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Neonatal Enteropathies: Defining the Causes of Protracted Diarrhea of Infancy

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Neonatal Enteropathies: Defining the Causes of Protracted Diarrhea of Infancy Journal of Pediatric Gastroenterology and Nutrition 38:16–26 © January 2004 Lippincott Williams & Wilkins, Inc., Philadelphia Invited Review Neonatal Enteropathies: Defining the Causes of Protracted Diarrhea of Infancy Philip M. Sherman, David J. Mitchell, and Ernest Cutz Research Institute, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada ABSTRACT chitect with intact villus-crypt axis. Neonatal enteropathies, The underlying causes of chronic diarrhea beginning early in by contrast, are characterized by blunting of the villi. These life are increasingly well defined. Infectious and post-infectious include microvillus inclusion disease, tufting enteropathy, enteropathies and food sensitive/allergic enteropathy account autoimmune enteropathy and IPEX syndrome - and it is for the majority of cases. Recent attention has focused on char- these conditions that are the subject of the current review. acterizing defined entities, which cause protracted diarrhea in JPGN 38:16–26, 2004. Keywords: Diarrhea—Infants— infants and young children. Disorders of intestinal ion transport Microvilli—Tufting—IPEX—Autoimmune—Epitheli- usually present at birth following a pregnancy complicated by um. © 2003 Lippincott Williams & Wilkins, Inc. polyhydramnios. Intestinal mucosal biopsies show normal ar- INTRODUCTION Causes of protracted diarrhea beginning early in life can be divided into those entities having a normal villus- Chronic and prolonged diarrhea is a symptom com- crypt axis and those associated with villus atrophy (Table plex with a variety of underlying etiologies. A recent 1). Congenital defects in the transport of sodium, chlo- medical position statement, which was published by the ride, glucose/galactose and bile acids, and congenital en- American Gastroenterological Association (1), provides terokinase deficiency each can cause prolonged diarrhea a comprehensive review of the subject in adults. How- dating to the early neonatal period (6). Often, a maternal ever, a different approach is required for evaluating in- history of polyhydramnios during the pregnancy is a clue fants and young children with protracted diarrhea. The to the diagnosis. Stool collection for the determination of increasingly well-characterized enteropathies that pre- fecal electrolyte concentrations should be undertaken sent in the neonatal period or early infancy (2) provide early on in the assessment because the results can prove the basis for this review. helpful in identifying the underlying molecular defect Intractable diarrhea of infancy is a term coined many (7). In recent years, major advances have been made in years ago by Avery (3) to describe chronic, unexplained understanding the molecular basis of these diseases (8,9). diarrhea in young children. The phrase has since been The value of identifying an underlying etiology of decried because it describes a symptom complex rather chronic protracted diarrhea is that it allows improved than a discrete disease entity (4). Protracted diarrhea has counseling of parents, families, referring physicians and been used more recently as a generic term to describe other health care professionals about long-term progno- infants with loose and frequent stools of sufficient se- sis and therapeutic options (6). In addition, since some of verity to require nutritional support, often in the form of these conditions appear to have a genetic basis, the po- parenteral alimentation (5). The emphasis on adequate tential risk of subsequent affected siblings can be better support of total caloric intake and nutritional rehabilita- assessed (10). tion has dramatically improved the survival of affected infants and children. Microvillus Inclusion Disease Address correspondence and reprint requests to Dr. Philip M. Sherman, Presentation Gastroenterology and Nutrition, Room 8409, Hospital for Sick Chil- dren, 555 University Avenue, Toronto, Ontario, M5G 1X8, Canada, Microvillus inclusion disease is a severe enteropathy (e-mail: [email protected]). with watery diarrhea often beginning on the first day of 16 NEONATAL ENTEROPATHIES 17 TABLE 1. Causes of protracted diarrhea beginning during of milder variants of microvillus inclusion disease that the first six months of life present later and in which the prognosis may be better (17). Indeed, in some cases advancing enteral nutrition Normal villus-crypt architecture: Transport defects has been possible over time (18). chloride-bicarbonate exchanger (chloride-losing diarrhea) sodium-hydrogen exchanger (congenital sodium diarrhea) ileal bile acid receptor defect Morphology sodium-glucose cotransporter (glucose-galactose malabsorption) Micronutrient deficiency