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Biomedical subjects

A F Attili

Publications and source records attributed to A F Attili.

At least 19 recordsLinked to original sources
PubMed2006

Management and outcomes of hepatic cirrhosis: Findings from the RING study.

BACKGROUND/AIM: Hepatic cirrhosis is a frequent reason for ordinary hospital admission (OA). The RING study collected hospital discharge files (HDF) from Italian hospital gastroenterology units (IGU). This caselist provides a broad picture of the patients admitted for this pathology. MATERIAL/METHODS: More than 50,000 HDF for OA were collected between 2001 and 2004 from 26 IGU. RESULTS: Eight thousand four hundred and eighty-seven HDF (16%) had a diagnosis of hepatic cirrhosis; Child-Pugh classes were 20.2% A, 34.8% B and 45.0% C. Patients' mean age was 63.7+/-12.1 years and 62.5% were male. A 61.1% of the cirrhosis cases had ascites, 29.9% portal-systemic encephalopathy, 29.2% hepatocellular carcinoma (HCC), 10% bleeding varices, 3.0% hepatorenal syndrome (HRS). Mortality for OA for cirrhosis was 5.7% versus 2.6% for other diagnoses. The proportion varied with the severity of the cirrhosis: 0% for Child A, 1.1% B, 10.5% C. Mortality was significantly associated with: Child-Pugh at admission (odds ratio: OR 9.2), HRS (OR 11.7), bleeding varices (OR 2.2), HCC (OR 1.8). CONCLUSIONS: Hepatic cirrhosis was found in 16% of the OA to IGU and mortality was double the rate for all the other pathologies in the same wards. Child-Pugh is a useful prognostic tool, higher classes implying a greater risk of death. HRS and bleeding varices were the complications with most influence on in-hospital mortality.

Journal Article↗
PubMed2005

Alpha-SMA expression in hepatic stellate cells and quantitative analysis of hepatic fibrosis in cirrhosis and in recurrent chronic hepatitis after liver transplantation.

BACKGROUND: The alpha isotype of actin expressed by hepatic stellate cells reflects their activation to myofibroblast-like cell and has been directly related to experimental liver fibrogenesis, and indirectly to human fibrosis in chronic liver disease. AIMS: To evaluate the changes in distribution and percentage of alpha-smooth muscle actin-positive hepatic stellate cells and the correlation with the degree of the fibrosis in cirrhotic livers, as well as in patients with recurrent HCV chronic hepatitis after liver transplantation. METHODS: Human liver biopsies were divided in four groups: (1) normal livers obtained from cadaveric liver donors (n=35), (2) cirrhosis post-HBV hepatitis (n=11), (3) cirrhosis post-HCV hepatitis (n=10), and (4) post-transplant recurrent HCV chronic hepatitis (n=13). Samples were stained with anti-alpha-smooth muscle actin antibody by immunoperoxidase method and semi-quantitatively evaluated. Liver fibrosis was assessed from specimens stained with Masson's trichrome and quantified by computer image analysis. RESULTS: The percentage of alpha-smooth muscle actin-positive hepatic stellate cells was significantly higher in the HBV cirrhosis, HCV cirrhosis and post-transplant HCV recurrent hepatitis groups (36.1+/-15.2, 23.8+/-19.7 and 27.8+/-16.4%, respectively) compared to the liver donor group (2.9+/-4.0%). The alpha-smooth muscle actin-positive hepatic stellate cells to fibrous tissue ratio were significantly higher in the post-transplant recurrent HCV hepatitis group (2.36+/-1.12) compared to both the donor livers and the HCV cirrhosis groups (0.74+/-1.09 and 1.03+/-0.91, respectively). The alpha-smooth muscle actin-positive hepatic stellate cell percentage and fibrosis correlated positively in the post-transplant recurrent HCV hepatitis group and negatively in the HCV cirrhosis group. No difference in the immunohistochemical and morphometrical variables was found between the HCV cirrhosis and HBV cirrhosis groups. CONCLUSIONS: These results indirectly confirm that, in vivo, alpha-smooth muscle actin expression is a reliable marker of hepatic stellate cells activation which precedes fibrous tissue deposition even in the setting of recurrent HCV chronic hepatitis after liver transplantation, and it could be useful to identify the earliest stages of hepatic fibrosis and monitoring the efficacy of the therapy. In the presence of advanced cirrhosis other factors, rather than alpha-smooth muscle actin-positive hepatic stellate cells, may sustain fibrosis deposition.

