Predictive value of the Rome criteria for diagnosing the irritable bowel syndrome.

OBJECTIVE: Our aim was to examine the predictive value of the Rome criteria and absence of so-called "red flags" of clinical practice for diagnosing irritable bowel syndrome. Red flags were relevant abnormalities on physical examination, documented weight loss, nocturnal symptoms, blood in stools, history of antibiotic use, and family history of colon cancer. METHODS: In retrospective studies, 98 patients who had one or more Rome criteria and lacked red flags were identified by chart review of a 1-yr period. In prospective studies, 95 patients were identified who met the Rome criteria and lacked red flags. Sensitivity, specificity, predictive value of Rome criteria, and absence of red flags were determined. Consultant's final diagnosis was the gold standard. Investigations before and after referral were recorded and reason for referral was determined in prospective studies. RESULTS: In the retrospective series, the Rome criteria and absence of red flags had a sensitivity of 65%, specificity of 100%, and positive predictive value of 100%. None of these patients required revision of their diagnosis during a 2-yr follow-up. In the prospective study, the positive predictive value was 98%. More than 50% of the patients in this group had been referred because of diagnostic uncertainty and 24% had had an abdominal ultrasound; 66% of those <45 yr old underwent at least partial colonic evaluation. CONCLUSIONS: These findings suggest that the Rome criteria combined with a lack of red flags have a very high predictive value for diagnosing irritable bowel syndrome. Application of these diagnostic criteria has the potential to alter utilization of health care resources.

Indium-111-labeled autologous leukocyte imaging and fecal excretion. Comparison with conventional methods of assessment of inflammatory bowel disease.

This study was designed to evaluate the role of 111In-labeled leukocyte imaging and fecal excretion in the assessment of inflammatory bowel disease. We compared these tests to various indices of disease activity in Crohn's disease, to Truelove's grading in ulcerative colitis, and to endoscopy, x-ray, and pathology in both diseases. Eleven controls, 16 patients with Crohn's disease, 13 with ulcerative colitis, and 3 with other types of acute bowel inflammation were studied (positive controls). Indium scanning was performed at 1, 4, and 24 hr. Fourteen of 16 patients with active Crohn's disease had positive scans but in only five was localization accurate. One patient had inactive ulcerative colitis, and the scan was negative. Of 12 patients with active ulcerative colitis, 10 had positive scans but disease localization was accurate in only four. Disease extent was correctly defined in 1 of the 3 Positive Controls. There was no significant difference in the accuracy of scanning at 1, 4, or 24 hr. 111In fecal excretion was significantly higher in patients with inflammatory bowel disease than in controls, and there was correlation between 111In fecal excretion and most of the indices of disease activity in Crohn's disease. In ulcerative colitis, 111In fecal excretion did not correlate with Truelove's grading but reflected colonoscopic assessment of severity. In conclusion, 111In-labeled leukocyte scanning lacks sensitivity with respect to disease extent, but fecal excretion of 111In correlates well with disease severity as determined by other methods.

Lower esophageal sphincter pressure and gastroesophageal pressure gradients in excessively obese patients.

The purpose of the present study was to investigate the relationship of the gastroesophageal pressure gradient (GEPG) to lower esophageal sphincter pressure (LESP) in normal and in severely obese subjects. Eight lean volunteers with no clinical evidence of gastroesophageal reflux and eight asymptomatic severely obese patients (at least 80% over their ideal weight) underwent esophageal manometric studies with measurements of the LESP and GEPG in both inspiration and expiration. The LESP/GEPG ratio was also calculated in both inspiration and expiration. Acid sensitivity was assessed by means of infusion of 0.1 N HCl subsequent to the baseline motility study. There was no significant difference between the LESP in obese patients (O.P.) and normal subjects (N.Sb.) in either inspiration (mean +/- SEM in mm Hg: N.Sb. = 16.4 +/- 1.6, O.P. = 18.7 +/- 2.5), or expiration (N.Sb. = 16.6 +/- 1.5, O.P. = 20.6 +/- 2.6). However, the GEPG in both inspiration (N.Sb. = 13.3 +/- 1.6, O.P. = 23.1 +/- 2.0; p less than 0.001) and in expiration (N.Sb. = 2.1 +/- 0.5, O.P. = 8.1 +/- 1.1; p less than 0.001) was significantly higher in obese patients than in controls. As a result, the GEPG/LESP ratios were also higher (expiration N.Sb. = 0.15 +/- 0.03, O.P. = 0.46 +/- 0.10; p less than 0.01) in obese patients; and for inspiration (N.Sb. = 0.86 +/- 0.13, O.P. = 1.33 +/- 0.12; p less than 0.01) in the obese patients the ratio was greater than 1. None of the normal subjects exhibited acid sensitivity, but 6 of the 7 obese patients tested developed heartburn during acid infusion. In conclusion, the GEPG/LESP ratio in inspiration was greater than unity for obese patients inspite of normal LESP. Such a change in the ratio could facilitate reflux in obese patients.

