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Involvement of the gastrointestinal (GI) tract is an infrequent extrathoracic presentation of sarcoidosis. We reviewed 305 cases of GI involvement reported in 238 patients, in whom GI sarcoidosis was the first sign of the disease in half the cases. The disease does not affect the GI tract uniformly, with a clear oral-anal gradient (80% of reported cases involved the esophagus, stomach, and duodenum). Clinicopathological mechanisms of damage may include diffuse mucosal infiltration, endoluminal exophytic lesions, involvement of the myenteric plexus, and extrinsic compressions. Ten percent of patients presented with asymptomatic or subclinical disease found on endoscopy. The diagnosis is relevant clinically because 22% of cases reviewed presented as life threatening. In addition, initial clinical/endoscopic findings may be highly suggestive of GI cancer. The therapeutic approach is heterogeneous and included wait-and-see or symptomatic approaches, glucocorticoid/immunosuppressive therapy, and surgery. Sarcoidosis of the gut is a heterogeneous, potentially life-threatening condition that requires a multidisciplinary approach and early clinical suspicion to institute personalized therapeutic management and follow-up.

Objectives: Celiac disease (CD) is a chronic inflammatory disease of the small bowel that is characterized by increased intraepithelial lymphocytes (IELs) and villous atrophy of the mucosa. It is unclear how often intraepithelial lymphocytosis in the absence of atrophy is a manifestation of gluten sensitive enteropathy. The objective of this study was to identify factors that discriminate patients with CD from those with lymphocytic duodenosis (LD, intraepithelial lymphocytosis without villous atrophy). We compared Class 2 HLA type, presenting symptoms, and serology in patients with LD and CD., Methods: Retrospective review of 124 systematically assessed patients with LD compared with 454 CD patients with villous atrophy. All patients had duodenal biopsies and Class 2 HLA typing performed. HLA type, symptoms, serology pattern, and response to a gluten-free diet were analyzed using univariate logistic regression modeling, adjusted for age and gender., Results: Half of the (63 (51%)) LD patients lack the Class 2 HLA genotypes encoding DQ2 or DQ8 whereas only 11 (2%) CD patients had neither DQ2 nor DQ8, P<0.001. The genes encoding DQ2 were much more prevalent in CD (91%) than that in LD (37%, P<0.001), however, the rate of carriage of DQ8 did not differ between the two groups (15% vs. 15%, P=0.9). Although diarrhea and weight loss were equally frequent in LD and CD patients, LD patients were less likely to be associated with anemia (P=0.007), malaise (P=0.006), skin disorder (P=0.007), or a family history of CD (P<0.001). The LD subjects were much less likely to have tissue transglutaminase or endomysial antibodies than were CD subjects (12% or 0% vs. 87% and 87%; P<0.001, respectively)., Conclusions: The LD cohort differs significantly in terms of HLA type, serology, and clinical features, suggesting that the majority of patients with LD do not belong in the spectrum of CD.

Objective: Description of the clinical, endoscopic, and histopathologic detailed profiles of duodenal affection in portal hypertensive patients., Methods: A total of 105 patients with chronic liver disease and portal hypertension (PH) were included, upper endoscopy was performed, and two duodenal biopsies were obtained from the bulb and distal to the ampulla, for histopathologic examination. Twenty dyspeptic patients with normal upper endoscopy were included as controls., Results: Of the portal hypertensive patients, 54 (51.4%) had endoscopic duodenopathy (ED) lesions including erythema, erosions, ulcers, telangiectasia, exaggerated villous pattern, duodenal varices, and mixed lesions. ED was significantly higher in patients having severe than mild gastropathy (56.8% vs 23.5%, P<0.05) with no relation to size of esophageal varices or variceal bleeding. ED was a source of overt bleeding in 6.7% and occult bleeding in 2.9% of patients. Histopathologically, vascular changes included either capillary congestion (in more than half of biopsies) or capillary angiogenesis (in more than one-quarter of biopsies). Nonvascular changes included increased apoptosis (in about 16% of biopsies), fibrous proliferation (in about 4% of biopsies), and villous changes (in 11.4% of distal biopsies). All changes were not statistically different between patients with and without ED. In dyspeptic patients, only minimal histopathologic changes were noted., Conclusions: ED is significantly higher in patients with severe gastropathy and causes gastrointestinal bleeding in 9.5% of patients. Capillary angiogenesis is an important vascular mechanism for adaptation to PH. The overall existence of histopathologic duodenopathy is much higher than that of ED and occurs with a similar prevalence in patients with and without ED.

