Clinical usefulness of serum pepsinogens I and II, gastrin-17 and anti-Helicobacter pylori antibodies in the management of dyspeptic patients in primary care

Germanà, B.; Mario, F. Di; Cavallaro, L.G.; Moussa, Ali Mahamat; Lecis, P.; Liatoupolou, S.; Comparato, G.; Carloni, C.; Bertiato, G.; Battiestel, M.; Papa, Nicoletta Del; Aragona, Giovanni; Cavestro, Giulia Martina; Iori, Veronica; Merli, R.; Bertolini, Simone; Caruana, Pietro; Franzè, A.

doi:10.1016/j.dld.2005.01.016

Cited by 57 publications

(58 citation statements)

References 41 publications

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“…This finding was confirmed by some previous researches which have been reported serum anti H pylori and pepsinogens were found to be useful in distinguishing subjects with non-atrophic gastritis from those with normal mucosa (Vaananen et al, 2003;Germana et al, 2005). Another studyshowed H Pylori can increase the serum gastrin level; and the elevation of serum gastrin level by H Pylori may be one of its carcinogenic mechanisms (Gisbert et al, 1996).…”

Section: Discussionsupporting

confidence: 77%

Screening of Precancerous Gastric Lesions by Serum Pepsinogen, Gastrin-17, Anti-Helicobacter Pylori and Anti-Caga Antibodies in Dyspeptic Patients over 50 years Old in Guilan Province, North of Iran

Mansour-Ghanaei¹,

Joukar²,

Rajpout³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 77%

Screening of Precancerous Gastric Lesions by Serum Pepsinogen, Gastrin-17, Anti-Helicobacter Pylori and Anti-Caga Antibodies in Dyspeptic Patients over 50 years Old in Guilan Province, North of Iran

Mansour-Ghanaei¹,

Joukar²,

Rajpout³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…2B, a significant inverse correlation was shown between serum G17 and the severity of antral atrophy in the coexistence of corpus atrophy. Consequently, coexisting corpus atrophy allows us to rule out the possibility of feed-back inhibition of G17 release by high intragastric acidity, making use of a low level of serum G17 as a more reliable biomarker to predict the presence of antral atrophy (Sipponen et al 1990(Sipponen et al , 2002bGermaná et al 2005). Indeed, in this study, serum G17 of less than 1 pmol/l was found only in one of 98 CPG patients, who had corpus atrophy but lacked antral atrophy.…”

Section: Discussionmentioning

confidence: 79%

“…Recent studies have reported that gastrin17 (G17) was exclusively secreted from antral G cells, and its serum level may reflect the severity of antral atrophy more accurately compared with serum total gastrin (Sipponen et al 2002a(Sipponen et al , 2002bVäänänen et al 2003;Germaná et al 2005). Consequently, the determination of G17 in combination with serum PG can yield a topographic assessment of atrophic gastritis (antrum-or corpuspredominant atrophic gastritis or multifocal atrophic gastritis), potentially serving as a serological risk assessment of gastric cancer.…”

mentioning

confidence: 99%

Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

Kikuchi

Abe

Iijima

et al. 2011

Tohoku J. Exp. Med.

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Atrophic gastritis (AG) is a well-recognized high-risk condition for developing gastric cancer (GC). Gastrin 17 (G17), a hormone secreted from antral G cells, regulates gastric acid secretion, and its serum level is a possible indicator of antral atrophy. Serum pepsinogen is well established as the indicator of AG involving the corpus. Here we investigated whether serum PG and G17 levels would be useful for determining the topographic pattern of AG and estimating the risk of GC. Enrolled were 122 Japanese patients with early GC (114 well-to moderate-differentiated cancers and 8 poorly-differentiated cancers). In addition, 178 subjects without GC were recruited as control from those undergoing endoscopic examination (non-GC group). All subjects were histologically assigned to the following four groups: non-AG, antrum-predominant AG, corpus-predominant AG, and multifocal AG, affecting the antrum and corpus. Serum concentrations of pepsinogen and G17 were determined using ELISA. Multifocal AG was more frequent in the GC group than in the adjusted non-GC group, and had the highest risk of GC (OR 25.1). Serum G17 was significantly decreased with the exacerbation of antral atrophy in the coexistence of corpus atrophy. Serum biomarker profiles showed that the low levels of pepsinogen and G17 could discriminate between multifocal AG and other types of AG, but not with pepsinogen level alone. Serologically defined multifocal AG had the highest cancer risk among other serologically defined AG groups (OR 26.9). In conclusion, the low serum levels of pepsinogen and G17 are predictive of extensive gastric atrophy with high-risk of early GC.

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“…Gastrin and PGs influence gastric physiology and thus reflect the functional state of the gastric mucosa [20]. Several investigators have reported that measurements of PGs and G17 in serum can be employed as useful biomarkers for understanding gastric pathologies, such as atrophic gastritis and drug-induced ulcer [21,22].…”

Section: Discussionmentioning

confidence: 99%

High Serum Pepsinogen I and beta Helicobacter pylori Infection Are Risk Factors for Aspirin-Induced Gastroduodenal Injury

Shan¹,

Lei²,

Wei³

et al. 2017

Dig Dis

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Background: Whether gastric hyperchlorhydria and Helicobacter pylori infection contribute to aspirin-induced gastroduodenal injury still lacks evidence. Because serum pepsinogens (PGs) and gastrin-17 (G17) can reflect gastric acid secretion, this study intended to elucidate whether serum PGs, serum G17, and H. pylori infection are associated with aspirin-induced gastrointestinal injury. Summary: A total of 60 patients taking low-dose aspirin for more than 1 month were enrolled in this study. Serum PG I, PG II, and G17 were determined using ELISA. A 14C-urea breath test was used for the detection of an H. pylori infection. The modified Lanza score was used to evaluate the degree of gastroduodenal injury under endoscopy. The median serum PG I level was significantly higher in the intensive gastroduodenal injury (IGI) group compared to that in the mild gastroduodenal injury group (155.0 vs. 116.6 ng/mL, p = 0.006). The H. pylori infection rate was significantly higher in the IGI group (73 vs. 40%, p = 0.037). Receiver operator characteristic curves analysis revealed that the cutoff value of PG I was 123 ng/mL, with 80% sensitivity and 61.4% specificity. H. pylori infection combined with PG I at >123 ng/mL had an OR (95% CI) of 15.8 (2.4 ± 104.5) for the prediction of aspirin-induced gastroduodenal injury. Key Messages: Serum PG I and H. pylori infection could be used to identify potential high-risk aspirin-induced gastroduodenal injury patients.

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Clinical usefulness of serum pepsinogens I and II, gastrin-17 and anti-Helicobacter pylori antibodies in the management of dyspeptic patients in primary care

Cited by 57 publications

References 41 publications

Screening of Precancerous Gastric Lesions by Serum Pepsinogen, Gastrin-17, Anti-Helicobacter Pylori and Anti-Caga Antibodies in Dyspeptic Patients over 50 years Old in Guilan Province, North of Iran

Screening of Precancerous Gastric Lesions by Serum Pepsinogen, Gastrin-17, Anti-Helicobacter Pylori and Anti-Caga Antibodies in Dyspeptic Patients over 50 years Old in Guilan Province, North of Iran

Low Serum Levels of Pepsinogen and Gastrin 17 Are Predictive of Extensive Gastric Atrophy with High-Risk of Early Gastric Cancer

High Serum Pepsinogen I and beta Helicobacter pylori Infection Are Risk Factors for Aspirin-Induced Gastroduodenal Injury

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