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This study aimed to investigate the cause of persistently increased serum gastrin concentration seen in some Graves' disease patients even when euthyroid during antithyroid drug treatment. The subjects studied consisted of three groups: 33 patients with a common-type of Graves' disease, 14 with triiodothyronine (T3)-predominant Graves' disease (characterized from previous studies as having potent immunologic abnormalities including greater concentrations of thyroid-stimulating antibodies together with larger goiter size), and a group of 20 normal subjects. Fasting serum gastrin concentrations in common Graves' disease patients were significantly higher than those of normal subjects (58.4 +/- 38.9 pmol/L vs. 37.8 +/- 18.9 pmol/L [mean +/- SD], p0.05). The serum gastrin concentrations were even greater in T3-predominant Graves' disease patients than common Graves' disease patients (162.9 +/- 224.0 pmol/L vs. 58.4 +/- 38.9 pmol/L, p.05). Serum pepsinogen I (PGI) concentrations were significantly lower in the T3-predominant patient group than the common Graves' group (24.0 +/- 12.9 ng/mL vs. 39.7 +/- 19.6 ng/mL, p.05). Serum ratios of PG I to PG II were significantly lower in the T3-predominant Graves' disease patients than normal subjects (3.59 +/- 2.66 vs. 5.97 +/- 1.56, p.01). The ratios also had a significant (p.05) inverse correlation with serum gastrin concentrations in T3-predominant Graves' disease patients. The results suggest that autoimmune gastritis is associated with Graves' disease, particularly in patients with potent thyroid-autoimmunity.

In this article we reported a female patient with type 1 gastric neuroendocrine tumor (NET). Gastroscopy showed the presence of multiple polyp-like lesions sized 0.2–1.5 cm in the fundus and body of stomach. The main clinical manifestations were belching and fullness after a meal. She had a history of autoimmune atrophic gastritis and laboratory tests showed increased serum gastrin and acid deficiency, which met the diagnostic criteria of type 1 gastric NET. Treatments included endoscopic resection, sandostatin, and traditional Chinese herbs, and no relapse was noted during follow-up visits. The patient also had rectal NET. By analyzing this case, we tried to explore the diagnostic algorithm and clinical typing of type 1 gastric NET; meanwhile, along with literature review, we described the relapse rate of this disease and the value of regular follow-up (every 6–12 months). Finally, we analyzed the value of somatostatin analogue (SSA) in treating multiple type 1 gastric NET and in this case we demonstrated that SSA was effective in dissolving NET.

A case of peripheral neuropathy in a patient with diabetes who had atypical clinical findings is presented. Because of the atypical initial manifestations and short duration of insulin-dependent diabetes, another cause of the neuropathy was suspected. The presence of vitiligo, hypothyroidism, and diabetes prompted a search for evidence of pernicious anemia. Despite a normal blood cell count, the diagnosis of pernicious anemia was confirmed on the basis of an increased serum gastrin level and antiparietal cell antibody titer. Treatment with vitamin B12 resulted in an arrest, but not a reversal, of the signs of peripheral neuropathy. In patients with diabetes, vitamin B12 deficiency should be suspected; its early diagnosis and treatment are important in minimizing neurologic damage.

In the present study we have investigated the effects of proglumide (PRO) and somatostatin analog (SMS 201-995) on the mitotic activity of colonic mucosa in rats under basal conditions and after omeprazole (OM). The stathmokinetic method was used. Proglumide and OM were administered for 5 days, twice daily, SMS 201-995 on the 5th day of the experiment only, also twice daily. It was found that: 1) OM enhanced the proliferation of colonic mucosa, as well as increased serum gastrin, when compared to controls, 2) OM and PRO, when applied jointly, decreased the mitotic activity of the colonic epithelium, 3) PRO alone increased the colonic cell proliferation.

Serum gastrin and serum calcium concentrations were measured in 9 hemodialysis patients treated with 1-alpha-hydroxy vitamin D3 and in 15 control patients. Serum calcium and serum gastrin concentrations were significantly increased after 1 and after 5 months of treatment with 1-alpha-hydroxy vitamin D3. It is concluded that serum gastrin concentration is sensitive to a rise in calcium concentration within physiological range in patients with chronic renal failure.

