc and this may contribute towards the zinc deficiency occasionally associated with alcoholism.     

Outcomes following liver transplantation for patients with alcohol- versus nonalcohol-induced liver disease.

OBJECTIVE: To document and compare the outcomes of adult patients who received liver transplants for alcohol- and nonalcohol-induced liver diseases who attended a liver transplantation follow-up clinic in an urban, nontransplantation centre at a time when no formal alcohol abuse program for transplant candidates and/or recipients was offered. PATIENTS AND METHODS: The study population comprised 10 alcoholic patients and 48 nonalcoholic patients followed for an average of 41 months (range five to 79 months) and 46 months (range two to 116 months), respectively. Primary outcome variables included rates of recidivism, duration of abstinence after transplantation and compliance with post-transplant medical follow-up visits. Time to discharge after transplantation, episodes of graft rejection, liver and renal biochemical abnormalities, diabetes, hypertension, sepsis, strictures, complications unrelated to transplantation and changes in psychosocial status were secondary outcome variables. RESULTS: Significant differences were found with respect to a higher incidence of recidivism (50% for alcoholic patients compared with 2% for nonalcoholic patients, P<0.0001), a shorter period of abstinence after transplantation (14.7+/-17.2 months for alcoholic patients compared with 26.3+/-23.0 months for nonalcoholic patients, P<0.05) and more missed office visits (2.7+/-3.5 for alcoholic patients compared with 1.0+/-1.9 for nonalcoholic patients, P=0.05) in the alcoholic group. The alcoholic group also had a lower incidence of rejection episodes (10% for alcoholic patients compared with 44% for nonalcoholic patients, P<0.05) but higher rates of post-transplantation diabetes (40% for alcoholic patients compared with 2% for nonalcoholic patients, P<0.05), more nontransplantation-related complications (20% for alcoholic patients compared with 0% for nonalcoholic patients, P<0.05), and higher serum creatinine but lower bilirubin and cyclosporine A levels (P<0.05, respectively). Marital separations were also more common in the alcoholic group (20% for alcoholic patients compared with 0% for nonalcoholic patients, P<0.05). CONCLUSIONS: In the absence of formal alcohol abuse programs, the post-transplantation outcome in alcoholic patients generally does not compare well with that of patients who undergo transplantation for nonalcohol-related liver diseases.     

Adrenal androgens and illness

We have studied the adrenal androgen status of medically ill patients, patients before and after cholecystectomy and during recovery from burns injury. In patients ill for less than 2 weeks, serum androstenedione concentrations (mean +/- SEM) were raised (7.94 +/- 0.98 nmol/l) as compared with a control group (4.83 +/- 0.38 nmol/l, P less than 0.005) or with patients ill for more than 2 weeks (5.21 +/- 0.46 nmol/l, P less than 0.02); serum dehydroepiandrosterone sulphate (DHAS) levels were lower in patients ill for more than 2 weeks (1.21 +/- 0.42 mumol/l) than in either the acutely ill group (5.98 +/- 1.06 mumol/l, P less than 0.001) or the control ill group (5.56 +/- 0.59 mumol/l, P less than 0.001). In post-operative patients serum DHAS levels fell to below pre-operative levels reaching a nadir at day 8 (0.54 +/- 0.19 vs 1.66 +/- 0.56 mumol/l, P less than 0.02). In burned patients serum cortisol levels were increased on admission (661 +/- 91 vs 359 +/- 30 nmol/l, P less than 0.005) and remained high over the study period. Serum androstenedione concentrations were also high on admission (7.5 +/- 1.0 vs 3.9 +/- 0.3 nmol/l, P less than 0.02). Serum DHAS concentrations were similar to control values on admission (6.8 +/- 1.2 vs 5.2 +/- 0.7 mumol/l), fell to low levels thereafter reaching a nadir during week 3 (1.6 +/- 0.6 mumol/l, P less than 0.001). Steroid synthesis in times of chronic illness may be diverted from adrenal androgen to corticosteroid pathways ensuring maintained secretion of cortisol, which is essential to the health of ill patients.     

Phenotype study of blood T lymphocytes in alcoholic hepatopathies

Peripheral blood T lymphocytes and T lymphocytes subsets have been quantified by an indirect immunofluorescence technique using monoclonal antibodies, in 10 patients with fatty liver, 8 with acute alcoholic hepatitis (AAH), 10 with inactive cirrhosis and 7 with cirrhosis and AAH. Twenty normal subjects were studied as controls. As compared to controls (1.81 +/- 0.56 10(9)/l), we found a reduced number of peripheral T lymphocytes (OKT3+) in patients with inactive cirrhosis (0.98 +/- 0.45, p less than 0.001) and in patients with cirrhosis and AAH (1.22 +/- 0.51, p less than 0.02). The OKT4 to OKT8 ratio was normal in patients with fatty liver or inactive cirrhosis, but it was significantly higher in patients with AAH with or without cirrhosis (2.83 +/- 0.79, p less than 0.01, and 2.10 +/- 0.56, p less than 0,02, respectively) than in controls (1.68 +/- 0.24). In both groups, this increased ratio was due to a decreased proportion of OKT8+ circulating lymphocytes (19.2 +/- 6.7 p. 100, p less than 0.01, and 21.8 +/- 4.6 p. 100, p less than 0.02, respectively) when compared to controls (27.1 +/- 4.1 p. 100). The T-cell imbalance observed in patients with liver cell necrosis may be of importance in the pathogenesis of alcoholic liver disease.     

