Colorectal cancer in inflammatory bowel disease: molecular and clinical features.

The two forms of inflammatory bowel disease (IBD), Crohn's disease and ulcerative colitis, are characterized by chronic and relapsing inflammation of the intestines. Initiating events presumably occur well before patients are symptomatic. Evidence gathered over the past decade from both IBD patients and animal models of intestinal inflammation have confirmed that IBD represents complex heterogenic forms of diseases, influenced by a combination of environmental, genetic, and immunologic factors working in concert to produce exaggerated immune responses, resulting in chronic and remitting inflammation.

Consultant strategies for the gastroenterologist.

Effective communication skills and the ability to respond to the needs of referring physicians are critical for the maintenance and enhancement of a referral base. One challenge is to determine the reason for the consultation and to respond to the referring physician's interests. The consultation letter should be formatted effectively and the "turn-around time" should be as brief as possible, perhaps by fax as well as mail.

Clinical intestinal gas syndromes.

Belching, flatulence, abdominal distention, and gas pains are common symptoms that may stimulate concern for the patient and from the physician. An understanding of the pathophysiology of intestinal gas syndromes should permit a more focused diagnostic and therapeutic approach.

Pharmacologic therapy for inflammatory bowel disease.

The pharmacologic management of ulcerative colitis and Crohn's disease is usually carried out in a stepwise fashion. Initially, oral sulfasalazine or 5-aminosalicylic acid (5-ASA) products are given and, for patients with rectal disease, treatment may include topical therapy with either 5-ASA enemas or hydrocortisone suppositories. Patients with more active inflammatory disorders may also require oral corticosteroid therapy.

Gastrin's trophic effect in the colon: identification of a signaling pathway mediated by protein kinase C.

In previous studies we have reported that gastrin exerts a trophic effect on rat colonic epithelial cells in vitro. The effect of gastrin appeared to be mediated through a protein kinase C mechanism. In this study, we have characterized the role of protein kinase C in the gastrin-induced stimulation.

Management of NSAID-induced ulcer disease.

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased risk of gastric and duodenal ulcers, especially in patients with previous ulcer disease, heavy smokers, patients who are taking steroids and those with other illnesses. In patients at risk for gastroduodenal complications, prophylactic therapy with misoprostol or an H2-receptor antagonist should be considered. If ulcers occur during NSAID therapy, the anti-inflammatory drug should be discontinued and standard ulcer-healing therapy instituted.

Azathioprine reduces extravasation and neutrophil trafficking in immune complex-mediated inflammation in the rat colon.

Azathioprine (AZ) has been used in the treatment of refractory inflammatory bowel disease. The mechanism by which AZ decrease colonic inflammation is not known. It is alluded that AZ may be effective in the maintenance of remission.

Helicobacter pylori: aggressor or innocent bystander?

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries.

Gastrin induction of mRNA expression in rat colonic epithelium in vitro.

A newly developed system of isolated rat colonic epithelial cells was utilized for a comprehensive study of protein synthesis influenced by gastrin. We found that synthetic human gastrin (0.01-100 nM) increased the incorporation of [35S]methionine into proteins within 2 hours.

Challenges in acid/peptic disorders: a symposium overview.

Before 1977, the treatment of peptic ulcer disease consisted primarily of dietary, antacid, and anticholinergic programmes. There were heated controversies regarding rigid vs. liberal ulcer diets, a variety of antacids and dosing patterns to choose from, and conflicting claims over the benefit of various anticholinergic therapies.

Hydrogen peroxide-induced alterations in prostaglandin secretion in the rat colon in vitro.

Although the specific cause(s) of inflammatory bowel diseases (IBD) has not been identified, one theory suggests ischemia as the early event that occurs in IBD and reperfusion causes sustained release of oxyradicals, leading to inflammation and ulceration. In this study, we have confirmed that H2O2 in the concentration seen during ischemia/reperfusion is primarily responsible for cellular membrane damage in the rat colonic fragments in vitro. Hydrogen peroxide caused a time and dose-dependent increase in 6-keto-PGF1 alpha and TXB2 release.

Omeprazole: a new approach to gastric acid suppression.

Omeprazole, one of a new group of antisecretory drugs, is a substituted benzimidazole that does not exhibit the anticholinergic or histamine H2 antagonistic properties of drugs such as cimetidine. This agent suppresses gastric acid secretion by inhibiting the proton pump mechanism, thereby blocking the final step of acid secretion. Omeprazole is significantly more effective than the histamine H2 receptor antagonists in eliminating acid secretion; thus, it may be beneficial in patients who are resistant to these agents.

Mucoepidermoid (adenosquamous) carcinoma arising in Barrett's esophagus.

A case of mucoepidermoid or adenosquamous carcinoma arising from the mucous epithelium of a Barrett's esophagus is presented. Immunohistologic examination demonstrated carcinoembryonic antigen (CEA) in both the glandular and squamous components, but keratin only in the latter. Although mucoepidermoid carcinoma of the esophagus is believed to arise from submucosal glands, heterotopic gastric surface epithelium may also give rise to this uncommon neoplasm.

Common bile duct obstruction: assessment by transcholecystic cholangiography.

Percutaneous transcholecystic cholangiography was performed in 20 patients. Fifteen patients had normal-sized bile ducts on sonograms and computed tomographic scans, and five had partial common bile duct obstruction. Gallbladder pressures were measured in 14 patients.

The esophagogastric polyp-fold complex.

A polyp-fold complex at the gastroesophageal junction is a rare finding. We made this diagnosis in a 51-year-old man who presented with abdominal discomfort after an episode of protracted vomiting. The esophagogastric polyp-fold complex is not always associated with reflux esophagitis, as was originally proposed.

Development of lymphoma in patients with Crohn disease.

The authors report 3 cases of lymphoma developing in patients with Crohn disease. Neither a cause-and-effect relationship nor a common etiology could be proven.

Bile acid and pancreatic trypsin outputs are parallel during intraduodenal infusion of essential amino acids.

There is disagreement as to whether contraction of the gallbladder occurs simultaneously with secretion of pancreatic enzymes during food ingestion. One study that employed exogenous cholecystokinin (CCK) alone showed dissociation of total bile acids (TBA) and trypsin outputs, while another study that employed exogenous CCK plus secretin showed parallel outputs of TBA and trypsin. Since previous studies have suggested that intraduodenal infusion of essential amino acids (EAA) evokes pancreaticobiliary secretion similar to that observed with food ingestion, we infused increasing doses of EAA intraduodenally in 10 subjects with intact gallbladder and in 10 subjects with previous cholecystectomy and measured total bile acids and trypsin outputs serially.

Gastric and pancreatic function in patients with end-stage renal disease.

Gastroduodenal disease such as peptic ulcer and duodenitis is increased in patients with end-stage renal disease. Gastric hypersecretion of acid proposed as the underlying mechanism has been disputed because peptic ulcer has occurred even in those with normal or low gastric acid secretion. We studied the pancreatic exocrine secretion of bicarbonate (HCO3) and the concentration of plasma pepsinogens in addition to gastric acid secretion in 15 patients on chronic hemodialysis, 10 patients wih previous renal transplantation and compared them with 10 subjects without gastrointestinal or renal disease.