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OBJECTIVES:In the largest head-to-head comparison between an oral and an intravenous (IV) iron compound in patients with inflammatory bowel disease (IBD) so far, we strived to determine whether IV iron isomaltoside 1,000 is non-inferior to oral iron sulfate in the treatment of iron deficiency anemia (IDA).METHODS:This prospective, randomized, comparative, open-label, non-inferiority study was conducted at 36 sites in Europe and India. Patients with known intolerance to oral iron were excluded. A total of 338 IBD patients in clinical remission or with mild disease, a hemoglobin (Hb) <12 g/dl, and a transferrin saturation (TSAT) <20% were randomized 2:1 to receive either IV iron isomaltoside 1,000 according to the Ganzoni formula (225 patients) or oral iron sulfate 200 mg daily (equivalent to 200 mg elemental iron; 113 patients). An interactive web response system method was used to randomize the eligible patient to the treatment groups. The primary end point was change in Hb from baseline to week 8. Iron isomaltoside 1,000 and iron sulfate was compared by a non-inferiority assessment with a margin of −0.5 g/dl. The secondary end points, which tested for superiority, included change in Hb from baseline to weeks 2 and 4, change in s-ferritin, and TSAT to week 8, number of patients who discontinued study because of lack of response or intolerance of investigational drugs, change in total quality of life (QoL) score to weeks 4 and 8, and safety. Exploratory analyses included a responder analysis (proportion of patients with an increase in Hb ≥2 g/dl after 8 weeks), the effect of regional differences and total iron dose level, and other potential predictors of the treatment response.RESULTS:Non-inferiority in change of Hb to week 8 could not be demonstrated. There was a trend for oral iron sulfate being more effective in increasing Hb than iron isomaltoside 1,000. The estimated treatment effect was −0.37 (95% confidence interval (CI): −0.80, 0.06) with P=0.09 in the full analysis set (N=327) and −0.45 (95% CI: −0.88, −0.03) with P=0.04 in the per protocol analysis set (N=299). In patients treated with IV iron isomaltoside 1,000, the mean change in s-ferritin concentration was higher with an estimated treatment effect of 48.7 (95% CI: 18.6, 78.8) with P=0.002, whereas the mean change in TSAT was lower with an estimated treatment effect of −4.4 (95% CI: −7.4, −1.4) with P=0.005, compared with patients treated with oral iron. No differences in changes of QoL were observed. The safety profile was similar between the groups. The proportion of responders with Hb ≥2 g/dl (IV group: 67% oral group: 61%) were comparable between the groups (P=0.32). Iron isomaltoside 1,000 was more efficacious with higher cumulative doses of >1,000 mg IV. Significant predictors of Hb response to IV iron treatment were baseline Hb and C-reactive protein (CRP).CONCLUSIONS:We could not demonstrate non-inferiority of IV iron isomaltoside 1,000 compared with oral iron in this study. Based on the dose–response relationship observed with the IV iron co...

rum bilirubin, and prothrombin time prolongation over The profiles of patients with fulminant hepatic failure controls at admission were related to survival (P õ . 01). (FHF) from developing countries have not been reportedThe rapidity of onset of encephalopathy and cause of earlier. The current study was conducted prospectively, FHF did not influence the outcome. Cox's proportional at a single tertiary care center in India, to document the hazard regression showed age ¢40 years, presence of demographic and clinical characteristics, natural cerebral edema, serum bilirubin ¢15 mg/dL, and procourse, and causative profile of patients with FHF as thrombin time prolongation of 25 seconds or more over well as to define simple prognostic markers in these pacontrols were independent predictors of outcome. tients. Four hundred twenty-three consecutive patients Ninety-three percent of the patients with three or more with FHF admitted from January 1987 to June 1993 were of the above prognostic markers died. The sensitivity, included in the study. Each patient's serum was tested specificity, positive predictive value, and the negative for various hepatotropic viruses. Univariate Cox's repredictive value of the presence of three or more of these gression for 28 variables, multivariate Cox's proporprognostic factors for mortality was 93%, 80%, 86%, and tional hazard regression, stepwise logistic regression, 89.5%, respectively, with a diagnostic accuracy of 87.3%. and Kaplan-Meier survival analysis were done to idenWe conclude that most of our patients with FHF might tify independent predictors of outcome at admission. Most reports on fulminant hepatic failure (FHF)from the latter group were tested for hepatitis E virus (HEV) RNA and HCV RNA. In 31 (62%), HEV could be have been predominantly from the West, 1-9 and particuimplicated as the causative agent, and isolated HCV larly from three countries: the United Kingdom, 1,2 Ja-RNA could be detected in 7 (19%). Two hundred eighty-pan, 3,4 and France. 5 Based on these geographically limeight (66%) patients died. Approximately 75% of those ited observations, a new classification of this disease who died did so within 72 hours of hospitalisation. One entity into hyperacute, acute, and subacute liver failquarter of the female patients with FHF were pregnant. ure has been suggested.2 These authors also suggested Mortality among pregnant females, nonpregnant fe-the adoption of this classification universally for a unimales, and male patients with FHF was similar (P ú .1). form terminology. The latter study has not been able The cause and rapidity of the onset of hepatic enceph-

Acute pancreatitis occurs in 5.65% of patients with acute viral hepatitis, it is mild and recovers with conservative management.

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