Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis.

BACKGROUND/AIMS: Impaired gallbladder motility has been suggested as a contributor to increased incidence of gallstones in patients with liver cirrhosis. The purpose of this study was to determine gallbladder function and its relation with autonomic neuropathy in liver cirrhosis. MATERIALS AND METHODS: Gallbladder function was measured using ultrasonography in 48 patients with liver cirrhosis and in 31 controls. Autonomic neuropathy tests were applied in patients with liver cirrhosis. Patients with liver cirrhosis were analyzed in subgroups according to the severity of disease using the Child-Pugh classification. RESULTS: Fasting gallbladder volume was 16.2 mL (range: 2.1 mL-71.9 mL) in patients and 17.6 mL (range: 4.9 mL-76.6 mL) in controls. There were no differences in fasting gallbladder volume among the study groups (p>0.05). Gallbladder ejection fraction was significantly higher in patients compared with controls (84% vs. 65%) (p<0.001). No correlation was found between gallbladder ejection fraction and autonomic neuropathy (p>0.05). CONCLUSION: Our results indicate that liver cirrhosis does not impair gallbladder emptying, and that there is no association between gallbladder motility and autonomic neuropathy. Further investigations are required to explain increased gallbladder motility in liver cirrhosis.

Ultrasonographic evaluation of gallbladder functions in patients with irritable bowel syndrome.

BACKGROUND: The aim of the present study was to evaluate gallbladder function in irritable bowel syndrome (IBS) patients. METHODS: The functions of gallbladder were investigated every 30 min for 4 h. In addition, ejection fraction of the gallbladder was calculated from the fasting and post-prandial volumes. RESULTS: In IBS patients and healthy controls, fasting gallbladder volumes were 19.64 +/- 3.09 mL and 20.04 +/- 1.82 mL, and residual volumes after 3 h were 3.36 +/- 6.82 mL and 9.74 +/- 1.50 mL. Except for the residual volume after 3 h, all these results were not statistically significant. Residual volume after 3 h was statistically significantly lower in the IBS patients than in the controls (P < 0.001). Ejection fraction of the gallbladder was significantly higher in the IBS patients than in the controls (84% vs 55%, P < 0.001). CONCLUSIONS: Gallbladder contraction in patients with IBS was not different from that of a control group at post-prandial second hour but was signigicantly more pronounced at the end of 3 h when compared with controls. Ejection fraction of the gallbladder was higher in IBS patients when compared with controls.

Helicobacter pylori eradication lowers serum homocysteine level in patients without gastric atrophy.

AIM: To determine whether Helicobacter pylori (H pylori)infection caused hyperhomocysteinemia by altering serum vitamin B(12), serum folate and erythrocyte folate levels and whether eradication of this organism decreased serum homocysteine level. METHODS: The study involved 73 dyspeptic H pylori-positive patients, none of them had gastric mucosal atrophy based on rapid urease test and histology. Out of 73 patients, 41 (56.2%) showed a successful eradication of H pylori 4 wk after the end of treatment. In these 41 patients, fasting serum vitamin B(12), folate and homocysteine levels, and erythrocyte folate levels before and 4 wk after H pylori eradication therapy were compared. RESULTS: The group with a successful eradication of H pylori had significantly higher serum vitamin B(12) and erythrocyte folate levels in the post-treatment period compared to those in pre-treatment period (210+/-97 pg/mL vs 237+/-94 pg/mL, P<0.001 and 442+/-212 ng/mL vs 539+/-304 ng/mL, P = 0.024, respectively), but showed no significant change in serum folate levels (5.6+/-2.6 ng/mL vs 6.0+/-2.4 ng/mL, P = 0.341). Also, the serum homocysteine levels in this group were significantly lower after therapy (13.1+/-5.2 micromol/L vs 11.9+/-6.2 micromol /L, P = 0.002). Regression analysis showed that serum homocysteine level was positively correlated with age (P = 0.01) and negatively with serum folate level before therapy (P = 0.003). CONCLUSION: Eradication of H pylori decreases serum homocysteine even in patients who do not exhibit gastric mucosal atrophy. It appears that the level of homocysteine in serum is related to a complex interaction among serum vitamin B(12), serum folate and erythrocyte folate levels.

Predictors of vitamin B12 deficiency: age and Helicobacter pylori load of antral mucosa.

BACKGROUND/AIMS: The aim of this study was to assess the frequency of vitamin B12 deficiency in patients with non atrophic gastric mucosa and any relationship between the presence of vitamin B12 deficiency and demographic, hematologic, and histopathologic parameters. METHODS: Three hundred and ten patients with no gastric mucosal atrophy on histologic evaluation were included in the study. Chronic inflammation, neutrophil activity and H. pylori load were scored using the Sydney classification system. Variables that might influence or predict the presence of vitamin B12 deficiency (age, gender, hemoglobin, mean corpuscular volume, serum folate level, scores of histologic parameters) were evaluated by univariate/multivariate analysis. RESULTS: The percentages of patients with vitamin B12 concentrations of < 250 pg/mL, < 200 pg/mL, and =100 pg/mL were 67.4%, 46.8% and 6.5% respectively. Patient age and all three histologic were inversely related to vitamin B12 deficiency (p<0.05). By multivariate analysis, factors independently associated with serum vitamin B12 deficiency were age and antral H. pylori load (p<0.05). CONCLUSIONS: The higher frequency of vitamin B12 deficiency in this study compared with a western study may be a reflection of the effect of H. pylori infection on serum vitamin B12 level. In addition, age was shown to be an independent risk factor for vitamin B12 deficiency irrespective of gastric atrophy. It is already known that the presence of H. pylori on gastric mucosa influence serum vitamin B12 levels. Hematologic parameters are not useful in predicting the deficiency of this vitamin.

Serum leptin level can be a negative marker of hepatocyte damage in nonalcoholic fatty liver.

BACKGROUND: The aim of this study was to determine whether leptin and insulin resistance (IR) showed differences between steatotic patients with and without elevated serum transaminases. METHODS: The study included 32 patients with fatty liver and high serum transaminase level (group I), 31 patients with fatty liver and normal serum transaminase level (group II), and 8 nonobese and nonsteatotic controls. The presence of steatosis was demonstrated by ultrasonography. Due to the effect of body mass index (BMI) on leptin levels, groups I and II were divided to form four subgroups for analysis (group IA, BMI 30; group IIA, BMI 30. RESULTS: The serum leptin levels in group IIB were significantly higher than the levels in group IB ( P = 0.017). Serum leptin was also higher in group IIA than in group IA, but this difference was not statistically significant ( P = 0.097). Logistic regression analysis revealed a significant negative correlation between serum leptin level and the presence of a high transaminase level (odds ratio, 0.97; 95% confidence interval, 0.95-0.99). The levels of IR in the four patient groups were comparable, but the controls had significantly lower IR levels than group IIA. CONCLUSIONS: Elevated serum leptin seems to be a feature of steatotic patients with normal transaminase levels, and the level of serum leptin seems to decrease as the hepatocyte injury develops. IR is a common feature of fatty liver disease, irrespective of the presence of hepatocellular necrosis.