Malignant small-bowel neoplasms: spectrum of disease on MR imaging.

Malignant neoplasms of the small bowel are among the rarest types of cancer, accounting for only 2% of all gastrointestinal neoplasms. Owing both to the intrinsic difficulty of common radiographic and endoscopic methods in visualising the entire small bowel and the lack of typical physical findings, a delay in diagnosis is common. Recently, magnetic resonance (MR) imaging has become a widely accepted imaging modality in the study of suspected small-bowel neoplasms due to its ability to depict, without exposure to ionising radiation and with excellent soft-tissue contrast, intraluminal disorders in conjunction with mural, extraparietal and regional abnormalities. The aim of this pictorial review is to illustrate the MR appearance of malignant small-bowel neoplasms.

[Control using omeprazole in a case of upper digestive hemorrhage, induced by erosive uremic hemorrhagic gastritis resistant to conventional therapy]. / Controllo mediante omeprazolo di un caso di emorragia digestiva superiore, indotta da gastrite erosiva emorragica uremica resistente alla terapia convenzionale.

Erosive and/or ulcerative lesions of the digestive tract often complicate chronic renal failure. These lesions usually cause only chronic bleeding. In the rare cases of massive digestive bleeding, conventional therapy is frequently unsatisfactory. A case of massive bleeding, due to anti-H2 therapy resistant erosive haemorrhagic uremic gastritis is reported, where repeated transfusions failed to correct a marked anaemia (Hb = 0.8 g/dl). Considerable improvement of the endoscopy, clinical and hemato-biochemical pictures was achieved with 40 mg/day omeprazole. Three-months follow-up confirmed the efficacy and safety of the drug.

Effect of omeprazole on gastroesophageal reflux in Barrett's esophagus.

Pattern of gastric and esophageal acidity were evaluated in 14 patients with endoscopically and histologically proven Barrett's esophagus, in 46 with slight-to-moderate esophagitis, and in 22 healthy subjects. In patients with Barrett's esophagus, LES pressure was considerably lower and percentage exposure to acid was considerably higher than in either patients with esophagitis or controls (p less than 0.001). Percentage of time with esophageal pH below 4 was 33.2% in patients with Barrett's esophagus, 14% in patients with slight-to-moderate esophagitis (p less than 0.001), and 3.4% in controls (p less than 0.001). In patients with Barrett's esophagus, the esophageal exposure to acid was similar in upright and supine positions, and the number of refluxes that lasted longer than 5 min was also greater in these patients than in uncomplicated esophagitis or controls (p less than 0.001). Accordingly, their acid-clearing capacity was markedly reduced (p less than 0.001 vs. control). Omeprazole 20 mg, given once daily, reduced both percentage of time with pH below 4 (p less than 0.001) and the number of episodes longer than 5 min (p less than 0.001), but had no effect on acid clearance. In patients with Barrett's esophagus, omeprazole lowered intragastric acidity by 77.8% (p less than 0.001). Median intragastric pH was 1.9 (1.7-2.1) pretreatment, and 4.5 (4.2-5) during omeprazole (p less than 0.001).

Comparison of faecal blood loss, upper gastrointestinal mucosal integrity and symptoms after piroxicam beta-cyclodextrin, piroxicam and placebo administration.

In order to evaluate the gastric tolerance of the new piroxicam formulation CHF 1194 (piroxicam complexed with beta-cyclodextrin), a double-blind randomized trial was carried out in 21 young healthy volunteers comparing CHF 1194 with piroxicam and placebo. Faecal blood loss measurement by the Cr-51 labelled red blood cell technique, upper gastrointestinal endoscopic evaluation, titration of gastric pH and gastric biopsies before, during and after treatment were used to assess drug tolerability. Four out of 7 volunteers in the piroxicam-treated group withdrew because of severe gastrointestinal symptoms and oesophageal and/or gastroduodenal lesions, while all subjects treated with CHF 1194 or placebo completed the treatment. There was a significant difference between the endoscopic scores of the piroxicam and placebo groups, whereas no differences were found between CHF 1194 and placebo, nor between piroxicam and CHF 1194. Daily mean gastrointestinal blood loss was greater in the piroxicam group than in either the CHF 1194 or placebo groups, but the difference was not significant, due to the small number of piroxicam-treated subjects who completed the study. When administered for a short period to healthy young subjects, CHF 1194 caused less gastric damage and was better tolerated than piroxicam.

Do anticholinergics interact with histamine H2 receptor antagonists on night intragastric acidity in active duodenal ulcer patients?