Actins↗
PubMed2003

Malnutrition is not related to alterations in energy balance in patients with stable liver cirrhosis.

BACKGROUND AND AIMS: Little information are available on the relationship between energy balance and the alterations in nutritional status occurring in cirrhotic patients. The aim of the present study was to evaluate the daily energy balance in clinically stable cirrhotic patients with or without malnutrition. PATIENTS: Seventy-four consecutive cirrhotic patients and nine healthy controls were studied. METHODS: Basal energy expenditure was measured by indirect calorimetry and adjusted according to the patients' physical activity to estimate the daily energy expenditure. Food intake was evaluated based on a 3-day dietary diary. Nutritional status and body composition were assessed using skinfold anthropometry and dual energy X-ray absorptiometry, respectively. RESULTS: Thirty-two patients in the cirrhotic group were classified as severely malnourished according to anthropometric parameters. Two different patterns of soft-tissue loss were observed in the malnourished cirrhotic group: a significant reduction in fat mass and in fat-free mass was observed in males, whereas, females showed a significant reduction in fat mass only. Basal energy expenditure was similar in all groups, while the non-protein respiratory quotient was lower in cirrhotics notwithstanding their nutritional status. This suggests that lipids were the preferred oxidized fuel in the post-absorptive state in these patients. No difference in the estimated daily energy expenditure and energy intake was observed among groups. Lipid content of the diet was significantly lower in malnourished cirrhotics than in controls (33.1+/-1% vs 37.8+/-1%, P=0.02). CONCLUSIONS: Cirrhotic patients in stable clinical condition with malnutrition show a normal energy balance.

Analysis of Variance↗
PubMed2003

Helicobacter pylori diagnosis in patients with liver cirrhosis.

BACKGROUND: In cirrhotics, Helicobacter pylori infection is the major cause of peptic lesions, which are an important cause of upper intestinal haemorrhage in these patients. However, some diagnostic methods are not accurate for H. pylori detection in cirrhotics. AIMS: The study assessed the accuracy of different diagnostic methods for H. pylori detection in cirrhotics with and without gastroduodenal lesions. METHODS: The study population comprised of 53 cirrhotics. All patients underwent upper endoscopy: three biopsies were taken in the antrum and three in the gastric body. Four biopsies were used for Giemsa staining, while two were used for a rapid urease test. A blood sample was obtained for serology using Western blotting, and a [13C]urea breath test was performed in all patients. Histological assessment was regarded as the gold standard for diagnosis of H. pylori infection. RESULTS: H. pylori infection was detected at histological assessment in 28 (52.8%) patients. The [13C]urea breath test, rapid urease test, and serology were positive in 27 (51%) patients, 23 (43.4%) patients, and 34 (64.1%) patients, respectively. Sensitivity and specificity were 92.9 and 96% for the [13C]urea breath test, 78.6 and 96% for the rapid urease test, and 78.6 and 52% for serology. CONCLUSIONS: The [13C]urea breath test is very accurate in cirrhotics, whilst both serology and the rapid urease test give disappointing results.

Antibodies, Bacterial↗
PubMed2002

Alfa and beta estrogen receptors and the biliary tree.

