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Biomedical subjects

B I Hirschowitz

Publications and source records attributed to B I Hirschowitz.

At least 37 records · Page 2Linked to original sources
PubMed1996

Long-term treatment with lansoprazole for patients with Zollinger-Ellison syndrome.

BACKGROUND: Normalization of gastric secretion and cure of associated upper gastrointestinal lesions by resection of gastrinoma is possible in approximately 20% of patients with Zollinger-Ellison syndrome, leaving approximately 80% dependent on medical treatment with proton pump inhibitors for acid suppression. METHODS: Lansoprazole was given for 3-48 months (median 28 months) to 26 Zollinger-Ellison syndrome patients with peptic ulcer manifestations in all and oesophagitis in 13. Starting with 60 mg/day. the dose was individualized to lower basal acid output to less than 5 mmol/h for those with intact stomachs and less than 1 mmol/h in those who had prior gastrectomy or with oesophagitis. The patients were studied every 3 months for 1 year and then every 6 months with gastric analysis (basal and maximal acid and pepsin output) and endoscopy with biopsy for enterochromaffin-like (ECL) cells. RESULTS: Lansoprazole inhibited basal acid output by 95%, pepsin output by 65% and remained effective at the initial mean (66 +/- 4.3 mg/day) or smaller doses (56 +/- 12 mg/day) at 48 months. Mucosal lesions healed and symptoms (ulcer-type pain, diarrhoea, heartburn, weight loss) resolved rapidly, usually within a few weeks. Serum gastrin and ECL cell populations, which were elevated before treatment, remained statistically unchanged but one of the three multiple endocrine neoplasia I (MEN-I) patients developed a small carcinoid. Of the three patients with metastatic gastrinoma at diagnosis one has died and one has progressed, while the third has had stable liver metastases for 26 years. Ulcer-type relapses occurred in three of the five post-gastrectomy patients, one with fatal jejunal ulcer perforation despite adequate acid suppression. No biochemical or clinical adverse events due to lansoprazole were encountered. CONCLUSION: Lansoprazole effectively inhibits acid and pepsin secretion in Zollinger-Ellison syndrome patients without any demonstrated side-effects. Despite strict acid control, post-gastrectomy Zollinger-Ellison syndrome patients were more liable to ulcer relapse, while oesophagitis was not a marker for therapeutic difficulty.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Long-term treatment with lansoprazole of patients with duodenal ulcer and basal acid output of more than 15 mmol/h.

BACKGROUND: About 10% of patients with duodenal ulcers have marked gastric acid hypersecretion with basal acid output (BAO) of more than 15 mmol/h, which is in the range found in Zollinger-Ellison syndrome. PATIENTS AND STUDY DESIGN: We report long-term, up to 4 years, prospective treatment using lansoprazole in nine male patients with duodenal ulcers and a BAO of more than 15 mmol/h whose results are compared with those in 10 male Zollinger-Ellison syndrome patients with intact stomachs reported in detail in an accompanying paper. RESULTS: All 19 subjects, except one Zollinger-Ellison syndrome patient who had gastric and oesophageal ulcers, had a history of duodenal ulcers; 22% of those with gastric acid hypersecretion had oesophagitis compared with 60% of those with Zollinger-Ellison syndrome. Each subject had the dose of lansoprazole adjusted to give a BAO of less than 5 mmol/h. At 3-month intervals to 1 year, and then at 6-monthly intervals, basal and pentagastrin stimulated secretions were studied, in addition to gastroscopy with biopsy for gastric mucosal morphology. Basal and maximal acid and pepsin secretions were not different between gastric acid hypersecretion and Zollinger-Ellison syndrome patients before treatment. During treatment, BAO was reduced by over 90% to less than 2 mmol/h, while peak acid output was reduced by 70% in those with gastric acid hypersecretion and 90% in Zollinger-Ellison syndrome patients. Four gastric acid hypersecretion patients had relapses during treatment, three times in one patient and twice in another patient, but all responded to continued treatment with lansoprazole. Of the seven ulcer-related relapses in the gastric acid hypersecretion patients, four occurred with a BAO of less than 2 mmol/h and three with a BAO of 7.1-7.3 mmol/h; five of the seven relapses occurred in the absence of Helicobacter pylori. Lansoprazole remained effective at an average dose of approximately 70 mg/day, without causing any side-effects. CONCLUSION: Lansoprazole is apparently safe and effective for treating hypersecretion, whether due to hypergastrinaemia (Zollinger-Ellison syndrome) or not (non-Zollinger-Ellison syndrome hypersecretors).

