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Biomedical subjects

J Caballería

Publications and source records attributed to J Caballería.

At least 55 records · Page 3Linked to original sources
PubMed1991

Effects of H2-receptor antagonists on gastric alcohol dehydrogenase activity.

Inhibition of gastric alcohol dehydrogenase (ADH) activity by cimetidine results in elevated blood levels of ethanol after moderate consumption. To search for alternative H2-blockers lacking such an effect, we compared cimetidine, ranitidine, nizatidine, and famotidine. They inhibited rat gastric ADH noncompetitively, with a Ki for ethanol oxidation of 0.68 mM for cimetidine, 0.5 mM for ranitidine, 1 mM for nizatidine, and 4.5 mM for famotidine. These concentrations are higher than therapeutic plasma levels, but intracellular concentrations in the gastric mucosa (assessed with [3H]cimetidine and [14C]famotidine) were at least 10- and 2-fold greater than in the blood, respectively. These results suggests that, given at therapeutic doses in vivo, the degree of inhibition by cimetidine and ranitidine should be significant and comparable, that by nizatidine should be smaller, and that by famotidine should be negligible. These drugs also exerted either mixed or competitive inhibition of rat hepatic ADH, but the effects of cimetidine and famotidine were observed at concentrations unlikely to occur in vivo. Thus, in alcoholics and in social drinkers who require treatment with H2-receptor antagonists, famotidine might be preferable to the other H2 blockers tested.

Alcohol Dehydrogenase↗
PubMed1991

Effect of parenteral amino acid supplementation on short-term and long-term outcomes in severe alcoholic hepatitis: a randomized controlled trial.

The effect of parenteral amino acid administration on nutritional state, liver function and mortality was assessed in patients with severe alcoholic hepatitis. Twenty-eight patients received 2 l/day of a solution of dextrose (65 gm/L) and amino acids (25.8 gm/L) for 1 mo, whereas 26 received only the dextrose solution. All patients were allowed to eat a standard hospital diet. During the month in the hospital, there were six deaths in the treatment group and five deaths in the control group. Nitrogen balance improved in the treated group, but not in the control group. Creatinine-height index, triceps skin fold measurement and levels of serum albumin and prealbumin increased similarly in both groups. Serum retinol binding protein increased more in the treatment group than it did in the control group, and transferrin was increased only in the treatment group. Serum bilirubin, type III amino-terminal procollagen peptide and aminopyrine clearance improved more in the treatment group than in the control group, whereas serum AST and prothrombin time improved in the treatment group but not in the control group. Cumulative 2-yr survival rates from the day of entry into the study were 42% and 38% in the treatment and control groups, respectively. Patients who survived 2 yr and patients in the treatment group who died during the 2-yr follow-up had continued improvement in serum retinol binding protein, transferrin, bilirubin and prothrombin time. These parameters were unchanged in patients in the control group who died during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hepatitis C virus antibodies in chronic alcoholic patients: association with severity of liver injury.

The prevalence of hepatitis C virus antibody and its relationship to the severity of liver disease in chronic alcoholic patients has been assessed, using a recently developed enzyme immunoassay and confirmed by a recombinant immunoblot assay, in 144 patients (mean age +/- S.D. = 44.4 +/- 11.3 yr) who had consumed greater than 80 gm/day ethanol for greater than 5 yr. Hepatic disease was evaluated by clinical and biochemical studies and by liver biopsy when appropriate. In addition, 76 liver biopsy specimens from these patients were analyzed to determine whether liver lesions were similar in alcoholic patients with and without hepatitis C virus antibodies. According to clinical and histological features alcoholic patients were divided into five groups: normal liver (45 patients), fibrosteatosis (20 patients), alcoholic hepatitis (14 patients), cirrhosis (61 patients) and chronic hepatitis (4 patients). Hepatitis C virus antibodies were present in 35 alcoholic patients (24.3%). The prevalence of hepatitis C virus antibodies correlated with the severity of liver injury: 2.2% in patients without liver disease, 20% in those with fibrosteatosis, 41.4% in those with alcoholic hepatitis and 42.6% in those with cirrhosis. Hepatitis C virus antibodies were found in one of the four patients with chronic hepatitis (p less than 0.001). Furthermore, patients positive for hepatitis C virus antibodies with normal liver or fibrosteatosis showed higher serum bilirubin and gamma-globulin concentrations and lower aminopyrine breath test scores than did patients negative for hepatitis C virus antibodies with normal liver or fibrosteatosis. Similar differences between patients with and without hepatitis C virus antibodies were observed in patients with alcoholic hepatitis or cirrhosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Influence of liver disease on hepatic alcohol and aldehyde dehydrogenases.

