No abstract

The presence of ascorbic acid in gastric juice may protect against gastric carcinoma and peptic ulceration. This study examined the effect of Helicobacter pylon (H pylon) on the secretion of ascorbic acid into gastric juice by measuring fasting plasma and gastric juice ascorbic acid concentrations in patients with and without the infection and also before and after its eradication. Gastric juice ascorbic acid concentrations in 19 H pylon positive patients were significantly lower (median 2*8, range 0-28*8 [ig/ml) than those in 10 H pylori negative controls (median 17-8, range 5*6-155*4 ,ug/ml) (p<0.0005) despite similar plasma ascorbic acid concentrations in both groups. The median gastric juice:plasma ascorbic acid ratio in the H pylon positive patients was only 1*16 (range 0.02-6.67), compared with a median ratio of 4*87 (range 0*76-21.33) in H pylon negative controls (p<001). In the patients with H pylon infection there was a significant negative correlation between the severity of the antral polymorphonuclear infiltrate and gastric juice ascorbic acid concentrations (correlation coefficient -0.52, p=002). After eradication of H pylori in 11 patients, gastric juice ascorbic acid concentrations rose from 2*4 (0-12.8 [tg/ml) to 11*2 (0-50

It is possible to differentiate between primary and secondary thyroid squamous cell carcinoma, on the basis of combined evidence from clinical examination and endoscopic, pathological and radiological evaluation. Such differentiation is important, as the prognosis for primary squamous cell carcinoma is uniformly poor irrespective of treatment, and the most suitable option may be supportive therapy. Treatment for secondary squamous cell carcinoma of the thyroid varies with the site and extent of spread of the primary tumour.

In the past five years 12 patients have been identified presenting with chronic duodenal ulcer (DU) disease and with no evidence of current or recent Helicobacter pylori (H pylori) infection. Four of them were taking regular non-steroidal anti inflammatory agents, one was subsequently found to have Crohn's disease of the duodenum, and one to have the Zollinger-Ellison syndrome. The remaining six patients with idiopathic DU disease were remarkable for their absence of the A1 blood antigen gene. Detailed studies of gastric function were performed in these six patients and compared with H pylon positive patients with DU and with healthy volunteers. The median integrated gastrin response in the patients with idiopathic DU (2810 (range 750-8750) ng/l min) was similar to that of the H pylori positive patients with DU (3355 (550-8725)) and higher than that of the H pylon negative healthy volunteers (560 (225-1125)). The median peak acid output in the patients with idiopathic DU (37 mmol/h, range 17-52) was similar to that of the H pylon positive patients with DU (40 (15-57)) and higher than that ofthe non-ulcer controls (22 (16-29)). The median percentage of a liquid meal retained in the stomach at 60 minutes was less in the patients with idiopathic DU (23 (15-33)) than in Hpyloni negative healthy volunteers (34 (30-53) p<0-01). The median percentage of a solid meal retained at 60 minutes was less in the patients with idiopathic DU (54 (9-83)) than in either H pylon negative healthy volunteers (87 (49-95) p<001) or H pylon positive patients with DU (79 (51-100) p<0-01). In conclusion, three abnormalities of gastric function are prevalent in patients with H pylon negative idiopathic DU disease -hypergastrinaemia, increased acid secretion, and the one feature distinguishing them from H pylon positive patients with DU -rapid gastric emptying of both liquids and solids. Each of these abnormalities will increase the exposure of the duodenal mucosa to acid and thus explain its ulceration. The absence of the blood group A1 antigen gene is consistent with a genetic basis for the disturbed gastric function linked to the ABO blood group antigen genes. (Gut 1993; 34: 762-768) More than 95% of patients with chronic duo-

Nine patients with Helicobacter pylori-related antral gastritis and history of duodenal ulceration were studied before and at 1 and 7 months after eradication of the infection by a 4-week course of tripotassium dicitrato bismuthate, metronidazole, and amoxycillin. The median basal gastrin concentration before eradication was 30 ng/l (range, 20-60) and fell to 20 ng/l (5-20) at 1 month (p less than 0.02) and 15 ng/l (5-20) at 7 months (p less than 0.01) after eradication. The integrated gastrin response to a peptide meal was 3650 ng/l.min (range, 1875-6025) before treatment compared with 1800 ng/l.min (range, 1200-3075) at 1 month (p less than 0.01) and 1312 ng/l.min (875-2625) at 7 months (p less than 0.03). Daytime intragastric pH (0900-2100 h) was similar before treatment (median, 1.4; range, 1.1-2.1) and at 1 month (1.4; 1.1-2.3) and 7 months (1.4; 1-2.2) after eradication. In five of the patients nighttime acid output (2300-0900 h) was also studied and was similar before (median, 86 mmol/10 h; range, 52-114) and at 1 month (76 mmol/10 h; 50-143) and 7 months (94 mmol/10 h; 63-106) after eradication. In conclusion, eradication of H. pylori is accompanied by a sustained fall in serum gastrin concentrations but is not accompanied by an early or late reduction of daytime intragastric acidity or nighttime acid output.