Accuracy and Cut-Off Values of Pepsinogens I, II and Gastrin 17 for Diagnosis of Gastric Fundic Atrophy: Influence of Gastritis

Nasrollahzadeh, Dariush; Aghcheli, K; Sotoudeh, Masoud; Shakeri, Ramin; Persson, E. Christina; Islami, Farhad; Kamangar, Farin; Abnet, Christian C.; Boffetta, Paolo; Engstrand, Lars; Dawsey, Sanford M.; Malekzadeh, Reza; W, Ye

doi:10.1371/journal.pone.0026957

Cited by 48 publications

(46 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Performance of this test was significantly improved when analysis of H. pylori antibodies has been included [10]. Similar cut-offs, although higher for the pepsinogen I/II ratio ( 5.0), have been identified by an Iranian group for the detection of atrophy [11]. The data also support the role of pepsinogen II being an adequate marker for non-atrophic pangastritis, which is also considered as a risk condition for GC development.…”

Section: Prevention and Screening Of Gastric Cancersupporting

confidence: 52%

Helicobacter pylori: Gastric Cancer and Extragastric Intestinal Malignancies

et al. 2012

View full text Add to dashboard Cite

The greatest challenge in Helicobacter pylori-related diseases continues to remain prevention of gastric cancer. New evidence supports the beneficial effect of H. pylori eradication not only on prevention of gastric cancer but also on the regression of preneoplastic conditions of the gastric mucosa. Concerning early detection of gastric cancer there are still no adequate means and there is urgent need to define appropriate markers, for example, by gen-ome-wide research approaches. Currently, the best available method is the "serologic" biopsy based on pepsinogen I and the pepsinogen I/II ratio for identification of patients with severe gastric atrophy at increased risk for gastric cancer development. The treatment of early gastric cancer by endoscopic techniques can be performed safely and efficiently, but patients need meticulous follow-up for detection of metachronous lesions. In case of advanced disease, laparoscopically assisted surgical procedures are safe and favorable compared to open surgery. Two phase III trials support the role of adjuvant systemic treatment with different regimens. Unfortunately, there is still only slow progress in the development of palliative treatment regimens or modification of the existing therapy protocols. There is accumulating evidence for a role of H. pylori infection also in colorectal carcinogenesis. Seropositive individuals are at higher risk for the development of colorectal adenomas and consequently adenocarcinomas of this anatomical region. This phenomenon can partly be attributed to the increase of serum gastrin as response to atrophic changes of the gastric mucosa. In 2012, the infection with Helicobacter pylori remains one of the most challenging infectious diseases of the world, causing high morbidity and mortality. The major burden in global health care is still given by H. pylori representing the main risk factor for gastric cancer (GC), the second leading cause of cancer-related death. During the past years, the progress in the clinical management of GC has been modest. Innovations are limited to modifications of the existing chemotherapy regimens in either palliative or perioperative settings. Furthermore, new data have been gained concerning the endoscopic treatment of early GC. This review summarizes recent clinical-and research-related advances in the field of H. pylori and GC that have been published between April 2011 and April 2012, including also recent insights concerning the association between H. pylori infection and colorectal neoplasias. Prevention and Screening of Gastric Cancer H. pylori infection leads in all infected individuals to a chronic active gastritis, which can proceed, via the so-called Correa cascade, to gastric mucosal atrophy and intestinal metaplasia (IM), and finally to the development of GC. Thus, atrophy and IM are considered as precancerous conditions, and H. pylori eradication therapy is considered as preventive for GC [1]. Several studies have proven that eradication therapy also improves, or at least prevents, progression of ...

show abstract

Section: Prevention and Screening Of Gastric Cancersupporting

confidence: 52%

Helicobacter pylori: Gastric Cancer and Extragastric Intestinal Malignancies

et al. 2012

View full text Add to dashboard Cite

show abstract

“…In a recent study , designed in our country , the best cutoff value in gastric atrophy assessment was calculated at PGI, 56 ng/ml (sensitivity: 61.9%, specificity: 94.8%) but we used the cutoff value of PGI <88.7 ng/ml (sensitivity and specificity of 64.4% and 43% respectively) for atrophy (Nasrollahzade et al, 2011). That work was an office based study and 309 persons were enrolled but present study was a population based survey on 1390 persons explaining the difference of cutoff between two studies.…”

