Zollinger-Ellison syndrome: presentation, response to therapy, and outcome.

Background: Recent series describing the clinical presentation, response to therapy, and long-term outcome of Zollinger-Ellison syndrome are limited.

Aims: To assess the clinical characteristics and long-term outcome of patients with Zollinger-Ellison syndrome.

Methods: Over a 20-year period, patients with Zollinger-Ellison syndrome were enrolled in a prospective trial evaluating the efficacy of lansoprazole.

Presentation, response to lansoprazole therapy, and outcome of Zollinger-Ellison syndrome-like gastric acid hypersecretors.

Objective: To evaluate the clinical characteristics, response to treatment and outcome of Zollinger?Ellison syndrome (ZES)-like gastric acid hypersecretors.

Methods: Over a 20-year period, patients with gastric acid hypersecretion in the absence of ZES were enrolled in an open label prospective trial evaluating the efficacy of lansoprazole. Following baseline evaluations, patients were treated with escalating doses of lansoprazole based on the results of gastric acid analysis.

Costs and risks in the management of patients with gastric acid hypersecretion.

Goals: To define both risks and costs of optimal care of patients with gastric acid hypersecretion.

Background: The management of Zollinger-Ellison syndrome and other gastric acid hypersecretory disorders remains challenging. The optimal strategy for follow-up including gastric acid analysis, laboratory studies, and endoscopy is unknown but important given the potential complications from uncontrolled acid secretion.

Treatment strategies for Zollinger-Ellison syndrome.

Background: Zollinger-Ellison syndrome (ZES) is a rare disorder caused by tumor secretion of the hormone gastrin, which results in gastric acid hypersecretion and secondarily complicated peptic ulcer and diarrhea. Until the development of H(2)-receptor antagonists and later proton pump inhibitors (PPIs), the disease was virulent, often associated with ulcer-related mortality, and the mainstay of treatment was total gastrectomy.

Objective: To evaluate current approaches to diagnosis and therapy, focusing on the role of PPIs.

Absence of gastrointestinal infections in a cohort of patients with Zollinger-Ellison syndrome and other acid hypersecretors receiving long-term acid suppression with lansoprazole.

Background: The relationship between proton pump inhibitor therapy and other acid suppressing medications and the risk of gastrointestinal infections remains controversial.

Methods: Patients enrolled in a long-term trial of lansoprazole for Zollinger-Ellison syndrome and other acid hypersecretory states had interval histories taken every six months regarding hospitalizations or other intercurrent medical conditions. All medications taken were also reviewed at each visit.

Vitamin B12 deficiency in hypersecretors during long-term acid suppression with proton pump inhibitors.

Background: Proton pump inhibitors (PPIs) may cause cyanocobalamin (vitamin B12) malabsorption, but measuring serum B12 alone may underestimate the prevalence. However, B12 deficiency elevates methylmalonic acid and homocysteine, both additional markers of B12 deficiency.

Aim: To determine the true prevalence of B12 deficiency and whether acid suppression by PPI caused it.

Chromogranin A in patients with acid hypersecretion and/or hypergastrinaemia.

Background: Chromogranin has been proposed as a marker for gastrin-dependent enterochromaffin-like cell proliferation.

Aim: To examine this question in three populations: acid hypersecretors with gastrinoma (Zollinger-Ellison), or without gastrinoma (non-Zollinger-Ellison), and also in pernicious anaemia with achlorhydria-caused hypergastrinaemia.

Methods: We measured serum chromogranin, gastrin, gastric secretion and counted and quantified hyperplasia of enterochromaffin-like cells in gastric biopsies from 38 Zollinger-Ellison and 13 non-Zollinger-Ellison patients being treated with lansoprazole, for 5 years (median) and again 2.

Comparison of 13C- urea blood test to 13C-breath test and rapid urease test for the diagnosis of Helicobacter pylori infection.

At present, the available methods to diagnose active H. pylori infection are endoscopy with biopsy for histology, culture, rapid urease tests, 13C or 14C urea breath test, urine antibody and the stool antigen test. The aims of this study were to simplify the 13C urea test by measuring 13C in blood rather than breath, and to evaluate the usefulness of the 13C urea blood test for the diagnosis of H.

Clinical outcome using lansoprazole in acid hypersecretors with and without Zollinger-Ellison syndrome: a 13-year prospective study.

Background & Aims: Unremitting gastric acid and pepsin hypersecretion causes serious persistent and relapsing lesions, but the natural history with medical treatment alone has not been well-defined. The aims of this study were to heal and prevent relapse of acid/peptic lesions during acid suppression and to analyze benefits and risks during long-term lansoprazole treatment.

Methods: Sixty-seven patients (49 with Zollinger-Ellison syndrome [ZES], 18 without), with basal acid output (BAO) >15 mmol/h or >5 mmol/h if post-antrectomy (n = 9, all ZES), were treated with individually optimized doses of lansoprazole (7.

Risk factors for esophagitis in extreme acid hypersecretors with and without Zollinger-Ellison syndrome.

Background & Aims: Whereas severe duodenal ulcer is the hallmark of acid hypersecretion in Zollinger-Ellison syndrome (ZE) and similar states, the esophagus also is at high risk. We quantified the incidence of esophagitis and various risk factors that might contribute to it.

