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The Pathology of Malabsorption: Current Concepts

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The Pathology of Malabsorption: Current Concepts Histopathology 2007, 50, 64–82. DOI: 10.1111/j.1365-2559.2006.02547.x REVIEW The pathology of malabsorption: current concepts S R Owens & J K Greenson1 Departments of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA and 1University of Michigan Health System, Ann Arbor, MI, USA Owens S R & Greenson J K (2007) Histopathology 50, 64–82 The pathology of malabsorption: current concepts Intestinal malabsorption results from a wide variety of such as systemic sclerosis. Finally, microbial causes of causes, which can most easily be organized into three malabsorption include bacterial overgrowth, Whipple’s groups. Maldigestion arises from problems with mix- disease, and numerous infections or infestations that ing or with digestive mediators, and includes post- are most frequently seen in immunocompromised gastrectomy patients and those with deficiencies of patients. An overview of the most common and pancreatic or intestinal enzymes, or of bile salts. interesting entities in each of these categories follows, Mucosal and mural causes of malabsorption are along with a discussion of current concepts. Mucosal abundant, and include gluten-sensitive enteropathy, conditions and microbial causes of malabsorption are tropical sprue, autoimmune enteropathy, and HIV/ given special attention. AIDS-related enteropathy, as well as mural conditions Keywords: autoimmune enteropathy, bacterial overgrowth, coeliac disease, giardiasis, gluten-sensitive enteropathy, malabsorption, sprue, Whipple’s disease Abbreviations: AE, autoimmune enteropathy; CD, Crohn’s disease; DH, dermatitis herpetiformis; EATCL, enteropathy associated T-cell lymphoma; ELISA, enzyme-linked immunosorbent assay; EM, electron microscopy; GFD, gluten-free diet; GSE, gluten-sensitive enteropathy; H&E, haematoxylin and eosin; HIV/AIDS, human immunodeficiency virus/acquired immunodeficiency syndrome; IBD, inflammatory bowel disease; IEL, intra- epithelial lymphocyte(s); NSAIDS, non-steroidal anti-inflammatory drugs; PIL, primary lymphangectasia; SI, small intestine; TPN, total parenteral nutrition; TS, tropical sprue; TTG, tissue transglutaminase; UC, ulcerative colitis; WD, Whipple’s disease Introduction contains numerous digestive enzymes on its surface, as well as an intricate network of lymphatics and blood The human gastrointestinal (GI) tract is the site of vessels providing access to the bloodstream. Adequate absorption of a wide variety of ingested nutrients, digestion and absorption depend on a multitude of including vitamins, proteins, carbohydrates and fats. factors, including mechanical mixing, enzyme produc- Much of this absorption occurs in the small intestine tion and activity, proper mucosal function, adequate (SI), where the high surface area provided by the blood supply, intestinal motility and even normal villous and microvillous architecture optimizes uptake microbial ecology. of dietary substances. The specialized SI mucosa Accordingly, malfunctions in any of these compo- nents can lead to failure to absorb nutrients from the diet, often resulting in some combination of diarrhoea, Address for correspondence: Joel K Greenson MD, Professor of Pathology, University of Michigan Medical School, Rm 2G332, Box steatorrhoea, malnutrition, weight loss and anae- 0054, 1500 E. Medical Center Drive, Ann Arbor, MI 48109–0054, mia. The resultant symptoms are known as the mal- USA. e-mail: [email protected] absorption syndrome(s), which can be grouped by Ó 2007 The Authors. Journal compilation Ó 2007 Blackwell Publishing Limited. Pathology of malabsorption 65 their aetiology into three broad categories. Thus, intestinal microbial ecology, the results of which are malabsorption may result from maldigestion, such as discussed below. occurs in inadequate mixing (e.g. after gastrectomy) or in enzyme or bile salt deficiencies, from mucosal insufficiency of digestive mediators or mural problems, such as various enteropathies or neuromuscular conditions, or from microbial causes, As suggested above, numerous digestive mediators such as bacterial overgrowth and various infections ⁄ are necessary for proper digestion and absorption of infestations. nutrients. Bile salts from the liver emulsify fats, The vast number of causes of intestinal malabsorp- opening them to lipolytic enzymes and ultimately tion precludes an exhaustive review. Therefore, we will allowing the absorption of lipids and of lipid-soluble attempt an overview of the most common and inter- nutrients. Proper enzymatic activity is essential, esting aetiologies in the three categories, with a more serving chemically to alter the nutrients for uptake complete discussion of a handful of entities in each, by the intestine. Pancreatic enzymes