The hepatic activities and the isoenzyme patterns of both alcohol dehydrogenase and aldehyde dehydrogenase have been studied in 60 alcoholics with varying degrees of liver damage (from normal tissue or minimal changes to cirrhosis with alcoholic hepatitis) and in 24 nonalcoholics with chronic hepatitis or cirrhosis in order to ascertain their association with liver damage. In alcoholics both alcohol dehydrogenase and low-Km aldehyde dehydrogenase activities decreased proportionally with the severity of liver disease. In contrast, in nonalcoholics, there was a reduction of low-Km aldehyde dehydrogenase activity related to the severity of liver injury, but alcohol dehydrogenase was similar in patients with chronic hepatitis and nonalcoholic cirrhosis. There were no significant changes in total and high-Km aldehyde dehydrogenase activities among the different histologic groups studied, although the lowest activities were observed in patients with more severe liver injury. The prevalence of atypical alcohol dehydrogenase was similar in alcoholic (6.6%) and in nonalcoholic (8.3%) liver disease. All patients exhibited isoenzyme aldehyde dehydrogenase II, whereas isoenzyme I was not detected in 39.5% of the alcoholic patients and in 9.5% of those with nonalcoholic liver disease. The lack of aldehyde dehydrogenase I was observed in cases with the lowest enzymatic activities. These results suggest that the decrease of alcohol and aldehyde dehydrogenase activities in alcoholics is not a primary defect and, therefore, their decrease is secondary to liver damage. It is speculated that the diminution of alcohol dehydrogenase, found particularly in alcoholics, could be due to centrilobular cell necrosis.

Alcohol Dehydrogenase↗
PubMed1989

Alcoholic foamy degeneration in Spain. Prevalence and clinico-pathological features.

Among 389 consecutive chronic alcoholics in whom a liver biopsy was performed for diagnostic purposes, nine patients (2.3%) had histological changes of "alcoholic foamy degeneration" (AFD), characterized by numerous small fat droplets in the swollen hepatocytes of the centrilobular area. In five cases, there were non-specific clinical features, while the other four cases presented acute hepatic decompensation with jaundice and a reduced prothrombin activity. Seven patients had high serum lipid concentrations including hypertriglyceridemia and hypercholesterolemia, which improved after withdrawal of alcohol intake. In conclusion, AFD has a broad clinicopathological spectrum including asymptomatic patients and other cases with severe liver decompensation manifested by jaundice and reduced prothrombin activity. AFD is usually associated with hyperlipemia.

Adult↗
PubMed1988

Urine ethanol assessment: a helpful method for controlling abstinence in alcoholic liver disease.

The usefulness of a urine-alcohol determination in the evaluation of abstinence in alcoholic liver disease has been investigated in 181 patients. Alcohol was tested in morning urine samples collected on a follow-up visit in 103 patients, and the results were compared with those in 78 patients, where three samples were collected within the same week; one in the morning and two in the evening. Although the percentage of urine samples containing alcohol measured in a morning sample was similar to the patients' self-report (31% and 34%, respectively), urine analysis identified an additional 7% of patients who denied alcohol intake. Alternatively, serial urine-alcohol determinations were significantly more effective than patient reports (54% and 35.9%, respectively, P less than 0.01), particularly when urine was collected in the evenings. This difference was due mainly to the reluctance of women to admit drinking (7.4% of positive self reports vs 51% of women with alcohol positive urine samples, P less than 0.001). We conclude that serial measurements of alcohol in urine were useful tests which should be used to complement personal interview in the control of abstinence in patients with alcoholic liver disease.