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Reversible prolonged skin bleeding time in acute gastrointestinal bleeding presumed due to NSAIDs.

The purpose of this research was to look for a possible mechanism whereby NSAIDs, and particularly ASA, might cause gastrointestinal bleeding. A total of 34 hospitalized GI bleeders and 29 age- and sex-matched controls were studied. Skin bleeding time (SBT) was measured within 6 h of coming to hospital and before any blood products were given. All patients and controls were questioned regarding current NSAID use. This history was supplemented by estimation of serum salicylate and of platelet cyclooxygenase activity to detect unreported current aspirin (ASA) use. Various aspects of platelet function were also tested by lumiaggregation in 28 controls and, after recovery, in 27 of the bleeders. Of 34 bleeders, 26 bled from the upper GI tract, (13 from peptic ulcer) and eight from the lower GI tract, 30 (88%) had a current intake of NSAIDs and of these 22 (73%) used ASA, some in combination with other NSAIDs, whereas 12 of 29 controls were using NSAID's, 11 of which were ASA. SBT in the bleeders was 9.0 +/- 1.02 min versus 4.8 +/- 0.42 min in the controls (p < 0.001). SBT measured 6.6 days later in 28 bleeders was 4.7 +/- 0.22 min (p < 0.0006), and of those tested after recovery all but one had fallen to 6.5 min or less. None had any residual constitutional platelet abnormalities as tested by lumiaggregation. By logistic regression, NSAID intake was strongly associated with prolonged SBT to > 6 min (odds ratio [OR], 16.7; p < 0.0002), whereas NSAID intake (OR 14.6; p < 0.0003) and SBT > 6 min (OR 1.8; p < 0.005) contributed to a bleeding outcome. Almost 90% of GI bleeders had recently consumed NSAIDs, mostly ASA, on an average 15 h before onset of bleeding. Although most of the nonbleeders who had used NSAIDs did not have a prolonged SBT, most of the bleeders who used NSAIDs had an abnormal elevation of SBT, suggesting a possible mechanism for GI bleeding. Retesting approximately 7 days after recovery from bleeding showed normalization of the SBT, indicating that the defect was transient and spontaneously reversible.

Acute Disease↗
PubMed1996

Nonsteroidal anti-inflammatory drugs and the gut.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for analgesic, anti-inflammatory, and antithrombotic indications. Such use carries the risk of significant side effects on nontarget organs, especially the gut. Some of these effects may be serious, especially among the elderly, whose NSAID use is proportionately greatest. Upper gastrointestinal mucosal lesions range from trivial (petechiae and superficial erosions) to significant and potentially serious (chronic peptic ulcers, esophagitis, and small and large gut ulcers). The most serious side effects are perforation of peptic or gut ulcers and gastrointestinal bleeding, which NSAIDs may promote from both ulcerous and nonulcerous lesions of both the upper and lower gastrointestinal tract, ie, both acid-dependent and non-acid-dependent. Symptoms may be independent of observable lesions, and serious lesions may occur without previous symptoms. NSAIDs may also delay healing of peptic ulcers, even to the extent of intractability, and may cause recurrence after gastric surgery. Until we can separate the mechanisms whereby NSAIDs both cause injury and provide therapeutic benefits, the problem of side effects and their prevention or treatment remains unresolvable.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Aspirin related gastrointestinal bleeders have an exaggerated bleeding time response due to aspirin use.