acrodermatitis enteropathica (zinc deficiency) Duodenal biopsies in classic microvillus inclusion dis- Enzyme deficiency ease show normoplastic villus atrophy with relatively enterokinase deficiency little crypt hyperplasia, and an absence of marked in- Congenital short bowel flammatory infiltrate in the lamina propria (Figure 1 A). Villus atrophy: microvillus inclusion disease On higher magnification, the surface enterocytes are fo- tufting enteropathy cally piled-up and disorganized, with extensive vacuol- autoimmune enteropathy ization of the apical cytoplasm and loss of brush border IPEX syndrome definition (Figure 1 B). As shown in Figure 1 C with infectious enteropathy post-infectious enteropathy periodic-acid Schiff (PAS) staining the apical brush bor- allergic enteropathy der is poorly defined and there is PAS-positive staining idiopathic of the apical cytoplasm of enterocytes that is not seen in normal small intestine (19). Immunohistochemistry for brush border enzymes demonstrates the presence of al- life which is characterized on transmission electron mi- kaline phosphatase within the apical cytoplasm as well as croscopy by microvillus inclusions in enterocytes and in circular structures corresponding to microvillus inclu- colonocytes. This entity has been variously referred to as sions (20). microvillus inclusion disease, congenital microvillus at- Immunostaining for various cytoplasmic and mem- rophy, familial microvillous atrophy and Davidson’s brane antigens is useful in supporting the diagnosis of syndrome (11). We prefer the term microvillus inclusion microvillus inclusion disease at the light microscope disease because it highlights the characteristic diagnostic level. For example, immunostaining for villin, a micro- feature unique to this disorder, whereas microvillus at- filament component of the microvillus core, clearly dem- rophy is a non-specific finding observed in various types onstrates the intracytoplasmic microvillus inclusions of intestinal injury. (Figure1 D). Similarly, antibodies against carcinoembry- In microvillus inclusion disease, diarrhea can be so onic antigen (CEA) and CD10, a leukemia antigen nor- watery that it is mistaken for urine. The fecal sodium and mally expressed in the brush border of enterocytes, are chloride concentrations approximate those of serum and both useful in demonstrating microvillus inclusions the volume of stool loss may be equal to or greater than (21,22). In cases of microvillus inclusion disease there is that observed during cholera infection. Ion flux studies increased epithelial cell turnover with both enhanced demonstrate a net secretory state which accounts for the proliferation (Ki67 staining) and increased programmed voluminous diarrhea (12). As a result, affected infants cell death (apoptosis detected by TUNEL assay) to levels will die of dehydration unless appropriate (often mas- higher than that observed in normal small bowel, but less sive) intravenous fluid replacement is provided. Once than seen in gluten-sensitive enteropathy (23). infection has been excluded, microvillus inclusion dis- The morphology of duodenal biopsies in the variant ease is the most common identified cause of severe pro- forms of microvillus inclusion disease is more variable tracted diarrhea beginning during the first week of life and may evolve with time. In the reported cases (17) and (13). In contrast to neonates with transport defects (for in our experience (unpublished data), duodenal biopsies example, congenital chloride-losing diarrhea), polyhy- may initially show total villus atrophy, but later in life dramnios is not a common prenatal complication. Micro- show relatively normal villi on routine histopathology villus inclusion disease has been identified in infants (Figure 2 A). However, in this setting PAS staining or from multiple ethnic backgrounds worldwide (14). Mul- immunostaining for CD10 will show patches of abnor- tiple siblings can be affected (11). The disease appears to mal enterocytes containing microvillus inclusions next to cluster in infants of Navajo descent (15,16) providing apparently normal small bowel epithelium (Figure 2 B). evidence in support of a genetic etiology. On transmission electron microscopy, intracytoplas- Our experience indicates that classic microvillus in- mic microvillus inclusions in surface epithelial cells are clusion disease is a severe and intractable enteropathy a characteristic and diagnostic feature of microvillus in- requiring total parenteral nutrition for the delivery of clusion disease (Figure 3 A) because such inclusions are fluids and calories and that the condition is inevitably not found in other small bowel enteropathies (24,25). fatal without continuous intravenous nutrition or intesti- Microvillus inclusions can also be identified in colono- nal transplantation (13). However, there are
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