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Diagnosis and Treatment of Chronic Intestinal Pseudo-Obstruction in Children: Report of Consensus Workshop

Rudolph, Colin; Hyman, Paul*; Altschuler, Steven; Christensen, James; Colletti, Richard§; Cucchiara, Salvatore§§; Di Lorenzo, Carlo; Flores, Alex; Hillemeier, A.**; McCallum, Richard‡‡; Vanderhoof, Jon#

Journal of Pediatric Gastroenterology & Nutrition: January 1997 - Volume 24 - Issue 1 - p 102-112
Consensus Report
Free

Children's Center for Motility Disorders, University of Cincinnati, Cincinnati, Ohio;*Department of Gastroenterology, Children's Hospital of Orange County, Orange, California; Division of Gastroenterology & Nutrition. The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; Division of Gastroenterology, Department of Medicine, University of Iowa, Iowa City, Iowa; §Department of Pediatrics, University of Vermont, Burlington, Vermont; Division of Pediatric Gastroenterology, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania;Department of Pediatrics, Newton-Wellesley Hospital, Waltham, Massachusetts;**Division of Pediatric Gastroenterology, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan Medical Center, Ann Arbor, Michigan; ††Division of Gastroenterology, Hepatology, and Nutrition, University of Virginia School of Medicine, Charlottesville, Virginia; and ‡‡Department of Pediatrics, Creighton University School of Medicine, Omaha, Nebraska, U.S.A., and §§Department of Clinical Pediatrics, Second School of Medicine, University of Naples, Naples, Italy

This article is accompanied by an editorial. Please see: Camilleri M: Intestinal Dysmotility: Does the X-ray Resolve the Real Dilemma?, p. 100.

Address correspondence and reprint requests to Dr. Paul E. Hyman at the Childrens' Hospital of Orange County, 455 South Main Street, Orange, California 92668, U.S.A.

The diagnostic term, chronic intestinal pseudo-obstruction (CIP) is often used with poor regard to its meaning. The resultant inconsistency in the use of the term has hampered the clinical investigation and management of children with disorders of gastrointestinal motility (1). In addition, inappropriate application of a diagnosis of CIP based on exaggerated symptoms and overinterpretation of diagnostic tests has resulted in the perpetuation of and inadvertent physician collusion in Munchausen syndrome-by-proxy (2-4). Therefore, a Consensus Working Group was convened to address these problems, arrive at a clear definition for CIP, and suggest approaches for the diagnosis and treatment of this disorder.

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DEFINITION AND CLASSIFICATION OF PSEUDO-OBSTRUCTION

Terminology, clinical presentation, causes, and diagnostic approaches to gastrointestinal pseudo-obstruction in adults was summarized in a 1990 working team report (5). The terms defined in the adult working team report are applicable to pediatric patients. The term pseudo-obstruction denotes signs and symptoms resembling a physical obstruction to luminal flow, but without a true mechanical obstruction. Pseudo-obstruction may occur in any and all regions of the gastrointestinal tract. Further, pseudo-obstruction may occur as an acute response, as in paralytic ileus, or as a chronic remitting or persistent disorder. Although the term was initially applied only to syndromes suggesting intestinal obstruction, this broader definition encompasses other region and specific segmental motor disorders of the gastrointestinal tract, including achalasia, gastroparesis, Hirschsprung disease, and slow-transit constipation. Diagnostic approaches to these segmental motor disorders are described in standard medical textbooks and are not addressed here.

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DEFINITION OF CIP

CIP is a rare, severe, disabling disorder characterized by repetitive episodes or continuous symptoms and signs of bowel obstruction, including radiographic documentation of dilated bowel with airfluid levels, in the absence of a fixed, lumen-occluding lesion.

If pseudo-obstruction is congenital and persists for the first 2 months of life, or if the disorder is acquired and persists for >6 months, it is considered chronic. The small intestine is always involved, and the esophagus, stomach, and colon may be affected as well. Use of the term does not imply that the cause of the disorder is unknown. CIP may occur in many of the irreversible disorders that are listed in Table 1. In a few congenital cases, the intestinal neuropathy is such that the stomach does not empty and the bowel does not dilate. In such cases, histopathological evidence (e.g., total aganglionosis) is sufficient for a diagnosis of CIP and the requirement for bowel dilation is omitted.

The proposed definition for CIP is purposefully narrow in order to prevent use of the term to describe other disorders of gastrointestinal motility, such as acute reversible forms of pseudo-obstruction or irritable bowel syndrome. There is concern that an over-use of the term CIP has confused the classification of gastrointestinal motility disorders, resulting in the unnecessary use of aggressive therapies, including parenteral nutrition in children with less severe disorders. Disorders that resemble CIP, but that do not meet the criteria of the above definition, are listed in Table 2. These disorders are usually less resistant to therapy and do not necessarily portend a chronic, lifelong disease process.

Although a definition requiring bowel dilation might delay the diagnosis of idiopathic CIP, such a delay should not necessarily adversely affect management. Children with CIP or other disorders of gastrointestinal sensory or motor function respond to a variety of therapeutic interventions depending on the region of bowel involved and the severity of disease. Treatment should not be withheld because the diagnostic criteria for CIP have not been manifested. However, an incorrect or premature assignment of the diagnosis of CIP may reinforce the sick role. The restricted definition of CIP is intended to prevent the overaggressive treatment of children with less severe gastrointestinal motility disorders and to encourage rigor in establishing explanations for symptoms. In addition, the definition can serve as a standard definition for future studies of the pathogenesis and treatment of CIP. Rather than using the term CIP, the term gastroparesis can be used to more accurately describe patients without dilated bowel but with disorders of gastric emptying.

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CLINICAL SPECTRUM OF CIP

CIP may be classified either as primary or secondary. In primary CIP, the disease usually is limited to the hollow viscera, whereas in secondary forms, CIP is associated with an existing systemic disorder (Table 1). Some conditions classified as primary CIP are associated with extragastrointestinal manifestations involving the urinary tract or autonomic, peripheral, and central nervous systems. This classification scheme does not imply that the gastrointestinal tract is normal in the so-called “secondary” disorders nor does it aid in understanding the underlying disease mechanisms.

