Non-alcoholic Liver Cirrhosis Research Articles

Colchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosis

Alcohol and hepatotropic viruses cause the majority of liver cirrhosis cases in the Western World. Colchicine is an anti-inflammatory and anti-fibrotic medication. Several randomised clinical trials have addressed the question whether colchicine has any efficacy in patients with alcoholic or non-alcoholic fibrosis and cirrhosis. To assess the beneficial and harmful effects of colchicine in patients with alcoholic or non-alcoholic fibrosis or cirrhosis, excluding primary biliary cirrhosis. The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Controlled Trials Register on The Cochrane Library, MEDLINE, EMBASE, Web of Science, and full text searches were combined (September 2004). Manufacturers and researchers in the field were also contacted. We included randomised trials irrespective of blinding, language, or publication status comparing per oral colchicine with placebo or no intervention for patients with fibrosis or cirrhosis induced by either alcohol, virus, or unknown factors (cryptogenic). The statistical package (RevMan Analyses) provided by The Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated. We could include fifteen randomised clinical trials in which 1714 patients were randomised. We found no significant effects of colchicine on mortality (relative risks (RR) 1.00, 95% confidence interval (CI) 0.87 to 1.16), liver-related mortality (RR 1.08, 95% CI 0.88 to 1.33), complications (RR 1.01, 95% CI 0.74 to 1.38), liver biochemistry, liver histology, and alcohol consumption (RR 1.03, 95% CI 0.77 to 1.39). Colchicine was associated with a significantly increased risk of adverse events (RR 4.35, 95% CI 2.16 to 8.77). Colchicine should not be used for alcoholic, viral, or cryptogenic liver fibrosis or liver cirrhosis outside randomised clinical trials.

Trends in liver disease prevalence in Mexico from 2005 to 2050 through mortality data

Background and Aims. The epidemiology of liver cirrhosis differs across sex, ethnic groups, and geographic regions. In 2000, chronic liver disease was the fifth leading cause of death in Mexico. Accurate knowledge of the demographics of liver disease is essential in formulating health-care policies. Our main aim was to project the trends in liver disease prevalence in Mexico from 2005 to 2050 based on mortality data. Methods. Data on national mortality reported for the year 2002 in Mexico were analyzed. Specific-cause mortality rates were calculated for a selected age population (≥25 years old) and classified by sex and projected year (2005–2050). The following codes of the International Classification of Diseases for liver diseases were included: non-alcoholic chronic liver disease and cirrhosis, alcoholic liver disease, liver cancer, and acute and chronic hepatitis B and C infection. The projected prevalence of a chronic liver disease was estimated using the following equation: P = (ID × T) / [(ID × T) + 1], where P = prevalence, ID = incidence density (mortality rate multiplied by 2), T = median survival with the disease (= 20 years). Results: Nearly two million cases of chronic liver disease are expected. Alcohol-related liver diseases remain the most important causes of chronic liver disease, accounting for 996,255 cases in 2050. An emergent syndrome is non-alcoholic liver disease, which will be more important that infectious liver diseases (823,366 vs 46,992 expected cases, respectively). Hepatocellular carcinoma will be the third leading cause of liver disease. Conclusions: Chronic liver disease will be an important cause of morbidity and mortality in the future. Preventive strategies are necessary, particularly those related to obesity and alcohol consumption, to avoid catastrophic consequences.

Low birth weight: a possible risk factor also for liver diseases in adult life?

Birth weight is a popular topic, because it is precisely recorded, a major determinant of infant survival, associated with infant mortality, and health outcomes later in life. Low birth weight (LBW) is a predisposing factor for metabolic abnormalities such as atherosclerosis, renal disease, non-insulin diabetes mellitus, asthma, low IQ, hypertension, obesity, psychological distress. They have all been reported to be more common among those who were small at birth. Due to lack of studies suggesting a linkage between LBW and diseases of liver; evidences, which support the hypothesis on the creation of a link between LBW, an indicator of unfavourable intrauterine environment, and liver diseases emerging in the adult life, and possible direct associations of LBW with liver diseases, e.g., hepatitis, non-alcoholic fatty liver disease, cirrhosis, hepatoblastoma, or hepatocellular carcinoma were discussed. The associations between LBW and hepatitis vaccination as well as paediatric parental nutrition were also noted.

