PubMed · 5262750
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F R Minanda. [Anemia].. https://pubmed.ncbi.nlm.nih.gov/5262750/
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OBJECTIVE: To compare the cost of recombinant human erythropoietin (rHuEPO) with that of blood transfusion in the treatment of chemotherapy-induced anemia from a healthcare system perspective. DESIGN: A decision analytic model. Baseline estimates were obtained from a review of clinical trials data and economic evaluation studies. SUBJECTS: Secondary data analyses of patients with advanced malignancies, excluding hematologic malignancies and metastasized solid tumors. INTERVENTIONS: Patients received either leukocyte-depleted packed red blood cells (PRBCs) or rHuEPO 150 units/kg s.c. three times per week for 6 months (24 wk). After 6 weeks, if rHuEPO recipients did not display a response, they received rHuEPO 300 units/kg s.c. three times weekly for the duration of therapy. If rHuEPO recipients still exhibited no response, they were given blood transfusions. MEASUREMENTS AND MAIN RESULTS: For a treatment period of 24 weeks, approximately 64% of rHuEPO recipients responded at an average expected cost of $12971 per patient. One hundred percent of transfusion recipients responded at a cost of $481; this resulted in a cost savings of $8490. Variation of response rates for rHuEPO or PRBCs did not appreciably lower costs. Lower rHuEPO dosages and higher numbers of transfused units of PRBCs yielded approximately equivalent costs; however, these strategies may not be clinically prudent. CONCLUSIONS: From a healthcare system cost and outcome perspective, blood transfusion is the preferred strategy for chemotherapy-induced anemia. However, rHuEPO may be considered an effective blood-sparing alternative for patients with non-stem cell disorders. Future cost-effectiveness analyses are needed to assess more completely both the clinical and quality-of-life benefits rHuEPO may contribute to individual patients' lives and to society overall.
Tumor necrosis factor (TNF) induced by Plasmodium berghei ANKA (PbA) infection was suggested to play an important role in the development of cerebral malaria (CM). We asked whether TNF-alpha/beta double-deficient mice, which have a complete disruption of the TNF-signaling pathways, are protected from CM and what might be the possible mechanisms of protection. PbA infection induces fatal CM in wild-type mice, which die within 5 to 8 days with severe neurological signs. In contrast, TNF-alpha/beta-deficient mice are completely resistant to PbA-induced CM. As PbA-induced up-regulation of endothelial intercellular adhesion molecule (ICAM)-1 expression as well as the systemic release of nitric oxide is found only in wild-type mice, TNF is apparently central for the recruitment of mononuclear cells and microvascular damage. Mononuclear cell adhesion to the endothelium, vascular leak and, perivascular hemorrhage are found only in the brain of wild-type mice. By contrast, the development of parasitemia and anemia is independent of TNF. Resistance to CM in TNF-alpha/beta-deficient mice is associated with reduced interferon-gamma and interleukin-12 expression in the brain, in the absence of increased T helper type 2 cytokines. In conclusion, TNF apparently is required for PbA-induced endothelial ICAM-1 up-regulation and subsequent microvascular pathology resulting in fatal CM. In the absence of TNF, ICAM-1 and nitric oxide up-regulation are reduced, and PbA infection fails to cause fatal CM.
2',3'-dideoxycytidine (ddC) is a synthetic pyrimidine nucleoside analogue approved for treatment of HIV-positive patients. Previous studies indicated that ddC has the potential to cause thymic lymphoma in C57BL/6 x C3H F1 (hereafter called B6C3F1) mice. In this study, we evaluated the carcinogenic potential of ddC in two different mouse models. B6C3F1 hybrid mice carry ecotropic endogenous proviral sequences that may be activated to cause lymphoma, whereas NIH Swiss mice lack proviral sequences that can be expressed. The mice were treated with ddC by gavage at 500 and 1000 mg/kg/day for up to 6 months (human dose, 2.25 mg/day) and evaluated for toxicity, plasma levels of ddC, and pathological changes. Lymphocyte cell markers from the thymic lymphomas were assessed by immunophenotyping. Expression of p53 protein was evaluated using immunohistochemical staining. Treatment-related thymic lymphomas were present in both mouse models with a higher incidence in NIH Swiss than in B6C3F1 mice. The lymphomas were more prevalent in females than in males of both mouse models. Most mice with thymic lymphoma died during the course of the study. In addition to the thymus, lymphoma was often present in lymph nodes, spleen, and other organs. Lymphomas arose more frequently in mice that lack endogenous ecotropic retroviral sequences and thus were not due to activation of endogenous provirus. During the third month of the study, a few NIH Swiss mice that died had granulosa cell tumors of the ovary. Treatment-related but reversible thymic atrophy was observed in both mouse models. There was a very high correlation between the internal dose of ddC and the incidence of thymic lymphoma in both mouse models. Most of the lymphocytes from control thymuses and ddC-induced lymphomas were positive for Thy-1.2 (pan-T), heat stable antigen, and CD4 and CD8 markers, with no marked differences in the lymphocyte markers of the tumors between sexes or dose groups. p53 protein was detected in only 20% (23/115) of the ddC-induced lymphomas with mostly minimal expression in scattered cells. Because ddC induced lymphomas in two different mouse models, the potential carcinogenic risk should be considered in long-term treatment of HIV-positive patients, especially children and adolescent patients treated with ddC.