Disorders associated with primary CIP are classified as either myopathy or neuropathy depending on histopathology. The term “idiopathic” is applied when the disorder does not fit a recognizable genetic syndrome, when there is no apparent secondary cause, and when affected tissues are unavailable or appear normal under histological examination. Further subclassification as congenital or acquired is based on the presence or absence of symptoms at birth. Congenital myopathies and neuropathies present with symptoms at birth or shortly after. In most cases of congenital CIP, disease severity is greatest at birth and tends to improve or plateau over the first months of life. In contrast, forms of noncongenital CIP present later in childhood or adulthood. Other noncongenital disorders may be acquired through infection or immune-mediated inflammation within the myenteric plexus. Acquired forms of CIP may worsen or improve over time. In most kindreds presenting with CIP, those affected develop symptoms requiring medical care after childhood that tend to worsen with time.

Disorders causing secondary CIP are classified according to presumed underlying pathophysiology to facilitate an organized approach to evaluation. There may be considerable overlap in pathogenesis. For example, infiltrative diseases (such as amyloidosis) may damage both gastrointestinal smooth muscle and nerves.

Symptoms include nausea, anorexia, dysphagia, regurgitation, vomiting, abdominal distension and pain, and constipation (6,7), depending on the regions of the gastrointestinal tract involved. Other symptoms may arise from secondary complications, such as diarrhea from bacterial overgrowth, or from involvement of other organ systems, such as the urinary tract. Symptoms may be intermittent or persistent. In some kindreds, asymptomatic individuals may have clear radiographic signs of bowel dilation prior to onset of symptoms, indicating a discordance between symptoms and clinical findings (8).

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DIAGNOSIS OF CIP

An algorithm for the diagnosis of CIP is shown in Fig. 1. In a patient with symptoms of gastrointestinal obstruction, evaluation begins with supine and upright plain radiographs of the abdomen. Documentation of intermittent or persistent bowel obstruction with characteristic radiographic findings of air-fluid levels and bowel distention is required for the diagnosis of idiopathic CIP (9,10). In symptomatic patients without these radiographic findings, other diagnostic possibilities, including functional abdominal pain (11), gastroparesis, aerophagia (12), functional constipation, and nonulcer dyspepsia (13), should be considered (Table 2).

An episode of radiographically documented obstruction calls for a complete blood cell count, measures of serum electrolyte concentrations (including calcium and magnesium), and drug screen. A careful history, particularly regarding possible familial pseudo-obstruction, should be obtained. Initial treatment includes nasogastric decompression and correction of abnormalities in fluid and electrolyte homeostasis. Drugs that slow gastrointestinal motility should be discontinued whenever possible. If bowel dilation persists despite correction of laboratory abnormalities and discontinuation of suspect drugs, then radiographic contrast studies should be performed. Enteroclysis may be necessary to rule out a partial mechanical obstruction (14,15).

In chronic cases, and after excluding mechanical obstruction, secondary causes of pseudo-obstruction should be considered (Table 1). In immunodeficiency states, including those induced by medication following organ transplantation, symptoms of CIP should prompt an evaluation for myenteric plexus neuritis due to cytomegalovirus or Epstein-Barr virus. Screening blood tests for diabetesmellitus (hemoglobin A1C or postprandial blood glucose concentration), connective tissue and skeletal muscle disorders (antinuclear antibody panel, creatine phosphokinase, aldolase), and hypothyroidism (16) should be performed. Other tests to consider include serology for Chagas disease, urinary cate-cholamines to rule out pheochromocytoma (17,18), urinary porphyrins, and enteric neuronal autoantibodies (19). Hirschsprung's disease is diagnosed with a suction rectal biopsy. A full-thickness rectal biopsy may be indicated to exclude the neuronal intestinal dysplasias (20,21), particularly those associated with multiple endocrine neoplasia, type 3 (22-25). Antiendomysial antibody testing or small intestinal biopsy may be considered to rule out celiac disease (26,27).

Further evaluation is not necessary after treatable causes of pseudo-obstruction have been ruled out. Antroduodenal manometry and full-thickness bowel biopsies may aid in clarifying pathophysiology and histology, respectively, but, in most cases, will not alter treatment (see below). If symptoms and signs of pseudo-obstruction persist for >2 months after birth or >6 months in a child presenting after birth, a firm diagnosis of idiopathic CIP is warranted.

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OTHER DIAGNOSTIC APPROACHES

At this time, no single diagnostic test is specific enough to assume an accurate diagnosis of idiopathic CIP. The use of motility testing is discussed briefly bwlow. Motility is a term that encompasses measures of both wall movements and luminal transit through the gastrointestinal tract.

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Measurement of Transit

Orally administered radio-opaque markers to measure transit through the colon may discriminate between slow-transit constipation and fecal with-holding in children (28,29). This method is not useful for the evaluation of small-bowel transit. Mouth-to-cecum transit can be measured by ingestion of substances that are degraded by bacteria in the colon to a product detectable in breath; the lactulose breath hydrogen test is an example of this approach (30). However, these methods are unreliable in pseudo-obstruction due to small bowel bacterial overgrowth and the wide variations in intestinal transit time in normal children (31).

Labeling of meals with radioactive isotopes and imaging with a gamma camera provides reliable measures of esophageal transit (32) and gastric emptying in children (33,34). The use of scintigraphy also has been validated for the measurement of small bowel and colon transit in adults (32,35). However, normal values are not established for children. These techniques offer useful preliminary information. If solid meals exit the stomach normally, it is unlikely that there is a serious underlying gastric motility disorder.

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Antroduodenal Manometry

Antroduodenal manometry is used extensively to assess the physiology that could explain symptoms of a motility disorder. Although there are only a few published studies in normal children, extensive data from healthy neonates (36), adults (37,38) and sick children (39) provide information sufficient to permit limited interpretation of data from children. Interpretation of antroduodenal motility studies in the context of the clinical history may provide information that can aid in management.

Antroduodenal manometric studies usually are abnormal in children with CIP, with more obvious abnormalities being observed in severely affected patients (40-42). Subtle or infrequent discrete abnormalities in manometric patterns may be observed in some children with gastroesophageal reflux (13), nonulcer dyspepsia (13,43), and recurrent functional abdominal pain (11). Motor patterns are affected by sleep, pain, anxiety and anger, various drugs, and prior surgery. There are a variety of artifacts that may confound data analysis.

Despite these reservations, antroduodenal manometry may be useful in guiding the management of patients with certain gastrointestinal motility disorders. In general, normal amplitude, uncoordinated contractions characterize neuropathies, and persistently low amplitude, coordinated contractions characterize myopathies. In children, presence of a normal migrating motor complex predicted successful enteral nutrition support (40,41). In adults, characteristic patterns of small bowel contraction, including postprandial cluster activity (44) and simultaneous broad-based contractions, may suggest mechanical obstruction (44,45). If these patterns are observed, more detailed radiographic evaluation with enteroclysis should be pursued. Antroduodenal manometry is also useful to distinguish between vomiting and rumination (46). Vomiting is an involuntary reflex with characteristic features that precede, accompany, and follow the event. Emesis with rumination is associated with brief increases in intraabdominal pressure evident as simultaneous short duration increases in pressure in all recording sites.

