Diagnostic accuracy of RPR, FIB-4, APRI and AAR in liver fibrosis patients with chronic hepatitis B / 中国实用内科杂志

OBJECTIVE: We intended to evaluate the diagnostic efficiency of red cell distribution width to platelet ratio(RPR),and compare it with other three markers of fibrosis-4(FIB-4), aspartate aminotransferase-to-platelet-ratio-index(APRI) and aspartateaminotransferase-to-alanine aminotransferase ratio(AAR) for judging liver fibrosis and fibrosis severity in patients with chronic hepatitis B(CHB). METHODS: who had not received antiviral treatment met the requirements of this cross-sectional study. Hematology,biochemistry, virology testing and liver biopsy were performed. Receiver-operating characteristic curves were constructed and the area under the ROC curve was calculated. RESULTS: The cut-off value for distinguishing F0-1, F2-3 and F4 was 0.079, 0.141 and 0.279,respectively(P<0.001) for RPR; 1.194, 3.703 and 4.383(P<0.001) for FIB-4; 0.384, 0.660 and 1.441, respectively(P<0.001) for APRI; and 0.915, 0.850 and 0.960(P=0.706) for AAR. The sensitivity was 76.09% for RPR, 78.26% for FIB-4, 97.83% for AAR and80.43% for APRI; specificity was 81.48% for RPR, 75.93% for FIB-4, 14.81% for AAR and 80.43% for APRI; the AUROC was 0.787 for RPR, 0.778 for FIB-4, 0.540 for AAR and 0.759 for APRI. The common cut-off value was 0.11, 1.94, 0.60 and 0.59 for RPR, FIB-4, AAR and APRI respectively. CONCLUSION: RPR, FIB-4 and APRI have good efficiency in appraising significant and severe fibrosis in patients with CHB, however RPR is superior to FIB-4 and FIB-4 is superior to APRI, therefore, RPR is a better index in evaluating liver cirrhosis.

Dietary modification in patients with nonalcoholic fatty liver disease / 中国实用内科杂志

Obesity is the greatest risk factor of nonalcoholic fatty liver disease(NAFLD),and the prevalence of NAFLD is over 90% in severe obesity. Losing weight can improve and even reverse NAFLD to varying degrees. Dietary modification is the most efficacious method in the weight reduction of NAFLD, for it can effectively reduce fatty and chang inflammation of liver cells by controlling calorie intake and regulating the proportion of nutrients, and the fibrillation can also be improved. In this paper, we discuss the calorie intake and dietary pattern of general population, the elderly and school-aged children, focusing on how NAFLD patients control their weight through dietary modification.

Changes in the intestinal microenvironment during development of alcoholic fatty liver disease and related effects of probiotic therapy / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the initial changes in the gut microenvironment that accompany intestinal endotoxemia related to alcoholic fatty liver disease (ALD) in order to explore the potential initiating factors and to observe the effect of probiotic therapy on these factors.</p><p><b>METHODS</b>Fifty Sprague-Dawley male rats were randomly divided into an ALD model group (alcoholic intragastric administration), an intervention group (ALD with probiotic intragastric administration), and a control group (physiological saline intragastric administration). Histological changes of the liver were evaluated using hematoxylin-eosin staining and light microscopy. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglycerides (TG), and plasma endotoxin and coli bacillus were determined. The structural integrity of intestinal mucosa and tight junctions were observed by transmission electron microscopy. Occludin protein expression in intestinal epithelial cells was detected by immunohistochemistry.</p><p><b>RESULTS</b>After four weeks, the three groups showed significant differences in the plasma endotoxin levels [control: (0.67+/-0.14) pg/ml, model: (4.42+/-1.28) pg/ml, and intervention: (2.88+/-0.83) pg/ml; F = 27.288, P = 0.000] and numbers of Escherichia coli [control: (2.31+/-0.39) lg3/ml, model: (3.23+/-0.41) lg3/ml, and intervention: (2.24+/-0.44) lg3/ml; F = 10.692, P = 0.001]. The plasma endotoxin level and E. coli number were significantly higher in the model group than in the control group and the intervention group (all P less than 0.05). The three groups showed no significant differences in the levels of ALT, AST, and TG at four weeks. After eight weeks, however, all three serum markers were significantly different between the three groups [ALT: control: (62.33+/-7.12) U/L, model: (95.50+/-8.73) U/L, and intervention: (81.33+/-6.19) U/L; F = 18.051, P = 0.000]; [AST: control: (90.50+/-10.67) U/L, model: (130.00+/-14.91) U/L, and intervention: (110.33+/-7.26) U/L; F = 30.170, P = 0.000]; [TG: control: (0.84+/-0.84) mmol/L, model: (1.40+/-0.17) mmol/L, and intervention: (1.10+/-0.17) mmol/L; F = 10.592, P = 0.001]. In addition, the three groups showed significant differences in E. coli number [control: (2.23+/-0.46) lg3/ml, model: (4.81+/-0.29) lg3/ml, and intervention: (3.61+/-0.50) lg3/ml; F = 23.579, P = 0.000] and plasma endotoxin level [control: (0.52+/-0.21) pg/ml, model: (12.46+/-2.61) pg/ml, intervention: (6.83+/-1.74) pg/ml; F = 30.731, P = 0.000]. The levels of ALT, AST, TG and endotoxin, and the number of E. coli were all significantly higher in the model group than in the control group and the intervention group (all P less than 0.05). Small intestinal epithelial cell structural failure was more apparent and intercellular gaps more broad after eight weeks than after four weeks for all three groups. However, the intervention group showed clearer cell connection structures and less extensive cell gap broadening than the model group at eight weeks. After eight weeks, the occludin protein had become significantly down-regulated and distributed in a non-continuous pattern in the model group, as compared with the control group. However, the occludin protein expression was higher in intervention group than in the model group.</p><p><b>CONCLUSION</b>Intestinal endotoxemia related to perturbations in the microenvironment occurs in the early phase of ALD, and the increased intestinal permeability appears to be the initial factor of elevated plasma endotoxin, which may lead to liver damage. Probiotic therapy can reduced plasma endotoxin levels and postpone ALD progression by altering the composition of the gut microbiota and up-regulating expression of the occludin protein in intestinal epithelial cells.</p>

