Effects of posterior staphyloma on choroidal structure in myopic adults: a retrospective study.

BACKGROUND: Studies on the choroid of myopic eyes with posterior staphyloma have shown that choroidal thickness decreased. This retrospective study further analysed the effects of posterior scleral staphyloma on choroidal blood vessels and matrix components compared to non-pathological myopia. METHODS: In this cross-sectional study, ninety-one eyes were divided into pathological (posterior staphyloma) and non-pathological myopia. The latter was further divided into three groups (Group 1: 26 mm ≤ axial length; Group 2: 24 mm ≤ axial length < 26 mm; Group 3: 22 mm ≤ axial length < 24 mm). Choroidal thickness, total choroidal area, luminal area, stromal area, and choroidal vascularity index were calculated. RESULTS: The CVI in N1, N2, I1, S2 of the posterior staphyloma group were lower than those of group 1 (both P < 0.05). The mean height of posterior staphyloma was associated with mean CT (Pearson correlation: r = -0.578, P = 0.039) but not with the mean CVI in posterior staphyloma group. In all groups, the mean choroidal thickness, total choroidal area, luminal area, and stromal area were significantly associated with axial length (P < 0.001), and the mean choroidal vascularity index was significantly associated with the mean choroidal thickness (P < 0.001). CONCLUSION: The choroidal structure of pathological myopia with posterior staphyloma and non-pathological myopia with longer axial length demonstrates alterations in which choroidal vessels are more impaired than the stroma. A lower choroidal vascularity index should be alert to pathological changes for myopia with axial length > 26 mm.

Current treatment of chronic hepatitis B: Clinical aspects and future directions.

Hepatitis B virus (HBV) infection is a public health threat worldwide, and there is no direct treatment yet available. In the event of infection, patients may present liver cirrhosis and cancer, which threaten the patients' health globally, especially in the Asia-Pacific region and China. In 2019, Chinese hepatopathologists updated the 2015 Guidelines for the Prevention and Treatment of Chronic Hepatitis B as the clinical reference. The other versions formulated by the American Association for the Study of Liver Diseases (2018 AASLD guidelines) (AASLD, 2018), European Association for the Study of the Liver (2017 EASL guidelines) (EASL, 2017), and Asian-Pacific Association for the Study of the Liver (2015 APASL guidelines) (APASL, 2015) also provide clinical guidance. However, there are still some issues that need to be addressed. In the present study, the following aspects will be introduced successively: (1) Who should be treated in the general population according to the guidelines; (2) Treatment of specific populations infected with HBV; (3) Controversial issues in clinical practice; (4) Perspective.

External validation of hepatocellular carcinoma risk scores in patients with chronic hepatitis B virus infection in China.

Several scores have been proposed in untreated or treated patients with chronic hepatitis B (CHB) to predict risks of hepatocellular carcinoma (HCC) occurrence. However, it is still unclear which score suits all chronic hepatitis B virus (HBV)-infected patients well, regardless of whether they are chronic carriers or CHB patients. In this study, we validated and compared the predictability of CU-HCC, REACH-B, PAGE-B and mPAGE-B in patients with chronic HBV infection in China. 1,786 patients with no history of HCC were recruited, with 978 carriers and 808 CHB patients on antiviral therapy. Patients were classified into low- and high-risk groups according to the predefined cut-off values of 5, 8, 10 and 9 for CU-HCC, REACH-B, PAGE-B and mPAGE-B. The median follow-up period was 43.7months, during which 18 (1.0%) patients developed HCC. The areas under the receiver operating characteristic curves (AUROCs) of CU-HCC, REACH-B, PAGE-B and mPAGE-B scores to predict HCC risk at 36 months were 0.815, 0.703, 0.794 and 0.825, respectively (all p < 0.05). No significant difference among AUROCs of these scores was observed except those of mPAGE-B and REACH-B at 36 months. The cumulative incidence of HCC in low- and high- risk groups based on CU-HCC, REACH-B, PAGE-B and mPAGE-B were 0.4% vs. 3.2%, 0.7% vs. 1.5%, 0.2% vs. 1.3%, and 0.2% vs. 1.7% at 36 months, respectively (all p < 0.05, except PAGE-B, log-rant test). Both CU-HCC and mPAGE-B scores accurately predict HCC risk in Chinese chronic HBV-infected patients. Patients with CU-HCC <5 or mPAGE-B <9 could be exempt from HCC surveillance within 36 months.