The absence of antroduodenal manometric abnormalities also may be useful in certain clinical situations. Normal antroduodenal manometry usually indicates that a gastrointestinal motility disorder does not underlie a child's symptoms. Instead, behavioral disorders in the child or the family, including Munchausen's syndrome-by-proxy and somatiform pain disorder (47), should be considered (Table 2). Documentation of abnormal antroduodenal manometry prior to intestinal transplantation may prove helpful in predicting the need for a feeding jejunostomy in the transplant recipient. Antroduodenal manometry may be helpful to rule out a generalized motility disorder in patients with intractable constipation who are being considered for colectomy.

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Electrogastrography

Surface electrogastrography measures the rhythm and amplitude of gastric electrical activity. In a clinical research setting, gastric antral dysrhythmias have been demonstrated, by this method, in some patients with CIP (48). This noninvasive technique requires further validation and development before it can be useful for the clinical assessment of CIP in infants and children.

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Histology

Abnormalities of gastrointestinal nerve and muscle have been demonstrated in children and adults with CIP (49-52). Demonstration of histologic abnormalities is not required for diagnosis of idiopathic CIP; however, if tissue can be obtained safely when surgery is performed for another indication, such as ostomy placement, histologic studies are warranted (53). Staining with conventional metachromatic dyes may demonstrate degenerative changes in smooth muscle and excess collagen deposition within the muscularis propria. Immunochemical staining for specific smooth muscle proteins, such as α-actin, may reveal specific deficits (54). Tangential sections stained with silver stains, acetylcholinesterase stains, and immunochemical stains may demonstrate degeneration of neurons and axons, hypoganglionosis, proliferation of neurons or nerve fibers in the lamina propria, or glial cell proliferation. As the pathogenesis of the various causes of CIP is clarified, more detailed histologic study may be useful for determining prognosis and guiding treatment.

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TREATMENT OF CIP

Optimal nutrition by enteral or parenteral routes is of utmost importance both for supporting normal growth and development, and for digestion. When gastroparesis prevents oral or intragastric tube feedings, a trial of postpyloric feedings is occasionally successful (55). Even when parenteral feedings are required, at least small volumes of enteral feeding are desirable to prevent cholestatic liver disease (56) and to maintain bowel mucosal integrity (57).

Bacterial overgrowth, a frequent complication of pseudo-obstruction (58,59), often causes malabsorption (60) and may be associated with increased mucosal permeability to macromolecules (61) and bacterial translocation across the bowel (62,63). Intermittent treatment of bacterial overgrowth provides symptomatic relief and may decrease the risk of hepatobiliary injury (64) and sepsis.

Cisapride may provide symptomatic improvement in some children with pseudo-obstruction (40,65). Erythromycin (66), metoclopramide (67,68), bethanechol (68), domperidone (69), and naloxone (70) have not been of proven benefit but may be useful in selected cases. Combined therapy with octreotide and erythromycin reduced nausea and abdominal pain in adult patients with idiopathic and scleroderma-associated intestinal pseudo-obstruction (71).

Bowel decompression by nasogastric suction is useful during acute exacerbations in patients with cyclical symptoms. Patients with frequent exacerbations or chronic distension often benefit from placement of a venting enterostomy (72-75). Patients who have severe disability due to bowel dilation and who have sepsis may occasionally benefit from subtotal enterectomy and parenteral nutrition (74). Small intestine transplant may offer a potential for cure in children with life-threatening disease due to bowel dilation and recurrent sepsis, or with serious complications of parenteral nutrition, including liver failure or limited central venous access (76).

Acknowledgment: The Consensus Workshop and subsequent manuscript preparation were supported through an Unrestricted Educational Grant provided by Janssen Pharmaceutica.