This manuscript summarizes recent data showing that estrogens and their receptors play an important role in modulating cholangiocyte proliferation. We have recently demonstrated that rat cholangiocytes express both estrogen receptors (ER)-alpha and -beta subtypes, while hepatocytes only express ER-alpha. ER and especially the ER-beta subtype, are overexpressed in cholangiocytes proliferating after bile duct ligation (BDL) in the rat, in association with enlarged bile duct mass and with enhanced estradiol serum levels. Cholangiocyte proliferation, during BDL, is impaired by estrogen antagonists (tamoxifen, ICI 182,780) which furthermore, induce the overexpression of Fas antigen and activate apoptosis of proliferating cholangiocytes. 17beta-estradiol stimulates, in vitro cholangiocyte proliferation, and this effect is individually blocked by tamoxifen or ICI 182,780. Cholangiocyte proliferation during BDL was associated with an enhanced protein expression of phosphorylated extracellular regulated kinases (ERK)1/2 which is, in contrast, negatively modulated by tamoxifen in association with its antiproliferative effect. This indicates a major involvement of the ERK system in the estrogen modulation of cholangiocyte proliferation.

Animals↗
PubMed2001

Gastric epithelial cell proliferation in patients with liver cirrhosis.

An increased risk for gastric cancer in patients with liver cirrhosis has recently been reported. This study was performed in order to determine gastric epithelial cell proliferation in cirrhotic patients and to evaluate the role of congestive gastropathy (CG) and Helicobacter pylori infection in this process. Thirty-six cirrhotic patients and 18 controls were enrolled in the study. All patients underwent endoscopy and three biopsies were performed in the antrum and three in the gastric body. The presence of H. pylori infection was assessed by a rapid urease test and histology. The antral biopsies were used for gastric cell proliferation assessment by an immunohistochemical analysis (Ki-67). There was no significant difference in epithelial cell proliferation between cirrhotics and controls. Gastric proliferation values were higher in patients with H. pylori infection compared with uninfected patients, both in cirrhotic (P = 0.003) and in control groups (P = 0.06). Among the cirrhotic group, we found a progressive increase in gastric cell proliferation values related to the degree of CG, the highest values being observed in cirrhotic patients with severe CG. Moreover, cirrhotics with both severe CG and H. pylori infection had the highest proliferation values when compared with all other subgroups. In conclusion, this study found that: (1) CG significantly affects epithelial cell proliferation in gastric mucosa in cirrhotic patients, (2) H. pylori infection plays a similar role in gastric cell proliferation in both cirrhotic and non-cirrhotic patients, and (3) CG and H. pylori could act synergistically in this process.

Adult↗
PubMed2000

Impaired human gallbladder lipid absorption in cholesterol gallstone disease and its effect on cholesterol solubility in bile.

BACKGROUND & AIMS: The role of the gallbladder in gallstone pathogenesis is still unclear. We examined the effects of gallbladder mucosal lipid absorption on lipid composition and cholesterol crystallization in bile. METHODS: The in vitro-isolated, intra-arterially perfused gallbladder model was used (1) to compare the absorption rates of lipids from standard bile by gallbladders obtained from 7 patients with cholesterol gallstones and 6 controls; and (2) to measure the microscopic cholesterol crystal detection time in cholesterol-enriched pig bile before and after lipid absorption by the pig gallbladder. RESULTS: Control gallbladders, but not cholesterol gallstone gallbladders, significantly reduced cholesterol (P < 0.02) and phospholipid (P < 0.01) and increased bile salt (P < 0.01) molar percentages in bile over a 5-hour period by efficient and selective cholesterol and phospholipid absorption. A histomorphometric study of the epithelial cells showed significantly higher values for nuclear density (P < 0.01) and nuclear (P < 0.05) and cytoplasmic (P < 0.05) areas in the cholesterol gallstone than the control group. Sequential microscopy of cholesterol-enriched pig bile showed significantly shorter cholesterol filament (P < 0.01) and typical cholesterol plate (P < 0. 02) detection times before than after exposure of bile to the gallbladder lipid absorption. CONCLUSIONS: In cholesterol gallstone disease, the human gallbladder epithelium loses its capacity to selectively and efficiently absorb cholesterol and phospholipids from bile, even if it is hyperplastic and hypertrophic. This epithelial dysfunction eliminates the positive effect that the normal gallbladder exerts on cholesterol solubility in bile and might be a pathogenetic cofactor for cholesterol gallstone formation.