Section: Discussionmentioning

confidence: 99%

Serum Gastrin and the Pepsinogen I/II Ratio as Markers for Diagnosis of Premalignant Gastric Lesions

Shafaghi

Ghanaei²,

Joukar³

et al. 2013

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

“…Cao et al found a high AUC (0.88) for PgI in patients with GA (Cao et al, 2007). Nasrollahzadeh et al (2011) similarly reported relatively high accuracy (AUC=0.78) for PgI as well as for the combination of PgI and PgI/II ratio (AUC=0.79) for diagnosis GA. Shikata et al (2012) reported a sensitivity and specificity of 71.0% and 69.2% for a combination of PgI and PgI/II ratio to discriminate GC. Miki et al (2003) reported a sensitivity of 80% and a specificity of 70% for the combination of PgI and PgI/II ratio to detect GC.…”

Section: Discussionmentioning

confidence: 93%

“…But, the results of some previous studies showed relatively high accuracy for G17 to differentiate GA or GC. Nasrollahzadeh et al (2011) reported an AUC of 0.77 for G17 to discriminate GA. Kikushi et al (2011) also suggested G17 as good biomarker for diagnosis GA. Regarding the role of G17 pathogenesis of GC (Copps et al, 2009), further studies are warranted to assess the validity of G17 to differentiate GA/GC.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Diagnostic Values of Serum Levels of Pepsinogens and Gastrin-17 for Screening Gastritis and Gastric Cancer in a High Risk Area in Northern Iran

Nejadi-Kelarijani

Roshandel²,

Semnani³

et al. 2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Background: Gastric cancer (GC) is the second cause of cancer related death in the world. It may develop by progression from its precancerous condition, called gastric atrophy (GA) due to gastritis. The aim of this study was to evaluate the accuracy of serum levels of pepsinogens (Pg) and gastrin-17 (G17) as non-invasive methods to discriminate GA or GC (GA/GC) patients. Materials and Methods: Subjects referred to gastrointestinal clinics of Golestan province of Iran during 2010 and 2011 were invited to participate. Serum levels of PgI, PgII and G17 were measured using a GastroPanel kit. Based on the pathological examination of endoscopic biopsy samples, subjects were classified into four groups: normal, non-atrophic gastritis, GA, and GC. Receiver operating curve (ROC) analysis was used to determine cut-off values. Indices of validity were calculated for serum markers. Results: Study groups were normal individuals (n=74), non-atrophic gastritis (n=90), GA (n=31) and GC patients (n=30). The best cut-off points for PgI, PgI/II ratio, G17 and HP were 80 μg/L, 10, 6 pmol/L, and 20 EIU, respectively. PgI could differentiate GA/GC with high accuracy (AUC=0.83; 95%CI: 0.76-0.89). The accuracy of a combination of PgI and PgI/II ratio for detecting GA/GC was also relatively high (AUC=0.78; 95%CI: 0.70-0.86). Conclusions: Our findings suggested PgI alone as well as a combination of PgI and PgI/II ratio are valid markers to differentiate GA/GC. Therefore, Pgs may be considered in conducting GC screening programs in high-risk areas.

show abstract

Accuracy and Cut-Off Values of Pepsinogens I, II and Gastrin 17 for Diagnosis of Gastric Fundic Atrophy: Influence of Gastritis

Cited by 48 publications

References 45 publications

Helicobacter pylori: Gastric Cancer and Extragastric Intestinal Malignancies

Helicobacter pylori: Gastric Cancer and Extragastric Intestinal Malignancies

Serum Gastrin and the Pepsinogen I/II Ratio as Markers for Diagnosis of Premalignant Gastric Lesions

Diagnostic Values of Serum Levels of Pepsinogens and Gastrin-17 for Screening Gastritis and Gastric Cancer in a High Risk Area in Northern Iran

Contact Info

Product

Resources

About