FIG. 1

FIG. 1

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REFERENCES

1. Rudolph CD, Glassman M. Diagnosis of pseudoobstruction in children. Am J Gastroenterol 1993;88:802-6.
2. Baron HI, Beck DC, Vargas JH, Ament ME. Overinterpretation of gastroduodenal motility studies: two cases involving Munchausen syndrome by proxy. J Pediatr 1995;126:397-400.
3. Hyman PE, Di Lorenzo C, Beck D, Hamilton A, Zeltzer L. Munchausen's syndrome-by-proxy and chronic intestinal pseudo-obstruction: overlapping phenotypes. [Abstract] J Pediatr Gastroenterol Nutr 1994;19:332A.
4. Ginies JL, Goulet O, Champion G, et al. Munchausen's syndrome by proxy and chronic intestinal pseudo-obstruction. Arch Fr Pediatr 1989;46:267-9.
5. Christensen J, Dent J, Malagelada JR, Wingate DL. Pseudo-obstruction. Gastroenterol Int 1990;3:107-19.
6. Glassman M, Spivak W, Mininberg D, Madara J. Chronic idiopathic intestinal pseudoobstruction: a commonly misdiagnosed disease in infants and children. Pediatrics 1989;83:603-8.
7. Byrne WJ, Cipel L, Euler AR, Halpin TC, Ament ME. Chronic idiopathic intestinal pseudo-obstruction syndrome in children-clinical characteristics and prognosis. J Pediatr 1977;90:585-9.
8. Faulk DL, Anuras S, Gardner GD, Summers RW, Christensen J. A familial visceral myopathy. Ann Intern Med 1978;89:600-6.
9. Schuffler MD, Rohrmann CA Jr, Templeton FE. The radiologic manifestations of idiopathic intestinal pseudoobstruction. Am J Roentgenol 1976;127:729-36.
10. Byrne WJ, Cipel L, Ament ME, Gyepes MT. Chronic idiopathic intestinal pseudo-obstruction syndrome: radiologic signs in children with emphasis on differentiation from mechanical obstruction. Diagn Imaging 1981;50:294-304.
11. Pineiro-Carrero VM, Andres JM, Davis RH, Mathias JR. Abnormal gastroduodenal motility in children and adolescents with recurrent functional abdominal pain. J Pediatr 1988;113:820-5.
12. Gauderer MW, Halpin TC Jr, Izant RJ Jr. Pathologic childhood aerophagia: a recognizable clinical entity. J Pediatr Surg 1981;16:301-5.
13. Cucchiara S, Bortolotti M, Colombo C, et al. Abnormalities of gastrointestinal motility in children with nonulcer dyspepsia and in children with gastroesophageal reflux disease. Dig Dis Sci 1991;36:1066-73.
14. Dixon PM, Roulston ME, Nolan DJ. The small bowel enema: a ten year review. Clin Radiol 1993;47:46-8.
15. Barloon TJ, Lu CC, Honda H, Berbaum KS. Does a normal small-bowel enteroclysis exclude small bowel disease? A long-term follow-up of consecutive normal studies. Abdom Imaging 1994;19:113-5.
16. Abbasi AA, Douglass RC, Bissell GW, Chen Y. Myxedema ileus: a form of intestinal pseudo-obstruction. JAMA 1975;234:181-3.
17. Khafagi FA, Lloyd HM, Gough IR. Intestinal pseudo-obstruction in pheochromocytoma. Aust NZ J Med 1987;234:181-3.
18. Mullen JP, Cartwright RC, Tisherman SE, Missage JR, Shapiro AP. Pathogenesis and pharmacologic management of pseudo-obstruction of the bowel in pheochromocytoma. Am J Med Sci 1985;290:155-8.
19. Lennon V, Sas D, Busk M, et al. Enteric neuronal antibodies in pseudoobstruction with small-cell lung carcinoma. Gastroenterology 1991;100:137-42.
20. Milla PJ, Smith VV. Intestinal dysplasia. J Pediatr Gastroenterol Nutr 1993;17:356-7.
21. Schofield DE, Yunis EJ. Intestinal neuronal dysplasia. J Pediatr Gastroenterol Nutr 1991;12:182-9.
22. Griffiths AM, Mack DR, Byard RW, Stringer DA, Shandling B. Multiple endocrine neoplasia IIb: an unusual cause of chronic constipation. J Pediatr 1990;116:285-8.
23. D'Amore ES, Manivel JC, Pettinato G, Niehans GA, Snover DC. Intestinal ganglioneuromatosis: mucosal and transmural types. A clinicopathologic and immunohistochemical study of six cases. Hum Pathol 1991;22:276-86.
24. Fuller CE, Williams GT. Gastrointestinal manifestations of type I neurofibromatosis (von Recklinghausen's disease). Histopathology 1991;19:1-11.
25. Shekitka KM, Sobin LH. Ganglioneuromas of the gastrointestinal tract. Relation to Von Recklinghausen disease and other multiple tumour syndromes. Am J Surg Pathol 1994;18:250-7.
26. Dawson DJ, Sciberras CM, Whitwell H. Coeliac disease presenting with intestinal pseudo-obstruction. Gut 1984;25:1003-8.
27. Cluysenaer OJ, van Tongeren JH. Pseudo-obstruction in coeliac sprue. Neth J Med 1987;31:300-4.
28. Hinton JM, Lennard-Jones JE, Young AC. A new method of studying gut transit times using radiopaque markers. Gut 1969;10:842-7.
29. Bautista Casasnovas A, Varela Cives R, Villanueva Jeremias A, Castro-Gago M, Cadranel S, Tojo Sierra R. Measurement of colonic transit time in children. J Pediatr Gastroenterol Nutr 1991;13:42-5.
30. von der Ohe MR, Camilleri M. Measurement of small bowel and colonic transit: indications and methods. Mayo Clin Proc 1992;67:1169-79.
31. Perman JA, Modler S, Barr RG, Rosenthal P. Fasting breath hydrogen concentration: normal values and clinical application. Gastroenterology 1984;87:1358-63.
32. Guillet J, Wynchank S, Basse-Cathalinat B, Christophe E, Ducassou D, Blanquet P. Pediatric esophageal scintigraphy. Results of 200 studies. Clin Nucl Med 1983;8:427-34.
33. Seibert JJ, Byrne WJ, Euler AR. Gastric emptying in children: unusual patterns detected by scintigraphy. Am J Roentgenol 1983;141:49-51.
34. Guillet J, Wynchank S, Christophe E, Basse-Cathalinat B, Ducassou D, Blanquet P. Gastro-oesophageal reflux and gastric emptying of liquid in paediatric patients. Int J Nucl Med Biol 1984;11:254-8.
35. Camilleri M, Colemont LJ, Phillips SF, et al. Human gastric emptying and colonic filling of solids characterized by a new method. Am J Physiol 1989;257:G284-90.
36. Berseth CL. Gestational evolution of small intestine motility in preterm and term infants. J Pediatr 1989;115:646-51.
37. Stanghellini V, Camilleri M, Malagelada JR. Chronic idiopathic intestinal pseudo-obstruction: clinical and intestinal manometric findings. Gut 1987;28:5-12.
38. Quigley EM, Donovan JP, Lane MJ, Gallagher TF. Antroduodenal manometry. Usefulness and limitations as an outpatient study. Dig Dis Sci 1992;37:20-8.
39. Hyman PE, Napolitano JA, Diego A, et al. Antroduodenal manometry in the evaluation of chronic functional gastrointestinal symptoms. Pediatrics 1990;86:39-44.
40. Hyman PE, Di Lorenzo C, McAdams L, Flores AF, Tomomasa T, Garvey TQ III. Predicting the clinical response to cisapride in children with chronic intestinal pseudo-obstruction. Am J Gastroenterol 1993;88:832-6.
41. Cucchiara S, Annese V, Minella R, et al. Antroduodenojejunal manometry in the diagnosis of chronic idiopathic intestinal pseudoobstruction in children. J Pediatr Gastroenterol Nutr 1994;18:294-305.
42. Boige N, Faure C, Cargill G, et al. Manometrical evaluation in visceral neuropathies in children. J Pediatr Gastroenterol Nutr 1994;19:71-7.
43. Di Lorenzo C, Hyman PE, Flores AF, et al. Antroduodenal manometry in children and adults with severe non-ulcer dyspepsia. Scand J Gastroenterol 1994;29:799-806.
