Endotheliopathy: A continuum of hemolytic uremic syndrome due to mitomycin therapy

Groff, James A.; Kozak, Mark; Boehmer, John; Demko, Trudy M.; Diamond, Jonathan R.

doi:10.1016/s0272-6386(97)90042-1

Cited by 25 publications

(17 citation statements)

References 9 publications

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“…This event is followed by adhesion of platelets and fibrin to the site. Groff et al have reported that MMC-initiated endothelial dysfunction can be manifested clinically by hemorrhage (17). The present case may also have involved a degree of platelet dysfunction.…”

Section: Discussionmentioning

confidence: 50%

Hemolytic Uremic Syndrome with Intracranial Hemorrhage Following Mitomycin C Administration.

et al. 2001

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Section: Discussionmentioning

confidence: 50%

Hemolytic Uremic Syndrome with Intracranial Hemorrhage Following Mitomycin C Administration.

et al. 2001

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“…Toxicity is cumulative and dose-dependent, and increases at a dose of >50 mg/m 2 (15)(16)(17), as shown in patient 1. Mitomycin-C-induced TMA results from endothelial damage (18), which is at least partly due to formation of platelet-aggregating immune complexes and complement-fixing circulating immune complexes (19). To the best of our knowledge, PRES was not previously reported following treatment with mitomycin-C and may possibly be related to the mitomycin-C-induced TMA.…”

Section: Mitomycin-c-induced Presmentioning

confidence: 80%

Neurological variability in chemotherapy‑induced posterior reversible encephalopathy syndrome associated with thrombotic microangiopathy: Case reports and literature review

et al. 2017

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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 immuno globulins, 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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“…HUS may be related to drug-related endothelial damage [2, 3, 4, 5]. MiC-related HUS was described for the first time in 1979 [6, 7].…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin Is Beneficial in Mitomycin-Induced Hemolytic-Uremic Syndrome

Catalano¹,

Gianesini²,

Fabbian³

2002

Nephron

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Mitomycin C is a powerful antineoplastic agent. If used at high dosage, it may cause a secondary form of adult hemolytic-uremic syndrome (HUS). Blood transfusions worsen the evolution of this peculiar form of HUS. We describe a patient who developed HUS after treatment with mitomycin C (total dose 144 mg/m²) due to a carcinoma of the ascending colon. Repeated blood transfusions were associated with rapidly evolving renal failure coupled with anemia and thrombocytopenia. Haptoglobin was undetectable. Soon after starting subcutaneous erythropoietin, the velocity of progression of renal failure slowed whilst no more blood transfusions were required and haptoglobin levels returned to normal. Thereafter, the patient’s renal function slowly worsened and she started chronic hemodialysis 5 years later. Up to now, all investigations have failed to show a relapse of her adenocarcinoma. A possible explanation of these data is that erythropoietin permitted the termination of blood transfusions which both triggered and perpetuated the syndrome. However, we cannot exclude a primitive effect of erythropoietin on the endothelium or on the platelets.

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Endotheliopathy: A continuum of hemolytic uremic syndrome due to mitomycin therapy

Cited by 25 publications

References 9 publications

Hemolytic Uremic Syndrome with Intracranial Hemorrhage Following Mitomycin C Administration.

Hemolytic Uremic Syndrome with Intracranial Hemorrhage Following Mitomycin C Administration.

Neurological variability in chemotherapy‑induced posterior reversible encephalopathy syndrome associated with thrombotic microangiopathy: Case reports and literature review

Erythropoietin Is Beneficial in Mitomycin-Induced Hemolytic-Uremic Syndrome

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