Effects of protein deficiency on liver trace elements and antioxidant activity in carbon tetrachloride-induced liver cirrhosis.

In liver cirrhosis, liver tissue becomes progressively substituted by fibrosis, ultimately leading to architectural distortion, liver circulatory changes, and liver failure. Some data support the hypothesis that protein undernutrition may play a role in the development and progression of nonalcoholic liver cirrhosis and that this progression is at least partially mediated by changes in glutathione peroxidase (GPX), superoxide dismutase (SOD), and other antioxidative systems, leading to an increase in lipid peroxidation. We analyzed the effects of protein deficiency on liver Cu, Fe, Zn, Mn, and Se in carbon tetrachloride (CCl4)-induced liver cirrhosis, the relation of protein undernutrition and these trace elements with the activity of some hepatic antioxidative enzymatic mechanisms, and the relation of all of them with morphological and biochemical changes in 40 male adult Sprague-Dawley rats divided in four groups. Liver cirrhosis was induced by intraperitoneal injection of CCl4 to 10 rats fed a 2% protein diet and another 10 fed a 18% protein control diet; two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. The study period lasted 6 wk. GPX, SOD, and lipid peroxidation products as well as Zn, Cu, Mn, Se, and Fe were determined in liver samples. We found that liver GPX and Se were reduced in the cirrhotic animals, especially in the low-protein-fed ones, protein deficiency, but not cirrhosis, exerting the main effects. A close correlation was found between liver GPX and serum albumin and weight loss and an inverse one among GPX and hepatocyte ballooning, liver fibrosis, and fat, histomorphometrically determined. These results suggest a pathogenetic role of decreased GPX in the progression of liver disease, which may become enhanced by concomitant protein undernutrition. In addition to iron, the levels of which were increased in the malnourished rats, no differences were found regarding the other trace elements, SOD activity, and lipid peroxidation products.

Factors influencing the prevalence of gallstones in liver disease: the beneficial and harmful influences of alcohol

OBJECTIVE: The Patient Treatment File of the Department of Veterans Affairs comprises the computerized records of all inpatients treated in all Veterans Affairs hospitals distributed throughout the United States. This database was used to study the association between liver disease and clinically manifest cholelithiasis. METHODS: The computerized medical records of 38,459 patients with various forms of liver disease and 69,336 controls without the diagnosis were extracted from the annual files between 1990 and 1993. In a multiple logistic regression analysis, the occurrence of cholelithiasis served as the outcome variable, whereas different forms of liver disease and demographic characteristics, such as age, gender, and ethnicity, served as predictor variables. RESULTS: Among the control population, cholelithiasis was reported in 5.2% (3,571 of 69,336) of subjects. Cholelithiasis occurred in 7.5% (2,898 of 38,459) of patients with all liver disease, 9.5% (1,642 of 17,287) of patients with alcoholic liver cirrhosis, 13.7% (981 of 7,149) of patients with nonalcoholic liver cirrhosis, and 9.1% (66 of 728) of patients with alcoholic fatty liver (χ 2 = 1059, df = 4, p < 0.001). In the logistic regression, the odds ratios (ORs) for cholelithiasis associated with various forms of liver disease were: in all liver diseases combined (OR = 1.31, 95% CI = 1.25–1.38), in alcoholic liver cirrhosis (OR = 1.62, 95% CI = 1.54–1.72), in nonalcoholic liver cirrhosis (OR = 2.07, 95% CI = 1.94–2.21), and in alcoholic fatty liver (OR = 1.40, 95% CI = 1.11–1.75). Other risk factors for cholelithiasis besides liver disease were: female gender (OR = 1.43, 95% CI = 1.25–1.63), older age (OR = 1.28 per age decade, 95% CI = 1.26–1.30), Native American (OR = 1.38, 95% CI = 1.12–1.72) or Hispanic ethnicity (OR = 1.25, 95% CI = 1.15–1.35), and presence of diabetes mellitus (OR = 1.43, 95% CI = 1.35–1.52). A history of alcoholism exerted a protective influence (OR = 0.92, 95% CI = 0.87–0.97). CONCLUSION: Gallstone disease occurs frequently in hospitalized patients with chronic liver disease or liver cirrhosis and contributes to the burden of the disease.

