Cisplatin neurotoxicity

Cersosimo, Robert J.

doi:10.1016/0305-7372(89)90041-8

Cited by 87 publications

(42 citation statements)

References 43 publications

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“…Paclitaxel dose >250 mg m-2 is strongly associated with the occurrence of neurotoxicity, which is dose limiting at doses >300 mg m-2 (Sarosy et al, 1992). Cisplatin-induced neurotoxicity is mainly observed after cumulative doses of 300 mg m-2 (Cersosimo, 1989). Rowinsky et al (1991) found a 27% incidence of neurotoxicity (n=44) for the combination of cisplatin and paclitaxel, compared with 44% in our study.…”

Section: Discussioncontrasting

confidence: 46%

“…A varying incidence of neurotoxicity has been reported for paclitaxel (4-52%) (Eisenhauer et al, 1994;Thigpen et al, 1994), for cisplatin (3-92%) (Cersosimo, 1989) and for the combination of paclitaxel and cisplatin (27-28%) (Rowinsky et al, 1991, McGuire et al, 1996. Both paclitaxel and cisplatin induced neurotoxicity are cumulative and dose related (Cersosimo, 1989;Sarosy et al, 1992;Eisenhauer et al, 1994). Paclitaxel dose >250 mg m-2 is strongly associated with the occurrence of neurotoxicity, which is dose limiting at doses >300 mg m-2 (Sarosy et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

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Paclitaxel, ifosfamide and cisplatin with granulocyte colony-stimulating factor or recombinant human interleukin 3 and granulocyte colony-stimulating factor in ovarian cancer: a feasibility study

Veldhuis

Willemse²,

Beijnen³

et al. 1997

Br J Cancer

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Summary The tolerability and efficacy of four courses of paclitaxel and ifosfamide plus cisplatin every 3 weeks was evaluated in patients with residual or refractory ovarian cancer. Additionally, supportive haematological effects of recombinant human interleukin 3 (rhlL-3) and recombinant human granulocyte colony-stimulating factor (G-CSF) were studied. Paclitaxel starting dose was 135 mg m-2 (day 1), with ifosfamide dose 1.2 g m-2 day-1 (days 2-4) and cisplatin dose 30 mg m-2 day-1 (days 2-4). All 16 patients received 5.0 9g kg-1 day-' G-CSF (days 7-16) and, in addition, eight patients were randomized to receive 10 gg kg-' day-' rhlL-3 (days 5-9). Paclitaxel and ifosfamide doses were reduced when grade IV haematological toxicity occurred. In the absence of grade IV haematological toxicity and normal recovery of haematopoiesis, paclitaxel dose was escalated. Toxicity was evaluable in 56 courses, with haematological effects in 52. Despite antiemetic treatment, nausea and vomiting (2 grade 1) occurred in 50 courses. Five patients had persisting peripheral neuropathy. Renal and liver function were not affected. Grade IV neutropenia occurred in 12 out of 52 courses, with neutropenic fever in two patients, both of whom died from fatal septicaemia. Grade IV thrombocytopenia without bleeding was observed in 15 courses. Grade IV haematological toxicity was associated with hepatic metastases and concurrent increases in alkaline phosphatase (P <0.001) and gamma-glutamyltransferase (P=0.007). No relation was found between haematological toxicity and pharmacokinetic parameters of paclitaxel. Patients treated with rhlL-3 showed a tendency to a faster platelet recovery (not affecting platelet nadir), and the cisplatin dose intensity was higher (P=0.025). Six of the nine evaluable patients had a tumour response. The overall median progression-free survival was 7 months and the overall mean survival was 13 months. In conclusion, this potentially interesting combination as second-line treatment showed a low tolerability with unexpected mortality, while rhlL-3 administration tended to induce a more rapid platelet recovery.

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Section: Discussioncontrasting

confidence: 46%

Section: Discussionmentioning

confidence: 99%

Paclitaxel, ifosfamide and cisplatin with granulocyte colony-stimulating factor or recombinant human interleukin 3 and granulocyte colony-stimulating factor in ovarian cancer: a feasibility study

Veldhuis

Willemse²,

Beijnen³

et al. 1997

Br J Cancer

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“…Once inside the low chloride environment of the cell, replacement of the chloro ligands with other ligands may occur, which may result in cytotoxic response to the cell. Although it is proposed that the mechanism of DDPinduced cytotoxicity against cancer cells is through its binding to DNA (Andrews and Howell, 1990), the mechanisms of DDP-induced nephrotoxicity and neurotoxicity are not known (Daugaard and Abildgaard, 1989;Cersosimo, 1989). There is some evidence to suggest that at least some of the DDP-induced damage in the kidney occurs in the cell membranes, with renal ATPase activity being affected (DaleyYates and McBrien, 1982;Uozomi and Litterest, 1985).…”

