Incidence and Predictors of an Abnormal Liver Function Test Among 674 Systemic Sclerosis Patients: A Cohort Study.

Background: Abnormal liver function tests (LFTs) can indicate cirrhosis or liver cancer leading to mortality among systemic sclerosis (SSc) patients. No recent studies have investigated the clinical predictors of an abnormal LFT in SSc. We aimed to determine the incidence of abnormal LFT (including from hepatitis and cholestasis) and to identify its clinical predictors in SSc patients. Methods: An historical cohort was conducted on 674 adult SSc patients who attended the Scleroderma Clinic, Khon Kaen University, between January 2012 and November 2019 and who underwent routine screening for LFT. A Cox regression was used to analyze the clinical predictors of abnormal LFT. Results: Four hundred and thirty cases, representing 4190 person-years, had abnormal LFTs (viz, from hepatitis, cholestasis, and cholestatic hepatitis) for an incidence rate of 10.2 per 100 person-years. The respective incidence of hepatitis, cholestasis, and cholestatic hepatitis was 20.5, 12.9, and 20.4 per 100 person-years. The respective median first-time detection of hepatitis, cholestasis, and cholestatic hepatitis was 3.0, 5.9, and 2.8 years, and none had signs or symptoms suggestive of liver disease. According to the Cox regression analysis, the predictors of an abnormal LFT in SSc were elderly onset of SSc (hazard ratio (HR) 1.02), alcoholic drinking (HR 1.74), high modified Rodnan Skin Score (mRSS) (HR 1.03), edematous skin (HR 2.94), Raynaud's phenomenon (HR 1.39), hyperCKaemia (HR 1.88), and methotrexate use (HR 1.55). In contrast, current sildenafil treatment (HR 0.63) and high serum albumin (HR 0.70) were protective factors. Conclusion: Occult hepatitis, cholestasis, and cholestatic hepatitis can be detected in SSc patients using LFT screening, especially in cases of early disease onset. The long-term outcome is uncertain, and more longitudinal research is required.

Genetic variation in the vitamin D pathway CYP2R1 gene predicts sustained HBeAg seroconversion in chronic hepatitis B patients treated with pegylated interferon: A multicenter study.

Evidence of a role of vitamin D in the immune system is increasing. Low serum vitamin D is associated with increased hepatitis B virus replication. Genome-wide association study (GWAS) data has revealed a number of the single nucleotide polymorphisms (SNPs) within the vitamin D synthetic pathway that affect vitamin D functions. We aimed to determine the association between SNPs in the vitamin D gene cascade and response to pegylated interferon (PegIFN) therapy in hepatitis B e-antigen (HBeAg)-positive patients. One hundred and eleven patients treated for 48 weeks with PegIFN-alfa 2a at 13 hospitals were retrospectively evaluated. Thirteen SNPs derived from vitamin D cascade-related genes, including DHCR7 (rs12785878), CYP27B1 (rs10877012), CYP2R1 (rs2060793, rs12794714), GC (rs4588, rs7041, rs222020, rs2282679), and VDR (FokI, BsmI, Tru9I, ApaI, TaqI), were genotyped. Thirty-one patients (27.9%) seroconverted to HBeAg after 24 weeks of treatment. Multivariate analysis found pretreatment qHBsAg <10,000 IU/mL (OR = 7.73, 95% CI: 2.36-25.31, P = 0.001), CYP2R1 rs12794714 TT genotype (OR = 4.16, 95% CI: 1.07-16.25, P = 0.04), and baseline ALT >2 times the upper limit of normal (OR = 3.83, 95% CI: 1.31-11.22, P = 0.014) predicted sustained HBeAg seroconversion after completion of PegIFN treatment. HBV DNA during study period tended to be lower with the rs12794714 CYP2R1 TT than the non-TT genotype. The rs12794714 CYP2R1 polymorphism may be a useful pretreatment factor predictive of sustained HBeAg seroconversion after PegIFN therapy. This study provides evidence that not only vitamin D level but also genetic variation of CYP2R1 in the vitamin D cascade influences host immune response in chronic HBV infection.

CT findings of liver and splenic abscesses in melioidosis: comparison with those in non-melioidosis.

OBJECTIVE: To compare the CT findings of liver and splenic abscesses in melioidosis (ML) with non-melioidosis (NML). MATERIAL AND METHOD: CT (computed tomography) images of 47 patients with liver and splenic abscesses were retrospectively reviewed. The 28 patients with ML abscesses and 19 with NML abscesses were recruited into the present study. The sizes, shapes, distributions, margins, enhancement patterns and internal architectures of abscesses on CT images were evaluated and analyzed by Chi-square and Fisher exact tests. RESULTS: Seven and 6 ML patients had liver and splenic abscesses alone respectively, and 15 patients had combined liver and splenic abscesses. All NML patients had only liver abscesses. For liver abscesses, there were 3 ML and 13 NML patients with abscess size > or = 3 cm. Eleven ML and no NML patients had abscesses < 3 cm (p = 0.00). The abscesses were multiple and discretely distributed in all 11 ML patients, but none in NML patients (p = 0.002). Seven ML and 13 NML patients had moderate to marked peripheral enhancement (95% CI: -0.7, -0.01). All splenic abscesses (21 patients) found that B. pseudomallei was the causative organism. They were mostly smaller than 3 cm in size (85.71%), multiple (95.24%), and had no or minimal enhancement (85.71%). CONCLUSION: The CT findings of liver abscesses that can help to differentiate ML from NML include sizes, distributions, and enhancement patterns. The features of ML splenic abscesses in the present study were small, multiple, with no or minimal contrast enhancement.