Elevated LDL-c may warn of the risk of gallbladder stones in the patients with metabolic dysfunction-associated steatotic liver disease: A case-control study.

PURPOSE: This study aimed to explore the relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and the development of new-onset gallbladder stone disease (GSD) and to identify factors that influence the occurrence of new-onset GSD in patients with MASLD. METHODS: In this retrospective case-control study, patients who underwent asymptomatic GSD screening during annual routine health check-ups at two hospitals in China between August 2017 and July 2022 were included. Patients with new-onset GSD and controls without GSD were matched 1:1 based on age, sex, race, occupation, diet, drinking habits, systolic blood pressure, diastolic blood pressure, and fasting blood glucose levels. RESULTS: The study comprised 1200 patients with new-onset GSD and 1200 controls without GSD. Patients with new-onset GSD had higher rates of MASLD (33.8% vs. 22.2 %, P < 0.001) and hypercholesterolemia (12.6% vs. 7.2 %, P < 0.001) compared to controls. Waist circumference (WC) (OR = 1.042, 95 % CI: 1.022-1.063, P < 0.001), high-density lipoprotein cholesterol (HDL-c) (OR = 0.048, 95 % CI: 0.037-0.062, P < 0.001), triglycerides (OR = 0.819, 95 % CI: 0.699-0.958, P = 0.013), and hypercholesterolemia (OR = 5.023, 95 % CI: 2.735-9.225, P < 0.001) were independently associated with new-onset GSD. Among patients with MASLD, WC (OR = 1.075, 95 % CI: 1.026-1.127, P = 0.003), total cholesterol (TC) (OR = 2.094, 95 % CI: 1.259-3.484, P = 0.004), HDL-c (OR = 0.088, 95 % CI: 0.054-0.142, P < 0.001), and low-density lipoprotein cholesterol (LDL-c) (OR = 4.056, 95 % CI: 2.669-6.163, P < 0.001) were independently associated with new-onset GSD. CONCLUSIONS: The findings indicate that hypercholesterolemia is independently associated with GSD. Among patients with MASLD, hypercholesterolemia also showed an independent association with GSD. Notably, this study is the first to identify serum LDL-c levels as potentially the most significant risk factor for GSD, highlighting that elevated LDL-c could serve as an important indicator for individuals with MASLD.

[The association of vitamin D receptor gene ApaI and BsmI polymorphism with systemic lupus erythematosus].

OBJECTIVE: To determine the distribution of vitamin D receptor (VDR) gene ApaI and BsmI polymorphism in systemic lupus erythematosus (SLE) and the association with SLE in Chinese Han patients. METHODS: Genomic DNA from 244 Chinese SLE patients and 162 sex and ethnically matched controls were typed for VDR ApaI and BsmI polymorphism combination by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Clinical characteristics were analyzed between different ApaI and BsmI genotypes. RESULTS: There was no significant difference between the distribution frequencies of allelic gene A and a in SLE patients and the controls, but the distribution frequency of genotypes heterozygote Aa in SLE patients was higher than that in the controls (38.9% vs 22.2%, χ(2) = 12.442, P = 0.000). There was no significant difference between the distribution frequency of allelic gene and genotypes of BsmI in SLE patients and the controls (P > 0.05). However, there was significant difference between the distribution frequencies of ApaI and BsmI genotypes combination in SLE patients and the controls (χ(2) = 18.226, P = 0.006). The distribution frequency of genotypes Aa-bb in SLE patients was higher than that in the controls (32.4% vs 17.9%, χ(2) = 10.449 P = 0.001), while the distribution frequency of genotypes Aa-bb in SLE patients was lower than that in the controls (30.3% vs 42.0%, χ(2) = 5.808, P = 0.016). Furthermore, analyzing the effect of VDR ApaI and BsmI polymorphism combination to the symptoms of SLE, significant difference was observed in SLE patients carrying Aa-bb genotypes involved in serositis (P = 0.003), hematological system disorder (P = 0.021), and anti-Sm antibodies (P = 0.01) compared with other genotypes. CONCLUSION: There is significant association between ApaI and BsmI gene polymorphism Aa-bb genotypes and the incidence of SLE in the Han population of China, and genotype Aa-bb is more involved in serositis, hematological system disorder and has a positive effect on production of antibodies.

[Detecting anti-megakaryocyte antibodies in serum of systemic lupus erythematosus patients by indirect immunofluorescence].

This study was purposed to investigate the mechanism of thrombocytopenia in patients with systemic lupus erythematosus (SLE) through detecting anti-megakaryocyte antibodies in SLE patients. The serum anti-megakaryocyte antibodies in 36 SLE cases with thrombocytopenia were detected by using indirect immunofluorescence, the detected results were compared with detected results of 30 SLE cases without thrombocytopenia and 30 healthy persons. The results showed that the positive incidences of anti-megakaryocyte antibody in serum of 36 SLE cases with thrombocytopenia, 30 SLE cases without thrombocytopenia and 30 healthy persons were 19.4% (7/36), 6.7% (2/30) and 3.3% (1/30) respectively. As compared with SLE patients without thrombocytopenia and healthy persons, SLE patients with thrombocytopenia had higher incidence of anti-megakaryocyte antibodies, moreover there was significant difference between SLE patients with thrombocytopenia and healthy persons (p < 0.05), while there was no significant difference between SLE patients with or without thrombocytopenia (p > 0.05). It is concluded that autoantibodies against megakaryocytes exist in SLE patients and may partially contribute to the incidence of thrombocytopenia in SLE patients. The detection of anti-megakaryocyte antibodies with a enough case number is needed to make a final conclusion on thrombocytopenia pathogenesis in SLE.

[Reflux of bile induces esophageal mucosal inflammation and apoptosis in rats].

OBJECTIVE: To investigate the esophageal mucosal inflammation and apoptosis induced by reflux of different duodenal or bile in rats. METHODS: Esophagus division in esophagogastric junction and then esophagoduodenostomy were performed on rats to make the models of duodenogastroesophageal reflux (DGER). Three kinds of reflux model, DGER (Group A), duodenoesophageal reflux without gastric juice (Group B) and DGER without bile (Group C) were made by adjusting the DGER models. 9 weeks after operation, the esophageal mucosal inflammation was examined under microscope, and the esophageal apoptosis was tested by DNA fragmentation in situ using TdT-mediated dUTP biotin nick end labling (TUNEL). Immunohistochemical method was used to detect the status of esophageal Fas protein (CD95) associated apoptosis. RESULTS: Evidences of reflux esophagitis were seen in all rats with different reflux models. Esophageal inflammation was most severe in group A, then in group B, and the slightest in group C. Barrett's esophagus was seen in group A and group B but not in group C, and the incidence was found to be of no difference between the A and B groups (P > 0.05). Esophageal mucosal apoptosis index in group A was (7.05 +/- 1.44)%, being significantly higher than that in group B (5.25 +/- 1.78)% and group C (2.84 +/- 1.36)%, (P < 0.01). The apoptosis index was significantly higher in group B than in group C (P < 0.01). Fas protein was negative in normal tissues and in all injured esophageal mucosal tissues. CONCLUSION: The DGER without bile inflicts the slighest injury on the esophageal mucosa. Bile may play a significant role in the induction of Barrett's esophagus. The apoptosis indices increase in groups A, B and C, but apoptosis is not correlated with Fas expression.