Alpha1-antitrypsin bodies, PiZ phenotype, and peptic ulcer.

Abstract

SUMMARY An association between chronic peptic ulcer and heterozygous a1-antitrypsin deficiency has been reported: this study found no evidence of such an association. The prevalence of a1-antitrypsin bodies in the liver was compared with the known prevalence of Pi Z phenotype in the population: there was no significant difference.The production of al-antitrypsin, the major trypsin inhibitor in the blood, is controlled by alleles-the normal being PiM. Probably all persons with a PiZ allele have typical periodic acid-Schiff positive, diastase resistant, rounded bodies in the cytoplasm of their hepatocytes (Blenkinsopp and Haffenden, 1977), and these bodies rarely occur in persons with normal PiMM phenotype (Bradfield and Blenkinsopp, 1977).Andre et al. (1974) reported that 10.5% of 114 patients with chronic duodenal ulcer, and 9-6 % of 83 with chronic gastric ulcer, had levels of al-antitrypsin in the heterozygous (PiMZ) range, compared with 3-3% of 118 controls. The figure for patients with duodenal ulcer was statistically significantly different from that for controls, but that for gastric ulcer was not. However, normal levels of al-antitrypsin in the serum are scattered over a wide range, and the arbitrary choice of a cut-off at 60% of the mean normal value may be unsatisfactory. The presence of al-antitrypsin bodies in the liver provides a sharp discriminant, and this was used to investigate in necropsy material whether there was an increased prevalence of al-antitrypsin deficiency in patients with peptic ulcer. MethodsParaffin sections of formalin-fixed liver tissue taken at necropsy from patients with chronic gastric ulcer (72), chronic duodenal ulcer (52), or acute gastric ulcer (25), and from 159 patients without peptic ulceration were stained with periodic acid-Schiff after

Alpha-1-Antitrypsin Phenotypes and Serum Concentrations in Duodenal Ulcer Patients in The Netherlands

“…In two other studies [9,11], the same conclusion was reached, but two previous publications [8,10] suggest a possible role of oti-AT in the etiology of peptic ulcer disease. Lieberman [8] described a more frequent history of pep tic ulcer disease in ai-AT-deficient patients with lung emphysema, while André et al [10] found more heterozygous ct|-AT defi ciency in gastric and duodenal ulcer carriers than in other hospitalized patients with other digestive complaints.…”

“…Only a few reports have been published con cerning this question [8][9][10][11], Three of these studies [8][9][10] are based on determination of serum levels, and one on the presence of PI bodies [11]. These studies did not result in a consistent unequivocal answer.…”