Factors influencing the prevalence of gallstones in liver disease: the beneficial and harmful influences of alcohol

The Patient Treatment File of the Department of Veterans Affairs comprises the computerized records of all inpatients treated in all Veterans Affairs hospitals distributed throughout the United States. This database was used to study the association between liver disease and clinically manifest cholelithiasis. The computerized medical records of 38,459 patients with various forms of liver disease and 69,336 controls without the diagnosis were extracted from the annual files between 1990 and 1993. In a multiple logistic regression analysis, the occurrence of cholelithiasis served as the outcome variable, whereas different forms of liver disease and demographic characteristics, such as age, gender, and ethnicity, served as predictor variables. Among the control population, cholelithiasis was reported in 5.2% (3,571 of 69,336) of subjects. Cholelithiasis occurred in 7.5% (2,898 of 38,459) of patients with all liver disease, 9.5% (1,642 of 17,287) of patients with alcoholic liver cirrhosis, 13.7% (981 of 7,149) of patients with nonalcoholic liver cirrhosis, and 9.1% (66 of 728) of patients with alcoholic fatty liver (chi2 = 1059, df = 4, p < 0.001). In the logistic regression, the odds ratios (ORs) for cholelithiasis associated with various forms of liver disease were: in all liver diseases combined (OR = 1.31, 95% CI = 1.25-1.38), in alcoholic liver cirrhosis (OR = 1.62, 95% CI = 1.54-1.72), in nonalcoholic liver cirrhosis (OR = 2.07, 95% CI = 1.94-2.21), and in alcoholic fatty liver (OR = 1.40, 95% CI = 1.11-1.75). Other risk factors for cholelithiasis besides liver disease were: female gender (OR = 1.43, 95% CI = 1.25-1.63), older age (OR = 1.28 per age decade, 95% CI = 1.26-1.30), Native American (OR = 1.38, 95% CI = 1.12-1.72) or Hispanic ethnicity (OR = 1.25, 95% CI = 1.15-1.35), and presence of diabetes mellitus (OR = 1.43, 95% CI = 1.35-1.52). A history of alcoholism exerted a protective influence (OR = 0.92, 95% CI = 0.87-0.97). Gallstone disease occurs frequently in hospitalized patients with chronic liver disease or liver cirrhosis and contributes to the burden of the disease.

Prognostic value of energy metabolism in patients with viral liver cirrhosis

The effect of energy malnutrition on survival in patients with non-alcoholic viral liver cirrhosis has not been well defined. We characterized energy metabolism at study entrance and prospectively analyzed its effect on subsequent survival in cirrhotics. One hundred nine consecutive patients with viral liver cirrhosis and 22 healthy control subjects participated in the study. By indirect calorimetry after overnight bedrest and fasting, resting energy expenditure (REE) was measured and non-protein respiratory quotient (npRQ) was calculated. Survival of cirrhotics were followed for up to 8 y. Survival rate was estimated with the Kaplan-Meier method. REE at entrance was significantly higher than the predicted basal metabolic rate (BMR) in cirrhotics ( P < 0.001). NpRQ was significantly lower in cirrhotics than in controls ( P < 0.001). Survival rate was significantly lower in patients with low npRQ ( < 0.85) than in patients with scores above 0.85 ( P < 0.01) and was significantly higher in normal metabolic patients (0.9 < REE/BMR < 1.1) than in hypometabolic (REE/BMR < 0.9) or hypermetabolic (1.1 < REE/BMR) patients ( P < 0.05). The proportional hazards model showed that npRQ (relative risk = 0.0003, 95% confidence interval = 0.0000–0.0970), REE/BMR (0.0199, 0.0007–0.5652), prothrombin time, and ammonia were independent significant factors determining survival. Thus evaluation of energy metabolism can be used to predict survival in patients with viral liver cirrhosis.