Background and Aims: Cystic dystrophy in heterotopic pancreas (CDHP) is an uncommon complication of pancreatic heterotopia, only described in surgical series, whose natural history is not known. The aim of this study was to determine clinical and morphological features of CDHP in a medical-surgical series of patients and to ascertain the relationship of CDHP with chronic pancreatitis (CP) in the pancreas proper., Methods: All patients who had duodenal CDHP diagnosed radiologically both with CT scan and endoscopic ultrasonography between 1995 and 2004 were included. The diagnosis was confirmed by surgical specimens when available., Results: One hundred five patients were included (91% men, 86% chronic alcoholic) with a median follow-up of 15 months. The median age at first symptoms was 46 yr. CDHP was associated with CP in the pancreas proper in 71% of patients. Presenting symptoms were pancreatic pain (91%), severe weight loss (73%), acute pancreatitis (45%), vomiting (30%), steatorrhea (23%), diabetes mellitus (20%), jaundice (13%), and upper gastrointestinal hemorrhage (5%). Cysts were multiple in 75% (median 3). The median diameter of the largest cyst was 10 mm. Endoscopy was normal in 36% of patients and showed duodenal stenosis in 52% (complete 6%, incomplete 46%). Surgical treatment was necessary in only 27% of patients (Whipple procedure 16%)., Conclusions: CDHP may arise in patients with or without CP and with or without chronic alcoholism. Symptoms may be severe but warrant surgery in less than one-third of patients.

Interstitial cells of Cajal (ICC) are fundamental regulators of GI motility. Here, we report the manometrical abnormalities and abnormalities of ICC distribution and ultrastructure encountered in a 30-yr-old patient with megaduodenum and pseudo-obstruction. Full thickness biopsies taken during laparoscopic placement of a jejunostomy showed vacuolated myocytes and fibrosis predominantly in the outer third of the circular muscle layer of the duodenum, suggestive for visceral myopathy. The distribution of ICC was also strikingly abnormal: by light microscopy, ICC surrounding the myenteric plexus were lacking in the megaduodenum, whereas ICC were normally present in the duodenal circular muscle and in the jejunum. By electron microscopy, very few ICC were identified around the duodenal myenteric plexus. These findings suggest that abnormalities in ICC may contribute to the disturbed motility in some myopathic forms of intestinal pseudo-obstruction.

Objective: The aim of the present study was to assess the presence of duodenal erosion and its clinical characteristics on endoscopy in patients with portal hypertension who had undergone endoscopic injection sclerotherapy and/or endoscopic variceal ligation for esophagogastric varices., Methods: The subjects were 440 patients with portal hypertension, 450 with chronic hepatitis as a related control group, and 450 who underwent upper endoscopic examination as part of their routine physical examination as the controls. The underlying hepatic disease, hepatic function, and endoscopic findings of duodenal erosion among the patients with portal hypertension were studied., Results: Duodenal erosion was found in 68 patients with portal hypertension (68 of 440, 15.5%), four patients with chronic hepatitis (four of 450, 0.9%), and two controls (two of 450, 0.4%). The incidence of duodenal erosion among the patients with portal hypertension was significantly higher than that in the other two groups (p < 0.01, p < 0.01, respectively). The lesions commonly observed in duodenitis are speckle erosions mainly located in the duodenal bulb. However, the most frequently seen form of duodenal erosion among the patients with portal hypertension extended from the superior portion to the descending portion, and tended to show a circular alignment along the Kerckring's folds. The patients with portal hypertension with reduced hepatic reserve capacity had more severe duodenal erosion. Endoscopic ultrasonography revealed thickening of the duodenal wall and proliferation of vascular structures within and around the wall. The histological findings of the duodenal erosion included edema and vascular dilation in the mucosal and submucosal layers., Conclusions: The location of duodenal erosion in patients with portal hypertension differs from that in patients with ordinary duodenitis. Duodenal erosion in patients with portal hypertension is considered to be one of the lesions of portal hypertensive duodenopathy.

