gastritis progress over years into atrophic type, which considerably increase the risk of gastric adenoma, cancer and MALT lymphoma [10]. Approximately 10% of patients suffering from gastritis caused by H. pylori develop severe Atrophic gastritis of the corpus [11,12]. An early diagnosis of atrophic gastritis and the eradication of H. pylori form bases for treatment of atrophic gastritis and the prevention of related diseases. The prevalence of H. pylori infection obtained (81.40%) and that for atrophic gastritis (8.1%). The finding is consistent with the reports that atrophic gastritis prevalence in the world is about 10% [11,12]. In the diagnosis of H. pylori infection by the GastroPanel test the sensitivity and specificity were 95.7% and 62.5% respectively, with 91.8% of PPV and 76.9% of NPV. Although the serological pattern of H. pylori infection was statistically similar to the histological pattern (p > 0.50) (Table 1), the low specificity and NPV are however, due to levels of H. pylori IgG which can remain elevated for up to six to twelve months even after eradication and thus not being able to distinguish between past and recent infection [1]. But in conjunction with pepsinogens and gastrin-17 it can serve to diagnose inflammation related to other causes such as autoimmunity and use of nonsteroidal anti inflammatory drugs [1,4].

A statististically significant decrease in the mean PGI concentrations with increasing atrophic stages in the corpus was observed (p = 0.003). These findings were consistent with the report of Pasechnikov et al. (2005) [10] that serum pepsinogens decrease as atrophic gastritis in the corpus worsens due to loss of mucosal glands and cells. The use of serum pepsinogen I levels as an assessment of gastric acid secretion was adopted as early as in 1985 [13,14]. The clinical significance of pepsinogen A and pepsinogen C and serum gastrin levels [15] and the role of serum pepsinogen I and serum gastrin in the screening of severe atrophic corpus gastritis had been studied [16] and in screening of atrophic pan gastritis with high risk of cancer [17]. PGI reflects the status of the mucosa of the corpus and fundus of the stomach and is a wellknown indicator of the corpus mucosa.

For the scoring of atrophy by the GastroPanel test the sensitivity, specificity, PPV and NPV were respectively 85.7%, 88.6%, 40.0% and 98.6%. These results are similar with what has been reported in many other countries for example Sipponen et al. (2002) [18] in Finland; Väänänen et al. (2003) [19] in Finland; Pasechnikov et al. (2004) [20] in Russia; Cavallaro et al. (2004) [21] in Italy respectively reported the accuracy, sensitivity and specificity of the GastroPanel test as (91%:89%:93:%); (81%:79%:91%); (84%:79%:96%) and (96%:78%:98%). There was however, a significant difference in the diagnosis of atrophic antrum gastritis between the GastroPanel and histology (p < 0.01). This difference also looking at the low PPV value may be due to false positive diagnosis of atrophic antrum gastritis. We used fasting gastrin levels which can not differentiate between atrophic antrum gastritis and high intragastric acid output. According to Di Mario et al. 2008 [1] and Sipponen et al. 2002 [19] high acid secretion may inhibit the release of G-17 from antral G-cells, resulting in low serum levels of G-17 and in false interpretation of the presence of antral atrophy. However, these may be the patients in whom the risk of acid -related duodenogastric or gastro-oesophageal diseases is highest. Differentiation between high acid output and atrophic antrum gastritis can be achieved with the measurement of stimulated gastrin after a protein drink [4]. None the less significant reduced levels of gastrin-17 (p = 0.037) with progression to antrum atrophy was observed implicating its role in atrum atrophy diagnosis.

5. CONCLUSION

The diagnosis of atrophic gastritis obtained with the blood test panel of G-17, PGI and H. pylori antibodies is in a strong agreement with the biopsy findings, and thus the GastroPanel test can be a useful non endoscopic assessment of stomach mucosal atrophy in patients with dyspepsia. Due to its high sensitivity for atrophic gastritis diagnosis, it can be used in the screening of patients at risk of gastric cancer and peptic ulcer disease. Similarly, because of its high specificity for detecting normal stomach mucosa and non atrophic gastritis (superficial gastritis), it can be used to avoid endoscopic examination. The latter of which is invasive, expensive and limited.

6. ACKNOWLEDGEMENTS

Special thanks to Dr. AWONO Parfait of OCEAC Cameroon.

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NOTES

*Corresponding author.

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