Sudden infant death syndrome: the colon connection.

The etiology of sudden infant death syndrome (SIDS) is not known. Various maternal and infant risk factors have been identified. Adoption of the non-prone position has reduced the incidence of SIDS but has not eliminated the problem. Some sulfate reducing bacteria in the colon produce hydrogen sulfide (H2S) which is as toxic as hydrogen cyanide. Normally, the colonic mechanism for metabolizing and detoxifying H2S is very effective and no H2S appears in the exhaled breath although small amounts are present in the flatus. We are putting forth the hypothesis that in some cases of SIDS colonocytic mechanism for detoxifying H2S may not have matured by the age of 3 months and H2S may be absorbed resulting in SIDS. The hypothesis can be tested by in vitro evaluation of colonic tissue from SIDS cases for its ability to detoxify H2S.

Pathogenesis of esophageal rings in eosinophilic esophagitis.

Eosinophilic esophagitis and eosinophilic gastroenteritis is being recognized more frequently among the adult patients. The disease is characterized by massive infiltration of the wall of gastrointestinal tract by sheets of eosinophils. The clinical features depend upon the site of involvement. They include dyspepsia, dysphagia, nausea, vomiting, chest pain, diarrhea and protein-losing enteropathy. Eosinophilic esophagitis may present as chest pain, dysphagia or dyspepsia. The characteristic endoscopic feature of eosinophilic esophagitis is the formation of fine concentric mucosal rings (corrugated esophagus). Regarding the pathogenesis of these mucosal rings our hypothesis is that mast cells in the esophageal wall in response to allergens release histamine, eosinophilic chemotactic factor and platelet activating factor, etc. which activate eosinophils to release toxic cationic proteins. Activation of acetyl choline by histamine may cause contraction of the muscle fibers in the muscularis mucosae resulting in the formation of esophageal rings. This hypothesis can be tested by demonstrating the contraction of muscle layers of muscularis mucosae with the use of high frequency endoscopic ultrasonic probe introduced via the biopsy channel of an endoscope.

Carcinoma of gastric stump causing afferent loop obstruction and acute pancreatitis.

We report a case of a 79-year-old man who had undergone partial gastrectomy with Billroth-II (B-II) anastomosis 42 years ago for benign peptic ulcer. He presented with abdominal pain, distention and acute pancreatitis. Esophagogastroduodenoscopy showed a malignant mass obstructing the afferent stoma; surgical resection was performed. Pathogenesis of acute pancreatitis in this case and the problem of gastric stump carcinoma are discussed.

Colonic preparation correlates with fasting breath hydrogen in patients undergoing colonoscopy.

BACKGROUND/AIMS: Fasting breath hydrogen has been reported to be low after fasting and polyethylene glycol ingestion. However, the relationship between fasting breath hydrogen and colonic preparation for colonoscopy has not been studied before. We evaluated fasting breath hydrogen in patients undergoing colonoscopy and correlated it with the quality of colonic preparation. METHODOLOGY: One day before colonoscopy, the patients ingested clear liquid diet and starting in the afternoon the day before colonoscopy they drank polyethylene glycol 8oz every 10 minutes for 3 hours. They fasted overnight. Fasting breath hydrogen was measured using an EC 60 gastrolyzer. Colonic preparation was rated as excellent, fair or poor. The colonoscopic findings were noted. RESULTS: There were 69 male patients. 89% had excellent or fair colonic preparation (Group A) 11% had poor preparation (Group B). Fasting breath hydrogen in Group B patients 14.5 +/- 1.5 ppm was significantly higher compared to that in Group A patients 2.2 +/- 0.2 ppm (p < 0.005 t-test). In other respects the two groups were similar. CONCLUSIONS: Patients undergoing colonoscopy after polyethylene glycol ingestion who have poor colonic preparation have higher fasting breath hydrogen compared to those who have excellent/fair colonic preparation. The clinical implication of this observation is discussed.

Circadian variation in portal pressure: appropriate use of non-selective beta blockers in the prevention of variceal bleed.

The circadian variation in some biologic functions may have clinical, fiscal and therapeutic implications. The authors discuss circadian variation in portal pressure in cirrhotic patients and nocturnal occurrence of bleeding from varices in these patients. The pathogenesis of the diurnal variation in portal pressure is presented. The authors submit the hypothesis that an optimal dosing regimen for non-selective beta blocker therapy in the prevention of variceal bleed must include an evening dose of beta blocker medication. In studies reporting comparative efficacy of beta blocker therapy with other modalities in the prevention of variceal bleeding, the optimal dosing schedule for beta blocker therapy must be emphasized.

Evaluation of pancreas and other abdominal organs by colonoscopic ultrasound.

We report a case where colonoscopic ultrasound was used to evaluate the pancreas. In this case the usual method of evaluating the body of the pancreas by upper gastrointestinal ultrasound was unsuccessful because of the presence of a large hiatal hernia. The other abdominal organs evaluated by colonoscopic ultrasound included the ileo-cecal valve, kidney, liver, spleen and prostate. To our knowledge this is the first case where ultrasonic colonoscope has been used to evaluate the body of the pancrease.