such as amy- along with a review of current concepts. Special lase, lipase, trypsin and chymotrypsin act in concert emphasis will be afforded to mucosal problems, as well with enzymes intrinsic to the intestinal mucosa, as to several microbial conditions. including lactase, maltase, sucrase and numerous others, resulting in the chemical modification of proteins, complex carbohydrates, lipids and disaccha- Maldigestion rides. Each of these components is a potential site inadequate mixing of disruption of proper digestion and can result in malabsorption of nutrients. A full discussion of the mechanics of digestion is Accordingly, a defect or deficiency in any of these beyond the scope of this review. Early digestion relies constituents may lead to maldigestion and malabsorp- on the mechanical disruption of ingested food by tion. Abnormal liver function may cause a decrease in chewing as well as mixing with initial digestive bile salt production. Structural abnormalities in the enzymes such as amylase in the saliva. Once the food biliary system may lead to a decrease in delivery of bile bolus is in the stomach, further mechanical disruption salts to the digestive stream. Examples of such condi- occurs as the viscus churns the semiliquid ingestate. tions are gallstone disease, inflammatory conditions Proper digestion relies on the appropriate transmission such as primary sclerosing cholangitis, and congenital of the disaggregated, liquefied food (‘chyme’) to the anomalies such as biliary atresia. duodenum via the pyloric sphincter. The adequate The myriad of enzymes involved in digestion provide mixing of chyme with bile salts and pancreatic ample sites for malfunction. The exocrine pancreas enzymes, as well as its exposure to endogenous secretes proteolytic and lipolytic enzymes (particularly intestinal enzymes on the mucosal surface, depends trypsin and lipase) crucial to proper digestion. Condi- on its piecemeal delivery to the duodenum in a tions such as chronic pancreatitis, commonly from controlled fashion.1,2 alcohol abuse or chronic biliary obstruction, and Several difficulties may arise with the loss of proper autoimmune pancreatitis may lead to a reduction in gastric function, as in patients who have undergone exocrine pancreatic mass and a resultant decrease total or partial gastrectomy, or who have had a in enzyme production.14 Similarly, surgical resection suboptimal result from other surgical procedures such of sizeable quantities of pancreatic tissue can cause as Nissen fundoplication or bariatric surgery.3–11 The such insufficiency. Clinically significant steatorrhoea functional or structural loss of the gastric reservoir and weight loss usually do not occur unless there leads to rapid transit of large quantities of inadequately is a considerable reduction in enzyme secretion mixed, osmotically active food into the small bowel. As (> 90%).15,16 Congenital conditions such as cystic a result, mixing of bile salts and pancreatic enzymes fibrosis may lead to exocrine pancreatic insufficiency with the ingestate is inadequate. The resultant osmotic by preventing the outflow of enzymes via mucus pressure can lead to large fluid shifts, increasing the plugging.15,17–19 liquid bulk of the digestive stream.12,13 The rapid The small intestinal mucosa contains many intrinsic transit of partially digested food through the tract digestive enzymes, particularly those involved in car- results in explosive diarrhoea and, possibly, mal- bohydrate digestion. Deficiencies have been described absorption of nutrients.13,14 Additionally, the passage in many mucosal disaccharidases.20 However, lactase of substantially intact liquid and solid food into the deficiency (‘hypolactasia’) is by far the most common. small bowel may result in disruptions of the normal In fact, adult-onset (primary) hypolactasia is present in Ó 2007 The Authors. Journal compilation Ó 2007 Blackwell Publishing Ltd, Histopathology, 50, 64–82. 66 S R Owens & J K Greenson 21 the majority of the world’s population. Lactase is a mucosal disease disaccharidase present on the surface of microvilli, which enzymatically cleaves lactose into its constituent Many of the entities commonly associated with mal- sugars, glucose and galactose. Normally, lactase levels absorption syndromes fall into this category. These are down-regulated in early childhood, corresponding diseases may cause malabsorption through a variety of with weaning. This process varies in its completeness, mechanisms discussed here, especially via an absolute and some people are left with nearly absent lactase or functional loss of mucosal surface area. Gluten- activity. Thus, lactase ‘deficiency’ is a result of sensitive enteropathy, tropical sprue, autoimmune decreased enzyme synthesis rather than of an enzyme enteropathy and intestinal lymphangiectasia will be defect.22–24
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