Small intestinal neoplasms.

Small intestinal neoplasms are uncommonly encountered in clinical practice. They may occur sporadically, in association with genetic diseases (e.g., familial adenomatous polyposis coli or Peutz-Jeghers syndrome), or in association with chronic intestinal inflammatory disorders (e.g., Crohn's disease or celiac sprue). Benign small intestinal tumors (e.g., leiomyoma, lipoma, hamartoma, or desmoid tumor) usually are asymptomatic but may present with intussusception. Primary malignancies of the small intestine-including adenocarcinoma, leiomyosarcoma, carcinoid, and lymphoma-may present with intestinal obstruction, jaundice, bleeding, or pain. Extraintestinal neoplasms may involve the intestine via contiguous spread or peritoneal metastasis. Hematogenous metastases to the intestine from an extraintestinal primary are unusual and are most typical of melanoma. Because the small intestine is relatively inaccessible to routine endoscopy, diagnosis of small intestinal neoplasms is often delayed for months after onset of symptoms. When the diagnosis is suspected, enteroclysis is the most useful imaging study. Small bowel endoscopy (enteroscopy) is increasingly widely available and may permit earlier, nonoperative diagnosis.

When to suspect ischemic colitis. Why is this condition so often missed or misdiagnosed?

Ischemic colitis is one of the most often seen disorders of the large intestine in the elderly. Common predisposing factors are atherosclerosis, shock, and congestive heart failure, but often, elderly patients have no obvious predisposing or precipitating factors. The typical clinical presentation is acute sudden abdominal pain and distention with bloody diarrhea. Common early radiographic signs are bowel-wall thickening with thumbprinting, and later, ulceration and strictures may be found. Endoscopy is valuable in revealing the sharp demarcation between viable and necrotic colonic mucosa that is a strong indicator of ischemia. Within 48 hours, most patients show favorable response to conservative measures consisting of intravenous hydration, bowel rest, antibiotic therapy, and correction of precipitating processes. Vasoconstricting drugs and corticosteroids are contraindicated. When surgical intervention is indicated, it usually consists of resection of the ischemic segment and exteriorization of the remaining ends of the bowel.

Protective effects of zinc in indomethacin-induced gastric mucosal injury: evidence for a dual mechanism involving lipid peroxidation and nitric oxide.

BACKGROUND: Indomethacin causes gastric mucosal injury, although the pathogenesis is not fully understood. Zinc, is known to have gastroprotective effects in both humans and experimental animals. AIM: To determine (i) the protective effects of zinc in indomethacin-induced gastric mucosal injury in rats, and (ii) whether these cytoprotective effects are mediated by changes in gastric lipid peroxidation and/or nitric oxide synthase activity. METHODS: Gastric lesions were induced in rats by the intragastric administration of indomethacin. Morphological changes, lipid peroxidation (malondialdehyde levels) and nitric oxide synthase activity were determined in animals pre-treated with zinc sulphate and in controls. RESULTS: Indomethacin significantly increased malondialdehyde levels and decreased NOS activity. These effects were attenuated by pre-treatment with zinc (P < 0.005 and 0.0001, respectively). The protective effects of zinc were readily abolished in animals pre-treated with N-nitro-L-arginine methyl ester (L-NAME). Morphologically, indomethacin induced large areas of mucosal ulcerations, which were completely prevented by zinc pre-treatment. CONCLUSIONS: Zinc provides protection against indomethacin-induced gastric mucosal injury. These protective effects result from the inhibition of lipid peroxidation and the preservation of mucosal nitric oxide synthase.

Effects of fructose-1,6-diphosphate on the activity of rat liver nitric oxide synthase in vitro.

Fructose-1,6-diphosphate (FDP) was found to cause significant stimulation of nitric oxide synthase (NOS) in rat liver homogenates in vitro. This effect was more pronounced for the inducible isoform than its constitutive counterpart. Furthermore, FDP restored rat liver inducible NOS levels following their depletion by carbon tetrachloride (CCl4). This finding may have further practical implications in hepatoprotection from various noxious chemical and biological agents.

Multiple synchronous primaries of the gastrointestinal tract: a molecular case report.

Six synchronous gastrointestinal primaries were identified in a 70 year old male with no known cancer predisposition syndrome or recognized risk factors except alcohol abuse. These specimens appeared to be independent and unrelated by gross and histopathological examination. In order to further evaluate the six tumors, we analyzed selected DNA sequences for alterations in the K-ras oncogene and p53 tumor suppressor gene. In addition, three loci were analyzed to determine microsatellite instability. Using the polymerase chain reaction, single stranded conformational polymorphism, and DNA sequencing, we demonstrated that each primary manifests genetic characteristics typical of the tissue of origin. In addition, one primary, a moderately differentiated colon adenocarcinoma, exhibited mutations not detected in the other specimens. This study suggests that these synchronous primaries arose independently and progressed along different carcinogenic pathways.

Gastric cancer and pernicious anemia appearing as pseudoachalasia.

An elderly black man was admitted to our institution with macrocytic anemia, dysphagia, and significant weight loss. Results of an esophagogram were suggestive of achalasia. Gastric adenocarcinoma infiltrating the gastric cardia was seen on gastroscopy. The mode of presentation of gastric cancer in this case has not been previously reported in association with pernicious anemia. Patients with pernicious anemia are at higher risk of having gastrointestinal neoplasms than is the general population. We review the current literature and address the controversy concerning the need to subject patients with pernicious anemia to surveillance with upper gastrointestinal endoscopy.