Dieulafoy lesions are uncommon sources of GI hemorrhage and predominantly occur in the proximal stomach. At one time a pathological diagnosis made postoperatively, Dieulafoy lesions are now routinely diagnosed and treated endoscopically. Their true incidence is unclear as quiescent Dieulafoy lesions are easily overlooked on endoscopy and bleeding lesions are occasionally misidentified. Over 6 yr (June 1993-November 1999), 40 Dieulafoy lesions were identified on upper endoscopy at our institution, of which seven were located in the duodenum and one in the right colon. Forty-seven percent of patients were hospitalized for other causes before onset of bleeding, and 17 of 40 were found to have other abnormal findings at endoscopy. In 90% of the cases, endoscopic treatment was successful. Seven patients died, but none as a result of hemorrhage. In 24 endoscopically-treated patients in whom follow-up data are available, Dieulafoy bleeding recurred in one patient. Dieulafoy lesions are rare and often difficult to diagnose, but must be considered in the evaluation of upper and lower GI tract hemorrhage, as they can usually be managed endoscopically.

Objective: The aim of this study was to investigate the separate effects of indigenous oropharyngeal- and colonic-type flora on small intestinal mucosal immunity and morphometry in small intestinal bacterial overgrowth (SIBO)., Methods: A duodenal aspirate and random biopsies of underlying mucosa were obtained from 52 adult subjects (age range, 18-90 yr; median, 60 yr) without disorders that may otherwise disturb small intestinal histology or mucosal immunity. Villus height, crypt depth, villus/crypt ratios, counts of intraepithelial lymphocytes (IELs) and lamina propria total mononuclear cells, IgA, IgM, and IgG plasma cells, mast cells, and B and T lymphocytes were determined in relation to the presence or absence of SIBO and the nature of the overgrowth flora in all subjects. CD4+ve and CD8+ve T-cell counts were determined in 24 subjects., Results: SIBO was present in 26 of 52 (50%) subjects. Overgrowth flora included colonic-type bacteria in 20 subjects and oropharyngeal-type flora alone in 6 subjects. Lamina propria IgA plasma cell counts were significantly increased in subjects with SIBO, irrespective of whether the overgrowth flora comprised oropharyngeal-type flora alone or included colonic-type bacteria. Neither villus height, crypt depth, villus/crypt ratios, nor total or other mononuclear cell counts in lamina propria differed significantly between subjects with and without SIBO, irrespective of the nature of the overgrowth flora. IEL counts were significantly higher than in culture-negative subjects only when the overgrowth flora included colonic-type bacteria. Even then, IEL counts were within a range currently considered normal. A significant, inverse correlation between advancing age and IEL counts became apparent after adjusting for the effect of SIBO of colonic-type flora., Conclusions: SIBO of oropharyngeal- and colonic-type flora are associated with differing disturbances of local duodenal mucosa. Nonetheless, these would not be readily apparent during routine histological assessment. Old age independently influences duodenal IEL counts.

Objective: The aim of this study was to characterize the clinical and motility findings in 62 patients with systemic sclerosis or related disorders referred for evaluation of upper gastrointestinal (GI) symptoms., Methods: Methods included retrospective clinical record review and quantitation of esophageal, LES antral, and duodenal motility (3 h fasting, 2 h fed) were compared with results of 10 symptomatic patients with normal gastric emptying., Results: A total of 46 patients had systemic sclerosis, eight mixed connective tissue disease, and eight polymyositis-systemic sclerosis overlap; systemic manifestations were almost invariably present. GI symptoms were: heartburn (77%), nausea/vomiting (58%), dysphagia (61%), diarrhea (53%), constipation (31%), and fecal incontinence (13%). Anatomical studies showed esophageal erosions or GERD (53%), aperistalsis (34%), stricture (29%), and Barrett's metaplasia (16%); megaduodenum, small bowel dilation, or diverticulae (42%); and pneumatosis intestinalis (8%). A total of 36 patients underwent esophageal and 26 esophagogastrointestinal manometry. Postprandial antral motility index was abnormal in 22 of 26; amplitudes and frequency in the antrum (34 +/- 3 mm Hg and 0.6 +/- 0.1/min, respectively) and duodenum (7.3 +/- 0.9 mm Hg and 1.8 +/- 0.5/min) were significantly lower than controls (p < 0.05)., Conclusion: In patients with GI symptoms associated with systemic sclerosis and related disorders, the amplitude and frequency of intestinal contractions are typically <10 mm Hg and <2/min. Antral amplitude is low (<40 mm Hg) when antral hypomotility is observed.