Ethanol↗
PubMed1987

Portal hypertension in primary biliary cirrhosis. Relationship with histological features.

The prevalence and type of portal hypertension (PH) in primary biliary cirrhosis (PBC) and their relationship with liver lesions have been investigated in 32 patients with the disease. Portal hypertension was considered when oesophageal or gastric varices were observed by endoscopy and/or when hepatic venous pressure gradient measured by hepatic vein catheterization was greater than 6 mmHg. Within 3 days of endoscopy, a liver biopsy was performed for histological staging and semiquantitative grading (0 to 3+) of portal and sinusoidal fibrosis, portal inflammation, piecemeal necrosis, lobular necrosis, cholestasis, as well as the presence of granulomas and Mallory's hyaline. Twenty patients (62.5%) had portal hypertension, five of them showing presinusoidal PH (15.5%) and the remaining 15 (47%) with sinusoidal component. The four patients in stage IV had sinusoidal PH and the only patient in stage I had no PH. The prevalence of portal hypertension was similar in patients in stage II (57%) and stage III (55%), but presinusoidal PH was only observed in patients in stage II. Patients with PH showed significantly higher portal inflammation and piecemeal necrosis than patients without PH. By contrast, there were no differences in portal and sinusoidal fibrosis, nor in the other histologic features. These results indicate that portal hypertension is common in PBC and it may be present in the early stages of the disease. The fact that presinusoidal PH was only observed in patients in stage II suggests that portal hypertension is initially of presinusoidal type, and then as the disease progresses is joined by a sinusoidal component.

Adult↗
PubMed1987

Lactitol versus lactulose in the treatment of acute portal systemic encephalopathy (PSE). A controlled trial.

Preliminary data suggest that lactitol (beta-galactoside-sorbitol), a new synthetic non-absorbable disaccharide, has beneficial effects on chronic portal systemic encephalopathy. To compare the efficacy of lactitol vs. lactulose in the treatment of acute portal systemic encephalopathy (PSE), 40 cirrhotic patients with an acute episode of PSE were randomly allocated to one of two groups: group A (20 patients) received lactulose (30 ml/6 h) and group B (20 patients) lactitol (12 g/6 h). These doses were adjusted daily to obtain two bowel movements per day. The duration of treatment was 5 days. Age, sex, hepatic and renal function, precipitating factors and level of PSE measured by clinical examination, EEG and number connection test were similar in the two groups. A complete clinical resolution of PSE occurred in 11 patients in each group. In 5 patients of the lactulose group and in 6 of the lactitol group there was a moderate improvement of PSE during the study. Finally, 4 patients in the lactulose group and 3 in the lactitol group did not respond to treatment. No side effects attributable to therapy were observed in either group. These results indicate that lactitol is as effective as lactulose in the management of patients with cirrhosis and acute PSE.

Acute Disease↗
PubMed1987

Hepatic alcohol and aldehyde dehydrogenases in liver disease.

To investigate the influence of liver injury on the activities of hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), these enzymes have been measured in tissue from alcoholic and non alcoholic patients with different severity of liver damage. ADH and ALDH activities decreased proportionatelly with the progression of liver disease in alcoholics. By contrast, in non-alcoholics, there was a reduction of Low-Km ALDH related with the severity of liver injury but ADH was similar in patients with chronic hepatitis and non-alcoholic cirrhosis. Furthermore, ADH was significantly lower in alcoholic than in non-alcoholic cirrhotics. These results suggests that the decreased ADH and ALDH in alcoholics are not primary abnormalities predisposing to alcoholism and alcoholic liver disease. The diminution of ADH found only in alcoholics could be due to the loss of the enzyme produced by centrolobulillar cell necrosis, that is often observed in alcoholic liver disease.

Adult↗
PubMed1986

Serum procollagen type III peptide as a marker of hepatic fibrogenesis in alcoholic hepatitis.

