In Indonesia, endoscopy services are limited and studies about gastric mucosal status by using pepsinogens (PGs) are rare. We measured PG levels, and calculated the best cutoff and predictive values for discriminating gastric mucosal status among ethnic groups in Indonesia. We collected gastric biopsy specimens and sera from 233 patients with dyspepsia living in three Indonesian islands. When ≥5.5 U/mL was used as the best cutoff value of Helicobacter pylori antibody titer, 8.6% (20 of 233) were positive for H. pylori infection. PG I and II levels were higher among smokers, and PG I was higher in alcohol drinkers than in their counterparts. PG II level was significantly higher, whereas PG I/II ratios were lower in H. pylori-positive than in H. pylori-negative patients. PG I/II ratios showed a significant inverse correlation with the inflammation and atrophy scores of the antrum. The best cutoff values of PG I/II were 4.05 and 3.55 for discriminating chronic and atrophic gastritis, respectively. PG I, PG II, and PG I/II ratios were significantly lower in subjects from Bangli than in those from Makassar and Surabaya, and concordant with the ABC group distribution; however, group D (H. pylori negative/PG positive) was the lowest in subjects from Bangli. In conclusion, validation of indirect methods is necessary before their application. We confirmed that serum PG level is a useful biomarker determining chronic gastritis, but a modest sensitivity for atrophic gastritis in Indonesia. The ABC method should be used with caution in areas with a low prevalence of H. pylori.

Dyspepsia still becomes a major challenge in upper gastrointestinal disease in Indonesia. This disease often correlated with Helicobacter pylori infection. However, the prevalence of this bacterium is generally low in Indonesia. Therefore, several considerations should be taken into consideration during the management of dyspepsia and H. pylori infection. “Management of dyspepsia and H. pylori infection in Indonesia: The Indonesian consensus report” comprises information gathered from 22 gastroenterology centers across Indonesia. The experts gathered to evolve a consensus, that consists of the statements, grades of recommendations, evidence levels, and rationales for the dyspepsia and H. pylori infection management for daily clinical practice. The report explains several aspects from the updated epidemiology information to comprehensive management therapy. After the experts worked together on all statements in the recommendations, the results are presented with the final agreement as a consensus to help clinicians in understanding, diagnosing, and treating dyspepsia and H. pylori infection patients in daily clinical practice in Indonesia.

Background. The host immune system plays an important role in hepatitis B virus (HBV) infection manifestation. Genetic polymorphisms of several inflammatory cytokines, including TNF-α and IL-10, have been associated with chronic hepatitis B (CHB) progression, although with contradicting results. CHB progression can be categorized into four phases, immune tolerance (IT), immune clearance (IC), low/no replicative (LR), and e-negative hepatitis (ENH), with HBeAg seroconversion as an important milestone. Here, we determined the association of TNF-α (rs1800629) and IL-10 (rs1800896 and rs1800872) SNPs in the context of CHB natural history progression, particularly to HBeAg seroconversion, in Indonesian CHB patients. Methods. A total of 287 subjects were recruited and categorized into distinct CHB phases based on HBeAg, viral load, and ALT levels. TNF-α and IL-10 SNPs were determined using PCR-RFLP and confirmed with direct sequencing. The association between SNP genotypes with CHB dynamics was determined using logistic regression presented as odds ratio (OR) with 95% CI. Results. No significant association was found between IL-10 -592A/C polymorphism and progression of IT and IC to LR, IT and IC to ENH, and LR to ENH phases in all the gene models. IL-10 rs1800896 and TNF-α rs1800629 could not be analyzed using logistic regression. Subjects’ age (≥40 years old) was significantly associated with IT and IC to LR (OR: 2.191, 95% CI 1.067–4.578, $P=0.034$ ), IT and IC to ENH (OR: 7.460, 95% CI 3.316–18.310, $P<0.001$ ), and LR to ENH (OR: 5.252, 95% CI 2.010–14.858, $P=0.001$ ). Male gender was associated with LR to ENH (OR: 4.077, 95% CI 1.605–11.023, $P=0.004$ ). Conclusions. Age and male gender were associated with CHB phase progression instead of the TNF-α and IL-10 polymorphisms. It would be beneficial to study not only the effect of host determinants but also the viral factor to understand the mechanisms of CHB phase progression.

