Obesity does not affect sodium picosulphate bowel preparation.

BACKGROUND: A previous study utilising oral polyethylene-glycol by Borg et al. concluded that obesity is an independent predictor of inadequate bowel preparation at colonoscopy. AIM: To compare bowel preparation quality between obese and non-obese individuals as assessed by Boston bowel preparation scale (BBPS) after using sodium picosulphate. METHODS: Prospective recruitment of patients at a day surgical unit in a New South Wales academic hospital. Bowel preparation was with Picoprep in all patients. Body Mass Index and epidemiological details were collected. Bowel preparation efficacy was assessed using the Boston Bowel Preparation Score. RESULTS: One hundred and four patients were enrolled prospectively. Five (4.8%) were excluded owing to poor mental capacity. Sixty-three (64%) were non-obese, and 36 (36%) were obese. Fifty-seven (90%) non-obese and 32 (89%) obese patients had good bowel preparation. There was no statistical difference for sodium picosulphate bowel preparation between obese and non-obese individuals (P > 0.99) using Fisher's exact probability tests. The BBPS score in the left colon predicted the overall BBPS score in all patients (P < 0.001). Three of 99 patients (3%) did not tolerate sodium picosulphate, with nausea being the most common side-effect. LIMITATIONS: Non-randomised study CONCLUSIONS: There was no difference in bowel preparation quality between obese and non-obese patients using a low-volume bowel preparation (sodium picosulphate) and without dose modification of the bowel preparation. Sodium picosulphate was a welltolerated and an effective bowel preparation for obese individuals. With an increasing incidence of obesity and expanding colonoscopic indications within Australia and other Western countries from government-sponsored programs, it is paramount that procedural quality not be compromised in the obese patient.

Flumecinol for the treatment of pruritus associated with primary biliary cirrhosis.

OBJECTIVE: To determine whether flumecinol (3-trifluoromethyl-alpha-ethylbenzhydrol, Zixoryn) is effective in ameliorating pruritus of cholestasis, particularly in primary bilary cirrhosis. METHODS AND RESULTS: 50 patients (46 with primary biliary cirrhosis, PBC) took oral flumecinol 600 mg or identical placebo once weekly for 3 weeks. Patients assessed pruritus by scoring a daily 100 mm visual analogue scale (VAS; 0 = no itch, 100 = severe, continuous, day and night intolerable itch). Quality of life was similarly measured. Patients scored the VAS daily for a 7-day baseline and for a further 21 days. Subjectively, pruritus improved in 13 of 24 on flumecinol and 10 of 26 on placebo (chi 2 = 1.24, P = 0.27). Median difference in fall in VAS pruritus score between baseline week (mean score for each individual used) and the last week was 8.0 [95% confidence interval (CI) -2.1 to 20.8] and for VAS quality of life was 5.0 (95% Cl 0.4 to 13.0) both in favour of flumecinol over placebo. Later, 19 patients (all PBC) were randomised to flumecinol 300 mg or placebo daily for 3 weeks. Subjectively, pruritus improved in 7 of 10 on flumecinol and 1 of 9 on placebo (Fisher's exact test, P = 0.02). Median difference in fall in VAS pruritus score was 19.8 mm (95% CI 3.3 to 40.7 mm) in favour of flumecinol over placebo and for quality of life was 3.5 mm (95% Cl -5.9 to 24.9 mm). Flumecinol did not significantly affect liver function tests, antipyrine clearance or serum total bile acids, and was not associated with any significant side-effects. CONCLUSION: Flumecinol was safe at the above doses and short term treatment with 300 mg daily, significantly ameliorated pruritus in primary biliary cirrhosis.

A two year controlled trial examining the effectiveness of ursodeoxycholic acid in primary biliary cirrhosis.

Forty-six patients with primary biliary cirrhosis from a single centre were studied in a randomized placebo-controlled trial to determine the effectiveness of ursodeoxycholic acid (UDCA) over a 2 year period. The two groups were well-matched at baseline. For each parameter, by calculating the difference between the median changes with time between the UDCA group and the placebo group, it was found that from entry, with respect to placebo, there were differences between median changes (MCD) favouring the UDCA group in bilirubin (MCD 5 mumol/L [95% confidence interval (CI) 1 to 12] at 1 year and 5 mumol/L (95% CI 1 to 9) at 2 years), alkaline phosphatase MCD 242 iu/L (95% CI 107 to 360) at 1 year and 268 iu/L (95% CI 146 to 424) at 2 years and aspartate aminotransferase MCD 26 iu/L (95% CI 12 to 41) at 1 year and 37 iu/L (95% CI 16 to 64) at 2 years. Within the UDCA group, there was long-term fall in alkaline phosphatase [median fall 116 iu/L (95% CI 93 to 378) at 2 years and aspartate aminotransferase [median fall 18 iu/L (95% CI 6 to 47) at 2 years; however, the major change in bilirubin was a modest rise over 2 years in the placebo group [median rise 2 mumol/L (95% CI 1 to 9)]. Changes in albumin, prothrombin ratio and immunoglobulins were generally minor and not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Factors influencing mortality from bleeding peptic ulcers.

