Zollinger-Ellison syndrome peptic ulcers

Less common causes of peptic ulceration include Zollinger-Ellison syndrome (ZES), cancer chemotherapy, radiation, and vascular insufficiency. ZES is caused by a gastrin-producing tumor called a gastrinoma and results in gastric acid hypersecretion. High-dose oral proton pump inhibitor (PPI) therapy is the initial treatment of choice for ZES intermittent intravenous PPI therapy may be required for any patient in whom oral therapy is contraindicated.1... 

Clissold, S. P., Campoli-Richaeds, D. M., Omeprazole. A preliminary review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in peptic ulcer disease and Zollinger-Ellison syndrome, Drugs 1986, 32, 15-47. 

Peptic ulceration occurs as an acute or chronic non-traumatic epithelial breach typically in the gastric or duodenal mucosa, but also in the oesophagus (see above) and occasionally in the small intestine with the Zollinger-Ellison syndrome of gastrin overproduction or with an acid-secreting Meckel s diverticulum. Symptoms overlap with those of non-ulcer dyspepsia and cancer and the diagnostic cornerstone is endoscopy. Biopsy may be necessary to distinguish ulcer from cancer. 

Muscarinic receptor stimulation increases gastrointestinal motility and secretory activity (see p. 29). Cholinergic antagonists, such as hyoscyamine, are used as adjuncts in the management of peptic ulcer disease and Zollinger-Ellison syndrome, particularly in patients... 

Zollinger-Ellison syndrome is characterised by increased levels of the hormone gastrin, causing the stomach to produce excess hydrochloric acid. Often the canse is a tnmonr (gastrinoma) of the duodenum or pancreas. Peptic ulcers occur in almost 95% of patients. 

H2-receptor antagonists are quite effective in some peptic acid disorders (duodenal ulcers, gastric ulcers), whereas their effectiveness in others is less apparent (Zollinger-Ellison syndrome, gastrooesophageal reflux disease) [22]. For such conditions, prolonged and potent reduction of acid secretion caused by H /K -ATPase inhibitors is necessary and results in superiority of omeprazole over H2-receptor antagonists [25, 26]. 

Ranitidine is indicated for therapy of peptic ulcer disease, gastroesophageal reflux disease, pathological hypersecretory conditions (e.g., Zollinger-Ellison syndrome), erosive esophagitis, and adjunctive treatment of acute allergic reactions. 

PER/I prescription event monitoring see epidemiology, peptic ulcer A disease state characterized by ulceration, initially of the mucosa of the alimentary tract, caused by the action of pepsin and hydrochloric acid. It may be in the body of the stomach (gastric ulcer), the duodenum (duodenal ulcer), jejunum Oejunal ulcer especially in Zollinger-Ellison syndrome) or of the oesophagus (oesophageal ulcer ... 

Zollinger-Ellison Syndrome — Cimetidine also blocks acid output in Z-E patients without causing side effects.This use of an -receptor antagonist, shown earlier for metiamide,represents an important advance in the treatment of this peptic ulcer disease condition. 

They are more effective than H2 blockers in peptic ulcer disease (PUD) and are also effective in GERD and Zollinger-Ellison syndrome. 

Tagamet is used to treat Zollinger-Ellison syndrome, a syndrome characterized by hypersecretion of gastric acid and the formation of peptic ulcers. 

Code concluded that the experiments incriminated gastric juice as the factor in the production of peptic ulcer, but only later did he realize that he had produced the experimental equivalent of the Zollinger-Ellison syndrome. Frank Mann was pleased by the results, for up to that time he had not been able to produce experimental ulcers in the duodenum as the result of action of the animal s own gastric juice. 

Recurrent anastomotic ulcers when they occur are usually found on the jejunal side of the anastomosis (Fig. 5.8a). In patients who present with persistent or complex duodenal or anastomotic ulcer, especially if associated with diarrhoea, weight loss, and liver metastasis, Zollinger-Ellison syndrome should be suspected. The syndrome consists of recurrent intractable peptic ulcers caused by hypergastrinae-mia produced by gastrin-secreting tumours of the pancreas (75%) or duodenum (15%) (Hirschowitz 1997). Tumour localisation is critical to aid in the identification of patients with potentially respectable disease (Berg and Wolfe 1991). Twenty percent of patients have multiple endocrine neoplasia type I which includes parathyroid, pituitary, and adrenal tumours. 

Further correlations between gastroduodenal ulceration and other related conditions noted the association of pancreatic tumors with peptic ulceration. The further elucidation of the neuroendocrine tumor source of gastrin and the consequences of acid hypersecretion led to the resolution of this relationship by Zollinger and Ellison. They identified the existence of a syndrome of pancreatic neuroendocrine tumors associated with a peptic ulcer diathesis. Similar observations in conditions such as basophil leukemia and mastocytosis noted the excessive production of histamine with consequent acid hypersecretion and peptic ulcer disease in such patients. 

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