Macrophage-inducible C-type lectin is associated with anti-cyclic citrullinated peptide antibodies-positive rheumatoid arthritis in men / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Macrophage-inducible C-type lectin (MINCLE) is an important member of C-type lectin superfamily, which has been shown evidence for susceptibility to arthritis in animal models. We aimed to investigate the possible association of MINCLE with rheumatoid arthritis (RA) susceptibility in Chinese Han population.</p><p><b>METHODS</b>Haplotypes from HapMap database (Chinese Han Beijing, CHB) were used to select tag-single nucleotide polymorphism (SNP) (r(2) = 0.8) residing in MINCLE gene. A total of 563 patients with RA and 404 healthy controls were TagMan genotyped for SNP rs10841845. Association analyses were performed on the whole data set and on RA subsets based on gender difference and the status of anti-cyclic citrullinated peptide (anti-CCP) antibody in RA patients. Association statistics were calculated by age and sex adjusted logistic regression.</p><p><b>RESULTS</b>Overall, MINCLE SNP rs10841845 was not associated with susceptibility to RA. However, following anti-CCP stratification, rs10841845 GG genotypes conferred a significantly protective effects against anti-CCP-positive RA (OR 0.65, 95%CI 0.430 - 0.995, P = 0.048). Following gender stratification, SNP rs10841845 G allele appeared to insert its RA protective effect only in male patients, both at allele level (G vs. A OR 0.66, 95%CI 0.46 - 0.93, P = 0.018) and at genotype level (GG vs. AA+AG, OR 0.429, 95%CI 0.20 - 0.95, P = 0.036). Notably, the male RA protective effect of rs10841845 G allele was only seen in anti-CCP-positive RA (G vs. A: OR 0.64, 95%CI 0.43 - 0.96, P = 0.029; GG vs. AA+AG: OR 0.375, 95%CI 0.14 - 0.94, P = 0.038). Furthermore, we observed a significant reduction of Disease Activity Score (DAS) 28 score (3.91 ± 0.70 vs. 5.66 ± 0.31, P = 0.022) and serum C-reactive protein levels (31.64 ± 24.13 vs. 91.80 ± 12.02, P = 0.012) in male anti-CCP-positive RA patients carrying rs10841845 GG genotype, compared with patients carrying AA+AG genotypes.</p><p><b>CONCLUSIONS</b>Our study provides the evidence for a gender specific association between MINCLE rs10841845 and RA susceptibility. The SNP rs10841845 G allele appears to have protective effect against anti-CCP-positive RA and confer reduced RA activity in men.</p>

Rs548234 polymorphism at PRDM1-ATG5 region susceptible to rheumatoid arthritis in Caucasians is not associated with rheumatoid arthritis in Chinese Han population / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>A previous study has shown that rs548234 polymorphism at PRDM1-ATG5 region is associated with rheumatoid arthritis (RA) in Caucasian populations. The aim of this study was to investigate the effect of rs548234 polymorphism at PRDM1-ATG5 region on susceptibility to RA in Chinese Han population.</p><p><b>METHODS</b>We genotyped 848 RA patients and 1431 matched healthy controls for rs548234 single-nucleotide polymorphism (SNP) with a predesigned TaqMan SNP genotyping assay. Association analyses were performed on the whole data set and on rheumatoid factors (RF) and anti-cyclic citrullinated peptides (anti-CCP) antibody. Finally, we carried out combined analysis of rs548234 association with RA based on the published data.</p><p><b>RESULTS</b>No significant difference in the genotype distribution between RA patients and healthy controls for rs548234 (C/T) polymorphism was found in Chinese Han population, neither in whole data set nor in stratified subsets, e.g. RF and anti-CCP status. Association analysis in different ethnic groups showed that rs548234 at PRDM1-ATG5 region was associated with RA in Caucasian ancestry but not in East Asian population.</p><p><b>CONCLUSIONS</b>Our results showed no involvement of rs548234 at PRDM1-ATG5 region in the susceptibility or clinical relevance of RA in Chinese Han population.</p>