BACKGROUND: Gastrointestinal bleeding is related to non-steroidal anti-inflammatory drug (NSAID) use, especially aspirin, but only a small subset of users bleed. AIM: To look for risk factors or mechanisms whereby aspirin may promote gastrointestinal bleeding. PATIENTS: Sixty one patients with previous aspirin related upper gastrointestinal bleeding and 61 matched controls. METHODS: Patients and controls were given 375 mg of aspirin and sequential skin bleeding time and blood aspirin levels were measured. Additional studies included platelet lumiaggregation, von Willebrand factor, Factor VIII, and coagulation studies. RESULTS: Baseline skin bleeding time was similar in bleeders and controls, but bleeders had a more prolonged skin bleeding time after aspirin use. Hyper-response was more frequent in bleeders (30% v 9.3%; p < 0.01) and was associated with more than one previous separate bleeding event and a lower packed cell volume during the preceding bleeding episode. No differences were found in other factors studied. Logistic regression analysis identified prolonged skin bleeding time after aspirin use as an independent factor contributing to aspirin related gastrointestinal bleeding (RR = 5.4; 95% CI: 1.8 to 17.1). CONCLUSIONS: 30% of patients with a history of aspirin related gastrointestinal bleeding have an exaggerated prolongation of skin bleeding time in response to aspirin, which may be a risk factor for bleeding. This intrinsic defect or to subclinical von Willebrand disease or different aspirin metabolism.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Pharmacological aspects of acid secretion.

The secretion of gastric acid is regulated both centrally and peripherally. The finding that H2-receptor antagonists are able to reduce or abolish acid secretion due to vagal, gastrinergic, and histaminergic stimulation shows that histamine plays a pivotal role in stimulation of the parietal cell. In the rat, the fundic histamine is released from the ECL cell, in response to gastrin, acetylcholine, or epinephrine, and histamine release is inhibited by somatostatin or by the H3-receptor ligand, R-alpha-methyl histamine. The parietal cell has a muscarinic, M3, receptor responsible for [Ca]i regulation. Blockade of muscarinic receptors by atropine can be as effective as H2-receptor blockade in controlling acid secretion. However, general effects on muscarinic receptors elsewhere produce significant side effects. The different receptor pathways converge to stimulate the gastric H+,K(+)-ATPase, the pump responsible for acid secretion by the stomach. This enzyme is an alpha,beta heterodimer, present in cytoplasmic membrane vesicles of the resting cell and in the canaliculus of the stimulated cell. It has been shown that acid secretion by the pump depends on provision of K+Cl- efflux pathway becoming associated with the pump. As secretion occurs only in the canaliculus, this K+Cl- pathway is activated only when the pump inserts into the canalicular membrane. Transport by the enzyme involves reciprocal conformational changes in the cytoplasmic and extracytoplasmic domain. These result in changes in sidedness and affinity for H3O+ and K+, enabling active H+ for K+ exchange. The acid pump inhibitors of the substituted benzimidazole class, such as omeprazole, are concentrated in the canaliculus of the secreting parietal cell and are activated there to form sulfenamides. The omeprazole sulfenamide, for example, reacts covalently with two cysteines in the extracytoplasmic loops between the fifth and sixth transmembrane and the seventh and eighth transmembrane segments of the alpha subunit of the H+,K(+)-ATPase, forming disulfide derivatives. This inhibits ATP hydrolysis and H+ transport, resulting in effective, long-lasting regulation of acid secretion. Therefore, this class of acid pump inhibitor is significantly more effective and faster acting than the H2 receptor antagonists. K+ competitive antagonists bind to the M1 and M2 transmembrane segments of the alpha subunit of the acid pump and also abolish ATPase activity. These drugs should also be able to reduce acid secretion more effectively than receptor antagonists and provide shorter acting but complete inhibition of acid secretion.

Amino Acid Sequence↗
PubMed1994

Ingestion of aspirin prevents platelet-induced human fibroblast growth. Implications for peptic ulcer healing.

Because aspirin (ASA) may affect peptic ulcer healing through actions on platelets (for example, by inhibiting release of growth factors), human foreskin fibroblast mitogenesis was used for two bioassays (24-h growth with 3H-thymidine incorporation and 5- to 6-day cell proliferation) for serum derived from collagen-aggregated platelet-rich plasma (PRP) or platelet-poor plasma (PPP) or from clotted whole blood (WBS). Blood was taken from five normal subjects before and 6 h after ingestion of ASA. After ASA ingestion serum (WBS or PRP) was less mitogenic (p < 0.01) by both bioassays, whereas PPP serum was not mitogenic either before or after ASA. In vitro, neither ASA nor salicylic acid alone at levels normally found in plasma with ASA use inhibited fibroblast growth. We conclude that ASA ingestion inhibits the mitogenic action of platelets on fibroblast culture by inhibiting the release of putative growth factors. Such an effect might explain the adverse effects of ASA on ulcer healing.

