Background: Liver dysfunction in pregnancy has serious consequences. Its frequency and characteristics have not been systematically documented in Britain. We have prospectively determined incidence, causes, and outcome of liver dysfunction in pregnancy in an obstetric unit in Southwest Wales, UK. Methods: A central laboratory identified all abnormal liver tests (bilirubin >25 µmol/l, aspartate transaminase >40 U/l, or γ glutamyl transpeptidase >35 U/l) from patients in antenatal clinics and wards of an obstetric unit serving a population of 250 000. Patients with abnormal liver tests were assessed and followed through after pregnancy. Medical advice was provided to obstetric teams. Findings: There were 4377 deliveries during the 15 month study. A total of 142 patients had abnormal liver tests. There were 206 contributing diagnoses, the great majority being pregnancy specific. Among the most important were pre-eclampsia (68), HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome (30), obstetric cholestasis (23), hyperemesis gravidarum (11), acute fatty liver of pregnancy (five), and hepatic infarct (one). Sepsis, postoperative factors, and placental pathology (51) were not uncommonly responsible but incidental or pre-existing hepatobiliary disease was infrequent (17). Sixty five patients were delivered early by induction or caesarean section because of liver dysfunction. Despite substantial liver related morbidity, there were no maternal deaths and only two intrauterine deaths. Conclusions: Liver dysfunction was seen in 3% of deliveries during a 15 month prospective study and was usually directly related to pregnancy with spontaneous recovery in the puerperium. Incidence of the most serious conditions, acute fatty liver of pregnancy and HELLP syndrome, was much greater than previously reported. Profound effects on maternal and infant health were observed but close medical and obstetric collaboration ensured low mortality.

Objectives: To determine if an educational intervention initiated in secondary care can influence prescribing of proton pump inhibitors (PPIs) in the community. Methods: A prospective study of PPI use in patients admitted to medical wards in a university hospital. A simple educational intervention was employed to reduce inappropriate prescribing of PPIs in the community. Results: In the pre-intervention analysis 66/271 (24%) patients were receiving treatment with a PPI prescribed in the community. In 36/66 (54%) patients the PPI had been prescribed inappropriately. Six months after the intervention 91/344 (26%) patients were prescribed a PPI in the community. In only 45 of these 91 (49%) patients was there a recommended indication. Conclusion: The intervention used in this study had no effect on the proportion of patients taking a PPI at the time of hospital admission or on the appropriateness of prescribing in the community.

Cel iac disease (CD) or gluten sensitive enteropathy is a permanent intolerance of dietary gluten leading to mucosal damage in the proximal small bowel in genetically susceptible individuals, characterized by inflammation, crypt hyperplasia and villous atrophy which regress on withdrawal of gluten from the diet. Recent population screening studies have shown the prevalence of CD in Western countries approaches 1% 1-3 but the condition is greatly under-diagnosed, partly because many cases are subclinical, but also because of its previously perceived rarity.CD should be considered in many clinical settings and detected early to prevent complications in later life. In a 6-year prospective study, Corrao et al 4 followed 1,072 consecutive CD patients and found a standard mortality ratio of 0.5 in those who complied with a strict gluten-free diet but a standard mortality ratio of 6.0 in the poor compliers. Using the general practice research database, West et al 5 identified 4,732 CD patients and found a modest increase in overall risks of malignancy and mortality compared to matched controls. 184Celiac disease (CD) or gluten sensitive enteropathy is relatively common in western populations with prevalence around 1%. With the recent availability of sensitive and specific serological testing, many patients who are either asymptomatic or have subtle symptoms can be shown to have CD. Patients with CD have modest increases in risks of malignancy and mortality compared to controls. The mortality among CD patients who comply poorly with a gluten-free diet is greater than in compliant patients.The pattern of presentation of CD has altered over the past three decades. Many cases are now detected in adulthood during investigation of problems as diverse as anemia, osteoporosis, autoimmune disorders, unexplained neurological syndromes, infertility and chronic hypertransaminasemia of uncertain cause.Among autoimmune disorders, increased prevalence of CD has been found in patients with autoimmune thyroid disease, type 1 diabetes mellitus, autoimmune liver diseases and inflammatory bowel disease. Prevalence of CD was noted to be 1% to 19% in patients with type 1 diabetes mellitus, 2% to 5% in autoimmune thyroid disorders and 3% to 7% in primary biliary cirrhosis in prospective studies. Conversely, there is also an increased prevalence of immune based disorders among patients with CD.The pathogenesis of co-existent autoimmune thyroid disease and CD is not known, but these conditions share similar HLA haplotypes and are associated with the gene encoding cytotoxic T-lymphocyte-associated antigen-4.Screening high risk patients for CD, such as those with autoimmune diseases, is a reasonable strategy given the increased prevalence.Treatment of CD with a gluten-free diet should reduce the recognized complications of this disease and provide benefits in both general health and perhaps life expectancy. It also improves glycemic control in patients with type 1 diabetes mellitus and enhances the absorption of medications for associated hypoth...

Background and aims-To ascertain the causes of raised aspartate aminotransferase (AST) presumed to be of hepatic origin in two hospitals and the local community served by a centralised biochemistry laboratory. Methods-From June 1996 to February 1997 all patients with AST greater than 400 U/l were identified by the biochemistry laboratory; the patients' clinical records were studied to determine the diagnosis, the clinical outcome, and whether the raised AST and its significance had been noted. Results-A total of 137 patients with a hepatic cause for the raised AST were found. The cause of the raised AST was hepatic ischaemia/hypoxia in 68, pancreatobiliary disease in 33, primary hepatocellular disease in 23, hepatic malignancy in five, and hepatic haematoma in one. In seven patients the diagnosis was unclear. The overall mortality was high (22%) with the highest mortality in the hepatic ischaemia group (37%). The recording and interpretation of the causes of raised AST was poor with only 48% having the correct diagnosis. In 38% the raised AST was apparently not noticed by the attending clinicians. Conclusions-The commonest cause of a hepatitis like biochemical picture was hepatic hypoxia (50%) followed by pancreatobiliary disease (24%). Drug induced hepatic necrosis (8.8%) was uncommon and viral hepatitis was rare (3.6%). AST concentrations returned towards normal most rapidly in patients with hepatic hypoxia and calculous biliary obstruction. Hepatitis, viral or otherwise, is an uncommon cause of a typical hepatitic biochemical result in this community. (Gut 1999;45:129-133)