Cisplatin-Induced Hemolysis

Getaz, E. P.; Beckley, S.; Fitzpatrick, J; Dozier, Askia

doi:10.1056/nejm198002073020607

Cited by 85 publications

(32 citation statements)

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“…This conclusion is further strengthened by a lack of effect of the platinum complexes on red cell half-lives (t12= 14 days), which, as it appears, are similar to those 0112=10-21 days) reviewed by Belcher and Harriss (1959) for normal rats. Drug-induced increase in osmotic fragility or reduction in survival time of red cells, however, could arise in rats after day 3 and may involve production of antibodies against red cells, as has been reported in patients receiving cis-platin (Getaz et al, 1980;Nguyen et al, 1981). Depression of erythropoietic activity as an alternate mechanism for the severe anaemia can almost certainly be ruled out, since, in this case, anaemia would develop slowly, if at all, as a result of the long mean red cell life span (21 days).…”

Section: Discussionmentioning

confidence: 87%

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Haematological toxicity of carboplatin in rats

Siddik¹,

Boxall²,

Harrap³

1987

Br J Cancer

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Summary In rats a maximal tolerated dose of carboplatin (60mg kg-1, i.v.) caused severe anaemia, leucopenia and thrombocytopenia. These indices of haematological toxicity were also observed with a maximal tolerated dose of cis-platin (6.5mgkg-1, i.v.), but reductions in blood cell counts were less than those observed with carboplatin. Anaemia was deduced to be the dose-limiting toxicity of carboplatin, since red cell transfusions afforded protection to rats receiving a lethal dose of this compound (80mgkg-1, i.v.). Anaemia did not appear to be due to an increase in the susceptibility of cis-platin-or carboplatin-exposed red cells to lysis, as concluded from results of osmotic fragility tests. These red cells, when tagged with 51Cr, also did not exhibit reductions in survival time. Administration of 5 Cr-labelled control red cells to rats, which had been treated with carboplatin 3 days earlier, resulted in substantial loss of the radiolabel from the circulation, indicating that internal haemorrhaging, as a result of thrombocytopenia, is probably the principle cause of drug-induced anaemia.

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Section: Discussionmentioning

confidence: 87%

“…Red cell lysis, however, cannot be ruled out as a contributory factor in anaemia arising from carboplatin administration since this toxic process is partly responsible for giving rise to cis-platin-induced anaemia (Getaz et al, 1980;Nguyen et al, 1981).…”

mentioning

confidence: 99%

Haematological toxicity of carboplatin in rats

Siddik¹,

Boxall²,

Harrap³

1987

Br J Cancer

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“…(24). The anemia occurs early, is cumulative, is disproportionate to white blood cell changes, and necessitates red cell transfusion in the vast majority of successfully treated cancer patients.…”

Section: Predictors Of Therapy-induced Anemiamentioning

confidence: 99%

Cisplatin-associated anemia: an erythropoietin deficiency syndrome.

Wood¹,

Hrushesky²

1995

J. Clin. Invest.

141

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Cisplatin-based therapy results in a cumulative anemia that is disproportionate to the effects on other blood cells. The severity of this treatment-induced anemia and the resultant transfusion requirement in cancer patients correlate with cisplatin-induced renal tubular dysfunction. Observed/expected serum erythropoietin (EPO) ratios decline with progressive cisplatin therapy and are proportionate to the degree of renal dysfunction. Recovery from anemia and of observed/expected serum EPO ratios in patients occurs after cessation of cisplatin therapy, along with restoration of renal tubular function. Creatinine clearance, however, remains permanently depressed. Cisplatin-treated rats develop progressive renal dysfunction and anemia that persists for many weeks, without effects on white blood cell counts. The anemia is also associated with a lack of expected EPO and reticulocyte response. With EPO administration, cisplatin-treated rats exhibit a greater reticulocyte response and hematocrit increment then non-cisplatin-treated rats given EPO, indicating minimal erythroid precursor cell damage from cisplatin. These results indicate the primary etiology of cisplatin-associated anemia is a transient, but persisting EPO deficiency state resulting from cisplatin-induced renal tubular damage, which can be prevented or treated by hormone (EPO) replacement. (J. Clin. Invest. 1995. 95:1650-1659

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“…Unfortunately, red cell morphology was not described in these studies. Recent ly, a case of Coombs-positive hemolytic anemia follow ing prolonged therapy with CP has been reported [10]. An immune mechanism is not operative in our patient since their anemia occurred on initial exposure to the drug and was Coombs-negative in type.…”

Section: Discussionmentioning

confidence: 59%

Hematologic Effect of cis-Platinum-Bleomycin Therapy

Najarian¹,

Miller²,

Zimelman³

et al. 1981

Oncology

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A prospective study of the hematologic findings in 19 patients receiving cis-platinum (C-P) bleomycin (B) for squamous cell carcinoma of the head and neck was performed. CP 3 mg/kg was given on day 1, B 15 mg/m² on day 3 and then by continous infusion from day 3 to 10. Hematocrits declined in all patients from a mean of 41.6 ± 3.9 to 36.6 ± 4.9 (p < 0.001) with the nadir seen by 10 days, reticulocyte count was unchanged. In 1 patient marked hemolysis occurred over 10-day period associated with the appearance of irregular spherocytes on smear, a situation similar to the index case which initiated this study. 5 other patients had spherocytes. A significant lymphopenia in the absence of neutropenia and thrombocytopenia was also observed.

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Cisplatin-Induced Hemolysis

Cited by 85 publications

References 1 publication

Haematological toxicity of carboplatin in rats

Haematological toxicity of carboplatin in rats

Cisplatin-associated anemia: an erythropoietin deficiency syndrome.

Hematologic Effect of cis-Platinum-Bleomycin Therapy

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