Thrombotic microangiopathy associated with α‐interferon therapy for chronic myeloid leukaemia (Case Report)

Gales̃ić, Kres̆imir; Božić, Borka; Račić, Ivana; Ščukaneć-Špoljar, Mira

doi:10.1111/j.1440-1797.2006.00524.x

Cited by 13 publications

(6 citation statements)

References 24 publications

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“…[58][59][60] Cytokine therapy and TMA Cytokine therapy with interferon-a in the setting of chronic myeloid leukemia has been linked with TMA in a number of case reports and case series. [61][62][63][64][65][66][67][68] It has also been reported in the treatment of Sezary syndrome 69 and hairy cell leukemia. 70 The pathophysiologic mechanism by which interferon-a induces TMA is thought to occur via increased leukocyte adhesion to endothelium, causing endothelial damage.…”

Section: Other Chemotherapeutic Agentsmentioning

confidence: 97%

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Antineoplastic agents and thrombotic microangiopathy

Garcia

Atallah

2016

J Oncol Pharm Pract

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Section: Other Chemotherapeutic Agentsmentioning

confidence: 97%

“…70 The pathophysiologic mechanism by which interferon-a induces TMA is thought to occur via increased leukocyte adhesion to endothelium, causing endothelial damage. 63,65 Positive antiphospholipid antibodies were noted in some cases, 61,69 and these may play a role in the development of TMA in a subset of patients.…”

Section: Other Chemotherapeutic Agentsmentioning

confidence: 99%

Antineoplastic agents and thrombotic microangiopathy

Garcia

Atallah

2016

J Oncol Pharm Pract

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“…For TMA, the glycosylation is likely not associated with the pathogenicity of interferon b. It remains unclear why interferon causes TMA [6,8,10,11]. Interferon has been reported to cause endothelial cell damage directly through a decrease in vascular endothelial growth factor production, or to generate ADAMTS-13 inhibitor through T cell activation [12][13][14].…”

Section: Case Reportmentioning

confidence: 99%

Thrombotic microangiopathy caused by interferon β-1b for multiple sclerosis: a case report

et al. 2016

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A 41-year-old man with a history of multiple sclerosis (MS) developed thrombotic microangiopathy after taking interferon b-1b for 10 years. Although the relapse of his MS was well controlled under normal blood pressure, he had persistent nausea, anorexia, gait disturbance and visual disorder 1 month before admission. He showed lethargy and high blood pressure (180/ 102 mmHg). Laboratory test results revealed anemia and thrombocytopenia, elevated LDH and renal dysfunction. Urinary dipstick showed a 2? result for proteinuria and 3? for hematuria. Schizocyte were present and haptoglobin decreased, and we diagnosed him with possible thrombotic microangiopathy (TMA). Magnetic resonance image indicated posterior reversible encephalopathy syndrome (PRES), which could be accelerated by TMA. After discontinuing interferon b-1b, high dose intravenous methylpredonisolone, anti-hypertension therapy and plasma exchange was started. Because a mild decrease in ADAMTS13 activity and absence of ADAMTS 13 inhibitor could not cause thrombotic thrombocytopenic purpura, plasma exchange was stopped. The patient's renal function recovered and PRES resolved, and he was discharged with slightly decrease of visual acuity. We suggest that his TMA was likely caused by interferon b-1b, resulting in PRES in a patient with multiple sclerosis. We report this rare case and also review the literature.

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“…[1] Among histological findings detected, there are some reports with renal thrombotic microangiopathy (TMA). [2–5] We report here a case of interferon-induced hemolytic uremic syndrome (HUS). A 36-year-old Caucasian woman was admitted for acute renal failure and pulmonary edema.…”

mentioning

confidence: 99%