Red blood cell status in alcoholic and non-alcoholic liver disease

Macrocytosis is most commonly associated with vitamin B12 and folic acid deficiency, followed by alcoholism, liver disease, and other pathologic conditions. We studied the red cell and vitamin status in 423 consecutive patients with various liver diseases, including 31 with acute viral hepatitis (AVH), 105 with chronic hepatitis (CH), and 134 with alcoholic liver disease (ALD), who consisted of 84 with non-cirrhotic alcoholic liver disease (NCALD) and 50 with alcoholic liver cirrhosis (ALC), 60 with non-alcoholic liver cirrhosis (NALC), and 93 with hepatocellular carcinoma (HCC). The mean corpuscular volume (MCV) and red cell distribution width (RDW) were significantly higher in patients with ALD and NALC, and among them macrocytosis occurred more frequently in patients with ALC. Macrocytic anemia was mostly found in cirrhotic patients, in which the Child-Pugh score was closely related to the development of macrocytic anemia. In ALD, the MCV was significantly correlated with the estimated alcohol consumption and inversely correlated with the serum folic acid level, which, however, was often maintained within the normal range in patients with macrocytic ALC. After abstinence from alcohol, the MCV and RDW were reduced significantly and were associated with an increasing serum folic acid level. This suggests that macrocytic anemia was a common feature of alcoholic and non-alcoholic liver cirrhosis and that alcohol abuse and folic acid deficiency play a secondary role in macrocytosis. (J Lab Clin Med 2001;138:332-7)

Coffee, Caffeine, and the Risk of Liver Cirrhosis

PURPOSE: To evaluate the effect of the consumption of caffeine-containing beverages on the risk of symptomatic liver cirrhosis (LC). METHODS: From 1994 to 1998, all the consecutive cirrhotic inpatients admitted in 19 collaborative hospitals for signs of liver decompensation in whom the diagnosis of liver cirrhosis was made for the first time (274 cases) and one or two gender, age, and place of residence pair matched individuals (458 controls) were recruited. Data on years of education, lifetime cigarette use, lifetime intake of alcohol- and caffeine-containing beverages, usual consumption of 180 food items, and on markers of hepatitis B and C viral infection were collected. RESULTS: A statistically significant trend toward lowered cirrhosis risk with increasing exposure to coffee was observed. The LC odds ratios decreased from 1.0 (reference category: lifetime abstainers from coffee) to 0.47 (95% confidence interval: 0.20, 1.10), 0.23 (0.10, 0.53), 0.21 (0.06, 0.74), and 0.16 (0.05, 0.50) in 1, 2, 3, and 4 or more cups of coffee drinkers, respectively. There was no convincing evidence that coffee consumption modifies the effects of the known risk factors of liver cirrhosis (alcohol intake and viruses infection). CONCLUSIONS: These findings support the hypothesis that coffee, but not other beverages containing caffeine, may inhibit the onset of alcoholic and nonalcoholic liver cirrhosis.

Colchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosis.