44. Summers RW, Anuras S, Green J. Jejunal manometry patterns in health, partial intestinal obstruction and pseudoobstruction. Gastroenterology 1983;85:1290-300.
45. Camilleri M. Jejunal manometry in distal subacute mechanical obstruction: significance of prolonged simultaneous contractions. Gut 1989;30:468-75.
46. Amarnath RP, Abell TL, Malagelada JR. The rumination syndrome in adults. A characteristic manometric pattern. Ann Intern Med 1986;105:513-8.
47. Zeltzer LK, Hyman PE, Heyman MB, et al. Persistent pain in adolescents. J Pediatr Gastroenterol Nutr (in press).
48. Devane SP, Ravelli AM, Bisset WM, Smith VV, Lake BD, Milla PJ. Gastric antral dysrhythmias in children with chronic idiopathic intestinal pseudoobstruction. Gut 1992;33:1477-81.
49. Krishnamurthy S, Schuffler M. Pathology of neuromuscular disorders of the small intestine and colon. Gastroenterology 1987;93:610-39.
50. Navarro J, Sonsino E, Boige N, et al. Visceral neuropathies responsible for chronic intestinal pseudo-obstruction syndrome in pediatric practice: analysis of 26 cases. J Pediatr Gastroenterol Nutr 1990;11:179-95.
51. Lake B. Observations on the pathology of pseudo-obstruction. In: Milla PJ, ed. Disorders of gastrointestinal motility in childhood. New York, NY: John Wiley & Sons, 1988.
52. Krishnamurthy S, Heng Y, Schuffler MD. Chronic intestinal pseudo-obstruction in infants and children caused by diverse abnormalities of the myenteric plexus. Gastroenterology 1993;104:1398-408.
53. Schuffler MD. Pathology of enteric neuromuscular disorders. In: Hyman PE, Di Lorenzo C, eds. Pediatric gastrointestinal motility. New York, NY: Academy Professional Information Services, Inc., 1994.
54. Smith VV, Lake BD, Damm MA, Nicholls RJ. Intestinal pseudo-obstruction with deficient smooth muscle alphaactin. Histopathology 1992;21:535-42.
55. Di Lorenzo C, Flores A, Buie T, Hyman P. Intestinal motility and jejunal feeding in children with chronic intestinal pseudo-obstruction. Gastroenterology 1995;108:1379-1385.
56. Balistreri W, Bucuvalas J, Farrell M, Bove K. Total parenteral nutrition-associated cholestasis: factors responsible for the decreasing incidence. In: Lentze MJ, Reichen J. Paediatric cholestasis: novel approaches to treatment. London: Kluwer Academic Publishers, 1991.
57. Alverdy JC, Aoys E, Moss GS. Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 1988;104:185-90.
58. Keshavarzian A, Isaacs P, McColl I, Sladen GE. Idiopathic intestinal pseudo-obstruction and contaminated small bowel syndrome-treatment with metronidazole, ileostomy, and indomethacin. Am J Gastroenterol 1983;78:562-5.
59. Vantrappen G, Janssens J, Hellemans J, Ghoos Y. The interdigestive motor complex of normal subjects and patients with bacterial overgrowth of the small intestine. J Clin Invest 1977;59:1158-66.
60. McEvoy A, Dutton J, James OF. Bacterial contamination of the small intestine is an important cause of occult malabsorption in the elderly. Br Med J 1983;287:789-93.
61. Pignata C, Budillon G, Monaco G, et al. Jejunal bacterial overgrowth and intestinal permeability in children with immunodeficiency syndromes. Gut 1990;191:879-82.
62. Van Leeuwen PA, Boermeester MA, Houdijk AP, et al. Clinical significance of translocation. Gut 1994;35(suppl 1):S28-34.
63. Berg RD. Bacterial translocation from the gastrointestinal tract. J Med 1992;23:217-44.
64. Lichtman SN, Keku J, Schwab JH, Sartor RB. Hepatic injury associated with small bowel bacterial overgrowth in rats is prevented by metronidazole and tetracycline. Gastroenterology 1991;100:513-19.
65. Di Lorenzo C, Reddy SN, Villanueva-Meyer J, Mena I, Martin S, Hyman PE. Cisapride in children with chronic intestinal pseudoobstruction. An acute, double-blind, crossover, pseudo-controlled trial. Gastroenterology 1991;101:1564-70.
66. Miller S, O'Dorisio T, Thomas E, Mekhijian H. Erythromycin exerts a prokinetic effect in patients with chronic idiopathic intestinal pseudoobstruction [Abstract]. Gastroenterology 1990;98:A375.
67. Lipton AA, Knauer CM. Pseudo-obstruction of the bowel. Therapeutic trial of metoclopramide. Am J Dig Dis 1977;2:263-5.
68. Vargars JH, Sachs P, Ament ME. Chronic intestinal pseudo-obstruction syndrome in pediatrics. Results of a national survey by members of the North American Society of Pediatric Gastroenterology and Nutrition. J Pediatr Gastroenterol Nutr 1989;7:323-32.
69. Turgeon D. Domperidone in chronic intestinal pseudoobstruction. Gastroenterology 1990;99:1194.
70. Schang JC, Devroede G. Beneficial effects of naloxone in a patient with intestinal pseudoobstruction. Am J Gastroenterol 1985;80:407-11.
71. Verne GN, Eaker EY, Hardy E, Sninsky CA. Effect of octreotide and erythromycin on idiopathic and scleroderma-associated intestinal pseudo-obstruction. Dig Dis Sci 1995;40:1892-1901.
72. Pitt HA, Mann LL, Berquist WE, Ament ME, Fonkalsrud E, DenBesten L. Chronic intestinal pseudo-obstruction. Management with total parenteral nutrition and a venting enterostomy. Arch Surg 1985;120:614-8.
73. Mansell PI, Tattersall RB, Balsitis M, Lowe J, Spiller RC. Megaduodenum due to hollow visceral myopathy successfully managed by duodenoplasty and feeding jejunostomy. Gut 1991;32:334-7.
74. Fonkalsrud EW, Pitt HA, Berquist WE, Ament ME. Surgical management of chronic intestinal pseudo-obstruction in infancy and childhood. Prog Pediatr Surg 1989;24:221-5.
75. Mughal MM, Irving MH. Treatment of end stage chronic intestinal pseudo-obstruction by subtotal enterectomy and home parenteral nutrition. Gut 1989;29:1613-7.
76. Starzl TE, Todo S, Tzakis A, Fung J. The transplantation of gastrointestinal organs. Gastroenterology 1993;104:673-9.
77. Kirtane J, Talwalker V, Dastur DJ. Megacystis, microcolon, intestinal hypoperistalsis syndrome: Possible pathogenesis. J Pediatr Surg 1984;19:206-8.
78. Oliveira G, Boechat MI, Ferreira MA. Megacystismicrocolon-intestinal hypoperistalsis syndrome in a newborn girl whose brother had prune belly syndrome: common pathogenesis? Pediatr Radiol 1983;13:294-6.
79. Berdon WE, Baker DH, Blanc WA, Gay B, Santulli TV, Donovan C. Megacystis-microcolon-intestinal hypoperistalsis syndrome: a new cause of intestinal obstruction in the newborn. Report of radiologic findings in five newborn girls. Am J Roentgenol 1976;126:957-64.
80. Amoury RA, Fellows RA, Goodwin CD, Hall RI, Holder TM, Ashcraft KW. Megacystis-microcolon-intestinal hypoperistalsis syndrome: a cause of intestinal obstruction in the newborn period. J Pediatr Surg 1977;12:1063-5.
81. Wiswell TE, Rawlings JS, Wilson JL, Pettett G. Megacystis-microcolon-intestinal hypoperistalsis syndrome. Pediatrics 1979;63:805-8.
82. Schuffler MD, Pagon RA, Schwartz R, Bill AH. Visceral myopathy of the gastrointestinal and genitourinary tracts in infants. Gastroenterology 1988;94:892-8.
83. Martin JE, Benson M, Swash M, Salih V, Gray A. Myofibroblasts in hollow visceral myopathy: the origin of gastrointestinal fibrosis? Gut 1993;34:999-1001.
84. Jayachandar J, Frank JL, Jonas MM. Isolated intestinal myopathy resembling progressive systemic sclerosis in a child. Gastroenterology 1988;95:1114-8.