Aspirin↗
PubMed1994

Effects of cholinergic, histaminergic, and peptidergic stimulation on pepsinogen secretion by isolated human peptic cells.

BACKGROUND: Whereas pepsin secretion by the human stomach has been extensively investigated, the characteristics of the peptide cell cannot be fully understood from in vivo studies. We therefore studied isolated human peptic cells to test directly cellular responses to different agents. METHODS: Eight endoscopic biopsy specimens yielded 10(6) cells, > 90% pure and > 95% viable. Secreted pepsinogen was measured with a sensitive hemoglobin digestion method at pH 2. RESULTS: Pepsinogen secretion was concentration-dependently stimulated by acetylcholine (ACh) (EC50 = 0.3 microM), cholecystokinin (CCK)-8 (2 nM), histamine (2 microM), and gastrin-I (30 nM) but not by bombesin or pentagastrin. ACh stimulation was inhibited 40 times more potently by atropine (IC50 = 12 nM) than by pirenzepine (IC50 = 0.5 microM). Histamine was inhibited by 10(-4) cimetidine. CCK-8 stimulation was inhibited 80% by the CCK-A-selective antagonist L364,718 (IC50 = 12 nM) but not by the CCK-B-selective antagonist L365,260. CONCLUSION: Isolated human peptic cells from endoscopic biopsy specimens secrete pepsinogen in response to ACh > CCK-8 > histamine > gastrin-I. The human peptic cell muscarinic-cholinergic receptor is not of the M1 subtype, and the CCK-8 response is predominantly mediated by a CCK-A receptor subtype.

Acetylcholine↗
PubMed1994

Nonsteroidal antiinflammatory drugs and the gastrointestinal tract.

Nonsteroidal antiinflammatory drugs (NSAIDs) are used in large amounts for analgesic, antiinflammatory, and antithrombotic indications. This use is not without side effects on the gut and other organs, and some of these side effects may be serious and even lethal. No NSAID has been shown to be without side-effect potential. Use increases with age, and age poses additional risks to patients with side effects. The most serious side effects are perforation of peptic and gut ulcers and gastrointestinal (GI) bleeding, which NSAIDs, and especially acetylsalicylic acid (ASA; aspirin), may promote from both ulcer and nonulcer lesions of both the upper and lower GI tract (i.e., both acid- and nonacid-dependent). Upper GI mucosal lesions range from trivial--petechiae and superficial erosions--to significant and potentially serious deep (chronic) peptic ulcers, esophagitis, and, less commonly, small and large gut ulcers. Symptoms may occur independently of observable lesions, and serious lesions may occur without any prior symptoms. The risk of ulceration due to therapeutic doses of NSAIDs is estimated at 5- to 10-fold. NSAIDs also delay healing of conventional peptic ulcers. Moreover, ASA abuse, often surreptitious and discoverable by serum salicylate level measurement, may cause totally intractable gastric or duodenal ulceration. Surgery is contraindicated because relapse is inevitable and progressively more serious. The rational use of NSAIDs is discussed, and prophylactic and treatment strategies are proposed. None seems entirely satisfactory, and the best prophylaxis would be to avoid the use of NSAIDs except for proven indications. Until the mechanisms whereby NSAIDs both cause injury and provide therapeutic benefits can be separated, the problem of side effects and their prevention or treatment remains unresolvable.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Vagal effects on acid and pepsin secretion and serum gastrin in duodenal ulcer and controls.

To study whether the vagus sustains basal secretion and stimulates acid and pepsin differently in duodenal ulcer (DU) and non-DU, we tested 144 patients with DU and 92 nonulcer controls, using 1-hr basal secretion followed by 15 min of modified sham feeding (MSF) and after 1 hr followed by a reference maximum elicited by 6 micrograms/kg pentagastrin given subcutaneously and observed for another 1 hr. Of all subjects, 97.5% responded to MSF by raising basal acid output (BAO) at least 15%. MSF added amounts of acid equal to 26-30% of peak acid output and 30-43% of peak pepsin output, regardless of diagnosis or level of basal secretion (including hypersecretors). Speed and duration of responses were similar in DU and controls. MSF did not substantially alter serum gastrin. Males secreted more acid and pepsin than females under all conditions, differences that persisted in DU but not in controls when outputs were corrected for body weight. Male DU but not female DU patients secreted more than corresponding controls. Sham feeding is an effective stimulus with similar characteristics in controls and DU patients. There was no evidence for saturation of vagal pathways in basal hypersecretors. MSF stimulation does not appear to involve gastrin. Hypersecretion in DU derives largely from responses in male DU.