Activity of gastric mucosal nitric oxide synthase in portal hypertensive gastropathy.

OBJECTIVE: The importance of portal hypertensive gastropathy, as a potentially bleeding lesion in cirrhotics with portal hypertension, has recently been appreciated. Histologically, dilation of the mucosal and submucosal vessels of the stomach is noted in this entity. The possibility of nitric oxide acting as a mediator for this mucosal vascular dilation has not been explored. METHODS: We determined, in a group of 10 male cirrhotic patients with esophageal varices and endoscopic changes consistent with severe portal hypertensive gastropathy (Group A), the gastric mucosal nitric oxide synthase activity. This was determined by measuring the rate of conversion of [3H]-arginine to [3H]-citrulline. Serum levels of nitrates and nitrites, the end products of nitric oxide, were also measured. The results were compared with those of a group of 10 male controls with no liver disease (Group B). RESULTS: Gastric mucosal constitutive and inducible nitric oxide synthase levels were significantly higher in group A (125.4 +/- 4.3 and 259.7 +/- 5.5 pmol/mg protein/minute, respectively) than in group B (88 +/- 8.6 and 130.8 +/- 6.6 pmol/mg protein/minute, respectively) ( p < 0.002 and < 0.0001, respectively). Serum nitrate/nitrite levels were 30.1 +/- 3.2 nmol/ml in group A and 15.5 +/- 0.09 nmol/ml in group B (p < 0.001). CONCLUSIONS: We conclude that the significantly increased gastric mucosal nitric oxide synthase activity, in patients with portal hypertensive gastropathy, suggests an important role for nitric oxide in the pathogenesis of this mucosal lesion.

Colonic ganglioneuroma presenting as filiform polyposis.

A 74-year-old man had an isolated colonic ganglioneuroma presenting endoscopically as filiform polyposis coli. Extensive workup failed to show either von Recklinghausen's neurofibromatosis or multiple endocrine neoplasia (MEN) 2b. We discuss the clinical implications of this and review the literature.

Eosinophilic gastro-enteritis associated with protein-losing enteropathy and protein C deficiency.

Reported below is a case of eosinophilic gastro-enteritis involving the colon, stomach and duodenum in a patient who was also found to have marked hypoalbuminaemia and protein C deficiency due to severe protein-losing enteropathy. The most recent literature is reviewed and the challenging differential diagnosis of the disease is discussed.

Biliary complications of Fasciola hepatica: the role of endoscopic retrograde cholangiography in management.

The parasite Fasciola hepatica resides in the biliary tree but rarely causes significant clinical sequelae. In this report, we review our experience with four patients in whom F. hepatica infection resulted in biliary complications, especially severe biliary colic and jaundice. The diagnosis was achieved with endoscopic retrograde cholangiography which demonstrated the worms in the extrahepatic bile ducts. Endoscopic sphincterotomy was performed uneventfully in all patients allowing balloon extraction of the parasites and resolution of their symptoms.

Serum gastrin levels in patients with colorectal cancer and adenomatous polyps: a prospective study.

Serum gastrin levels were measured by radioimmunoassay in 62 patients with colorectal neoplasms (40 with adenomatous polyps and 22 with cancer) and 40 controls. Fasting serum gastrin in both the polyp (73.93 +/- 6.5 pg/ml) and the cancer (99 +/- 19.7 pg/ml) groups was significantly higher than those of the control group (42.65 +/- 2.2 pg/ml). These findings suggest that hypergastrinemia may be an etiologic factor in colorectal neoplasia.

Case reports: pseudomelanosis duodeni: association with systemic hypertension.

Two male patients with mild gastrointestinal bleeding had peculiar dark pigmentation of their duodenum on upper endoscopy. These pigmented lesions were still present 3 months after the original endoscopy and after resolution of all other mucosal lesions. Both patients had other medical problems, including hypertension. They have been on multiple antihypertensive medications for many years. Biopsies of these duodenal lesions showed the pigment to be present inside the macrophages found in the lamina propria and in between the epithelial cells. Electron microscopy revealed a lysosomal localization of this pigment. This melanin-like pigment proved to contain varying amounts of iron, sulfur, and calcium. This pigmentation is closely associated with systemic hypertension, even in the pediatric population.

Syndrome of inappropriate ADH secretion and diplopia: oat cell (small cell) rectal carcinoma metastatic to the central nervous system.

Extrapulmonary small cell carcinoma is being increasingly recognized as a distinct clinical entity. We report a patient with small cell carcinoma of the rectum metastatic to the brain, presenting with diplopia and inappropriate antidiuretic hormone syndrome.

Experimental autoimmune hepatitis in mice following immunization with syngeneic liver proteins.

In this study, we describe the successful induction of experimental autoimmune hepatitis by immunizing inbred strains of mice with syngeneic liver antigens. Hepatic lesions, presumably based on autoimmune mechanisms, induced after 3 weekly immunizations were of only moderate degree. Of the various mouse strains used, C57BL/6 mice showed the most prominent histological changes of the liver, which were accompanied by elevated serum alanine aminotransferase levels. This system offers a potential model for further investigating experimental autoimmune hepatitis.