GALAD score and a proposal for GALADUS model for detecting hepatocellular carcinoma in Vietnamese patients with chronic liver disease.

OBJECTIVE: The GALAD score, a serum biomarker-based model, predicts the likelihood of hepatocellular carcinoma (HCC) in patients with chronic liver disease. We evaluated the performance of the GALAD score compared to that of liver ultrasound in detecting HCC. PATIENTS AND METHODS: This study recruited a group of 136 patients with HCC and a control group of 436 patients with cirrhosis or chronic hepatitis B or hepatitis C. The performance of the GALAD score and ultrasound in detecting HCC in these patients was analyzed using the area under the receiver operating characteristic curve (AUC). The sensitivity and specificity of the optimal GALAD score were compared to those of ultrasound. RESULTS: The AUC of the GALAD score for detecting HCC was 0.940 [95% confidence interval (CI) 0.92-0.96], higher than that of ultrasound [0.939 (0.91-0.96), p < 0.001]. At a threshold of 1.24, the GALAD score had a sensitivity of 91.2% and a specificity of 81.9% for detecting HCC. The AUC of the GALAD score for early HCC detection was 0.75 (95% CI 0.71-0.80, p < 0.001; threshold 1.13, sensitivity 87.5%, specificity 67.8%, p < 0.001). The combination of GALAD and ultrasound (GALADUS score) showed further improvement, achieving an AUC of 0.97 (95% CI 0.96-0.99; cut-off point 1.37, sensitivity 95.6%, specificity 89.2%, p < 0.001). CONCLUSIONS: In our study, the GALADUS score showed improved performance compared to the GALAD score. Therefore, we suggest that the performance of the GALAD score should be reconsidered and that it should be evaluated in combination with ultrasound for HCC detection.

Relationship between PET/CT images and KRAS gene mutations in colorectal cancer in Vietnamese patients.

OBJECTIVE: We conducted this study to determine the relationship among standardized uptake value (SUV), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) indexes of Flourine-18 fluorodeoxyglucose positron emission tomography/computed tomography18 (FDG-PET/CT) imaging and Kirsten rat sarcoma (KRAS) gene mutations in colorectal cancer (CRC). PATIENTS AND METHODS: This cross-sectional study was conducted in Bach Mai Hospital from 2020 to 2022. It included newly diagnosed CRC patients who underwent PET/CT examination prior to primary tumor resection. The maximum SUV (SUVmax - SUVmean), MTV, and TLG were considered. All pathologically confirmed CRC patients were accepted with further KRAS mutation status analysis. RESULTS: We enrolled 63 newly diagnosed CRC patients who underwent PET/CT examination prior to primary tumor resection. Among them, 31 (49.2%) patients had KRAS gene mutation. Patients with KRAS mutation status showed significantly different and higher SUVmax (p-value = 0.025), SUVmax t/b (p-value = 0.013), SUVmax t-b (p-value = 0.014), MTV (p-value = 0.023), and TLG (p-value = 0.011) than patients with WT KRAS. Other characteristics, including age, gender, tumor location, SUVb, SUVmean, SUVmax of lymph nodes, and SUVmax of liver metastasis, were insignificantly different between the two groups of patients with KRAS mutation status. Receiver operating curve analysis showed that the area under the curve was 0.672 for SUVmax (p-value = 0.019), SUVt/b (p-value = 0.045), and SUVt-b (p-value = 0.020). CONCLUSIONS: We observed a relationship, considering the quantitative parameters (SUVmax, SUVmax, SUVmax t-b, MTV, and TLG), between 18FDG-PET/CT images and the KRAS gene mutation in CRC by analyzing 63 patients prior to treatment.

MARCO variants are associated with phagocytosis, pulmonary tuberculosis susceptibility and Beijing lineage.

Macrophage receptor with collagenous structure (MARCO) has an important role in the phagocytosis of Mycobacterium tuberculosis (M. tuberculosis). We hypothesized that MARCO polymorphisms are associated with phagocytosis, tuberculosis (TB) disease susceptibility and presentation, and infecting lineage. We used a human cellular model to examine how MARCO genotype mediates the immune response; a case-control study to investigate tuberculosis host genetic susceptibility; and a host-pathogen genetic analysis to study host-pathogen interactions. Two MARCO heterozygous (AG) genotypes (single-nucleotide polymorphisms rs2278589 and rs6751745) were associated with impaired phagocytosis of M. tuberculosis trehalose 6,6'-dimycolate-cord factor and ß-glucan-coated beads in macrophages. The heterozygous genotypes of rs2278589 and rs6751745 were also associated with increased risk of pulmonary TB (PTB; rs2278589, P=0.001, odds ratio (OR)=1.6; rs6751745, P=0.009, OR=1.4), and with severe chest X-ray abnormalities (P=0.007, OR=1.6). These two genotypes were also associated with the Beijing lineage (rs2278589, P=0.001, OR=1.7; rs6751745, P=0.01, OR=1.5). Together, these results suggest that MARCO polymorphisms may regulate phagocytosis of M. tuberculosis and susceptibility and severity of PTB. They also suggest MARCO genotype and Beijing strains may interact to increase the risk of PTB.