85. Lowsky R, Davidson G, Wolman S, Jeejeebhoy K, Hegele RA. Familial visceral myopathy associated with a mitochondrial myopathy. Gut 1993;34:279-83.
86. Alstead EM, Murphy MN, Flanagan AM, Bishop AE, Hodgson HJ. Familial autonomic visceral myopathy degeneration of muscularis mucosae. J Clin Pathol 1988;41:424-9.
87. Fitzgibbons PL, Chandrasoma PT. Familial viscera myopathy. Evidence of diffuse involvement of intestinal smooth muscle. Am J Surg Pathol 1987;11:846-54.
88. Jacobs E, Ardichvili D, Perissino A, Gottignies P, Hanssens JF. A case of familial visceral myopathy with atrophy and fibrosis of the longitudinal muscles layer of the entire small bowel. Gastroenterology 1979;77:745-50.
89. Schuffler MD, Lowe MC, Bill AH. Studies of idiopathic intestinal pseudo-obstruction: I. Hereditary hollow visceral myopathy: clinical and pathological studies. Gastroenterology 1977;73:327-38.
90. Schuffler MD, Pope CE II. Studies of idiopathic intestinal pseudo-obstruction: II. Hereditary hollow visceral myopathy: family studies. Gastroenterology 1977;73:339-44.
91. Stafford SJ, Ulshen MH, Mandell J. Familial visceral myopathy. J Urol 1984;131:978-80.
92. Jones SC, Dixon MF, Lintott DD, Axon AT. Familial visceral myopathy: a family with involvement of four generations. Dig Dis Sci 1992;37:464-9.
93. Nonaka M, Goulet O, Arahan P, Fekete C, Ricour C, Nezelof C. Primary intestinal myopathy, a cause of chronic idiopathic intestinal pseudoobstruction syndrome (CIPS): clinicopathological studies of seven cases in children. Pediatr Pathol 1989;9:409-24.
94. Law D, Eyck RT. Familial megaduodenum and megacystis. Am J Med 1962;33:911-22.
95. Cheng SC, Sanderson CR, Way NJ, Yoong RM. Familial idiopathic megaduodenum. Aust NZ J Surg 1987;57:879-82.
96. Anuras S, Mitros FA, Nowak TV, et al. A familial visceral myopathy with external ophthalmoplegia and autosomal recessive transmission. Gastroenterology 1983;84:346-53.
97. Ionasescu VV, Thompson HS, Aschenbrener C, Anuras S, Risk WS. Late-onset oculogastrointestinal muscular dystrophy. Am J Med Genet 1984;18:781-8.
98. Ionasescu V, Thompson HH, Ionasescu R, et al. Inherited ophthalmoplegia with intestinal pseudo-obstruction. J Neurol Sci 1983;59:215-28.
99. Cervera R, Bruix J, Bayes A, Blesa R, Illa I, Coll J, Garcia-Puges AM. Chronic intestinal pseudoobstruction and ophthalmoplegia in a patient with mitochondrial myopathy. Gut 1988;29:544-7.
100. Li V, Hostein J, Romero NB, et al. Chronic intestinal pseudoobstruction with myopathy and ophthalmoplegia. A muscular biochemical study of a mitochondrial disorder. Dig Dis Sci 1992;37:456-63.
101. Kim JJ, Armstrong DD, Fishman MA. Multicore myopathy, microcephaly, aganglionosis, and short stature. J Child Neurol 1994;9:275-7.
102. Qualman SJ, Murray R. Aganglionosis and related disorders. Hum Pathol 1994;25:1141-9.
103. Ponder BA. The gene causing multiple endocrine neoplasia type 2 (MEN 2). Ann Med 1994;26:199-203.
104. Singh G, Hershman MJ, Loft DE, et al. Partial malrotation associated with pseudo-obstruction of the small bowel. Br J Clin Prac 1993;47:274-5.
105. Devane SP, Coombes R, Smith VV, et al. Persistent gastrointestinal symptoms after correction of malrotation. Arch Dis Child 1992;67:218-21.
106. Tanner MS, Smith B, Lloyd JK. Functional intestinal obstruction due to deficiency of argyrophil neurones in the myenteric plexus. Familial syndrome presenting with short bowel, malrotation and pyloric hypertrophy. Arch Dis Child 1976;51:837-41.
107. Kern IB, Leece A, Bohane T. Congenital short gut, malrotation, and dysmotility of the small bowel. J Pediatr Gastroenterol Nutr 1990;11:411-15.
108. Vasikanskas E, Piccoli DA, Flores AF, Di Lorenzo C, Hyman PE. Chronic intestinal pseudo-obstruction in fetal alcohol syndrome [Abstract]. Gastroenterology 1994;106:A637.
109. Vanderwinden JM, Dassonville M, Vander Veken E, Cadranel S, De Laet MH. Post-necrotising enterocolitis pseudo-obstruction treated with Cisapride. Z Kinderchir 1990;45:282-5.
110. Faber J, Fich A, Steinberg AF, et al. Familial intestinal pseudoobstruction dominated by a progressive neurologic disease at a young age. Gastroenterology 1987;92:786-90.
111. Hirschowitz BI, Groll A, Ceballos R. Hereditary nerve deafness in three sisters with absent gastric motility, small bowel diverticulitis and ulceration and progressive sensory neuropathy. Birth Defects 1972;8:27-41.
112. Mayer EA, Schuffler MD, Rotter JI, Hanna P, Mogard M. Familial visceral neuropathy with autosomal dominant transmission. Gastroenterology 1986;91:1528-35.
113. Schuffler MD, Bird TD, Sumi SM, Cook A. A familial neuronal disease presenting as intestinal pseudoobstruction. Gastroenterology 1978;75:889-98.
114. Steiner I, Steinberg A, Argov Z, Faber J, Fich A, Gilai A. Familial progressive neuronal disease and chronic idiopathic intestinal pseudo-obstruction. Neurology 1987;37:1046-50.
115. Barnett JL, McDonnell WM, Appelman HD, Dobbins WO. Familial visceral neuropathy with neuronal intranuclear inclusions: diagnosis by rectal biopsy. Gastroenterology 1992;102:684-91.
116. Camilleri M, Carbone LD, Schuffler MD. Familial enteric neuropathy with pseudoobstruction. Dig Dis Sci 1991;36:1168-71.
117. Roy AD, Bharucha H, Nevin NC, Odling-Smee GW. Idiopathic intestinal pseudo-obstruction: A familial visceral neuropathy. Clin Genet 1980;18:291-7.
118. Bagwell CE, Filler RM, Cutz E, et al. Neonatal intestinal pseudoobstruction. J Pediatr Surg 1984;19:732-9.
119. Kleckner FS. Dermatomyositis and its manifestations in the gastrointestinal tract. Am J Gastroenterol 1970;53:141-6.
120. Magill HL, Hixson SD, Whitington G, Igarashi M, Hannissian A. Duodenal perforation in childhood dermatomyositis. Pediatr Radiol 1984;14:28-30.
121. Cacoub P, Benhamou Y, Barbet P, et al. Systemic lupus erythematosus and chronic intestinal pseudoobstruction. J Rheumatol 1993;20:377-81.
122. Marshall JB, Kretschmar JM, Gerhardt DC, et al. Gastrointestinal manifestations of mixed connective tissue disease. Gastroenterology 1990;98:1232-8.
123. Rohrmann CA Jr, Ricci MT, Krishnamurthy S, Schuffler MD. Radiologic and histologic differentiation of neuromuscular disorders of the gastrointestinal tract: visceral myopathies, visceral neuropathies, and progressive systemic sclerosis. Am J Roentgenol 1981;143:933-41.
124. Sjogren RW. Gastrointestinal motility disorders in scleroderma. Arthritis Rheumatol 1994;37:1265-82.
125. Sato T, Ito H, Miyazaki S, Komine S, Hayashida Y. Megacystis and megacolon in an infant with Ehlers-Danlos syndrome. Acta Paediatr Japan 1993;35:358-60.
    126. Leon SH, Schuffler MD, Kettler M, Rohrmann CA. Chronic intestinal pseudo-obstruction as a complication of Duchenne's muscular dystrophy. Gastroenterology 1986;90:455-9.
    127. Nowak TV, Ionasescu V, Anuras S. Gastrointestinal manifestations of the muscular dystrophies. Gastroenterology 1982;82:800-10.