Absorption↗
PubMed2000

Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection.

BACKGROUND: The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM: To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS: A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS: Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS: These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.

Adult↗
PubMed2000

A new highly effective short-term therapy schedule for Helicobacter pylori eradication.

BACKGROUND: Although triple therapy regimens suggested in the Current European guidelines give fairly good results, several studies have reported an unsatisfactory Helicobacter pylori eradication rate (< 80%). AIM: To evaluate the efficacy of a new short-term treatment sequence on H. pylori eradication. METHODS: A total of 52 patients with H. pylori infection and either non-ulcer dyspepsia (34 patients) or peptic ulcer (18 patients) were enrolled to receive a 10-day therapy: omeprazole 20 mg b.d. plus amoxycillin 1 g b.d. for the first 5 days, followed by omeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. for the remaining 5 days. H. pylori infection at entry was assessed by rapid urease test and histology on biopsies from the antrum and the corpus. Bacterial eradication was assessed by endoscopy (peptic ulcer patients) or 13C urea breath test (non-ulcer dyspepsia patients) 4-6 weeks after therapy had ended. RESULTS: All patients completed the study. H. pylori eradication was achieved in all but one patient, with an eradication rate of 98% (95% CI: 94.3-100) with intention-to-treat analysis. Patient compliance was good (consumption of prescribed drugs > 95%) for all but one patient, who took the triple therapy regimen for 4 days instead of 5 days. No major side-effects were reported but three (6%) patients complained of mild side-effects. CONCLUSIONS: The use of this 'five plus five' therapy schedule as an initial treatment for H. pylori deserves further investigation.

Administration, Oral↗
PubMed2000

Ascorbic acid and intestinal metaplasia in the stomach: a prospective, randomized study.

BACKGROUND: Intestinal type metaplasia plays a role in intestinal type gastric carcinoma development. Ascorbic acid demonstrates a protective effect against gastric carcinogenesis, due to its ability to inactivate oxygen free-radicals as well as its nitrite-scavenging effects. AIM: To assess whether long-term ascorbic acid administration following Helicobacter pylori eradication could affect intestinal metaplasia regression in the stomach. METHODS: Sixty-five patients were included in the study. The inclusion criterion was the presence of intestinal metaplasia on the gastric mucosa after H. pylori eradication. An upper gastrointestinal endoscopy was performed and 3 biopsy specimens were taken in the antrum, 3 in the gastric body, and 2 in the incisura angularis. Patients were randomized to receive 500 mg of ascorbic acid o.d., after lunch (32 patients) for 6 months or no treatment (33 patients). All patients underwent to endoscopic control at the end of the 6 months. RESULTS: H. pylori infection recurrence was detected in 6 (9.4%) patients (three from each group), and these patients were excluded from further analysis. We were unable to find evidence of intestinal metaplasia in any biopsied site of the gastric mucosa in 9/29 (31%) patients from the ascorbic acid group and in 1/29 (3.4%) of the patients from the control group (P=0.006). Moreover, a further six (20.7%) patients from the ascorbic acid group presenting chronic inactive pangastritis with widespread intestinal metaplasia at entry, showed less extensive antritis with intestinal metaplasia at control, whilst a similar finding was only seen in one patient from the control group (P=0.051). CONCLUSION: The administration of ascorbic acid significantly helps to resolve intestinal metaplasia of the gastric mucosa following H. pylori eradication, and its use as a chemoprevention treatment should be considered.

Adult↗
PubMed2000

Clinical and histologic predictors of Helicobacter pylori infection recurrence.