Objectives: Diagnosis of unrecognized celiac disease is potentially important. The prevalence of celiac disease in patients with insulin-dependent diabetes mellitus is uncertain. We report the prevalence of celiac disease in a stratified random sample (n = 101) of adult insulin-dependent diabetic patients (age, 18-59 yr) attending our clinic, and in an age- and sex-matched control group (n = 51)., Methods: Screening was by anti-endomysial antibody, measured by indirect immunofluorescence using sections of human umbilical cord., Results: Celiac disease had not been suspected in any patient at the time of screening. Eight patients tested positive for anti-endomysial antibody, all of whom had a distal duodenal biopsy performed. Five patients had histologic evidence of celiac disease. One patient with negative histology was receiving immunosuppressive therapy for a renal-pancreas transplant. Of the five patients with abnormal histology, two improved on gluten restriction, one was unable to comply, one refused treatment, and one was lost to follow-up. No control subject tested positive for endomysial antibody., Conclusions: Patients with insulin-dependent diabetes have an increased prevalence of celiac disease. Because most cases are clinically unrecognized, consideration should be given to screening all insulin-dependent diabetes mellitus patients with endomysial antibodies.

Objective: Our objective was to compare the clinical characteristics of 72 patients with proximal Crohn's disease (PCD), i.e., from mouth through jejunum, with those of 242 patients with distal Crohn's disease (DCD), i.e., from ileum through rectum., Methods: The diagnosis of Crohn's disease was made on established criteria, e.g., radiology, histology, etc., Results: All but one patient with PCD eventually had DCD as well. Twenty-seven of the 72 patients in the PCD group had manifest PCD at the time of diagnosis. For the 45 PCD patients who, at first, had only distal lesions, 5.0 +/- 4.2 yr passed before a proximal localization was detected. After the diagnosis had been established, the average follow-up time was 19.2 yr in the PCD group and 23.1 yr in the DCD group. The age at onset of disease was significantly (p < 0.01) lower in the PCD group (19.1 yr) than in the DCD group (24.3 yr). However, the time from onset of first symptoms to diagnosis was almost identical in the two groups (PCD group 3.8 yr vs. DCD group 3.4 yr). When complaints began in 1970 or later, after introduction of the flexible endoscope, there was a significant difference between length of time-to-diagnosis in the PCD and DCD groups, i.e., 2.7 and 1.6 yr, respectively, (p < 0.05). Remarkable differences were found in initial symptoms at the onset of disease. Abdominal pain and/or cramps and general malaise were found more often in patients with PCD (respectively, 82% and 21%) than in patients with DCD (respectively, 70% and 10%) (both p < or = 0.05). Although small-bowel resections were performed comparably often in the two groups, in the PCD group, the average length of resected small bowel was significantly greater (77.3 cm, p < 0.002) (n = 53) than in the DCD group (48.1 cm, n = 165)., Conclusions: We conclude that PCD differs from DCD in its clinical presentation, particularly with regard to abdominal pain and/or cramps and general malaise. Patients with PCD are younger at the onset of symptoms, at diagnosis, and when the first abdominal operation is performed, but there is no difference in lag times compared with those of DCD patients. During the course of the illness, more small bowel is resected from PCD patients.

Ménétrier's disease is a rare cause of hypertrophic gastropathy, usually confined to gastric body and fundus, which is characterized by giant rugae, hypoalbuminemia, and foveolar hyperplasia. The etiology of this disease is still unknown. We report a case of a 74-yr-old man who had dyspepsia, hypoalbuminemia, weight loss, and diffuse polypoid, nodular lesions affecting the whole stomach and proximal duodenum on gastroscopy and barium meal study. The histology of gastric and duodenal mucosal lesions fulfilled the diagnosis of Ménétrier's disease, that was not described to involve duodenum in the literature. The disease resolved clinically, endoscopically, and pathologically after therapy with famotidine for 3 months. We speculated that extensive pyloric metaplasia and then foveolar hyperplasia of duodenum in this patient might be a variant of Ménétrier's disease with favorable clinical course.