The effect of acid and bethanechol stimulation in patients with symptomatic hypertensive peristaltic (nutcracker) esophagus. Evidence that this disorder may be a precursor of diffuse esophageal spasm.

The hypertensive peristaltic (nutcracker) esophagus represents a motility disorder characterized clinically by squeezing retrosternal chest pain and manometrically by high amplitude esophageal peristaltic contractions. This study was designed to examine whether the nutcracker esophagus is: (a) a distinct entity, (b) a member of the spectrum of primary esophageal dysmotilities (e.g., diffuse esophageal spasm and achalasia), or (c) is secondary to reflux-induced acid sensitivity. Thirteen patients with a nutcracker esophagus by baseline manometry were subsequently studied after acid perfusion and bethanechol stimulation (0.08 mg/kg). Records were analyzed for symptomatic response and motility changes. Eight of 13 (62%) experienced chest pain during acid perfusion, but none had significant motility changes documented during this period. After bethanechol injection, chest pain occurred in six of 12 (50%) patients; two had burning pain and in the other four (33%) their squeezing chest pain was reproduced. Changes in the motility tracing with evidence of disordered motility suggestive of diffuse esophageal spasm were seen after bethanechol in seven of the 12 tracings analyzed (58%), including all six patients who developed chest pain. We conclude that patients with nutcracker esophagus on baseline manometry may develop motility patterns consistent with diffuse esophageal spasm after provocation with bethanechol. We take this to suggest that the nutcracker esophagus is part of the continuum of primary motility disorders and may actually be a precursor of diffuse esophageal spasm.

Ultrasound in the diagnosis of sphincter of Oddi spasm.

Biliary colic from spasm of the sphincter of Oddi has been a difficult diagnosis to prove. We describe a patient in whom the diagnosis was arrived at using a pharmacological provocative test employing codeine to reproduce pain and a change in liver and pancreatic serum enzymes, and ultrasound to demonstrate a transient increase in common bile duct diameter. Testing carried out before surgical sphincteroplasty reproduced symptoms, and brought about marked pancreatic and liver enzyme elevation and an increase in common bile duct diameter measured by ultrasound (0.4 to 1.0 cm). Such events did not occur after sphincteroplasty. This case study suggests that codeine may be a useful provocative agent and that ultrasound measurements of changes in common bile duct diameter may provide a useful method in the diagnostic approach to Sphincter of Oddi Spasm.

Simultaneous estimation of arteriolar, capillary, and shunt blood flow of the gut mucosa.

Microspheres of 15 and 9 microns diameter were injected simultaneously into the left ventricle of the dog, and the entrapment of these microspheres in different layers of the gut wall was measured under resting conditions, vasoconstriction, and subsequent vasodilation. Results show that some of the 9-microns spheres passed into the portal blood through all layers of the gut wall, whereas 15-microns spheres were completely entrapped in the tissue. The pattern of entrapment of 15-microns spheres during vasoconstriction and during subsequent vasodilation suggests that these microspheres measure adequately the arteriolar inflow of the muscularis, submucosa, and mucosa (i.e., villus plus crypt) but, due to series arrangement between the arterioles of the villus and the crypt, cannot measure the arteriolar flow of the villus and crypt separately. The entrapment of 9-microns microspheres in the muscularis, submucosa, crypt, and villus that occurred during vasoconstriction did not change during subsequent vasodilation. This suggests that these microspheres became lodged in the precapillary sphincter or capillary and therefore measured the capillary flow of these layers. Accordingly, the difference between the arteriolar (measured by 15 microns) and the capillary (measured by 9 microns) flow of the muscularis, submucosa, and mucosa may provide an estimate of the noncapillary (shunt) flow of these layers.

