Villous damage induced by suction biopsy and by acute ethanol intake in normal human small intestine

Abstract

Previous studies by us indicated that ethanol in concentrations of 2.0-4.8% produced subepithelial blebs in the jejunum of the hamster. In the rat, due to rupture of the blebs, there was denudation of the villus tip epithelium. There are nos similar data on humans. Ethanol, in quantities equivalent to 4.8-6.4 ounces of 80 proof whiskey (diluted to 20% w/v), was infused into stomachs of 20 normal human volunteers. Subjects were divided into groups (Gr) according to the amount or type of alcohol given, and site of biopsies (SB). Gr 1:60 g ethanol, SB = jejunum. Gr 2:45 g ethanol, SB = jejunum. Gr 3:45 g ethanol, SB = duodenum. Gr 4:45 g ethanol as 4.8 oz 80 proof whiskey, SB = duodenum. To compare the morphology in the absence and presence of ethanol, biopsies were obtained from each volunteer before ethanol administration (control period), immediately after peak ethanol concentration in the duodenum or jejunum (ethanol period), and when intraluminal ethanol concentration fell towards zero (recovery period). The mean peak intraluminal ethanol concentrations in the four groups varied between 5.69% and 9.37% (w/v). Ethanol-induced damage was evaluated using strict preset criteria. Coded slides were evaluated by two observers. Suction biopsy damaged 18% of the villi even in biopsies obtained during the control period. Ethanol produced a statistically significant increase in the number of damaged villi (mean of all groups 45%, range: 32% in Gr 2 to 62% in Gr 3). During the recovery period the number of damaged villi fell to that seen in control period biopsies. Ethanol, in quantities equivalent to those ingested during moderate drinking, may produce transient damage to the upper small intestine of man. Conversely, ethanol may simply increase the susceptibility of the mucosa to the unavoidable trauma of suction biopsy. However, the histological and ultrastructural changes were similar to those induced by ethanol in small laboratory animals.

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

“…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).…”

Prevention of Alterations in Intestinal Permeability Is Involved in Zinc Inhibition of Acute Ethanol-Induced Liver Damage in Mice

“…other studies were from several hours to several days following acute ethanol exposure (Worthington et al, 1978;Keshavarzian et al, 1994). It is imperative to examine tissue before repair has taken place, and clearly the intestine is capable of restoring both morphological alterations and decreases in barrier function during recovery from alcohol challenge (Millan et al, 1980;Tamai et al, 2000). Ileal intestine from mice treated acutely with ethanol in our study suffered gross morphological anomalies, where many intestinal villi had breaches in the epithelial layer.…”

Alcohol and the digestive system – should it always be blamed?

“…Jak wykazały badania Millana i wsp. [66], po dożołądkowej aplikacji whisky rozcień-czonej do 20% lub wodnego roztworu etanolu o takim samym stężeniu w treści dwunastniczej stężenie alkoholu etylowego mieściło się w granicach 6,46-9,37 g/100 ml (8,2-11,9%), a w jelicie czczym 5,69-6,35 g/ 100 ml (7,2-8,0%). Stężenia te były wystarczająco duże do wywołania morfologicznego uszkodzenia kosmków jelitowych [66].…”

“…[66], po dożołądkowej aplikacji whisky rozcień-czonej do 20% lub wodnego roztworu etanolu o takim samym stężeniu w treści dwunastniczej stężenie alkoholu etylowego mieściło się w granicach 6,46-9,37 g/100 ml (8,2-11,9%), a w jelicie czczym 5,69-6,35 g/ 100 ml (7,2-8,0%). Stężenia te były wystarczająco duże do wywołania morfologicznego uszkodzenia kosmków jelitowych [66]. W nowszych badaniach wykazano, że inkubacja komórek nabłonka jelitowego w roztworach etanolu w przedziale 5-10 g/100 ml skutkuje indukcją w nich apoptozy [67].…”