| Autor: |
Loong TH; Unit of Gastroenterology and Hepatology, Department of Medicine, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Soon NC; Unit of Gastroenterology and Hepatology, Department of Medicine, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Nik Mahmud NRK; Unit of Upper Gastrointestinal and Bariatric Surgery, Department of Surgery, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Naidu J; Unit of Gastroenterology and Hepatology, Department of Medicine, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Rani RA; Unit of Gastroenterology and Hepatology, Department of Medicine, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia.; Faculty of Medicine, Universiti Teknologi MARA, 40450 Shah Alam, Selangor, Malaysia., Abdul Hamid N; Department of Physiology, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia.; Faculty of Medicine and Health Sciences, Universiti Sains Islam Malaysia, 71800 Negeri Sembilan, Malaysia., Elias MH; Department of Physiology, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Mohamed Rose I; Department of Pathology, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Tamil A; Department of Community Health, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Mokhtar NM; Department of Physiology, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia., Raja Ali RA; Unit of Gastroenterology and Hepatology, Department of Medicine, Pusat Perubatan Universiti Kebangsaan Malaysia, Bandar Tun Razak, 56000 Kuala Lumpur, Malaysia. |
| Abstrakt: |
There is a lack of non-invasive screening modalities to diagnose chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). Thus, the aim of the present study was to determine the sensitivity and specificity of serum pepsinogen I (PGI), PGI:II, the PGI:II ratio and gastrin-17 (G-17) in diagnosing CAG and IM, and the correlations between these serum biomarkers and pre-malignant gastric lesions. A cross-sectional study of 72 patients (82% of the calculated sample size) who underwent oesophageal-gastro-duodenoscopy for dyspepsia was performed in the present study. The mean age of the participants was 56.2±16.2 years. Serum PGI:I, PGI:II, G-17 and Helicobacter pylori antibody levels were measured by enzyme-linked immunosorbent assay. Median levels of PGI:I, PGI:II, the PGI:II ratio and G-17 for were 129.9 µg/l, 10.3 µg/l, 14.7 and 4.4 pmol/l, respectively. Subjects with corpus CAG/IM exhibited a significantly lower PGI:II ratio (7.2) compared with the control group (15.7; P<0.001). Histological CAG and IM correlated well with the serum PGI:II ratio (r=-0.417; P<0.001). The cut-off value of the PGI:II ratio of ≤10.0 demonstrated high sensitivity (83.3%), specificity (77.9%) and area under the receiver operating characteristic curve of 0.902 in detecting the two conditions. However, the sensitivity was particularly low at a ratio of ≤3.0. The serum PGI:II ratio is a sensitive and specific marker to diagnose corpus CAG/IM, but at a high cut-off value. This ratio may potentially be used as an outpatient, non-invasive biomarker for detecting corpus CAG/IM. |
