Quantitative Histomorphometric Study of the Jejunal Mucosa in Chronic Alcoholics

Bode, J C; Knüppel, Hans-Peter; Schwerk, W. B.; Lorenz-Meyer, H; Dürr, H. K.

doi:10.1159/000198760

Cited by 32 publications

(20 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Either loss of the epithelial cells or disruption of the tight junctions will lead to an increase in intestinal permeability. Clinical studies demonstrated that acute alcohol administration can cause apparent histopathological changes in the proximal part of the small intestine, whereas chronic alcohol consumption only induces minor histopathological changes (9,12,34). Our previous study (30) also showed that intestinal histopathological alterations, such as loss of epithelial cells at the top of the intestinal villi, were associated with acute alcohol intoxication-induced intestinal barrier disruption in mice (30).…”

Section: Discussionmentioning

confidence: 87%

The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction

Zhong

McClain²,

Cave

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

188

165

View full text Add to dashboard Cite

Disruption of the intestinal barrier is a causal factor in the development of alcoholic endotoxemia and hepatitis. This study was undertaken to determine whether zinc deficiency is related to the deleterious effects of alcohol on the intestinal barrier. Mice were pair fed an alcohol or isocaloric liquid diet for 4 wk, and hepatitis was detected in association with elevated blood endotoxin level. Alcohol exposure significantly increased the permeability of the ileum but did not affect the barrier function of the duodenum or jejunum. Reduction of tight-junction proteins at the ileal epithelium was detected in alcohol-fed mice although alcohol exposure did not cause apparent histopathological changes. Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species. Caco-2 cell culture demonstrated that alcohol exposure increases the intracellular free zinc because of oxidative stress. Zinc deprivation caused epithelial barrier disruption in association with disassembling of tight junction proteins in the Caco-2 monolayer cells. Furthermore, minor zinc deprivation exaggerated the deleterious effect of alcohol on the epithelial barrier. In conclusion, epithelial barrier dysfunction in the distal small intestine plays an important role in alcohol-induced gut leakiness, and zinc deficiency attributable to oxidative stress may interfere with the intestinal barrier function by a direct action on tight junction proteins or by sensitizing to the effects of alcohol.

show abstract

Section: Discussionmentioning

confidence: 87%

The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction

Zhong

McClain²,

Cave

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

188

165

View full text Add to dashboard Cite

show abstract

“…[19][20][21][22][23] In alcoholic liver disease, villous atrophy is frequently observed; reduction in villous height in relation to crypt depth and lower mucosal surface have been detected by light microscopy in alcoholics, even in the absence of cirrhosis. [24][25][26] Following the introduction of capsule endoscopy, mucosal abnormalities of the small intestine in liver cirrhosis patients with portal hypertension have been well documented and include inflammatory-like abnormalities (oedema, erythema, granularity and friability) as well as vascular lesions (cherry red spots, telangiectasias or angiodysplasia-like lesions and varices). 27 The reduced recovery of mannitol in all our study patients would be consistent with these findings.…”

Section: Discussionmentioning

confidence: 99%

Increased intestinal permeability in malnourished patients with liver cirrhosis

Norman

Pirlich

et al. 2012

Eur J Clin Nutr

View full text Add to dashboard Cite

BACKGROUND/OBJECTIVE: Malnutrition is a prominent feature in liver cirrhosis, with deleterious impact on clinical outcome. The objective of this study is to investigate whether malnutrition is associated with increased gastrointestinal permeability in liver cirrhosis reflected by altered urinary excretion of non-metabolizable sugar probes. SUBJECTS/METHODS: Patients with advanced liver cirrhosis (Child Pugh Score B or C) were recruited. Nutritional status was determined according to the Subjective Global Assessment. Intestinal permeability was assessed by measuring the urinary excretion of orally administered, non-metabolized sugar probe molecules. The lactulose/mannitol ratio served as marker for intestinal permeability and reflects non-carrier-mediated transcellular and paracellular transport of the small intestine during the first 5 h. Sucrose recovery in urine within the first 5 h reflects gastroduodenal permeability; sucralose recovery in urine 5-26 h after consumption reflects colonic permeability. RESULTS: Sixty-four patients (56.7±10.8 years; 33% female) were included in the study. Twenty-one patients were considered well nourished according to the Subjective Global Assessment, 23 moderately nourished and 20 patients severely malnourished; 74% had alcoholic liver disease and 67% had cirrhosis stage Child C. Gastroduodenal and colonic permeability was significantly increased in patients with liver cirrhosis compared with 63 healthy controls (0.23±0.22 and 1.37±1.42% vs 0.14±0.10 and 0.41±0.72% in controls), but not different between well and malnourished subjects. Small intestinal permeability (lactulose/ mannitol ratio) was increased in all patients (0.069 ± 0.055%) and further increased in malnourished patients (0.048 ± 0.031% vs 0.084 ± 0.061%, P ¼ 0.004) due to decreased mannitol recovery only. CONCLUSIONS: Gastric, small intestinal and even colonic permeability was altogether increased in liver cirrhosis, and malnutrition was associated with further increased small intestinal permeability indicative of villous atrophy.

show abstract

“…Morphometric studies have shown [21,23] that villus height and mucosal surface area are reduced in alcoholic as compared to nonalco holic patients. The data obtained in the present study, i.e.…”

Section: Discussionmentioning

confidence: 99%

Comparative Effects of Intestinal Absorption of Folic Acid and Methyltetrahydrofolic Acid in Chronic Ethanol-Fed-Rats

Carreras

Vázquez²,

Rubio³

et al. 1994

Ann Nutr Metab

View full text Add to dashboard Cite

This study concerns in vivo folic acid and methyltetrahydrofolic acid (MTHF) absorption by the whole intestinal surface after 20 weeks of 30% ethanol ingestion in drinking water. The results were compared with control rats fed ad libitum. The total intestinal serosal areas were similar in ethanol-fed and control rats. Significant increases in intestinal length, and decreases in tissue wet and dry weights were found in ethanol-fed rats. Serum folic acid concentrations were significantly less in the animals which had ingested ethanol than in the control rats. Intestinal folic acid absorption was significantly increased at lower substrate concentrations (0.5 and 1 µM), while no difference was observed at 2.5 µM in the ethanol-fed rats. Folic acid absorption relative to tissue wet weight showed significant increases at all tested concentrations in the ethanol-fed rats. Intestinal MTHF absorption showed no significant changes at 0.5 µM MTHF concentration, and an increase was observed in the absorption values at 1 and 2.5 µM concentrations in the ethanol-fed rats. When expressed as tissue wet weight, MTHF absorption values in ethanol-fed rats increased at 1 and 2.5 µM but did not differ at 0.5 µM substrate concentrations. The above results indicate compensatory responses in the folic acid and MTHF intestinal absorption after chronic ethanol ingestion. These effects are observed when the whole intestinal surface is evaluated.

show abstract

Quantitative Histomorphometric Study of the Jejunal Mucosa in Chronic Alcoholics

Cited by 32 publications

References 9 publications

The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction

The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction

Increased intestinal permeability in malnourished patients with liver cirrhosis

Comparative Effects of Intestinal Absorption of Folic Acid and Methyltetrahydrofolic Acid in Chronic Ethanol-Fed-Rats

Contact Info

Product

Resources

About