Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal failure in cancer patients is a common problem in oncology; this complication is frequently multifactorial in origin. Several antineoplastic agents are potentially nephrotoxic; previous renal impairment as well as combinations with other nephrotoxic drugs may increase the risk of nephrotoxicity during administration of chemotherapy. Methotrexate-related renal damage most frequently occurs with high-dose therapy and can be avoided by forced alkaline diuresis and administration of folinic acid. Renal dysfunction secondary to semustine (CH3-CCNU) is clearly related to cumulative doses in excess to 1,200 mg/m2; the onset may be delayed and renal failure progress despite drug discontinuation. Streptozotocin is also nephrotoxic and may cause proteinuria and renal tubular acidosis; progressive renal failure can be predicted by a close monitoring of proteinuria and prevented by drug discontinuance. Mitomycin-associated renal failure frequently presents with signs of microangiopathic hemolytic anemia; renal failure is usually delayed but occasionally, it may be rapidly progressive despite drug discontinuance. Cisplatin nephrotoxicity is clearly dose-related and used to be considered dose limiting. Renal insufficiency can be prevented by hydration and forced diuresis; in addition, hyperhydration with mannitol-induced saline diuresis may allow administration of high doses and thus circumvent the dose-limiting effect of cisplatin-induced renal toxicity. Cisplatin-induced renal magnesium wasting occurs frequently and should be supplemented. Other approaches to reduce cisplatin nephrotoxicity are currently under investigation and are discussed.
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PMID:Nephrotoxicity induced by cancer chemotherapy with special emphasis on cisplatin toxicity. 353 60

Twenty-two children with malignant histiocytosis ranging in age from 2 to 13 1/2 years are described. In 10 cases, the correct diagnosis was only made retrospectively. The most salient pathologic features were found in lymph node biopsy specimens. Fever and wasting were the most prominent symptoms in 21 cases, and abdominal pains were striking in 9. Peripheral lymphadenopathy, mostly of the cervicoaxillary type, was present in 21 patients, with marked tenderness in 14. Abnormal mediastinal and/or paraaortic lymph nodes were detected radiographically in two-thirds of the patients. Other prominent features included subcutaneous inflammatory infiltration in 12 patients and skin nodules in 8. Pleural effusions were seen in 8 children. The haematologic findings are described. Only 5 of 19 children had bonemarrow involvement. Fifteen patients died, one to 45 months from onset of their illness (median survival time, five months). Nine patients are alive with no evidence of disease 21 to 46+ months (median, 40 months) after the time of diagnosis and 8 have currently been off treatment for periods ranging from three to 29 months; they all have been treated with vincristine, prednisone, cyclophosphamide, and adriamycin and 4 have achieved remission after treatment with vinblastine, bleomycin, and CCNU or cytosine-arabinoside. It is concluded from this study that clearly delineated clinical features of malignant histiocytosis in childhood should allow more rapid determination of the proper diagnosis and should result in early treatment by means of intensive systemic combination chemotherapy, which has dramatically improved the prognosis.
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PMID:Malignant histiocytosis in childhood: clinical study and therapeutic results in 22 cases. 737 13