Immunohemolytic anemia following oxaliplatin administration

Garufi, Carlo; Vaglio, Stefania; Brienza, S.; Conti, Laura; Dattino, R; Girelli, Gabriella; Terzoli, E.

doi:10.1023/a:1008336108007

Cited by 46 publications

(33 citation statements)

References 5 publications

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“…All cases were reversible upon oxaliplatin withdrawal and corticosteroid administration. Such reactions have also been described by other investigators that recommend definitive drug withdrawal [33, 34]. …”

Section: Discussionsupporting

confidence: 56%

Clinical Features of Hypersensitivity Reactions to Oxaliplatin: A 10-Year Experience

Polyzos

Tsavaris²,

Gogas³

et al. 2008

Oncology

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Background: Oxaliplatin has become one of the major cytotoxic agents for the treatment of gastrointestinal tumors. As a result, several cases of the so-called oxaliplatin-associated hypersensitivity reaction have been documented. Patients and Methods: We have retrospectively evaluated and characterized these reactions in our patient group by reviewing the files of 1,224 patients exposed to an oxaliplatin-containing regimen in order to provide useful clinical information for diagnosis and management. Results: Three hundred and eight (308) patients who have never been exposed to platinum compounds developed symptoms compatible with a reaction to oxaliplatin that was verified by manifestation of at least similar symptoms on rechallenging. The reactions occurred after the first 5 courses, with a median course number of 9 (range 1–24). These reactions could be distinguished as (1) mild reactions occurring in 195 (63%) patients manifesting with itching and small area erythema either during treatment or within the next hours, and (2) severe reactions occurring in 113 (37%) patients within minutes of drug infusion manifesting with diffuse erythroderma, facial swelling, chest tightness, bronchospasm and changes in blood pressure. Oxaliplatin withdrawal was not required in patients with a mild reaction. Forty-eight (42%) patients having a severe reaction with appropriate premedication and prolongation of the infusion duration could tolerate 2–4 subsequent courses. For the remaining 65 (58%) patients, oxaliplatin withdrawal was inevitable because of the very severe reactions occurring on rechallenging. In addition, 3 patients presented with thrombocytopenia and 3 others with hemolytic anemia, all reversible upon oxaliplatin discontinuation. Conclusions: Hypersensitivity reactions to oxaliplatin are underestimated. Although the reactions are not frequent during first courses, in extensively pretreated patients, they may become a serious problem. In the majority of patients, drug discontinuation might not be necessary. In patients manifesting a severe reaction, re-exposure to oxaliplatin should be considered only if the patient can tolerate the reaction and there has been clinical benefit from this therapy. Physicians and nursing staff should be aware of the risk and be well prepared.

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Section: Discussionsupporting

confidence: 56%

Clinical Features of Hypersensitivity Reactions to Oxaliplatin: A 10-Year Experience

Polyzos

Tsavaris²,

Gogas³

et al. 2008

Oncology

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“…51 Moreover, dynamin-related protein 1, a protein that catalyzes the process of mitochondrial fission with the consequent ROS production, is involved in chemotherapy-induced neuropathy in rats. 16 By contrast, a low relevance of ROS production from inflammatory cells could be hypothesized since another side effect related to prolonged oxaliplatin use is a nonmyelosuppressive hematologic toxicity, which includes hemolysis, 18 thrombocytopenia, 5 and pancytopenia. 48 It is of fundamental importance that, to be clinically useful, the antineuropathic agents must reduce the neurotoxic effect of the chemotherapeutic agent maintaining its full anti-tumor efficacy.…”

Section: Discussionmentioning

confidence: 99%

Oxaliplatin-Induced Neuropathy: Oxidative Stress as Pathological Mechanism. Protective Effect of Silibinin

Mannelli

Zanardelli

Failli

et al. 2012

The Journal of Pain

156

120

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Oxaliplatin is the standard treatment for advanced colorectal cancer. Its dose-limiting toxicity is the development of a painful neuropathic syndrome sustained by unclear mechanisms. Although the oxidative hypothesis is a matter of debate, direct data about oxidative damage induced in vivo by anticancer agents are lacking and the efficacy of the available antioxidant compounds are unsatisfactory. In a rat model of painful oxaliplatin-induced neuropathy (2.4 mgkg À1 i.p., daily for 21 days), we described an important component of oxidative stress. In the plasma of oxaliplatin-treated rats, the increases in carbonylated protein and thiobarbituric acid reactive substances were the index of the resultant protein oxidation and lipoperoxidation, respectively. The same pattern of oxidation was revealed also in the sciatic nerve, and in the spinal cord where the damage reached the DNA level. The antioxidant compound silibinin (100 mgkg À1 per os), administered once a day, starting from the first day of oxaliplatin injection until the 20th, prevented oxidative damage as did a-tocopherol. Repetitive administration of silibinin, as well as a-tocopherol, reduced oxaliplatin-dependent pain induced by mechanical and thermal stimuli. Antioxidants were also able to improve motor coordination. The antineuropathic effect of both molecules improved by about 50% oxaliplatin-induced behavioral alterations.Perspective: This study characterizes oxidative stress parameters in a rat model of oxaliplatininduced neuropathy. A relationship between the improvement of oxidative alterations and pain relief is established in rats treated with natural antioxidant compounds like a-tocopherol and silibinin. Silibinin could be a valid therapeutic option for chemotherapy-induced neuropathy.

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“…However, two independent pathogenetic mechanisms have been proposed for this toxicity. Some authors described the formation of autoantibodies to erythrocytes and, more rarely, to platelets and neutrophils as a result of l-OHP adsorption on blood cells [6,7,10,12,14], suggesting that the mechanism for this adverse event should be a peripheral immuno-mediated blood cells disruption which resembles the Evans' syndrome [13]. By contrast, other authors reported high levels of cytokines (i.e.…”

Section: To the Editormentioning

confidence: 99%

Life-threatening oxaliplatin-induced acute thrombocytopenia, hemolysis and bleeding: A case report

et al. 2008

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Immunohemolytic anemia following oxaliplatin administration

Cited by 46 publications

References 5 publications

Clinical Features of Hypersensitivity Reactions to Oxaliplatin: A 10-Year Experience

Clinical Features of Hypersensitivity Reactions to Oxaliplatin: A 10-Year Experience

Oxaliplatin-Induced Neuropathy: Oxidative Stress as Pathological Mechanism. Protective Effect of Silibinin

Life-threatening oxaliplatin-induced acute thrombocytopenia, hemolysis and bleeding: A case report

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