The majority of liver fibrosis and liver cirrhosis cases in the Western World is caused by alcohol and hepatotoxic viruses. Colchicine is an anti-inflammatory and anti-fibrotic medication. Several randomised clinical trials have addressed the question whether colchicine has any efficacy in patients with alcoholic as well as non-alcoholic fibrosis and cirrhosis. The objectives were to assess the efficacy of colchicine on mortality, clinical symptoms and complications, liver biochemistry, liver fibrosis markers, liver histology, alcohol consumption, quality of life, and health economics in patients with alcoholic and non-alcoholic fibrosis or cirrhosis, excluding primary biliary cirrhosis and other rarer forms of fibrosis/cirrhosis. Also adverse events were assessed. The Cochrane Hepato-Biliary Group Controlled Trials Register, The Cochrane Library, MEDLINE, and full text searches were combined. Only randomised clinical trials were included studying patients with alcoholic fibrosis, alcoholic hepatitis and/or alcoholic cirrhosis as well as patients with viral induced or cryptogenic fibrosis and/or cirrhosis according to the diagnostic work-up of the individual trial. Interventions encompassed peroral colchicine at any dose versus placebo or no intervention. The trials could be double-blind, single-blind or unblinded. The trials could be unpublished or published and no language limitations were applied. All analyses were performed according to the intention-to-treat method. The statistical package (RevMan and MetaView) provided by the Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated by the Jadad-scale. Combining the results of 14 randomised clinical trials including 1150 patients demonstrated no significant effects of colchicine on mortality (Peto odds ratio (OR) 0.90, 95% confidence interval (CI) 0.63 to 1.29), liver related mortality (OR 1.05, 95% CI 0.61 to 1.80), complications (OR 1.01, 95% CI 0.63 to 1.62), liver biochemistry, liver histology, and alcohol consumption (OR 1.02, 95% CI 0.58 to 1.79). Colchicine was associated with a significantly increased risk of adverse events (OR 4.92, 95% CI 2.66 to 9.10; P< 0.001). Colchicine should not be used for alcoholic, viral, or cryptogenic liver fibrosis or liver cirrhosis outside randomised trials.

Changes in platelet serotonin (5-HT) content in patients with alcoholic and non-alcoholic liver cirrhosis

Changes in platelet serotonin (5-HT) content in patients with alcoholic and non-alcoholic liver cirrhosis

Changes in platelet serotonin (5-HT) content in patients with alcoholic and non-alcoholic liver cirrhosis

Changes in platelet serotonin (5-HT) content in patients with alcoholic and non-alcoholic liver cirrhosis

Colchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosis.

Colchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosis.

Low plasma levels of docosahexaenoic acid in patients with liver cirrhosis and its correction with a polyunsaturated fatty acid-enriched soft oil capsule.

Plasma levels of docosahexaenoic acid (DHA, C22:6 omega 3) were found to be decreased in 11 patients with alcoholic and non-alcoholic liver cirrhosis depending on the severity of liver damage. In this reduction, we found impaired metabolism of omega-3 long-chain polyunsaturated fatty acids in the cirrhotic liver and poor dietary intake of DHA to involved in the reduction of DHA plasma levels. The deficiency of this fatty acid, which is concentrated in the nervous tissues, may be related to the impaired neural function observed in hepatic encephalopathy of these patients. Oral DHA supplementation was supplied in the form of a polyunsaturated fatty acid-enriched soft oil capsule (omega 3/omega 6 ratio = 0.91, and P/S ratio = 1.87). Twelve capsules per day (containing 408 mg DHA, which corresponds to one-fourth of the DHA content in a normal daily diet) improved the DHA contents in the plasma phospholipid fractions of 5 alcoholic patients with low DHA levels.

Role of substance P in the pathogenesis of spider angiomas in patients with nonalcoholic liver cirrhosis.