Heterotopic gastric tissue in the duodenal bulb.

Heterotopic gastric tissue in the duodenal bulb is a rare congenital lesion. Its prevalence has been reported to be 0.5-2%. It must be differentiated from gastric metaplasia of the duodenal bulb because the two entities have different clinical implications. During one year, we found three cases of gastric heterotopia of the duodenal bulb. In one of the cases, active acid-secreting gastric mucosa was documented by performing the pentagastrin Congo red dye test. The differences between gastric heterotopia of the duodenal bulb and gastric metaplasia of the duodenal bulb have been discussed.

In cirrhotic patients variceal bleeding is more frequent in the evening and correlates with severity of liver disease.

BACKGROUND/AIMS: It has been observed that the portal pressure in cirrhotic patients shows circadian variation and is at a maximum at night. Our aims in this study were a) to evaluate the frequency of upper gastrointestinal (UGI) bleeding from esophageal/gastric varices or portal congestive gastropathy during the day, evening or night shift, and b) to correlate the frequency of bleeding during various shifts with severity of liver disease. METHODOLOGY: At our institution, during the period from January 1997 to June 1995, 15,000 gastrointestinal (GI) endoscopic reports and consultations were evaluated. Episodes of bleeding due to portal hypertension (PH), i.e., esophageal varices, gastric varices or congestive gastropathy, were noted. The time of occurrence of bleeding from PH in various shifts, e.g., day shift (DS), evening shift (ES) or night shift (NS) was determined. The severity of liver disease was classified as A, B or C according to Child's classification. RESULTS: There were 221 episodes of UGI bleeding due to PH in 144 patients. 75.5% of patients presented with hematemesis, whereas 24.5% presented with melena (p < 0.025). Bleeding started during the DS in 39/221 (17.6%), during the ES in 122/221 (55.2%), and during the NS in 60/221 (27.1%). There were 29 (13.1%) patients in Child's A, 75 (33.9%) in Child's B, and 117 (52.9%) in Child's C. Among the 122 bleeders during ES, 85 (69.6%) were in category C. It seems that in these patients UGI bleeding is more frequent during the ES compared to DS and NS (p < 0.0001; chi square; 95% CI: 0.52-0.58). Child's C patients are more likely to bleed during ES compared to Child's A or B patients (p < 0.0001; Odds Ratio: 4.8%; 95% CI: 2.7-8.5). CONCLUSIONS: 1) The majority of the cirrhotic patients with PH who develop UGI bleeding present with hematemesis rather than melena. 2) The bleeding in these patients is more likely to occur during the ES. 3) Child's C patients are more likely to bleed during the ES.

The safety of hot biopsy forceps in the removal of small colonic polyps.

Nine hundred and seven polyps (mean size 3.7 mm; range 2-8) from 460 patients (mean age 67 years; range 34-94) were removed with monopolar electrocoagulation forceps ('hot biopsy forceps'). Sixty-three percent of the polyps were adenomatous and 36% were hyperplastic. In this series there were 3 cancers and 1 neurofibroma. About 42% of the polyps were in the sigmoid-rectum region; the rest were evenly distributed in the remaining part of the colon. There were no complications. Specifically there were no cases of perforation or massive bleeding after removal of these polyps. Within the guidelines mentioned, hot biopsy removal of small colonic polyps is safe.

Effect of clonidine on gastrointestinal transit time.

BACKGROUND/AIMS: Orocecal time can be measured by lactulose H2 breath test. Duodenal entry time can be evaluated by measuring D-xylose; the duodeno-cecal time can be derived by subtracting duodenal entry time from orocecal time. In this study we established the normal value of these parameters for our laboratory in males and also evaluated the effect of clonidine on these parameters. METHODOLOGY: In 9 healthy male volunteers orocecal time was measured by the lactulose H2 breath test. Duodenal entry time was established by measuring blood D-xylose. Duodenocecal time was derived by subtracting duodenal entry time from orocecal time. RESULTS: The mean orocecal time was 54.44 + 3.77 minutes; the mean duodenal entry time was 17.22 + 3.15 minutes and the mean duodenocecal time was 37.22 + 3.16 minutes. CONCLUSIONS: Oral clonidine prolonged orocecal, duodenal entry and duodenocecal times in only 33% of the subjects.

Enterokinase.

Enterokinase is a glycoprotein and is now designated enteropeptidase (E.C.3.4.4.8.). It is present in the duodenal and jejunal mucosa. Pancreatic proteolytic enzymes are secreted as proenzymes. Enterokinase converts trypsinogen to trypsin in the duodenal lumen. Duodenopancreatic reflux of duodenal enterokinase may be important in the pathogenesis of experimental and clinical acute pancreatitis. Congenital enterokinase deficiency is a distinct clinical entity characterized by diarrhea, failure to thrive, hypoproteinemia, and edema. Acquired enterokinase deficiency may occur in some diffuse small bowel diseases. Steatorrhea of celiac spruce may be due partly to the fact that deficiency of secretin and cholecystokinin may interfere with the action of enterokinase. The interrelationship between secretin, cholecystokinin, enterokinase, and bile salts is not completely understood.