Adult↗
PubMed1992

Objective evidence of aspirin use in both ulcer and nonulcer upper and lower gastrointestinal bleeding.

To obtain the best evidence for nonsteroidal anti-inflammatory drug (NSAID) use in gastrointestinal (GI) bleeding, a detailed patient history was supplemented with objective tests of aspirin use, i.e., high-performance liquid chromatography of plasma and platelet cyclo-oxygenase inhibition, which detect aspirin intake within 24 and 120 hours, respectively. Seventy-one patients consecutively admitted for upper or lower GI bleeding and 138 age- and sex-matched controls were studied. Five bleeders were excluded for confounding factors, e.g., warfarin. Of the other 66 bleeders, 45 had upper GI bleeding (28 from peptic ulcer, 14 from duodenal ulcer, and 14 from gastric ulcer) and 21 lower GI bleeding. Evidence of current NSAID use (of which 89% was aspirin) was found in 80% of bleeders vs. 24.3% of controls (P less than 0.0001), for an odds ratio of 13.7 (95% confidence interval, 6.39-27.27). The cyclo-oxygenase test uncovered 21.5% more aspirin users than history alone. Severity of bleeding was not different in acetylsalicylic acid users. The surprisingly high association of current intake of NSAIDs, especially aspirin, with nonulcer GI bleeding including colonic bleeding, changes the conventional view of the following hierarchy of the risk: NSAID----peptic ulcer----bleeding to: NSAIDs----GI bleeding. This view has important implications for current ulcer cotherapy prophylactic strategies, which could fail to prevent greater than 50% of GI bleeding episodes.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1992

Two doses of omeprazole versus placebo in symptomatic erosive esophagitis: the U.S. Multicenter Study.

Two hundred thirty patients with reflux symptoms and endoscopically proven erosive esophagitis were enrolled from 15 U.S. centers into a randomized, double-blind, dose-ranging study comparing placebo with omeprazole, 20 or 40 mg given once daily in the morning. Esophagitis grade 2 was present in 44% of patients, grade 3 in 37% of patients, and grade 4 in 19% of patients. Endpoints, defined as complete relief of heartburn and complete esophageal mucosal healing, were assessed after 4 and 8 weeks of treatment. Both omeprazole doses were significantly superior to placebo in complete endoscopic healing. After 8 weeks of treatment, 73.5% of patients in the 20-mg omeprazole group and 74.7% in the 40-mg omeprazole group, compared with 14.0% in the placebo group, had complete healing of the esophageal mucosa. At the end of the study, complete relief of daytime heartburn was obtained in 79.5% of patients in the 20-mg omeprazole group, 81.6% in the 40-mg omeprazole group, and 37.2% in the placebo group (P less than or equal to 0.05). Complete relief of nighttime heartburn was noted by 79.5% of patients in the 20-mg omeprazole group, 85.1% in the 40-mg omeprazole group, and 34.9% in the placebo group (P less than or equal to 0.05). The median time to complete relief of daytime and nighttime heartburn occurred earlier in the 40-mg group than in the 20-mg group (9 vs. 17 days and 9 vs. 20 days, respectively); however, these differences were not statistically significant. Relief of acid regurgitation and dysphagia also occurred earlier in the 40-mg group. Omeprazole was well tolerated in this group of patients. No unexpected adverse experiences occurred. The results of this study confirm those of six multicenter, international trials in which omeprazole in doses of 20-60 mg provided a degree of esophageal mucosal healing and complete relief of reflux symptoms superior to any other medical treatment.

Adult↗
PubMed1992

Influence of smoking on basal and on vagally and maximally stimulated gastric acid and pepsin secretion.