Factors influencing Helicobacter pylori infection recurrence still have not been fully clarified. The aim of this study was to determine whether, after eradication of H. pylori, any clinical or histologic features could yield information on infection relapse. We enrolled in the study 72 patients successfully treated for H. pylori infection by either dual (n = 49) or triple (n = 23) therapy. H. pylori eradication was defined as a negative bacterial finding by rapid urease test and histologic assessment at least 4 weeks after cessation of therapy. Upon eradication, gastritis grading was performed and patients were asked to return for an endoscopic control 6-8 months later. The recurrence of H. pylori infection was observed in 12 of 72 (16.7%) patients. The infection recurrence rate resulted significantly higher in nonulcer dyspepsia patients (p = 0.01 ) and in women (p = 0.03), whereas infection relapse did not differ between patients treated with dual or triple therapy. There was a strong (p = 0.0001 ) relationship between the persistence of chronic active gastritis after H. pylori eradication and recurrence of infection, whereas gastritis grade and metaplasia were not related to recurrence. In conclusion, this study found that H. pylori infection recurrence after successful dual or triple therapy is fairly high and that gastroduodenal disease, gender, and gastritis activity seem to affect infection relapse.

Adult↗
PubMed2000

Cholelithiasis: genetic hypothesis.

In inbred mice gallstone susceptibility is determined by Lith (lithogenic) genes which promote cholesterol hypersecretion in bile as a response to a high-fat diet. At least three major classes of proteins can be considered as candidate genes: (a) enzymes involved in cholesterol metabolism regulation; (b) trans-membrane carrier proteins from hepatocyte into bile; (c) cytosolic transfer proteins which regulate intrahepatocyte trafficking. The main candidates are: Spgp, a transmembrane protein which produces bile salt transport. Its gene map in Lith 1 region (Chromosome 2) and its expression is increased in susceptible inbred strains of mice (C57L) of inbred mice. Cmoat is a carrier protein that promotes the secretion of conjugated substances in bile. Its gene map in Lith 2 region (Chromosome 19) and its expression is increased in susceptible inbred strains of mice fed on a lithogenic diet. HGMR is the enzyme that regulates de novo synthesis of cholesterol in the liver. Its activity increases in resistant strains fed on a lithogenic diet and unvaries in susceptible strains. Its gene does not reside in any Lith region, but one Lith gene could be responsible for its activity regulation. To date, the hypothesis of a genetic basis of cholelithiasis in men has only been investigated in one study, in which the association of cholelithiasis and a mutation in the C7AH gene was documented in a group of Mexican patients.

Journal Article↗
PubMed1999

Helicobacter pylori eradication with proton pump inhibitor-based triple therapies and re-treatment with ranitidine bismuth citrate-based triple therapy.

BACKGROUND: It has been suggested that short-term triple therapy comprising a proton pump inhibitor, plus clarithromycin and amoxycillin be used as first choice in treating H. pylori infection, while eradication failure patients should be further treated with a quadruple therapy. Nevertheless, conflicting results have been reported using these treatment regimens in different countries. METHODS: A total of 278 patients with H. pylori infection were randomised to receive one-week triple therapy, comprising clarithromycin 500 mg b.d., amoxycillin 1 g b.d., and either omeprazole 20 mg b.d. (OAC; 90 patients), or pantoprazole 40 mg b.d. (PAC; 95 patients), or lansoprazole 30 mg b.d. (LAC; 93 patients). H. pylori infection at entry, and eradication 4-6 weeks after therapy had ended, were assessed by rapid urease test and histology on biopsies from the antrum and the corpus. When eradication did not occur, patients were given a 2-week treatment comprising ranitidine bismuth citrate 400 mg b.d., tetracycline 500 mg t.d.s. and tinidazole 500 mg b.d. (RBTT). Eradication in these patients was assessed 4-6 weeks after conclusion of treatment by a further endoscopy. RESULTS: Six patients were lost to the follow-up. At the end of the first course of treatment, the overall H. pylori eradication rate was 78% (95% CI: 73-83) and 79% (95% CI: 75-84) at 'intention-to-treat' (ITT) and 'per protocol' (PP) analysis, respectively, without any statistically significant difference between treatment regimens, although a trend for better results with the omeprazole combination was observed. Moreover, H. pylori eradication was achieved in 82% (95% CI: 75-97) (ITT) and 86% (95% CI: 69-94) (PP) of 38 patients re-treated with RBTT regimen. CONCLUSIONS: Our data found that this short-term triple therapy is not a satisfactory treatment (< 80% eradication rate) for H. pylori infection. The 2-week triple therapy used as re-treatment in eradication failure patients yielded more promising results.

