Methods: This study included patients with biopsy-proven non-alcoholic fatty liver disease (NAFLD) diagnosed between November 2012 and October 2015. Serum cathepsin D levels were measured using the CatD enzyme-linked immunosorbent assay (USCN Life Science, Wuhan, China) using stored samples collected on the same day of the liver biopsy procedure. The performance of cathepsin D in the diagnosis and monitoring of NASH was evaluated using receiver operating characteristic analysis.
Results: Data for 216 liver biopsies and 34 healthy controls were analyzed. The mean cathepsin D level was not significantly different between NAFLD patients and controls; between NASH and non-NASH patients; and across the different steatosis, lobular inflammation, and hepatocyte ballooning grades. The area under receiver operating characteristic curve (AUROC) of cathepsin D for the diagnosis of NAFLD and NASH was 0.62 and 0.52, respectively. The AUROC of cathepsin D for the diagnosis of the different steatosis, lobular inflammation, and hepatocyte ballooning grades ranged from 0.51 to 0.58. Of the 216 liver biopsies, 152 were paired liver biopsies from 76 patients who had a repeat liver biopsy after 48 weeks. There was no significant change in the cathepsin D level at follow-up compared to baseline in patients who had histological improvement or worsening for steatosis, lobular inflammation, and hepatocyte ballooning grades. Cathepsin D was poor for predicting improvement or worsening of steatosis and hepatocyte ballooning, with AUROC ranging from 0.47 to 0.54. It was fair for predicting worsening (AUROC 0.73) but poor for predicting improvement (AUROC 0.54) of lobular inflammation.
Conclusion: Cathepsin D was a poor biomarker for the diagnosis and monitoring of NASH in our cohort of Asian patients, somewhat inconsistent with previous observations in Caucasian patients. Further studies in different cohorts are needed to verify our observation.
Methods: Colectomy samples were obtained from 11 adults (mean age 45.7, six males) who were residents of Northeastern Peninsular Malaysia. Microplastics were identified following chemical digestion of specimens and subsequent filtration. The samples were then examined for characteristics (abundance, length, shape, and color) and composition of three common polymer types using stereo- and Fourier Transform InfraRed (FTIR) microscopes.
Results: Microplastics were detected in all 11 specimens with an average of 331 particles/individual specimen or 28.1 ± 15.4 particles/g tissue. Filaments or fibers accounted for 96.1% of particles, and 73.1% of all filaments were transparent. Out of 40 random filaments from 10 specimens (one had indeterminate spectra patterns), 90% were polycarbonate, 50% were polyamide, and 40% were polypropylene.
Conclusion: Our study suggests that microplastics are ubiquitously present in the human colon.
Methods: Lactase activity was measured with a 13CO2 lactose breath test using an infrared spectrometer. Each subject took 25 g of lactose naturally enriched in 13CO2 together with 250 mL of water after an overnight fast. Breath samples were collected at baseline and at 15-min intervals for 180 min. Subjects were asked to report gastrointestinal (GI) symptoms following ingestion of the lactose test meal.
Results: Of the 248 subjects tested, 216 (87.1%) were lactase deficient. We found no significant differences in the presentation of LD between gender and races. LD was found in 87.5% of males and 86.8% of females (P = 0.975) and in different races: Chinese (88.5%) versus Malay (83.1%) (P = 0.399), Indian (90.5%) versus Malay (P = 0.295), and Chinese versus Indian (P = 0.902). LI was diagnosed in only 49 (19.8%) subjects; 35 patients had diarrhea, while the remainder had at least two other GI symptoms after the lactose meal.
Conclusion: The prevalence of LD was high in all three major ethnic groups-Malays, Chinese, and Indians. Ironically, the prevalence of LI was low overall.