Published data show that smokers have greater basal or peak acid and pepsin outputs, but the mechanisms underlying these effects are unknown. To confirm this and to determine whether these findings extend to, and implicate, any vagal overactivity, gastric secretions collected for 1 h basally, 1 h after 15 min of modified sham feeding (MSF), and 1 h after pentagastrin (6 micrograms/kg subcutaneously) were analyzed for acid and pepsin content in 204 subjects, 104 with duodenal ulcer (66 smokers) and 101 without (57 smokers). Maximal acid outputs (MAO, mu eq/kg/h, means +/- SEM) were higher in smokers than in non-smokers in both duodenal ulcer (DU) (623 +/- 35 versus 491 +/- 35, p less than 0.005) and non-DU (502 +/- 32 versus 376 +/- 20, p less than 0.005). Basal and MSF secretions were generally increased in smokers but, when expressed as a percentage of MAO, were not different in smokers and non-smokers (18% versus 17% and 43% versus 39%, respectively, in DU, and 13% versus 16% and 40% versus 36% in non-DU). Maximal pepsin outputs (units x 10(-2)/kg/h) were also higher in smokers than in non-smokers (DU, 129 +/- 7.9 versus 105 +/- 9.5, p = 0.05, and non-DU, 101 +/- 7.5 versus 77 +/- 10, p = 0.05). Basal and MSF secretions as a percentage of maximal pepsin output were not different in smokers versus non-smokers. Multivariate logistic regression shows that smoking was most strongly associated with MAO and sham feeding outputs, but the duration-intensity (pack-years) of smoking was associated only with elevated MAO.(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenal Ulcer↗
PubMed1992

Acid and pepsin secretion in patients with esophagitis refractory to treatment with H2 antagonists.

The basis for treatment of esophagitis is suppression of gastric acid secretion. To determine whether lack of healing with standard treatment with H2 antagonists might be due to abnormal gastric secretion, 30 patients who remained unhealed after 12 weeks' therapy with histamine H2 antagonists were compared with 20 patients who healed after 6 or 12 weeks' therapy. The groups were matched with regard to age, weight, sex, and presence of hiatal hernia or duodenal ulcer. There were no significant differences in fasting gastric juice volume, pH, or acid or pepsin concentrations. All 30 refractory patients had basal acid output (BAO) less than 10 meq/h, and 16 of 30 had BAO less than 2 meq/h--that is, there was no evidence of hypersecretion in any refractory patients. Moreover, basal and maximal acid and pepsin outputs were not higher in non-healing patients. Refractory patients had a higher prevalence of initial severe (grade 3 or 4) esophagitis (80% versus 35% in those who healed, p less than 0.01) and of strictures (73 versus 15%, p less than 0.001), both of which serve as markers for refractoriness to treatment. Thus 77% of patients who presented with severe esophagitis failed to heal versus 32% of those with mild or moderate esophagitis (p less than 0.01). Refractoriness of esophagitis is not related to gastric acid or pepsin hypersecretion but represents a constitutional susceptibility to esophagitis and requires both short- and long-term treatment strategies that are not yet well defined.

Esophagitis↗
PubMed1992

Rapid regression of enterochromaffinlike cell gastric carcinoids in pernicious anemia after antrectomy.

In rats, hypergastrinemia due to achlorhydria produced by antisecretory drugs or resection of the gastric fundus leads to enterochromaffinlike (ECL) cell hyperplasia and gastric carcinoids. In humans, achlorhydria due to pernicious anemia may also lead to ECL cell hyperplasia and multicentric gastric carcinoids in as many as 5% of cases. To examine the apparent gastrin dependence of gastric ECL carcinoids, three patients were studied (2 men aged 59 and 73 years; 1 woman aged 45 years) who had pernicious anemia, serum gastrin concentrations of greater than 1000 ng/L (greater than 1000 pg/mL), and multicentric gastric carcinoids. Antrectomy resulted in normalization of serum gastrin levels within 8 hours and disappearance of carcinoids in 6-16 weeks. In each of the three patients, a focus of microcarcinoid was found at 12-18 months. Further follow-up in each of the three patients 21-30 months after antrectomy again showed no carcinoids or ECL cell hyperplasia. It is concluded that multicentric ECL gastric carcinoids in patients with pernicious anemia and achlorhydria appear to be gastrin dependent and disappear after normalization of serum gastrin by antrectomy. Antrectomy rather than total gastrectomy may be the most appropriate treatment for this condition.

Aged↗