ArticleMolecular and clinical oncology2018
Neurological variability in chemotherapy-induced posterior reversible encephalopathy syndrome associated with thrombotic microangiopathy: Case reports and literature review.
Article in Molecular and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Role of inflammation and oxidative stress in chemotherapy-induced neurotoxicity.Immunologic research · 2022Review
- Fatal Thrombotic Microangiopathy and Posterior Reversible Encephalopathy Syndrome in a Patient with Anti-melanoma Differentiation-associated Gene 5 Antibody-positive Dermatomyositis.Internal medicine (Tokyo, Japan) · 2021Article
- Chemotherapy and Immunosuppressant Therapy-Induced Posterior Reversible Encephalopathy Syndrome.Cureus · 2020Review
- Thrombotic thrombocytopenic purpura with reversible splenial lesion syndrome: a case report.BMC neurology · 2020Article
- Posterior reversible encephalopathy syndrome associated with the use of chemotherapeutic agents: a rare complication after treatment with vinorelbine.BMJ case reports · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Posterior reversible encephalopathy syndrome (PRES) is a clinical syndrome characterized by headaches, seizures, a confusional state and visual disturbances associated with transient predominantly bilateral posterior white mater magnetic resonance imaging lesions. It is primarily reported in the setting of hypertension, acute renal failure, peripartum eclampsia, autoimmune disease, immunosuppression and chemotherapy. Thrombotic microangiopathy (TMA), including hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) has also been reported as potential PRES inducer. The present study reviews two cases of patients with PRES, associated with TMA caused by chemotherapy. Their clinical and imaging data, and the relevant literature were reviewed. Patient 1 presented with TMA-induced PRES following mitomycin-C for metastatic colon adenocarcinoma. Treatment with steroids, plasma exchange, intravenous immunoglobulins, aspirin, antihypertensive drugs, and diuretics resulted in resolution of the neurological and imaging deficits. Patient 2 presented with TMA-induced PRES following gemcitabine for metastatic breast carcinoma. Treatment was ineffective and the patient deteriorated despite verapamil, dexamethasone, and plasma exchange. In this report, the relevant literature regarding pathogenesis, treatment and prognosis of chemotherapy-induced PRES associated with TMA was reviewed. We conclude that several chemotherapy agents may cause PRES through various pathogenic mechanisms, leading to clinical variability and divergent response to therapy.
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