Methods: Sixty-eight acid hypersecretors (basal acid output >15 mmol/h), 50 patients with ZE, and 18 patients without ZE with normal gastrin levels were studied by gastric analysis, serum gastrin levels, and endoscopy.

Atypical and aggressive upper gastrointestinal ulceration associated with aspirin abuse.

Background: Unusual resistance to treatment in 5% to 7% of 1,845 peptic ulcers examined under endoscopy from 1987 to 1996 prompted a search for unusual causes. Although some ulcers were caused by Zollinger-Ellison syndrome (ZES), an atypical clinical course in other patients, especially with those with multiple ulcers, suggested abuse of aspirin.

Study: Patients who did not have ZES were questioned closely regarding aspirin use and were tested for serum salicylate to detect surreptitious abuse.

Minor effects of Helicobacter pylori on gastric secretion and dose of lansoprazole during long-term treatment in ZE and non-ZE acid hypersecretors.

Background: Helicobacter pylori infection may increase or decrease acid secretion and may augment proton pump inhibitor efficacy. Pepsin effects have not been reported. In Zollinger-Ellison syndrome (ZE) specifically, H.

Long-term lansoprazole control of gastric acid and pepsin secretion in ZE and non-ZE hypersecretors: a prospective 10-year study.

Background: The majority of patients with Zollinger-Ellison syndrome require lifelong treatment with proton pump inhibitors.

Aims: To determine the efficacy of lansoprazole control of acid and pepsin secretion over the long term in Zollinger-Ellison syndrome and non-Zollinger-Ellison syndrome hypersecretors.

Methods: Sixty-three hypersecretors (basal acid output > 15 mmol/h), 46 Zollinger-Ellison syndrome and 17 non-Zollinger-Ellison syndrome, with a total history of 15.

Questions regarding future research on aspirin and the gastrointestinal tract.

Despite great proven and potential benefits, aspirin also has adverse side effects on all parts of the gastrointestinal tract including ulceration, bleeding, perforation, and stenosis. Because of widespread and growing use, there is a need to understand and, if possible, prevent the adverse effects of aspirin while maintaining its benefits. This article is part of a report from a consensus meeting in 1999 on nonsteroidal anti-inflammatory drugs, and examines possible mechanisms of each of the risks of normal and low-dose aspirin use including areas of uncertainty.

Helicobacter pylori effects on gastritis, gastrin and enterochromaffin-like cells in Zollinger-Ellison syndrome and non-Zollinger-Ellison syndrome acid hypersecretors treated long-term with lansoprazole.

Background: Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor.

Aims: To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger-Ellison syndrome) or normal gastrin (non-Zollinger-Ellison syndrome) before and during long-term treatment with lansoprazole.

Pepsin and the esophagus.

Esophagitis results from excessive exposure of the esophagus to gastric juice through an ineffective or dysfunctional lower esophageal sphincter mechanism. A possible role of pepsin in damaging the esophageal mucosa with consequent esophagitis may be examined directly by testing pepsin under various conditions in experimental models of esophagitis. Since gastric juice contains both acid and pepsin, all experiments examine separately effects of perfusion of the esophagus by acid without and with pepsin in various combinations.

Study of outcome after targeted intervention for peptic ulcer resistant to acid suppression therapy.

Objective: Different factors might affect outcome in ulcers resistant to antisecretory therapy. The aim of the study was to define the odds of resistant ulcers being associated with NSAID use, and/or Helicobacter pylori (H. pylori) infection, or neither.

Minimizing the risk of NSAID-induced GI bleeding.

Although nonsteroidal anti-inflammatory drugs (NSAIDs) have definite indications and can offer relief for many conditions, many patients have severe gastrointestinal problems after taking them. Physicians should prescribe these drugs more selectively and advise patients to limit their use of over-the-counter NSAIDs. For patients at high risk who need an NSAID, a prophylactic drug or a cyclooxygenase 2-selective NSAID can decrease the risk.

Association of obesity with hiatal hernia and esophagitis.

Objective: Although weight loss is commonly recommended for symptoms of gastroesophageal reflux, a relationship between excessive body weight and esophageal reflux has not been established. The aim of this study was to determine whether obesity is associated with the presence of a hiatal hernia (HH) and/or an endoscopic diagnosis of esophagitis.

Methods: Retrospective case control studies were done using 1389 patients who underwent gastric analysis and upper GI endoscopy between 1974 and 1995.

Clinical aspects of ECL-cell abnormalities.

ECL cell hyperplasia results from hypergastrinemia, and in man this occurs due to achlorhydria in atrophic gastritis (pernicious anemia [PA]) and gastrinoma (Zollinger-Ellison syndrome [ZES]). Progression to neoplasia, i.e.

Toxicity of NSAIDs in the stomach and duodenum.

NSAIDs are widely used for analgesic, anti-inflammatory and anti-thrombotic indications. Such use carries the risk of gastrointestinal complications (1% over 6 months) which NSAIDs may promote from both ulcerous and nonulcerous lesions. Symptoms are poor predictors of serious lesions and complications, which may occur without previous symptoms.