Cutaneous spider angioma is a common sign observed in patients with liver cirrhosis, but its pathogenesis is still unclear. Increased plasma levels of estrogen, vascular dilation, and neovascularization are possible etiologies. This study was designed to investigate the relationship of spider angiomas in patients with nonalcoholic liver cirrhosis to the plasma levels of sex hormones and various vasodilators and hemodynamic parameters. A total of 60 patients with nonalcoholic liver cirrhosis and 20 healthy subjects were included in this study. The number, size, and location of the spider angiomas were recorded. Plasma levels of estradiol, testosterone, substance P, calcitonin gene-related peptide, and nitrate/nitrite and forearm hemodynamics were measured. Cirrhotic patients showed higher plasma estradiol/testosterone ratios (28.3+/-47.2 x 10(-3), median 10.5 x 10(-3) vs 8.2+/-8.3 x 10(-3), median 5.7 x 10(-3), p = 0.003) and levels of nitrate/ nitrite (29.9+/-17.5, median 23.8 vs 21.4+/-10.0, median 20.6 micromol/L, p = 0.01) and substance P (47.5+/-62.5, median 29.2 vs 15.2+/-7.7, median 12.3 pg/ml, p < 0.001) than healthy controls. Sixteen (27%) of the 60 cirrhotic patients had spider angiomas. Cirrhotic patients with spider angiomas disclosed higher plasma levels of substance P (84.7+/-105.3, median 53.1 vs 34.5+/-30.7, median 25.8 pg/ml, p = 0.006) and serum levels of bilirubin (3.9+/-3.8, median 1.9 vs 1.9+/-1.9, median 1.2 mg/dl, p = 0.02) than those without. Stepwise logistic regression showed substance P was the only significant and independent predictor associated with the presence of spider angiomas in cirrhotic patients (odds ratio = 3.0, 95% confidence interval = 1.4-6.6, p = 0.01). Plasma levels of substance P are elevated in patients with nonalcoholic cirrhosis and may play an important role in the pathogenesis of spider angiomas.

Role of substance P in the pathogenesis of spider angiomas in patients with nonalcoholic liver cirrhosis

Objective:Cutaneous spider angioma is a common sign observed in patients with liver cirrhosis, but its pathogenesis is still unclear. Increased plasma levels of estrogen, vascular dilation, and neovascularization are possible etiologies. This study was designed to investigate the relationship of spider angiomas in patients with nonalcoholic liver cirrhosis to the plasma levels of sex hormones and various vasodilators and hemodynamic parameters. Methods: A total of 60 patients with nonalcoholic liver cirrhosis and 20 healthy subjects were included in this study. The number, size, and location of the spider angiomas were recorded. Plasma levels of estradiol, testosterone, substance P, calcitonin gene-related peptide, and nitrate/nitrite and forearm hemodynamics were measured. Results: Cirrhotic patients showed higher plasma estradiol/testosterone ratios (28.3 ± 47.2 × 10 −3, median 10.5 × 10 −3 vs 8.2 ± 8.3 × 10 −3, median 5.7 × 10 −3, p = 0.003) and levels of nitrate/nitrite (29.9 ± 17.5, median 23.8 vs 21.4 ± 10.0, median 20.6 μmol/L, p = 0.01) and substance P (47.5 ± 62.5, median 29.2 vs 15.2 ± 7.7, median 12.3 pg/ml, p < 0.001) than healthy controls. Sixteen (27%) of the 60 cirrhotic patients had spider angiomas. Cirrhotic patients with spider angiomas disclosed higher plasma levels of substance P (84.7 ± 105.3, median 53.1 vs 34.5 ± 30.7, median 25.8 pg/ml, p = 0.006) and serum levels of bilirubin (3.9 ± 3.8, median 1.9 vs 1.9 ± 1.9, median 1.2 mg/dl, p = 0.02) than those without. Stepwise logistic regression showed substance P was the only significant and independent predictor associated with the presence of spider angiomas in cirrhotic patients (odds ratio = 3.0, 95% confidence interval = 1.4–6.6, p = 0.01). Conclusion: Plasma levels of substance P are elevated in patients with nonalcoholic cirrhosis and may play an important role in the pathogenesis of spider angiomas.