The case described herein underscores the importance of early endoscopy when intramural gastric air is detected by radiography. Although gastric pneumatosis is an uncommon finding, when it is detected, clinicians must be aggressive in determining the underlying etiology so that appropriate interventions are initiated in a timely manner. In this case, the gross endoscopic appearance of the mucosa and the unique histological findings were critical in establishing the correct diagnosis. Although gastric pneumatosis has been found in surgically resected specimens, the first description of histological findings associated with gastric pneumatosis in endoscopically obtained biopsies is presented in this report. This report also documents how rapidly both endoscopic and histological abnormalities, associated with this entity, can resolve.

Hereditary megaduodenum is a rare disease with autosomal dominant transmission characterized by visceral myopathy that involves the digestive and urinary tracts, and usually presents as intestinal pseudo-obstruction. Recently, a high rate of spontaneous chromosomal damage was found in blood lymphocytes of patients with hereditary megaduodenum, predictive of an increased cancer risk. Clinical manifestations of the disease vary, ranging from severe pseudo-obstruction to asymptomatic family members; recurrent urinary tract infections are common. Histology reveals vacuolar degeneration and fibrosis of the longitudinal layer of gastrointestinal muscle. This disease should be suspected in patients with an enlarged duodenum but no mechanical obstruction. Treatment is symptomatic and based on diet and control of bacterial overgrowth. Enteral or parenteral nutrition may be needed. Laterolateral duodenojejunostomy and gastrojejunostomy may sometimes be helpful to relieve obstructive symptoms. The risk of cancer in patients with hereditary megaduodenum is still unknown. This paper describes a family with hereditary megaduodenum in which one of the three affected members died of esophageal carcinoma and reviews the literature on the disease with particular attention to reports of cancer.

We document a patient with a penetrating peptic ulcer of the first part of the duodenum, that extended into the main portal vein forming a fistula. This is the first reported case of a duodenoportal fistula secondary to peptic ulcer disease. The fistula was complicated by massive gastrointestinal hemorrhage, extra- and intrahepatic portal vein thrombosis, hepatic parenchymal infarction, and intrahepatic portal vein foreign body granulomas containing vegetable matter.

We report a case of brown-black pigmentation of the duodenum found in an elderly female during endoscopy for unrelated reasons. Melanin-like pigmentation of the duodenum is a rare endoscopic entity of uncertain etiology and significance. Various theories related to the etiology and pathogenesis, as well as histochemical and electron microscopic characteristics, are discussed.

Double pylorus is either a congenital abnormality or an acquired complication of peptic ulcer disease. We had followed two patients for 3 and 5 yr, respectively, to observe the processes of formation and the prognosis of double pylorus. Initially, duodenal ulcer was found in one patient with diabetes mellitus and chronic renal failure, and gastric ulcer was found in the other with chronic obstructive pulmonary disease. Both developed double pylorus with refractory courses. In spite of intensive medical treatment, both of them had persistent ulcers in the fistulous tract and failed to develop reepithelization. Helicobacter pylori was found in all of the specimens of gastroduodenal biopsies in both cases. Therefore, we believe that the refractory courses of double pylorus may be related to the underlying diseases and/or the presence of H. pylori. Antibacterial treatment of H. pylori or surgical intervention should be considered for patients with this condition.

Objectives: The aim of this study was to characterize the clinical presentation, pathological features, and outcome of a series of patients with Brunner's gland hamartomas., Methods: We reviewed the clinical and pathological features of 27 patients who presented with Brunner's gland hamartomas, and we obtained follow-up information., Results: Patients (12 men and 15 women) presented predominantly in the fifth and sixth decades of life either with gastrointestinal hemorrhage (n = 10) or obstructive symptoms (n = 10); there were also patients whose tumors were discovered as an incidental finding (n = 7). The tumors were generally pedunculated, were located in the first portion of the duodenum, and were in the range of diameter from 1 to 6 cm. Histologically, the hamartomas were characterized by the presence of nondysplastic, lobulated Brunner's glands with intervening bands of fibrous tissue and variable adipose and lymphoid tissue. Focal sclerosis was found in 93% of the hamartomas, possibly mimicking an adenocarcinoma. Whether managed surgically (24 patients) or endoscopically (three patients), the outcome was uniformly favorable. After a median period of 7-yr-follow-up, no tumors recurred, and no additional morbidity was identified., Conclusions: Brunner's gland hamartomas are rare duodenal tumors occurring in middle age that present either with gastrointestinal hemorrhage, obstructive symptoms, or as an incidental finding. Surgical or endoscopic excision is uncomplicated, and the long-term outcome is favorable.

