Diagnosis and treatment of iron deficiency anemia in patients with inflammatory bowel disease and gastrointestinal bleeding: iron deficiency anemia working group consensus report.

Iron deficiency (ID) and iron deficiency anemia (IDA) are important signs of gastrointestinal (GI) hemorrhage. Therefore, the evaluation of the GI tract should be a part of the diagnostic protocol in patients with IDA. GI hemorrhage is not a disease but a symptom, which might have different underlying causes. ID and IDA have significant negative impacts on the life quality and work ability, and they may lead to frequent hospitalization, delay of discharge, and increased healthcare costs. Therefore, an optimal management of the disease causing GI hemorrhage should include iron replacement therapy, along with the treatment of the underlying condition. IDA in inflammatory bowel disease (IBD) has received particular attention owing to its high prevalence, probably due to a number of other factors such as chronic hemorrhage, reduced dietary iron intake, and impaired absorption of iron. Historically, in IBD and in patients with GI hemorrhage, the diagnosis and management of IDA have been suboptimal. Options for iron replacement include oral and intravenous (IV) iron supplementation. Oral iron supplementation frequently results in GI side effects, and theoretically, it may exacerbate IBD activity; therefore, IV iron supplementation is usually considered in patients not responding to or not complying with oral iron supplementation or patients having low hemoglobin concentration and requiring prompt iron repletion. The aim of this report was to review the diagnostic and therapeutic considerations of IDA in IBD and GI hemorrhage with a multidisciplinary group of experts and to formulate necessary practical recommendations.

Adjuvant therapeutic plasma exchange in liver failure: assessments of clinical and laboratory parameters.

BACKGROUND: Therapeutic plasma exchange (TPE) seems to be an effective approach for clearing toxins, immune-mediated antigens, and other particles from the circulation. The aim of this study was to analyze the positive effects of TPE on clinical and biochemical parameters of liver failure. PATIENTS AND METHODS: Between January 2001 and March 31, 2005 individuals (men/women, 17/14; median age, 42.7+/-15.8 y) with acute and chronic liver failure who underwent a total of 113 TPEs (median session 3.7) were retrospectively reviewed. TPE was performed using the Fresenius AS-TEC 204 cell separator (Fresenius AG, Germany). The indication for TPE was severe coagulopathy (prothrombin time >20 s), severe hepatic encephalopathy, hyperbilirubinemia, and candidacy for liver transplantation. All patients were examined before and immediately after the last TPE session. RESULTS: When compared with baseline, there was significant improvement in hepatic encephalopathy stage (from median score 3.0 to 1.0, P=0.001), serum prothrombin time (from median 26.0 to 20.0 s, P=0.003), aminotransferases (P<0.001), and total bilirubin levels (from median 35.0 to 23.3 mg/dL, P<0.001) after TPE. Thirteen of the thirty-one individuals (41.9%) died in the hospital. The mean follow-up period of 18 survival patients was 35.9+/-5.6 months and 10 of those survived (55.6%, 10/18). No serious adverse effect of TPE was observed in any of the patients during or after completion of TPE. Only 6 patients experienced minor transfusion reactions. CONCLUSIONS: TPE seems to be effective in improving hepatic encephalopathy stage and liver tests in individuals with acute and chronic liver failure. The data suggest that TPE is safe and tolerable in such individuals, however, overall survival remains poor despite TPE.