Adolescent↗
PubMed1999

Helicobacter pylori infection, plasma ammonia levels, and psychometric testing in cirrhotic patients.

OBJECTIVE: The role of Helicobacter pylori (H. pylori) infection as a cause of hepatic encephalopathy is still debated. This study focused on the relationship between H. pylori, plasma ammonia levels, and intellectual function in cirrhotic patients. METHODS: Forty-seven cirrhotics with latent or mild hepatic encephalopathy were enrolled in the study, upon H. pylori assessment at endoscopy. Plasma ammonia level determinations and psychometric testing were performed at entry in all patients. Patients with H. pylori infection received a 2-wk standard dual therapy and bacterial eradication was assessed at endoscopy 6-8 wk later. On this occasion, plasma ammonia levels and psychometric assessments were repeated. Patients without H. pylori infection at entry were also studied after 6-8 wk for ammonia level assessment and psychometric testing, as a control group. Patients receiving lactulose therapy and those without therapy were grouped separately for statistical analysis. RESULTS: Among 21 patients without lactulose therapy (group A), basal plasma ammonia levels and psychometric testing scores did not significantly differ between 13 infected and eight uninfected patients. Similarly, among 26 patients undergoing lactulose therapy (group B), basal plasma ammonia concentration and psychometric testing scores did not significantly differ between 13 infected and 13 uninfected patients. Moreover, in group B, both the prevalence of previous overt hepatic encephalopathy episodes and the mean daily dose of lactulose therapy were similar between infected and uninfected patients. In addition, no significant reduction in the plasma ammonia concentrations and in psychometric testing scores emerged in both groups A and B after bacterial eradication. CONCLUSIONS: This study failed to find a relationship between H. pylori, plasma ammonia levels, and psychometric testing scores in cirrhotic patients with latent or mild hepatic encephalopathy.

Adult↗
PubMed1999

Effect of lactitol on blood ammonia response to oral glutamine challenge in cirrhotic patients: evidence for an effect of nonabsorbable disaccharides on small intestine ammonia generation.

OBJECTIVE: Nonabsorbable disaccharides are widely used to decrease blood ammonia concentration. Their principal mode of action is the modification of pH and bacterial flora in the colon. The aim of the present study was to test the hypothesis that these drugs may also reduce small intestine ammonia generation. METHODS: Eight male cirrhotics without overt hepatic encephalopathy received 20 g of glutamine in 100 ml of water. Venous samples for whole blood ammonia were taken before, 30 and 60 min after the load. Immediately after the last blood sample the patients were submitted to the following psychometric tests: number connection test, Posner's attention test, and Sternberg paradigm. After the first glutamine load, patients were started on lactitol (initial dose 20 g, three times a day). Once two bowel movements/day were obtained and maintained for at least 5 days, oral glutamine challenge and psychometric tests were repeated. RESULTS: Ammonia increased significantly after the glutamine load (from 83 +/- 13 to 164 +/- 30 microg/dl at 30 min and 210 +/- 29 microg/dl at 60 min; mean +/- SE; p = 0.006 analysis of variance) but not after glutamine load after lactitol treatment (from 77 +/- 17 to 111 +/- 21 microg/dl and 142 +/- 24 microg/dl; p = not significant). The peak increment (127 +/- 24 vs 65 +/- 18 microg/dl; p = 0.008) of ammonia elevation was significantly smaller during lactitol administration. The patients' psychometric performance after the glutamine load did not differ significantly after lactitol treatment. CONCLUSIONS: Lactitol reduces the elevation in blood ammonia that follows oral glutamine challenge. Because enterally administered glutamine is efficiently absorbed in the jejunum and, in part, metabolized to ammonia we suggest that lactitol affects small intestine ammonia generation probably by shortening the residence time of intestinal contents.

Administration, Oral↗