The effect of administering low doses of famotidine or ranitidine alone or in combination with an M1-receptor-selective antagonist, pirenzepine, on night intragastric acidity was evaluated in 16 active duodenal ulcer patients to verify 1) whether anticholinergics and H2-antagonists have a synergic effect on inhibition of night gastric acidity, and 2) whether patients with vagal hypertone are more sensitive to anticholinergics than the remainder of the duodenal ulcer population. The endogastric pH was continuously recorded for 12 h (8 PM-8 AM) after random, single-blind administration of one of the following drug regimens: 20 mg famotidine, 150 mg ranitidine, 50 mg pirenzepine, 20 mg famotidine plus 50 mg pirenzepine, and 150 mg ranitidine plus 50 mg pirenzepine. Six patients with a basal acid output:peak acid output BAO:PAO greater than 0.3 were considered "vagal hypertone" subjects. Night gastric acidity inhibition was -39.6% with pirenzepine (p less than 0.001) and -73.7% and -71.5% with famotidine or ranitidine (p less than 0.001 vs. pirenzepine). The simultaneous administration of pirenzepine with famotidine or ranitidine provoked only a slight, insignificant increase in percent suppression, 5.1% and 6.3%, respectively, and did not modify either the time lag to onset of anti-H2 action or the duration of action. Patients with a BAO:PAO greater than 0.3 were not more sensitive to anticholinergic treatment than other duodenal ulcer patients. Our study furnishes evidence that combined administration of anti-H2 and anticholinergics is not significantly better than anti-H2 alone, in active duodenal ulcer patients.

Colonic mass movements in idiopathic chronic constipation.

As relatively little is known of human colonic motor activity either in health, or in pathological conditions, we investigated mass movements in 14 chronically constipated patients and 18 healthy volunteers. Mass movements were recorded from proximal and distal colon during 24 h (12 noon-12 noon) by a colonoscopically positioned multilumen manometric probe and low compliance infusion system. Patients and controls differed significantly in the number (mean 2.6 (0.7) v 6.1 (0.9) (SE), p = 0.02) and duration (mean 8.2 (1.6) v 14.1 (0.8) s, p = 0.04) of mass movements. The data suggest that one pathophysiological mechanism of constipation may be decreased propulsive activity. A circadian pattern, with a significant difference between day and night distribution, was documented in both groups. The patients reported decreased defecatory stimulus concomitant with the mass movements.

Functional dyspepsia and chronic idiopathic gastric stasis. Role of endogenous opiates.

Chronic idiopathic gastric stasis can be responsible for unexplained dyspepsia. Because exogenous opiates inhibit gastric emptying and endogenouslike substances are present in the gastrointestinal tract, we tested the hypothesis that increased endogenous opiate activity may be responsible for chronic idiopathic gastric stasis. Eighteen patients with chronic idiopathic gastric stasis and ten healthy volunteers were studied by gastrointestinal manometry. Scintigraphic technique also was used, during which either intravenous saline or naloxone hydrochloride were infused. Manometry showed gastric hypomotility in ten patients and duodenal hyperdyskinesia in the remaining eight patients. Naloxone did not alter gastric emptying in healthy subjects or corrected gastric stasis in patients with gastric hypomotility, while it normalized gastric emptying in patients with duodenal dyskinesia. It seems that either gastroparesis or duodenal dyskinesia can promote gastric stasis and chronic dyspepsia, and endogenous opiates participate in the pathogenesis of gastric stasis in patients with duodenal dyskinesia.

Nifedipine reduces the colonic motor response to eating in patients with the irritable colon syndrome.

Patients with the irritable colon syndrome have an exaggerated and/or prolonged colonic motor response to eating. This is believed to be the cause of their postprandial complaints. Since the flux of calcium ions across cell membranes plays a major role in the contractions of the gastrointestinal smooth muscle, we investigated the effect of nifedipine, a calcium channel blocker, on the gastrocolonic response in nine patients with the irritable colon syndrome. Colonic myoelectric and contractile activity was recorded during fasting and after a 1000-cal mixed meal, either with or without nifedipine (20 mg sublingually) administration. Nifedipine reduced the postprandial increase of both spike potential activity and motility index. This effect of acute administration of the drug provides rational support to test nifedipine in clinical trials as a possible means for treating the irritable colon syndrome.

The relationship between aminopyrine breath test and severity of liver disease in cirrhosis.

Twenty-two patients with cirrhosis were evaluated by the 2 hr.-(C14)-aminopyrine breath test, the conventional liver tests and two systems for grading the severity of liver disease. Twenty-three patients with noncirrhotic liver disease and 15 controls were also studied. Reduced 14CO2 values were found in 21 of the 22 cirrhotic patients and seven of those had noncirrhotic liver disease associated with severe functional reserve impairment. The values in patients with minor liver diseases or cholestasis were normal. In the cirrhotic patients 2 hr.-(C14)-aminopyrine breath test scores correlated with prothrombin time, retention of bromosulfalein, fasting serum bile acid, albumin, bilirubin, serum aspartate aminotransferase and, above all, with the scores of the two clinical rating systems. The 2 hr.-(C14)-aminopyrine breath test was superior to conventional tests in quantifying the degree of hepatic functional reserve and forecasting the prognosis.