Hepatic encephalopathy - a physostigmine-reactive central anticholinergic syndrome?

This report describes an association between hepatic encephalopathy and central anticholinergic syndrome (CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade Child B. Suspecting upper gastrointestinal bleeding, she was intubated for gastroduodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resulting from ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.

Small bowel motility in primary biliary cirrhosis.

Previous studies have shown small bowel motor activity abnormalities in patients with liver cirrhosis of different etiologies, but motility has not been studied in patients with primary biliary cirrhosis. Our aim was to investigate proximal small bowel motility in these patients. Twenty-five female patients presenting clinical, biochemical, serological, and histological findings compatible with primary biliary cirrhosis, 10 female patients with nonalcoholic liver cirrhosis, and 10 normal female controls were studied. Motility of the upper small bowel was measured in the fasted state by means of perfused manometric catheters, connected to external transducers and positioned in the small bowel under fluoroscopy. The average amplitude of contractions was significantly decreased in patients with primary biliary cirrhosis compared with other liver cirrhosis (20.2+/-1.0 vs 32+/-2.9 mm Hg). Also, a significantly increased frequency of cluster of contractions and an increased duration of phase II of the migrating motor complex as seen in liver cirrhosis was observed when compared with normals. We conclude that primary biliary cirrhosis patients present motor abnormalities of the small intestine similar to those of patients with liver cirrhosis of other etiologies. In addition, a decrease in the amplitude of small bowel contractions was also found in these patients, suggesting a myogenic involvement.

Small bowel motility in primary biliary cirrhosis

Objective: Previous studies have shown small bowel motor activity abnormalities in patients with liver cirrhosis of different etiologies, but motility has not been studied in patients with primary biliary cirrhosis. Our aim was to investigate proximal small bowel motility in these patients. Methods: Twenty-five female patients presenting clinical, biochemical, serological, and histological findings compatible with primary biliary cirrhosis, 10 female patients with nonalcoholic liver cirrhosis, and 10 normal female controls were studied. Motility of the upper small bowel was measured in the fasted state by means of perfused manometric catheters, connected to external transducers and positioned in the small bowel under fluoroscopy. Results: The average amplitude of contractions was significantly decreased in patients with primary biliary cirrhosis compared with other liver cirrhosis (20.2 ± 1.0 vs 32 ± 2.9 mm Hg). Also, a significantly increased frequency of cluster of contractions and an increased duration of phase II of the migrating motor complex as seen in liver cirrhosis was observed when compared with normals. Conclusion: We conclude that primary biliary cirrhosis patients present motor abnormalities of the small intestine similar to those of patients with liver cirrhosis of other etiologies. In addition, a decrease in the amplitude of small bowel contractions was also found in these patients, suggesting a myogenic involvement.

Plasma somatostatin response to an oral test meal in liver transplant patients

Ten liver transplant patients were studied in basal conditions and after ingestion of a standard mixed test meal. Control groups included 10 normal subjects, 10 patients with nonalcoholic liver cirrhosis, and seven kidney transplant patients. Plasma somatostatin, blood glucose, and plasma insulin, C-peptide, and glucagon were determined before and 15, 30, 45, 60, 90, 120, and 180 minutes after the start of the meal. In liver transplant patients, basal somatostatin and insulin levels were significantly lower than in cirrhotics and were comparable to those recorded in controls and in kidney transplant patients. The time course of the somatostatin secretory response after the meal was similar in any group, but the increase, evaluated as the incremental area above baseline, was significantly higher in liver transplant patients than in controls and cirrhotics and comparable to that recorded in kidney transplant patients. Insulin incremental areas were also lower than in cirrhotics and comparable to those recorded in controls and kidney transplant patients. The data suggest that in liver transplant patients an increased somatostatin response to a meal may be related to a relative β-cell secretory defect, which in turn seems consequent to immunosuppressive treatment.