Total and individual free fatty acid concentrations in liver cirrhosis

The finding of high plasma free fatty acid (FFA) levels in cirrhotic patients has been attributed either to decreased hepatic clearance or to enhanced fat mobilization. To better clarify these hypotheses, total and individual FFA and glycerol levels were determined in 21 cirrhotic patients with different degrees of hepatocellular damage (evaluated by liver function tests), portal hypertension (evaluated by endoscopy and clinical signs), and nutritional status (evaluated by anthropometric and biohumoral parameters) and in 10 age- and sex-matched healthy subjects. Glucose tolerance and insulin and glucagon levels were determined in all individuals. Well-nourished and malnourished patients were identified within the cirrhotic group. Plasma FFA and glycerol concentrations were well correlated (r = 0.47, P less than 0.05), levels being significantly higher in cirrhotic individuals than in controls (746.6 +/- 46.29 SE v 359.22 +/- 40.82 mumol/L, P less than 0.001 for plasma FFA; 150.1 +/- 3.12 v 82.5 +/- 9.2 mumol/L, P less than 0.01 for glycerol). Plasma FFA and glycerol showed no correlation with the liver function test results or portal hypertension parameters. Interestingly, plasma levels of FFA and glycerol were influenced by the nutritional status, significantly higher FFA levels being observed in the well-nourished than in the malnourished patients (842.5 +/- 47.5 v 563.4 +/- 78 mumol/L, P less than 0.005). Furthermore, a positive correlation was found between plasma glycerol level and percentage of triceps skinfold (r = 0.45, P less than 0.05). No correlation was found between plasma levels of FFA or glycerol and glucose tolerance, insulin and glucagon.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between unexplained elevations in alanine aminotransferase and serum leptin in U.S. adults: results from the Third National Health and Nutrition Examination Survey (NHANES III)

INTRODUCTION: There has been an interest to explore whether serum leptin plays any role in the pathogenesis of chronic liver disease. We conducted a case-control study to evaluate the relationship between unexplained elevations in ALT and serum leptin in NHANES III participants. METHODS: A total of 6343 adults who had fasting serum leptin and ALT measured as part of NHANES III constituted our study group. From this database, we have constructed cohorts of patients with unexplained elevations in ALT according to published criteria and compared their serum leptin levels to matched controls without liver disease and matched controls with hepatitis C. Leptin was also compared between patients with unexplained elevations in ALT with and without metabolic syndrome. RESULTS: Serum leptin in 288 patients with unexplained elevations in ALT was 13.3 +/- 9.9 ng/mL and was not significantly different than 720 controls without liver disease (13.6 +/- 11.9 ng/mL, P = 0.6). Serum leptin in another group of patients with unexplained elevations in ALT and hepatitis C controls was also not significantly different (8.0 +/- 4.8 vs. 8.8 +/- 7.4 ng/mL, respectively, P = 0.5). There was no independent relationship between the presence of metabolic syndrome and serum leptin in individuals with unexplained elevations in ALT (P = 0.8). CONCLUSIONS: Individuals with unexplained elevations in ALT did not have higher levels of serum leptin than the matched controls. As unexplained elevations in ALT may signify the presence of nonalcoholic fatty liver disease in NHANES III participants, our data provide indirect evidence against a role for serum leptin in the pathogenesis of nonalcoholic fatty liver disease.     

老年2型糖尿病合并非酒精性脂肪性肝病患者Vaspin水平的变化

目的研究老年T2DM合并非酒精性脂肪性肝病（NAFLD）患者血清Vaspin水平的变化及其临床意义。方法测定老年T2DM合并NAFLD患者44例（T2DM＋NAFLD组）,老年T2DM不合并NAFLD患者40例（T2DM组）,老年糖耐量正常的NAFLD患者40例（NAFLD组）与老年正常对照41名（NC组）的Vaspin水平。结果T2DM＋NAFLD组、T2DM组、NAFLD组血清Vaspin水平均明显高于NC组（1．46±0．43、1．03±0．27、0．76±0．28vs0．36±0．13）ng／ml,差异有统计学意义（P〈0．01或P％0．05）。多元逐步回归分析显示Fins、内脏脂肪厚度（VFT）、HbA1c是Vaspin水平的独立影响因素,Vaspin、VFT和TG是老年T2DM合并NAFLD的危险因素。结论血清Vaspin水平的变化可能在老年T2DM合并NAFLD的发生发展中起一定作用。     

Intestinal zinc absorption in cirrhotic patients

We studied intestinal zinc absorption and daily urinary zinc excretion in 13 healthy controls and 27 cirrhotic patients (14 alcoholics, 13 non-alcoholics) with normal serum creatinine levels. Intestinal zinc absorption was determined by the oral zinc tolerance test. Serum levels were significantly lower in cirrhotics, whether alcoholic or non-alcoholic, than in healthy controls (6.2 +/- 2.1 mumol/L vs. 11.6 +/- 2.1 mumol/L; p less than 0.001). Daily urinary zinc excretion was significantly higher in alcoholic cirrhotics (17.6 +/- 9.4 mumol/d vs. 11.4 +/- 4.1 mumol/d; p less than 0.05). Intestinal zinc absorption was significantly reduced in cirrhotics and correlated with the degree of liver dysfunction. During the oral tolerance test, urinary zinc excretion was not significantly higher in cirrhotics than in controls. We conclude that the low serum zinc levels in cirrhotics are of multifactorial origin. Impaired intestinal absorption seems to play a role, particularly in patients with more severe liver dysfunction, but increased urinary excretion may contribute to zinc deficiency in alcoholics.