A study was made of the effect of a synthetic enkephalin analog and cimetidinee on experimental duodenal ulcer in rats induced by cysteamine administration. The ulcers were demonstrated to heal within 4 weeks. It was noted that ulcer occurrence was preceded by the increased serum gastrin level. Administration to rats of the enkephalin analog accelerated ulcer healing to a greater extent than that of cimetidin. It is suggested that one of the mechanisms of enkephalin analog protective action might involve the prevention of the gastrin increased level.

Gastric emptying time of a solid meal was estimated on X-ray in 7 patients with a normal duodenal loop, 7 patients with a proximal duodenal anomaly, and 12 patients with a distal duodenal anomaly. A determination coefficient between gastric emptying time and duration of serum gastrin increase was calculated. The food-stimulated serum gastrin secretory pattern was studied in 9 patients with a normal duodenal loop, 6 with a proximal duodenal anomaly, and 13 with a distal duodenal anomaly. The various groups presented significantly different gastric emptying times; thus patients with normal duodenal loop had a mean gastric emptying time of 6 h, patients with proximal duodenal anomalies ahd a mean gastric emptying time of 4.5 h, and patients with distal duodenal anomalies had a mean gastric emptying time of 9 h. Gastric emptying time and duration of increased serum gastrin secretion was positively correlated (R2 = 0.89). The food-stimulated serum gastric secretory pattern was equal in patients with proximal duodenal anomalies and those with distal duodenal anomalies and furthermore, reached significantly higher serum gastrin concentrations than in patients with a normal duodenal loop.

The relative importance of thought, sight, smell, and taste of food in the cephalic phase of gastric acid secretion has not been studied systematically. We found that discussing appetizing food for 30 min (without sight, smell, or taste) increased acid secretion from 4 to 13 mmol/h in healthy human subjects (p less than 0.001) and also increased serum gastrin concentrations significantly (p less than 0.02). Discussing food resulted in an acid secretory response that averaged 66% +/- 10% of the response to modified sham feeding, which activates thought, sight, smell, and taste. Discussing topics other than food (e.g., current events, sports) did not increase acid secretion significantly. The sight of appetizing food (without smell or taste), the smell of appetizing food (without sight or taste), or the combination of sight and smell (without taste) also increased acid secretion and serum gastrin concentrations significantly. However, sight and smell were significantly less potent stimulants of acid secretion than sham feeding, with responses averaging only 23%-46% of the response to sham feeding. These studies indicate that thinking about food is a potent stimulant of gastric secretion in healthy humans. Moreover, the sight and smell of food increase gastric acid secretion and serum gastrin concentrations, probably by provoking thoughts related to food.

Intravenous infusion of bombesin in humans results in increased serum gastrin levels and increased lower esophageal sphincter pressure. To differentiate a gastrin- from a nongastrin-mediated mechanism, the effect of intravenous bombesin infusion on lower esophageal sphincter pressure was studied in 5 healthy subjects and in 5 antrectomized patients. Lower esophageal sphincter pressure was recorded by three continuously perfused catheters with side-openings located 5 mm apart. Blood samples were taken at regular intervals during the study periods to assay gastrin and pancreatic polypeptide. Manometric tracings and blood samples were coded and evaluated blindly. Lower esophageal sphincter pressure increased during bombesin infusion both in normal and antrectomized subjects. The increase had a delayed onset and persisted after discontinuation of bombesin. No correlation was found between lower esophageal sphincter pressure and serum gastrin or pancreatic polypeptide values. These data indicate that the effect of bombesin on lower esophageal sphincter pressure is not gastrin or pancreatic polypeptide mediated.

Whereas 67 patients with duodenal ulcer had fasting and 30-minute postprandial mean serum gastrin levels not substantially different from 32 normal subjects, they had substantially higher fasting and histamine-stimulated gastric acid secretion. The increased acid secretion found in patients with duodenal ulcer is not caused by increased serum gastrin levels. Ten patients with recurrent ulcer, after incomplete vagotomy and gastric resection, had high gastric acid secretion and normal serum gastrin levels. Three patients with recurrent ulcer following complete vagotomy and gastric resection, but with retained antrum, had both high gastric acid secretion and high fasting and postprandial secrum gastrin levels. Three patients with Zollinger-Ellison tumors had even higher basal acid outputs and serum gastrin levels. The combination of basic gastric acid secretory studies and serum gastrin determinations may identify three causes of recurrent ulcer: incomplete vagotomy, retained antrum, and Zollinger-Ellison tumor.