Nodular duodenum, frequently described as nodular duodenitis, is endoscopically characterized by multiple erythematous nodules in the proximal duodenum and may represent a variant of duodenal inflammation. This study examines the incidence, clinical presentation, histologic correlates, natural history, and response to therapy of nodular duodenum in 83 patients who presented with epigastric pain, heartburn, early satiety, bloating, nausea, vomiting, or gastrointestinal bleeding. There was a previous history of peptic ulcer disease in 58% of patients and gastroesophageal reflux in 33%. None of the patients had associated end-stage renal disease. Endoscopically, in addition to nodular duodenum, esophagitis was found in 17% of patients and gastritis in 32%. Histology of duodenal nodules revealed chronic inflammation in 58% of patients, Brunner's gland hyperplasia in 9%, gastric heterotopia in 7%, and normal mucosa in 26% of patients. In a group of 34 patients studied prospectively, high dosage (300 mg orally bid) therapy with the H2-antagonist ranitidine for 8 wk significantly improved symptoms and endoscopic appearance (p < 0.05). In 26 patients who completely or partially failed H2-antagonist therapy, continuation of therapy with omeprazole (40 mg orally qd) for 8 wk significantly improved symptoms and endoscopic findings (p < 0.05) in 10 patients. These therapeutic approaches led to improvement in the endoscopic findings, but to no statistically significant changes in the underlying histologic appearance of the duodenum. We conclude that nodular duodenum is an endoscopically distinct entity that may respond clinically to antisecretory therapy, but remains difficult to eradicate completely.

Ninety-one normal, healthy volunteers participated in a single-center, double-blind, placebo-controlled, randomized, parallel group study: 1) to compare the prostaglandin E1 analog, misoprostol, given at a dose of 200 micrograms bid, with the recommended dose of 200 micrograms qid in protecting the gastroduodenal mucosa against injury due to anti-inflammatory doses of aspirin (3900 mg/day); and 2) to determine whether the reduced dose was associated with a lesser incidence of gastrointestinal (GI) side effects, particularly diarrhea. All subjects received 975 mg of aspirin qid with meals and at bedtime. They were concurrently administered either misoprostol 200 micrograms qid, misoprostol 200 micrograms bid and placebo bid, or placebo qid. All subjects were endoscopically normal at the onset of the study and were re-endoscoped on the morning of the 7th day of therapy, 2 h after the morning dose of medications. Gastric and duodenal mucosa were assessed separately on a 0-7 scale which gave a greater weight to erosions than to hemorrhages. GI symptoms, especially bowel habits, were assessed by means of diary cards. Subjects in both misoprostol groups had significantly less gastric and duodenal mucosal injury than subjects who received placebo (p less than 0.007 for each pairwise comparison). There was no statistically significant difference between the two misoprostol groups (p less than 0.093). Subjects in the misoprostol 200 micrograms qid group had significantly more loose and watery bowel movements than the subjects in the misoprostol 200 micrograms bid group (p less than 0.013), whereas there were no significant differences in bowel habits between the misoprostol 200 micrograms bid and placebo groups (p less than 0.122). More subjects in the misoprostol 200 micrograms qid group reported abdominal pain, loose stools, watery stools, flatulence, dyspepsia, and nausea than in the misoprostol 200 micrograms bid and placebo groups. In conclusion, the adverse events in the misoprostol 200 micrograms bid group were not significantly different from those in the placebo group, and were significantly better than in the misoprostol 200 micrograms qid group. The lower dose retained mucosal protective activity that was statistically indistinguishable from that of misoprostol 200 micrograms qid.

