An historical note on chemotherapy of bacterial infections (Gerhard Domagk).
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Biomedical subjects
Publications and source records attributed to G M Forbes.
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Administration of home parenteral nutrition (HPN) to patients with intestinal failure requires attention to caloric content of feeds, fluid, electrolyte balance, and micronutrient status. Peripheral blood estimations of vitamins and trace elements may be abnormal, but their clinical significance in relation to deficiency or toxicity states is not always clear. We sought to determine the incidence and nature of clinical micronutrient abnormality in our HPN program. Clinical assessment and case record review of 49 patients actively receiving HPN was undertaken, and, in 32 of these patients, serum micronutrient levels were assayed. Clinical evidence of micronutrient deficiency was identified in 16 patients (33%). Iron deficiency anemia occurred in 14 patients which resolved after iron supplementation in all except 1 patient who had persistent intestinal blood loss. Anemia was precipitated in six patients by identifiable clinical events (acute gastrointestinal disease in five and menorrhagia in one), and in two others folate deficiency coexisted. Biotin deficiency developed in three patients, manifested by dry eyes and angular cheilitis or hair loss. Vitamin A deficiency resulting in visual disturbance developed in one patient who was not receiving multivitamin supplements at that time. Serum levels of zinc, copper, selenium, manganese, vitamin A, and vitamin E were measured in 32 patients. No patient had normal levels of all six micronutrients. Nevertheless, there was no clinical evidence of toxicity or deficiency in any of these patients at the time assays were performed. In conclusion, abnormalities of micronutrient status are common in HPN patients, but serious sequelae appear to be unusual.
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Hepatic dysfunction following bone marrow transplantation (BMT) may present complex management issues. The incidence and aetiology of abnormal liver function following allogeneic and autologous BMT was reviewed over a 2 year period in Royal Perth Hospital and these findings were related to management decisions and patient outcome. Abnormal serum liver biochemistry during the first 12 post-transplant months occurred in all allogeneic (n = 31) and 14 of 23 (61%) autologous transplant patients; 13 (41%) allogeneic and three (13%) autologous patients developed severe hepatic dysfunction. In allogeneic transplants, the most common causes of liver disease were graft-versus-host disease (33%), drug hepatotoxicity (19%) and posttransplant viral hepatitis (15%); in autologous patients, disease recurrence (28%) and sepsis (17%) were the most frequent identifiable cause of abnormal liver function. The aetiology of abnormal liver biochemistry was not determined in 13 instances, but this did not adversely affect patient outcome. Percutaneous liver biopsy or endoscopic cholangiography were only required in three patients. Liver disease contributed to death in two allogeneic patients with multiple causes for liver dysfunction, and in one patient with refractory severe hepatic graft-versus-host disease. It was concluded that hepatic dysfunction is common after BMT, the cause of which can be determined in many cases with simple non-invasive tests used in conjunction with the clinical setting. Specific treatment, where necessary, is then able to be commenced in a majority of patients without the need for invasive investigation.
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