Duodenal-Ulcer Disease Associated with Elevated Serum Pepsinogen I

Ji, Rotter; Jq, Sones; Im, Sungbin; Ct, Richardson; Jm, Gursky; Jh, Walsh; Dl, Rimoin

doi:10.1056/nejm197901113000203

Cited by 161 publications

(42 citation statements)

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“…The human stomach expresses two isozymogens, PGI and PGII, with different biochemical and immunological properties (13). Histological studies based on immunohistochemistry using specific antibodies or in-situ hybridization have clearly identified cells that produce PGI and PGII (14)(15)(16) (17)(18)(19)(20)(21)(22)(23). It is important to note that, during the process of chronic atrophic gastritis, mucosal atrophy advances from the side of the pyloric gland towards the oral side, and that PGI levels and PGI/PGII ratios decrease with advancement in mucosal atrophy (18)(19)(20)23) (Fig.…”

Section: Pepsinogen Testingmentioning

confidence: 99%

Serum Pepsinogen and Gastric Cancer Screening

et al. 2007

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Section: Pepsinogen Testingmentioning

confidence: 99%

Serum Pepsinogen and Gastric Cancer Screening

et al. 2007

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“…5% of women in the Caucasian western population are expected to have some form of ulcer disease during their lifetime. This unchanged trend is genetically programmed: 30-59% of ulcer patients have a positive family history in contrast to 5-15% of control persons (2)(3)(4)(5). DU and GU follow separate genetic pathways.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology and modern treatment of ulcer disease (Review)

Holle¹

2010

Int J Mol Med

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Abstract. This is an overview of the pathophysiological abnormalities of gastroduodenal (GD) ulcers [duodenal ulcer (DU), gastric ulcer (GU) and Dragstedt ulcers (combined DU and GD)], as well as the effects of the different treatments (surgical, medicinal and physiological) described since the introduction of stomach resections. The intention is to demonstrate whether the peptic ulcer diseases are a homogeneous entity with a characteristic pathophysiology or whether they represent the final expression of many heterogeneous causes including impairment of upper gastrointestinal motility. The review also asks whether DU and GU have a common or different pathogenesis and whether ulcers in the stomach might be predominantly due to impaired mucosal resistance and the DU to gastric hypersecretion. The symptoms of both diseases are also compared with the findings in the normal controls.

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“…The serum pepsinogen levels were highly elevated in the blood group 0 patients when compared with other blood group A, B and AB patients. According to Hanley's report 1 • the extent of peptic secretory cell mass is influenced by sex, by ABO blood genes, and the serum pepsinogen levels and probably reflects the size of the gastric secretory cell mass. Their experimental resultsis revealed that the gastric secretory cell mass is larger in group 'O' phenotypes than in group 'A' phenotypes.…”

Section: Discussionmentioning

confidence: 99%

Genetic Markers in Duodenal Ulcer Disease

Ali¹,

Habibullah²,

Salahuddin³

1988

J Islam Med Assoc

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A study has been carried out on 100 endoscopically proven duodenal ulcer patients and in 100 healthy controls to examine the role of genetic factors in the development of duodenal ulcer disease. Serum pepsinogen levels, serum alpha-J-antitrypsin, haptoglobin phenotyping and ABO blood groups served as genetic markers.Hyperpepsinogenemia, deficiency of alpha-1-antitrypsin, haptoglobin 2-2 typing and '0' blood group were found to be associated with duodenal ulcer disease.Key words: Duodenal ulcer, genetic markers, association.The role of genetic factors in the pathogenesis of duodenal ulcer has been described by several workers 1 -3, who have reported an increased frequency of the disease in first degree relatives of patients, and greater concordance between monozygotic twins than dizygotic twins.3 Other markers such as ABO blood groups,• secretor and non secretor status, 5HLA typing' and serum pepsinogen 1 • 7 have been studied. But, there has been no report of multiple markers studied in the same individual. The present study was carried out by taking four markers (serum pepsinogen, serum alpha-1-antitrypsin, haptoglobin phenotyping (Hp) and ABO blood groups) in the same patients as well as in healthy controls, to see the role of these markers, in the predisposition to duodenal ulcer disease. MethodsOne hundred duodenal ulcer patients of both sexes and aged between 22 and 58 years (mean age 37 .6 ± 11.2) were studied at the Department of Gastroenterology, Osmania General Hospital, Hyderabad. The presence of a duodenal ulcer was confirmed by endoscopy. One hundred healthy age and sex matched individuals, none of whom had a history of duodenal ulcer, dyspepsia or any other disease, were selected as controls.From the Department of Gastro-enteralogy Osmania General Hospital Hyderabad, (A.P.) Blood samples were collected from patients and controls for the estimation of serum pepsinogen, serum alpha-1-antitrypsin and for the analysis of ABO blood groups and haptoglobin phenotypes. The ABO blood group frequencies of the general population of Hyderabad reported by Padma et al' were used as controls against which the blood group frequencies of duodenal ulcer patients were compared. Serum alpha-1-antitrypsin was estimated in the form of serum trypsin inhibitor capacity (STIC) by the method of Jaccobson 9 using hemoglobin as a substrate. Serum pepsinogen levels were determined by the method of Mirsky et al 10 using hemoglobin as a substrate. The slide agglutuation technique was fallowed for the analysis of ABO blood groups. Haptoglobin phenotypes were analysed by the method of Clark. 12The statistical significance of the difference in distribution of STIC and total serum pepsinogen in controls and patients as determined by student 't' tests. Pearson's correlation coefficient was calculated for the relationship between STlC and serum pepsinogen levels. Scatter diagrams showed the relationship between these two and appropriate regression lines were fitted in lhe figure. The frequency of blood groups and Hp types in ...

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Duodenal-Ulcer Disease Associated with Elevated Serum Pepsinogen I

Cited by 161 publications

References 14 publications

Serum Pepsinogen and Gastric Cancer Screening

Serum Pepsinogen and Gastric Cancer Screening

Pathophysiology and modern treatment of ulcer disease (Review)

Genetic Markers in Duodenal Ulcer Disease

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