A syndrome of acute self-limiting ulcerative esophagitis in young adults probably due to herpes simplex virus.

Five healthy young adults developed an acute self-limiting ulcerative esophagitis. Two had definite evidence of herpes virus being present and a third one had appropriate changes in herpes simplex viral titer. All cases followed a characteristic and similar course consisting of sudden onset of odynophagia, multiple discrete small ulcers in the esophagus and herpetiform lesions elsewhere in the skin or mouth. Although most previous reports of herpes esophagitis indicate that it is an "opportunistic" infection in debilitated hosts, the present report indicates that this infection, in patients who are otherwise well, may occur more frequently than one would have previously suspected. Therefore, herpes simplex virus should be considered as a possible etiological agent in the differential diagnosis in patients presenting with a sudden onset of odynophagia.

Transition from diffuse esophageal spasm to achalasia.

A 19-year-old man first presented with clinical, radiological, and manometric features of diffuse spasm. Within a year his motility disorder progressed to "vigorous" and, finally, classic achalasia. After pneumatic dilatation and subsequent long myotomy, the features of classic achalasia disappeared and he again exhibited radiological and manometric evidence of "vigorous" achalasia. The evolution of this patient's disease provides evidence that diffuse spasm and achalasia are different stages of the same disease and lie at opposite ends of a spectrum of related esophageal motility disorders.

Improvement in esophageal abnormalities in a patient with scleroderma and features of polymyositis.

A patient with clinical features of both scleroderma and polymyositis, including esophageal dysfunction typical of scleroderma is described. Regression of her illness occurred along with manometric improvement in the esophageal dysfunction. Improvement in esophageal abnormalities in scleroderma has not been previously reported.

Herpes simplex ulcerative esophagitis in a healthy subject.

A 20-year old white male developed a self-limited ulcerative esophagitis followed by a transient vesicular skin eruption due to infection by herpes simplex virus Type I (HSV-I). While herpetic esophagitis has been described previously, this case appears to be unique in that there was no concomitant serious delibitating illness or pharmacological immunosuppression. Herpes simplex Type I should be included in the differential diagnosis of unusual esophageal ulceration in otherwise healthy patients.

Atheromatous embolization to the stomach: an unusual cause of gastrointestinal bleeding.

This is a case report of an 80-year-old female with persistent blood loss from what was initially considered to be "hemorrhagic gastritis." Distal gastrectomy showed extensive atheromatous embolism and resultant ischemic lesions of the stomach--the apparent cause of the chronic bleeding. The patient has remained well without further blood loss during a 15-month follow-up period. While a small number of cases of gastric hemorrhage associated with atheromatous embolism have been reported, they all have been diagnosed at autopsy. This case is unusual in that the lesion was successfully delt with by surgical resection of the involved area.

Duodenoscopy in the diagnosis of upper gastrointestinal disease.

Duodenoscopy was undertaken in 143 patients with upper gastrointestinal tract symptoms. There were no complications of the procedure. The duodenum was successfully entered in 98% of attempts, and in 90% of patients the examination was judged to be technically successful. When compared with radiological assessment, the findings at duodenoscopy significantly altered diagnosis and management in 21% of patients. The endoscopic appearance of the non-ulcerated duodenal mucosa could not be consistently correlated with changes found in biopsy tissue obtained under direct vision. Duodenoscopy is a valuable adjunct in the clinical assessment of upper gastrointestinal tract symptoms suspected to be due to pathological changes in the duodenum.