    128. Tada S, Iida M, Yao T, Kitamoto T, Yao T, Fujishima M. Intestinal pseudo-obstruction in patients with amyloidosis: clinicopathologic differences between chemical types of amyloid protein. Gut 1993;34:1412-7.
    129. McDonald GB, Schuffler MD, Kadin ME, Tytgat GN. Intestinal pseudo-obstruction caused by diffuse lymphoid infiltration of the small intestine. Gastroenterology 1985;89:882-9.
    130. Arist-Nasr J, Gonzalez-Romo M, Keirns C, Larriva-Sahd J. Diffuse lymphoplasmacytic infiltration of the small intestine with damage to nerve plexus. A cause of intestinal pseudo-obstruction. Arch Pathol Lab Med 1993;117:812-9.
    131. Robinson MH, Dowling BL, Clark JV, Mason CH. Brown bowel syndrome: an unusual cause of massive dilatation of the colon. Gut 1989;30:882-4.
    132. Lin CN, Huang AH, Hsu SI, Lee C, et al. Brown bowel syndrome: report of two cases. J Formos Med Assoc 1993;92:1090-4.
    133. Ruchti C, Eisele S, Kaufmann M. Fatal intestinal pseudoobstruction in brown bowel syndrome. Arch Pathol Lab Med 1990;114:76-80.
    134. Axelrod F. Familial dysautonomia. In: Gellis SE, Kagan AR, eds. Gellis current pediatric therapy. Philadelphia: WB Saunders, 1986.
      135. Udassin R, Seror D, Vinograd I, Zamir O, Gadfrey S, Nissan S. Nissen fudoplication in the treatment of children with familial dysautonomia. Am J Surg 1992;164:332-6.
      136. Cohen J, Low P, Fealey R, Sheps S, Jiang NS. Somatic and autonomic function in progressive autonomic failure and multiple system atrophy. Ann Neurol 1987;22:692-9.
      137. Low PA, Dyck PJ, Lambert EH, et al. Acute panautonomic neuropathy. Ann Neurol 1983;13:412-7.
      138. Feldman M, Schiller LR. Disorders of gastrointestinal motility associated with diabetes mellitus. Ann Intern Med 1983;98:379-84.
        139. Reid B, Di Lorenzo C, Travis L, Flores AF, Grill BB, Hyman PE. Diabetic gastroparesis due to postprandial antral hypomotility in childhood. Pediatrics 1992;90:43-6.
        140. Yoshid MM, Krishnamurthy S, Wattchow DA, Furness JB, Schuffler MD. Megacolon in myotonic dystrophy caused by degenerative neuropathy of the myenteric plexus. Gastroenterology 1988;95:820-7.
        141. Nowak TV, Anuras S, Brown BP, Ionasescu V, Green JB. Small intestinal activity in myotonic dystrophy patients. Gastroenterology 1984;86:808-13.
        142. Lenard HG, Goebel HH, Weigel W. Smooth muscle involvement in congenital myotonic dystrophy. Neuropadiatrie 1977;8:42-52.
        143. Brunner HG, Hamel BC, Rieu P, Howeler CJ, Peters FT. Intestinal pseudo-obstruction in myotonic dystrophy. J Med Genet 1992;29:791-3.
        144. Dimmick JE, Bove KK. Cytomegalovirus infection of the bowel in infancy: Pathogenetic and diagnostic significance. Pediatr Pathol 1984;2:95-102.
        145. Sonsino E, Mouy R, Foucaud P, et al. Intestinal pseudoobstruction related to cytomegalovirus infection of myenteric plexus. N Engl J Med 1984;311:196-7.
        146. Oldfield EE III. Colonic pseudo-obstruction: a complication of herpes zoster. Am J Gastroenterol 1994;89:2092-3.
        147. Tribble DR, Church P, Frame JN. Gastrointestinal visceral motor complications of dermatomal herpes zoster: report of two cases and review. Clin Infect Dis 1993;17:431-6.
        148. Press MF, Riddell RH, Ringus J. Cytomegalovirus inclusion disease. Its occurrence in the myenteric plexus of a renal transplant patient. Arch Pathol Lab Med 1980;104:580-3.
        149. Bassotti G, Pagliacci MC, Nicoletti I, Pelli MA, Morelli A. Intestinal pseudoobstruction secondary to hypothyroidism. Importance of small bowel manometry. J Clin Gastroenterol 1992;14:56-8.
        150. Miyake T, Kawamori J, Yoshida T, Nakano H, Kohno S, Ohba S. Small bowel pseudo-obstruction in Kawasaki disease. Pediatr Radiol 1987;17:383-6.
        151. Chinn JS, Schuffler MD. Paraneoplastic visceral neuropathy as a cause of severe gastrointestinal motor dysfunction. Gastroenterology 1988;95:1279-86.
        152. Roman RJ, Loeb PM. Massive colonic dilatation as initial presentation of mesenteric vein thrombosis. Dig Dis Sci 1987;32:323-6.
        153. Perino LE, Schuffler MD, Mehta SJ, Everson GT. Radiation-induced intestinal pseudoobstruction. Gastroenterology 1986;91:994-8.
        154. Husebye E, Hauer-Jensen M, Kjorstad K, Skar V. Severe late radiation enteropathy is characterized by impaired motility of proximal small intestine. Dig Dis Sci 1994;39:2341-9.
        155. Barry RE, Chow AW, Billesdon J. Role of intestinal microflora in colonic pseudoobstruction complicating jejunoileal bypass. Gut 1977;18:356-9.
        156. Eck SL, Morse JH, Janssen DA, Emerson SG, Markovitz DM. Angioedema presenting as chronic gastrointestinal symptoms. Am J Gastroenterol 1993;88:436-9.
        157. Couse N, Tyrrell D, McMurray N, Tanner WA. Tuberculous peritonitis in association with pancytopenia and pseudo-obstruction of the colon. J R Soc Med 1987;80:318-9.
        158. Rex DK, Acute colonic pseudo-obstruction (Ogilvie's syndrome). Gastroenterologist 1994;2:233-8.
        159. Milner G, Gastro-intestinal side effects and psychotropic drugs. Med J Aust 1969;2:153-5.
        160. McMahon AJ, Amitriptyline overdose complicated by pseudo-obstruction and caecal perforation. Postgrad Med J 1989;65:948-9.
        161. Urso FP, Urso MJ, Lee CH. The cathartic colon: pathological findings and radiological/pathological correlation. Radiology 1975;116:557-9.
        162. Muller-Lissner SA. Adverse effects of laxatives: fact and fiction. Pharmacology 1993;47(suppl 1):138-45.
        163. Riemann JF, Schmidt H, Zimmerman W. The fine structures of colonic submucosal nerves in patients with chronic laxative abuse. Scand J Gastroenterol 1980;15:761-8.
        164. Sandgren JE, McPhee MS, Greenberger NJ. Narcotic bowel syndrome treated with clonidine. Resolution of abdominal pain and intestinal pseudo-obstruction. Ann Intern Med 1984;101:331-4.
        165. Schultz HS, Vernon B. Intestinal pseudo-obstruction related to using verapamil. West J Med 1989;151:556-8.
        166. Santagelo WC, Richey JE, Rivera L, Fordtran L, Fordtran JS. Surreptitious ipecac administration simulating intestinal pseudo-obstruction. Ann Intern Med 1989;110:1031-2.
        167. Calloway SP, Fonagy P, Pounder RE, Morgan MM. Behavioral techniques in the management of aerophagia in patients with hiatus hernia. J Psychosom Res 1983;27:499-502.
        168. Kellow JE, Eckersley CM, Jones MP. Enhanced perception of physiological intestinal motility in the irritable bowel syndrome. Gastroenterology 1991;101:1621-7.
        169. Stanghellini V, Ghidini C, Macarini MR, Paparo GF, Corinaldesi R, Barbara L. Fasting and postprandial gastrointestinal motility in ulcer and non-ulcer dyspepsia. Gut 1992;33:184-90.
        170. Sutphen JL, Saulsbury FT. Intentional ipecac poisoning: Munchausen syndrome by proxy. Pediatrics 1988;82:453-6.
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        1997 Pediatric Gastroenterology Certifying Examination