Soy diet for nonalcoholic fatty liver disease: A meta-analysis of randomized controlled trials.

INTRODUCTION: The efficacy of soy diet for nonalcoholic fatty liver disease remains controversial. We conduct a systematic review and meta-analysis to explore the influence of soy diet vs placebo on the treatment of non-alcoholic fatty liver disease. METHODS: We search PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through October 2020 for randomized controlled trials assessing the efficacy of soy diet vs placebo for nonalcoholic fatty liver disease. This meta-analysis is performed using the random-effect model. RESULTS: Five randomized controlled trials are included in the meta-analysis. Overall, compared with control group for nonalcoholic fatty liver disease, soy diet is associated with significantly reduced HOMA-IR (standard mean difference [SMD] = -0.42; 95% confidence interval [CI] = -0.76 to -0.08; P = .01), increased insulin (SMD = -0.64; 95% CI = -0.98 to -0.30; P = .0002) and decreased malondialdehyde (SMD = -0.43; 95% CI = -0.74 to -0.13; P = .005), but demonstrated no substantial impact on body mass index (SMD = 0.17; 95% CI = -0.20 to 0.53; P = .37), alanine aminotransferase (SMD = -0.01; 95% CI = -0.61 to 0.60; P = .98), aspartate-aminotransferase (SMD = 0.01; 95% CI = -0.47 to 0.49; P = .97), total cholesterol (SMD = 0.05; 95% CI = -0.25 to 0.35; P = .73) or low density lipoprotein (SMD = 0; 95% CI = -0.30 to 0.30; P = .99). CONCLUSIONS: Soy diet may benefit to alleviate insulin resistance for nonalcoholic fatty liver disease.

Surfactant protein A expression and distribution in human lung samples from smokers with or without chronic obstructive pulmonary disease in China.

Cigarette smoking is considered the main risk factor for chronic obstructive pulmonary disease (COPD), although the mechanism remains unknown. surfactant protein A (SP-A) is thought to protect the lung from smoking-induced damage, but related studies performed in China are scarce. The aim of the study is to assess alterations of SP-A expression and distribution in lung samples from Chinese smokers with or without COPD.This cross-sectional study assessed 45 men in Wuhan Tongji Hospital after lobectomy for lung cancer in June 2010 to September 2010. Peripheral lung specimens were collected from control nonsmokers without airflow obstruction (nonsmoking group, n = 15), smokers without airflow obstruction (smoking group, n = 15), and patients with COPD (COPD group, n = 15). SP-A expression levels in lung tissue samples and its distribution in lung cells, type II pneumocytes (PNII), and alveolar macrophages (MACR) were determined by immunoblotting and immunohistochemistry.SP-A levels were significantly decreased in the COPD group (1.00 ±â€Š0.25) compared with the smoking (2.31 ±â€Š0.64) and nonsmoking (8.03 ±â€Š2.80) groups; the smoking group also showed significantly reduced levels compared with the nonsmoking group (P < .05). PNII expressing SP-A were less abundant in the COPD group (39.3% ±â€Š7.1%) compared with the smoking group (76.2% ±â€Š29.8%), whereas SP-A MACR were more abundant (92.4% ±â€Š7.1% vs 68.5% ±â€Š20.2%) (all P < .05). Among the 30 smokers, forced expiratory volume in one second (% predicted) was positively correlated with SP-A levels (r = 0.739) and the rate of SP-A+ PNII (r = 0.811), and negatively correlated with the rate of SP-A+ MACR (r = -0.758) (all P < .05).Changes in SP-A expression and distribution in lung tissues may be involved in COPD pathogenesis in smokers.