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1.
World J Gastroenterol ; 28(28): 3706-3719, 2022 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-36161052

RESUMO

BACKGROUND: Helicobacter pylori (H. pylori) has characteristics of family cluster infection; however, its family-based infection status, related factors, and transmission pattern in central China, a high-risk area for H. pylori infection and gastric cancer, have not been evaluated. We investigated family-based H. pylori infection in healthy households to understand its infection status, related factors, and patterns of transmission for related disease prevention. AIM: To investigate family-based H. pylori infection status, related factors, and patterns of transmission in healthy households for related disease prevention. METHODS: Blood samples and survey questionnaires were collected from 282 families including 772 individuals. The recruited families were from 10 selected communities in the greater Zhengzhou area with different living standards, and the family members' general data, H. pylori infection status, related factors, and transmission pattern were analyzed. H. pylori infection was confirmed primarily by serum H. pylori antibody arrays; if patients previously underwent H. pylori eradication therapy, an additional 13C-urea breath test was performed to obtain their current infection status. Serum gastrin and pepsinogens (PGs) were also analyzed. RESULTS: Among the 772 individuals examined, H. pylori infection rate was 54.27%. These infected individuals were from 246 families, accounting for 87.23% of all 282 families examined, and 34.55% of these families were infected by the same strains. In 27.24% of infected families, all members were infected, and 68.66% of them were infected with type I strains. Among the 244 families that included both husband and wife, spouse co-infection rate was 34.84%, and in only 17.21% of these spouses, none were infected. The infection rate increased with duration of marriage, but annual household income, history of smoking, history of alcohol consumption, dining location, presence of gastrointestinal symptoms, and family history of gastric disease or GC did not affect infection rates; however, individuals who had a higher education level showed lower infection rates. The levels of gastrin-17, PGI, and PGII were significantly higher, and PGI/II ratio was significantly lower in H. pylori-infected groups than in H. pylori-negative groups. CONCLUSION: In our study sample from the general public of central China, H. pylori infection rate was 54.27%, but in 87.23% of healthy households, there was at least 1 H. pylori-infected person; in 27.24% of these infected families, all members were infected. Type I H. pylori was the dominant strain in this area. Individuals with a higher education level showed significantly lower infection rates; no other variables affected infection rates.


Assuntos
Infecções por Helicobacter , Helicobacter pylori , Neoplasias Gástricas , Gastrinas , Infecções por Helicobacter/diagnóstico , Infecções por Helicobacter/epidemiologia , Humanos , Pepsinogênio A , Pepsinogênios/uso terapêutico , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/prevenção & controle , Ureia
2.
Biochem Biophys Res Commun ; 238(1): 17-20, 1997 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-9299443

RESUMO

We isolated, by the subtraction cloning method, a pepsinogen C (PGC) gene fragment (the sequence between the 968th and 1179th base pairs) from a rat gastric mucosal cDNA library as a cDNA clone encoding a substance that promotes growth of the normal rat gastric mucosal cell line RGM1. Northern blot analysis revealed that PGC gene expression was enhanced not only in acetic acid-induced chronic gastric ulcers but also in indomethacin-induced gastric mucosal lesions. PGC gene expression was also increased in the Helicobacter felis-infected stomachs. Thus, the PGC gene may play a role in gastric epithelial cell growth during gastric mucosal healing.


Assuntos
Mucosa Gástrica/enzimologia , Substâncias de Crescimento/genética , Substâncias de Crescimento/fisiologia , Pepsinogênios/genética , Pepsinogênios/fisiologia , Ácido Acético , Animais , DNA Complementar/isolamento & purificação , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Gastrite/induzido quimicamente , Gastrite/enzimologia , Gastrite/genética , Regulação da Expressão Gênica , Substâncias de Crescimento/uso terapêutico , Helicobacter/fisiologia , Masculino , Pepsinogênios/uso terapêutico , RNA Mensageiro/biossíntese , Ratos , Ratos Sprague-Dawley , Úlcera Gástrica/induzido quimicamente , Úlcera Gástrica/enzimologia , Úlcera Gástrica/genética
3.
G E N ; 44(2): 191-8, 1990.
Artigo em Espanhol | MEDLINE | ID: mdl-2152275

RESUMO

Duodenal ulcer is a common disease. It has always been said that it results from an imbalance between aggressive forces (HC1 and pepsin) and defensive forces that act on the mucosa. More attention has traditionally been paid to acid and relative less interest to pepsin. Two types of pepsinogen have been recognized as precursors of peptic activity in the lumen. Pepsinogen I has been more frequently implicated in ulcerogenesis. The aim of this review is to consider the different current pathophysiologic and clinical aspects, and to take into account its importance as a predictive and genetic marker in duodenal ulcer disease, which is always a challenge in the daily practice of gastroenterologists.


Assuntos
Úlcera Duodenal/etiologia , Pepsinogênios/fisiologia , Úlcera Duodenal/sangue , Úlcera Duodenal/dietoterapia , Ácido Gástrico/metabolismo , Marcadores Genéticos , Humanos , Pepsinogênios/sangue , Pepsinogênios/genética , Pepsinogênios/uso terapêutico , Prognóstico
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