Pepsinogen II
Code:14002
| Includes | Pepsinogen II |
|---|
Analysis details
Methodology
- Chemiluminescent immunoassay (CLIA)
Expected Turnaround Time
1 day
Special Instructions
- Do not consume alcohol for 24 hours before the blood draw.
- Avoid high-fat foods during the 24 hours before collection.
- Adults: fast for at least 12 hours; water is allowed.
- Children <1 year: withhold feeds for 30–40 minutes before collection.
- Children 1–5 years: withhold feeds for 2–3 hours before collection.
- For 30 minutes before collection, avoid strenuous exercise and minimize emotional stress.
- Refrain from smoking for 30 minutes before collection.
How to use
The Pepsinogen II (PG II; pepsinogen C) test assists in evaluating H. pylori–associated antral gastritis, atrophic gastritis, and pangastritis; in assessing peptic ulcer disease; and in identifying patients at elevated risk for gastric adenocarcinoma when combined with pepsinogen I, the PGI/PGII ratio, and H. pylori testing. It can be used to track response after H. pylori eradication and mucosal healing in gastritis or ulcer disease. Pepsinogen II measurement may support the workup of suspected gastrinoma (Zollinger–Ellison syndrome). In oncology, pepsinogen C expression serves as a tumor-associated and prognostic marker in a subset of breast adenocarcinomas.
Limitations
Pepsinogens are inactive precursors of pepsin, and their serum concentrations reflect functional and structural states of the gastric mucosa, including inflammation, atrophy, metaplasia, and neoplasia. Pepsinogen I is produced by oxyntic (corpus) mucosa, whereas pepsinogen II is produced by oxyntic, cardiac, and pyloric mucosa and by Brunner glands. H. pylori–associated gastritis increases circulating pepsinogen II. Antral-predominant infection yields hypergastrinemia with increased acid output and elevated pepsinogen secretion and is linked to duodenal ulceration. In contrast, corpus-predominant disease causes oxyntic atrophy with reduced pepsinogen I, persistent hypergastrinemia, and a relative rise in pepsinogen II from non-oxyntic mucosa. Consequently, the PGI/PGII ratio falls in atrophic gastritis and correlates with disease severity. Concurrent measurement of pepsinogen I, pepsinogen II, gastrin-17, and H. pylori status provides a noninvasive “serologic biopsy” for global assessment of gastric pathology. Atrophic gastritis compromises vitamin B12 absorption and other nutrient uptake, which can result in macrocytic anemia and neurologic complications; affected patients carry increased risk for gastric adenocarcinoma. Pepsinogen II is also elevated in gastrinoma and is produced by a subset of tumors (for example, estrogen receptor–positive, well-differentiated breast adenocarcinoma), where its expression has been associated with a more favorable prognosis.
| Reference interval |
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| Indications | Workup of suspected antral-predominant H. pylori gastritis with acid hypersecretion (postprandial and fasting epigastric pain, heartburn, nocturnal cough)., Assessment for possible atrophic gastritis presenting with epigastric discomfort, early satiety, or nausea., Evaluation of vitamin B12 deficiency and related complications (macrocytic anemia, neurologic deficits, diarrhea)., Evaluation of probable duodenal ulcer disease with nocturnal and fasting epigastric pain, postprandial pain 1.5–2 hours after meals, heartburn, or diarrhea., Evaluation of probable gastric ulcer disease with immediate postprandial epigastric pain, early satiety, or weight loss., Risk stratification for gastric adenocarcinoma in individuals with atrophic gastritis, high intake of smoked foods or alcohol, tobacco exposure, family history, or premalignant gastric conditions., Supportive testing in suspected gastrinoma/Zollinger–Ellison syndrome (severe epigastric or back pain, prominent reflux, refractory diarrhea)., Monitoring after H. pylori eradication therapy and during recovery of gastric mucosa in gastritis or peptic ulcer disease., Prognostic evaluation in breast adenocarcinoma to inform therapeutic planning. |
Possible Causes of Abnormal Results
Increased levels
- aging
- renal dysfunction
Specimen Requirements
| Specimen | Serum |
|---|---|
| Container | Gold/Tiger Top (SST, Gel Separator) |
References
Atherton JC. The pathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Annu Rev Pathol. 2006;1:63-96.
He CY, Sun LP, Gong YH, Xu Q, Dong NN, Yuan Y. Serum pepsinogen II: a neglected but useful biomarker to differentiate between diseased and normal stomachs. J Gastroenterol Hepatol. 2011 Jun;26(6):1039-46.
Vizoso F, Sánchez LM, Díez-Itza I, Merino AM, López-Otín C. Pepsinogen C is a new prognostic marker in primary breast cancer. J Clin Oncol. 1995 Jan;13(1):54-61.
Agréus L, et al. Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers. Scandinavian Journal of Gastroenterology. 2012;47:136-147.
DeVita VT, Lawrence TS, Rosenberg SA, eds. DeVita, Hellman, and Rosenberg’s Principles and Practice of Oncology. 8th ed. Lippincott Williams & Wilkins; 2008.