Gastrointestinal tuberculosis is still rampant in underdeveloped countries and can mimic other gastrointestinal (GI) disorders. Herein we report four cases of isolated proximal duodenal tuberculosis, without involvement of other parts of the GI tract. The clinical presentation in three of them resembled that of peptic ulcer disease, and one had features of gastric outlet obstruction. On investigation, one of these patients had a pyeloduodenal fistula. The limitations of clinical evaluation, radiology, and endoscopy are stressed, and the value of surgical biopsy is highlighted.

A patient with a symptomatic duodenal duplication cyst demonstrated by endoscopic retrograde cholangiopancreatography (ERCP) is presented. This lesion usually does not communicate with duodenal lumen but should be added to the list of cystic duodenal lesions demonstrable by ERCP. ERCP preoperatively is helpful to the surgeon in isolating adjacent duct structures but cyst wall histology is mandatory for correct anatomic diagnosis as this lesion has often been confused with Type III choledochal cysts.

In 18 of 27 cases a duodenal diverticulum, which usually occurs at "weak" spots in the bowel wall, penetrated the pancreas. Of these, 14 cases (77.8%) extended along the embryological fusion line of the ventral and dorsal components, which is considered to be the so-called "locus minoris resistantiae." In four cases the diverticulum penetrating the ventral pancreas was in close approximation to the locus minoris resistantiae.

An unusual case of infarcted duodenal duplication cyst is presented. Our case is the first ever reported. Total excision followed by duodenojejunostomy successfully cured the patient.

Nonspecific duodenitis exists as a clinical entity distinct from duodenal ulcer disease. Duodenoscopic findings take two general forms: 1. nodularity and erythema, 2. erosions and friability. Both forms usually tend to improve with time but do not necessarily disappear. Although frequently a mild illness, the hemorrhagic erosive form of duodenitis is a potentially serious complication causing marked gastrointestinal bleeding and should be considered in patients taking aspirin-alcohol or following severe physiologic stress. Lastly, most patients initially seem to respond to anticholinergic, tranquilizer or antacid therapy but clinical correlation with long-term treatment will require controlled studies.

This is a case report of a patient with a variant of idiopathic intestinal pseudo-obstruction (IIPO). The patient, a 53-year old female with polycystic kidney disease, had intermittent episodes of intestinal distention with megaduodenum and megasigmoid noted at roentgen study and postmortem examination. The etiology of this abnormality is unclear and no significant changes in the innervation of the bowel were noted on gross or histologic study.

A case of tuberculous stricture of the third part of the duodenum was detected by duodenoscopy. Endoscopic biopsy, however, failed to reveal the histological diagnosis. The possible role of endoscopic follow-up of tubercular strictures is indicated.

To determine the effect of an acute dose of ethanol on the stomach and duodenum, seven alcoholic subjects with previously normal upper gastrointestinal endoscopy were reevaluated with endoscopy and directed biopsy three hours after the oral ingestion of ethanol (1 gm./kg. body weight) as a 35 gm./100 ml. solution. After ingestion of alcohol, all seven subjects had moderate to severe antral erythema and friability and two had patchy erosions and hemorrhage in the antrum and fundus of the stomach. Five of seven subjects had changes in the duodenal bulb consisting of erythema similar to that in the antrum of the stomach. Microscopically after alcohol, four of seven demonstrated focal subepithelial hemorrhage and another had frank mucosal hemorrhage in the antrum. In the duodenal bulb, four of seven subjects demonstrated focal subepithelial hemorrhage in the tips of bulbar villi and four of seven had striking infiltration of eosinophils in the subepithelial stroma. These histologic alterations were not present in prealcohol biopsies or in biopsies in two additional subjects given club soda alone or beef bouillon, or in repeat biopsies in two subjects re-endoscoped three days after the ingestion of alcohol when the endoscopic findings were again normal. It is concluded that a single dose of alcohol consistently causes macroscopic and microscopic antral and duodenal alterations.

At present, tuberculosis of the intestinal tract is rare in the United States. When gastrointestinal disease is seen, 85--90% of cases involve the ileocecal area. A case of tuberculosis of the duodenum unassociated with pulmonary disease is described. Although fiberoptic enndoscopy, abdominal ultrasonography and computerized axial tomography were used, the diagnosis required laprotomy with biopsy. The clinical manifestations, diagnostic investigations and treatment of the 49 previously reported cases of duodenal tuberculosis are also reviewed.