Non-Alcoholic Fatty Liver Disease (NAFLD) is chronic liver disease with poor outcome, especially in subjects with liver fibrosis. NAFLD is an independent cardiovascular risk factor for the development of Chronic kidney disease (CKD). CKD prevalence in NAFLD subjects are twice higher than non-NAFLD subjects, especially in patients with liver fibrosis. This study aims to evaluated relationship between liver fibrosis and CKD in NAFLD subjects.

Objective The present study evaluated the profile of endoglin (CD105) and vascular endothelial growth factor (VEGF) based on staging and histopathological grading of colorectal cancer as well as their relationship with bevacizumab therapy. Methods A total of 88 cases of colorectal adenocarcinoma were included in the present study. The levels of VEGF and CD105 protein were evaluated with enzyme-linked immunosorbent assay (ELISA). Results There was a significant difference in the level of CD105 (p = 0.002) between metastases and non-metastases subjects, showing that CD105 was higher in metastases subjects (4.59 ng/ml). There was no significant difference in the level of VEGF based on the presence of metastasis (p = 0.625). There was a significant difference in the levels of CD105 (p = 0.038) and VEGF (p = 0.010) between the subjects who received chemotherapy and those who did not. The CD105 level was higher in the subjects who received chemotherapy (4.43 ng/ml); conversely, the level of VEGF was lower in subjects who received chemotherapy (543.65 pg/ml). There was a statistically significant difference in the levels of CD105 (p = 0.003) and VEGF (p = 0.002) between subjects who received bevacizumab therapy and subjects who did not. The levels of CD105 were higher in subjects who received bevacizumab therapy (5.11 ng/ml); in contrast, the level of VEGF was higher in subjects who did not receive bevacizumab therapy (645.92 pg/ml). There was a significant positive correlation between CD105 and VEGF in subjects who did not receive bevacizumab (p < 0.01). Conclusion The results of this study support a hypothesis of “escape mechanism” in the failure of anti-angiogenesis therapy (anti-VEGF).

Introduction: One of the chronic kidney disease (CKD) manifestations is mineral disorder, such as phosphate and calcium. Phosphatonin levels are regulated by the hormone phosphatonin, which the most commonly associated with CKD is fibroblast growth factor-23 (FGF-23), mainly synthesized by bone cells. The increase in FGF-23 in CKD subjects is a physiological response to stabilize phosphate levels. Several conditions can increase FGF-23 levels including age, body mass index (BMI), diabetes mellitus (DM), and hypertension. Objectives: This study aims to test the correlation between FGF-23 levels at various stages of glomerular filtration rate (GFR) in CKD. Patients and Methods: This study is observational with a cross-sectional approach conducted at Wahidin Sudirohusodo and Unhas hospitals of Makassar. Subjects are CKD patients which meet inclusion criteria. Intact serum FGF-23 levels were measured using an ELISA (enzyme-linked immunosorbent assay) kit (Immutopics). Statistical analysis was conducted using ANOVA test, Mann-Whitney U, and Spearman’s correlation tests. Statistical results are considered significant if P<0.05. Results: The research was conducted on 78 subjects with CKD stages 3, 4 and 5, which consisted of 40 men and 38 women. The correlation test showed that the lower the GFR, the higher the FGF-23 level (P0.05). Conclusion: We found that every increase in the CKD stages and decrease of GFR, would be associated with an increase in the plasma levels of FGF-23. However, FGF-23 plasma concentration had no significant correlation with age, BMI, DM, and hypertension.