BACKGROUNDProton pump inhibitors (PPIs) are widely prescribed, often without clear indications. There are conflicting data on its association with mortality risk and hepatic decompensation in cirrhotic patients. Furthermore, PPI users and PPI exposure in some studies have been poorly defined with many confounding factors.AIMTo examine if PPI use increases mortality and hepatic decompensation and the impact of cumulative PPI dose exposure.METHODSData from patients with decompensated liver cirrhosis were extracted from a hospital database between 2013 to 2017. PPI users were defined as cumulative defined daily dose (cDDD) ≥ 28 within a landmark period, after hospitalisation for hepatic decompensation. Cox regression analysis for comparison was done after propensity score adjustment. Further risk of hepatic decompensation was analysed by Poisson regression.RESULTSAmong 295 decompensated cirrhosis patients, 238 were PPI users and 57 were non-users. PPI users had higher mortality compared to non-users [adjusted HR = 2.10, (1.20-3.67); P = 0.009]. Longer PPI use with cDDD > 90 was associated with higher mortality, compared to non-users [aHR = 2.27, (1.10-5.14); P = 0.038]. PPI users had a higher incidence of hospitalization for hepatic decompensation [aRR = 1.61, (1.30-2.11); P < 0.001].CONCLUSIONPPI use in decompensated cirrhosis is associated with increased risk of mortality and hepatic decompensation. Longer PPI exposure with cDDD > 90 increases the risk of mortality.
BACKGROUND Autoimmune markers including plasma cells (PC), anti-smooth-muscle antibody (ASMA), anti-nuclear antibody (ANA), and raised immunoglobulin G (IgG) are commonly observed in non-alcoholic steatohepatitis (NASH), however their clinical significance is unknown. AIM To determine if autoimmune markers in NASH patients are independently associated with poorer clinical outcomes. METHODS Consecutive patients with biopsy proven NASH from Christchurch Hospital, New Zealand and Singapore General Hospital (SGH) were included between 2005 to 2016 in a prospective multi-centre cohort study. Patients with other causes of chronic liver disease were excluded. IgG > 14 g/L or globulin fraction > 50%, ANA ≥ 1:40, SMA ≥ 1:40 were considered positive. Multivariate analysis was performed to assess which markers were independently associated with mortality and hepatic decompensation. RESULTS Total 261 patients were included of which 201 were from SGH. The median age was 53 and 51.9% were male. Advanced fibrosis was present in 31.4% at diagnosis. PC, ASMA, ANA and raised IgG were observed in 13.1%, 4.9%, 27.8% and 30.1% of patients respectively. After multivariate analysis, elevated IgG [Hazard Ratio (HR) 6.79, 95%CI: 2.93-17.15] and fibrosis stage (HR 1.37, 95%CI: 1.03-1.87) were found to be independently associated with increased risk of liver decompensation. Age (HR 1.06, 95%CI: 1.02-1.10) and elevated IgG (HR 3.79, 95%CI: 1.90-7.68) were independent factors associated with higher mortality risk. CONCLUSION Elevated IgG, rather than ANA, ASMA or plasma cells, is independently associated with increased risk of hepatic decompensation and mortality in NASH. It could hence be important for prognostication.
Eosinophilic cholangitis is a rare cause of deranged obstructive liver function tests. It has been described as a great mimicker for malignant biliary strictures and bile duct obstruction. There are only case reports available on treatment experience for eosinophilic cholangitis. A large proportion of patients present with biliary strictures for which they have undergone surgery or endoscopic treatment and a small proportion was given systemic corticosteroid. We share our treatment experience using budesonide which has fewer systemic side effects to prednisolone and avoids invasive management.
Evidence for an unidentified steroid in a child with apparent mineralocorticoid hypertension. J Clin Endocrinol Metab 1977;44:924-33. 4 Case report A girl, aged 2-years at the time of this report, had been observed since birth. Her mother was known to have a sporadic form of HR with severe bone abnormalities (osteomalacia) and dwarfism, and had been treated during infancy with combined phosphates and vitamin D3 without any improvement. The pregnancy was normal, and a caesarean section was performed for maternal indications.Our patient's birthweight was 3-3 kg and her length was 52 cm. A physical examination at age 2 months showed her to be normal-weight and height at the 25th centile. Laboratory investigations at that time found the following: hypophosphataemia-phosphate 1 13 mmol/l (3 5 mg/dl), normal range for our laboratory I 29-2-09 mmol/l; normal serum calcium 2-23 mmol/l (9-2 mg/dl), normal range 2-1-2-6 mmol/l; raised alkaline phosphatase-56 KA units, normal range 7-5-32*5 KA units; hypocalciuria-0 0365 mmol/kg/24 hours (1 46 mg/kg/24 hours); hyperphosphaturia-45-54 mmol/l 73m2/24 hours (1 41 mg/ 173m2/24 hours); and a reduction in renal tubular reabsorption of phosphate-60 %.
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