The mortality, causes of death, and the factors that are influencing deaths from bleeding acute and chronic peptic ulcers were evaluated retrospectively. During a 2-year period (1986-87) 272 patients were endoscoped for acute gastrointestinal hemorrhage and were found to have bled from a peptic ulcer (chronic gastric ulcers, 90; chronic duodenal ulcers, 114; acute gastroduodenal ulcers, 66; stomal ulcers, 2). The overall mortality was 9.6% (n = 26) (gastric ulcers, 6.7%; duodenal ulcers, 11.4%; acute ulcers, 10.6%). Statistically significant factors adversely affecting prognosis for gastric ulcer were re-bleeding, need for operation and serious intercurrent illness; for duodenal ulcer were units of transfused blood, re-bleeding, signs of recent hemorrhage at endoscopy, need for operation, and serious intercurrent illness; and for acute ulcer were increasing age, shock, units of transfused blood, re-bleeding, and serious intercurrent illness. Multivariate analysis was only attempted for duodenal ulcers because of sample sizes; it suggested that active bleeding or visible vessel at endoscopy, re-bleeding, and serious intercurrent illness were independent factors for mortality. From this study it is apparent that the major determinants of a fatal outcome in bleeding peptic ulcer diseases were serious intercurrent illness and rebleeding. As it must be anticipated that patients with these particular problems are at high risk of a poor outcome, it follows that it is important they have access to skilled treatment as provided by a specialist team in an intensive care ward. It also follows that every effort should be made to keep ulcers in remission to free the ulcer patient of potentially lethal complications.

Primary biliary cirrhosis. Quantitation of autoantibodies to purified mitochondrial enzymes and correlation with disease progression.

Primary biliary cirrhosis is characterized by the presence of antimitochondrial antibodies. Recently, six of the autoantigens have been identified as components of the 2-oxo acid dehydrogenase multienzyme complexes located within mammalian mitochondria. Immunoblotting studies have shown that two of these components, namely E2 and protein X of pyruvate dehydrogenase complex, are the major antigenic polypeptides recognized by autoantibodies. This study shows the development of an enzyme-linked immunosorbent assay to detect and quantitate antibodies to these two purified antigens. Coded serum samples from 166 patients with primary biliary cirrhosis, 140 patients with other liver and/or autoimmune disease, and 52 normal women were analyzed for reactivity using this immunoassay. These results indicate that this rapid, simple method has a 93% sensitivity and 96% specificity in the diagnosis of primary biliary cirrhosis. The titer of immunoglobulin G autoantibodies correlated not only with antimitochondrial antibody titer measured by indirect immunofluorescence (P less than 0.0001) but also with histological stage of disease (P less than 0.04) and prognostic biochemical variables such as higher serum bilirubin and lower serum albumin levels (P = 0.038 and 0.028, respectively). There was no significant correlation between titer of autoantibodies and serum globulin or immunoglobulin G levels, indicating that the positive correlation with disease progression was not secondary to hypergammaglobulinemia.

Prolonged hepatic cholestasis after flucloxacillin therapy.

A severe prolonged illness that was characterized by deep jaundice and debilitating pruritus occurred in five patients after the use of flucloxacillin. The symptoms and signs of liver disease took at least two months to resolve; after four- to nine-months' follow-up, liver enzyme activities have remained abnormal in all patients. Examination of liver biopsy specimens showed severe cholestasis in all cases, with evidence of significant bile-duct injury in three cases. In one patient, in whom symptoms have persisted for nine months, examination of a liver biopsy specimen showed marked bile-duct depletion. All patients were seen during a four-month period and it is felt that flucloxacillin-induced liver disease probably has been under-diagnosed and underreported. The use of flucloxacillin has been increasing rapidly and it is anticipated that more cases of flucloxacillin hepatotoxicity will occur in the future.

The E1 alpha and beta subunits of the pyruvate dehydrogenase complex are M2'd' and M2'e' autoantigens in primary biliary cirrhosis.

1. Sera from 76 patients with primary biliary cirrhosis (PBC) and 66 control subjects (53 with chronic liver disease and 13 healthy normal women) were immuno-blotted against purified E1 component of bovine pyruvate dehydrogenase complex (PDC) and bacterial PDC. 2. Thirty-one out of seventy-six (41%) sera from PBC patients showed a positive response to bovine E1 alpha, and five of these 31 (7% of total) reacted with bovine E1 beta. None of the control sera reacted with bovine E1 alpha or beta. 3. None of the PBC sera that recognized bovine E1 subunits reacted with bacterial PDC E1. 4. In the PBC patients there was no correlation between presence of antibodies to E1 alpha and beta subunits and histological stage of the disease. 5. Our data demonstrate that the E1 alpha and beta components of mammalian PDC are the M2'd' and 'e' mitochondrial autoantigens, respectively.