C O N T E N T S
Relations between serum pepsinogen levels, pepsinogen phenotypes, ABO blood groups, age and sex in blood donors
Pals G, Defize J, Pronk JC, Frants RR, Eriksson AW, Westerveld BD, Meuwissen SG, Biemond I
Ann Hum Biol 1985 Sep;12(5):403-411
Serum pepsinogen A (pepsinogen I) levels and urinary pepsinogen A phenotypes were studied in relation to ABO blood group, age and sex in 700 healthy blood donors. There was no relation between urinary pepsinogen A phenotypes and serum pepsinogen A levels. It is concluded that serum PGA levels and PGA phenotypes are independent factors in predisposition to gastroduodenal disorders. Serum pepsinogen A levels were higher in males than in females and rose with increasing age. Blood group O individuals showed higher serum pepsinogen A levels compared with blood group A. Pepsinogen A phenotypes with intensity of fraction 5 were more frequent in males compared with females.
Genetic markers and duodenal ulcer.
Shahid A, Zuberi SJ, Siddiqui AA, Waqar MA JPMA J Pak Med Assoc 1997 May;47(5):135-137 PMRC Research Centre, Jinnah Postgraduate Medical Centre, Aga Khan University, Karachi.
Serum pepsinogen?, Alpha 1-antitrypsin (A1AT) and blood groups were studied as genetic markers in 32 patients with endoscopically proven duodenal ulcer and 44 control subjects with no family history of ulcer disease. Serum pepsinogen was determined by the modified method of Edward et al, alpha 1-AT by single radial immunodiffusion (RID) and phenotyping was carried out by isoelectric focusing (IEF). Duodenal ulcer patients with hyper- pepsinogenemia (28%) and low serum alpha 1-AT (35%) had a dominant blood group O, lower mean age, an early onset of disease, a higher frequency of gastrointestinal (GI) bleeding and ulcer perforation. These parameters were found considerably different in patients with normal serum pepsinogen and alpha 1-AT. Phenotype analysis of alpha 1-AT revealed that four duodenal ulcer patients had partial deficiency of the protease inhibitor and none of the normal exhibited the deficiency pattern. The etiology of the disease appears to be genetic anomaly in 28% of patients while the rest (72%) had ulcers as a result of neuroendocrinological or environmental factors.
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