Section: Discussionmentioning

confidence: 99%

“…However, DDP causes both nephrotoxicity and a peripheral neuropathy. The nephrotoxicity can be alleviated by hydration and the administration of mannitol, but peripheral neuropathy is now often dose limiting (Cersosimo, 1989;Daugaard and Abildgaard, 1989). The neuropathy can be crippling and appears to be related to the cumulative dose of DDP (Borch and Markman, 1989).…”

mentioning

confidence: 99%

Pressure tuning infrared spectroscopic study of cisplatin-induced structural changes in a phosphatidylserine model membrane

Taylor

Goel²,

Shirazi³

et al. 1995

Br J Cancer

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Summary The dynamic effect of cis-diamminedichloroplatinum(II) (DPP) and its aquated metabolite (DDP-OH) on a dimyristoylphosphatidylserine (DMPS) model membrane was investigated by pressure tuning vibrational spectroscopy. The native species (DDP-C1) and the aquated species (DPP-OH) were both observed to bind to the carboxylate group of the serine as evidenced by a frequency shift of 1622-1620 cm '. However, only DDP-OH was observed to bind to the phosphate group (PO2-). The binding of either drug to DMPS resulted in an increased pressure required to halt the reorientational fluctuations of the acyl chains, indicating that the distance between the chains was increased. The two drugs did not partition into the matrix of the hydrophobic section in the model membrane. Collectively, these data suggest that DDP-C1 and DDP-OH are capable of binding to the polar head group of DMPS, resulting in an enlargement of the area of the head and a subsequent increase in the intermolecular distance between the acyl chains.

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“…Protective measures against nausea, vomiting and renal dysfunction have created the opportunity to increase the (individual and cumulative) cisplatin dose. With mild to moderate myelosuppression during conventional 3-or 4-weekly therapy, neurotoxicity (Cersosimo, 1989) and ototoxicity (Laurell and Jungnelius, 1990) have emerged as the remaining major dose-limiting side effects.…”

mentioning

confidence: 99%

Weekly high-dose cisplatin is a feasible treatment option: analysis on prognostic factors for toxicity in 400 patients

et al. 2003

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In the present study we describe the toxicity of weekly high-dose (70 -85 mg m À2 ) cisplatin in 400 patients (203 men, 197 women; median age 54 years) with advanced solid tumours treated in the period 1990 -2001 who took part in phase I/II trials, investigating the feasibility and efficacy of weekly cisplatin alone, or in combination with paclitaxel or etoposide. Cisplatin was administered in 250 ml NaCl 3% over 3 h, for six intended administrations. The mean number of administrations was 5.3 (range, 1 -6 administrations).Reasons not to complete six cycles were disease progression (7.5%), haematological toxicity (9%), nephrotoxicity (7%), ototoxicity (2.5%), neurotoxicity (1%), gastrointestinal toxicity (1%), cardiovascular complications (0.5%) or a combination of reasons including noncompliance and patient's request (5.5%). Logistic regression analysis was used to evaluate baseline parameters for prognostic value regarding toxicity. Leukopenia correlated with etoposide cotreatment, and thrombocytopenia with cisplatin dose and prior (platinum-based) chemotherapy. Risk factors for nephrotoxicity were older age, female gender, smoking, hypoalbuminaemia and paclitaxel coadministration. Neurotoxicity 4grade 1 (11% of patients) was associated with prior chemotherapy and paclitaxel coadministration. Symptomatic hearing loss occurred in 15% with anaemia as the predisposing factor. We conclude that weekly highdose cisplatin administered in hypertonic saline is a feasible treatment regimen.

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Cisplatin neurotoxicity

Cited by 87 publications

References 43 publications

Paclitaxel, ifosfamide and cisplatin with granulocyte colony-stimulating factor or recombinant human interleukin 3 and granulocyte colony-stimulating factor in ovarian cancer: a feasibility study

Paclitaxel, ifosfamide and cisplatin with granulocyte colony-stimulating factor or recombinant human interleukin 3 and granulocyte colony-stimulating factor in ovarian cancer: a feasibility study

Pressure tuning infrared spectroscopic study of cisplatin-induced structural changes in a phosphatidylserine model membrane

Weekly high-dose cisplatin is a feasible treatment option: analysis on prognostic factors for toxicity in 400 patients

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