To evaluate if serum procollagen type III peptide levels reflect the extent of liver fibrosis and hepatic collagen synthesis, we have studied 19 patients with histologically proven alcoholic hepatitis and 9 chronic alcoholics with normal liver histology or minimal steatosis. Serum procollagen peptide type III was measured at the time of liver biopsy, and determination of hepatic prolyl-hydroxylase activity, as an index of collagen synthesis, was performed in all liver samples. Hepatic prolyl-hydroxylase activity and serum procollagen peptide levels were significantly higher in patients with alcoholic hepatitis (959 +/- 115 cpm/mg and 33.2 +/- 5.3 ng/ml, respectively) than in alcoholics from the control group (537 +/- 62 cpm/mg and 10.9 +/- 1.5 ng/ml, respectively) (p less than 0.05 and p less than 0.01, respectively). All patients with alcoholic hepatitis had fibrosis (10 mild and 9 severe). Prolyl-hydroxylase activity and procollagen peptide levels were significantly higher in alcoholic hepatitis patients with severe fibrosis than in those with mild fibrosis (1208 +/- 154 cpm/mg vs. 734 +/- 138 cpm/mg, p less than 0.05 and 49.1 +/- 8.8 ng/ml vs. 20.4 +/- 2.6 ng/ml, p less than 0.01). Furthermore, a close correlation was found between the hepatic prolyl-hydroxylase activity and the serum level of procollagen peptide (r = 0.76, p less than 0.001). We conclude that the serum procollagen peptide level is a good marker of hepatic fibrogenesis in alcoholic hepatitis; thus, its serial measurement could be useful in identifying patients in progress to cirrhosis and in assessing the therapeutic efficiency of antifibrogenic drugs.

Adult↗
PubMed1986

Histological course of alcoholic hepatitis. Influence of abstinence, sex and extent of hepatic damage.

The factors influencing the histological evolution of alcoholic hepatitis without cirrhosis have been evaluated in 26 patients (14 males and 12 females) submitted to repeated liver biopsies over a mean period of 1.7 years (1-3). Drinking habits during follow-up were checked by inquiries to patients and relatives and by serial determination of ethanol in urine. At the end of the follow-up, 9 patients (34.6%) had progressed to cirrhosis, 5 (19.2%) still had alcoholic hepatitis and 12 (46.1%) had normal liver or only minimal changes. Nine patients continued drinking heavily, 4 reduced their daily intake markedly and 13 stopped drinking. Improvement of liver lesions was observed in 9 of the abstainers and in 3 non-abstainers that had markedly reduced their alcohol consumption. Among the 9 patients with persistent heavy alcohol consumption, 5 developed cirrhosis and 4 still showed alcoholic hepatitis in their last biopsy. Cirrhosis also developed over 1-2 years in 4 females who had stopped drinking, indicating a marked influence of sex on the course of alcoholic hepatitis. Progression of the disease to cirrhosis despite abstinence occurred in a high proportion of women (4/7) but not in men (0/6). These observations indicate that discontinuation of heavy alcohol consumption often results in improvement of liver lesion in patients with alcoholic hepatitis. However, the risk of progression to cirrhosis remains elevated in women.

Adult↗
PubMed1985

Lymphocytotoxic antibodies in primary biliary cirrhosis.

Sera of 30 patients with primary biliary cirrhosis (PBC) and 72 normal subjects matched for age and sex were examined for the presence of lymphocytotoxic antibodies (LCAs) against B and T cells at 4 degrees C and 37 degrees C. Patients were prospectively screened for: Sjögren's syndrome, scleroderma, Hashimoto's thyroiditis, and rheumatoid arthritis, in which LCAs have been described. Seventeen patients with PBC (56.6%) had LCAs against B cells as compared with only 11 of the 72 normal subjects (P less than 0.001). Five PBC patients (16.6%) also reacted against T cells as compared with none in control group (P less than 0.01). Clinical and biochemical features and the histological stage of PBC were similar in patients with and without LCA. Sjögren's syndrome was present in 13 patients--two with scleroderma and another with Hashimoto's thyroiditis. No patient had rheumatoid arthritis. The prevalence of LCAs was similar in PBC patients with or without autoimmune associated disease (54% vs 59%). We conclude that in PBC a high incidence of LCA is unrelated to the presence of an associated disease. LCA in PBC might be a nonspecific marker of an immune disorder.

Adult↗