        The American Board of Pediatrics (ABP) will administer the Certifying Examination in Pediatric Gastroenterology on Tuesday, August 5, 1997, in Chapel Hill, Philadelphia, Chicago, and San Francisco. You must have a current general pediatrics certificate to take a subspecialty examination. Late registration begins December 2, 1996. The late registration fee of $1,585 includes a $225 non-refundable penalty fee. The final deadline for applications is December 31, 1996. Applications postmarked after this date will not be accepted for the 1997 examination. On January 2, 1997, re-registration material will be mailed to those active candidates who meet the examination requirements. A copy of a valid, unrestricted license must be returned with the re-registration material. Regular registration begins on January 2, 1997, and extends through February 28, 1997. Qualified individuals who do not receive the material by January 15 should request the material from the ABP. The re-registration fee is $1,260. The re-registration fee must accompany the completed re-registration form and be postmarked by February 28, 1997. Late re-registration begins March 1, 1997. The late re-registration fee of $1,485 includes a $225 non-refundable penalty fee. The final deadline for postmark of re-registration material is March 31, 1997. Each application will be considered individually and must be acceptable to the Subboard of Pediatric Gastroenterology. Please contact the ABP for eligibility requirements. Site assignment is based on the date of receipt of the application or the re-registration material. There may be limited seating at some sites, so early registration is suggested. Please direct inquiries to: American Board of Pediatrics, 111 Silver Cedar Court, Chapel Hill, NC 27514-1651. Telephone: (919) 929-0461; Facsimile: (919) 929-9255.

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