Bortezomib-induced thrombotic thrombocytopaenic purpura: Figure 1

Mehta, Neha; Saxena, Ashish; Niesvizky, Rubén

doi:10.1136/bcr-2012-006461

Cited by 24 publications

(29 citation statements)

References 11 publications

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“…DITMA attributed to PI is a relatively recently appreciated complication of PI, and a review of the literature reveals nine previous case reports of systemic TMA attributed to PI (Table ). The first five reports describe patients treated with bortezomib‐based regimens who develop TMA . However, two cases were complicated by a history of allogeneic HSCT and subsequent use of calcineurin inhibitors, which may confound the finding of TMA.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, in these initial studies of carfilzomib, half of the cases of renal impairment were noted in conjunction with disease progression. No mention of DITMA is made in these initial studies, but recent case reports have noted the presence of TMA in patients treated with PI . Below, we summarize the current literature and expand on these findings with our own case series.…”

Section: Introductionmentioning

confidence: 87%

“…Two distinct mechanisms of action have been described: an immune‐mediated mechanism and dose‐dependent toxicity mechanism. Recently, case reports have arisen of DITMA occurring in patients receiving proteasome inhibitors (PI) as treatment for multiple myeloma (MM) .…”

Section: Introductionmentioning

confidence: 99%

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Proteasome inhibitor associated thrombotic microangiopathy

et al. 2016

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A variety of medications have been implicated in the causation of thrombotic microangiopathy (TMA). Recently, a few case reports have emerged of TMA attributed to the proteasome inhibitors (PI) bortezomib and carfilzomib in patients with multiple myeloma. The aim of this case series was to better characterize the role of PI in the etiology of drug‐induced TMA. We describe eleven patients from six medical centers from around the world who developed TMA while being treated with PI. The median time between medication initiation and diagnosis of TMA was 21 days (range 5 days to 17 months). Median laboratory values at diagnosis included hemoglobin—7.5 g dL−1, platelet count—20 × 109/L, LDH—698 U L−1, creatinine—3.12 mg dL−1. No patient had any other cause of TMA, including ADAMTS13 inhibition, other malignancy or use of any other medication previously associated with TMA. Nine patients had resolution of TMA without evidence of hemolysis after withdrawal of PI. Two patients had stabilization of laboratory values but persistent evidence of hemolysis despite medication withdrawal. One patient had recurrence of TMA with rechallenge of PI. There is a strong level of evidence that PI can cause DITMA. In evaluating patients with suspected TMA, PI use should be recognized as a potential etiology, and these medications should be discontinued promptly if thought to be the cause of TMA. Am. J. Hematol. 91:E348–E352, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 87%

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Proteasome inhibitor associated thrombotic microangiopathy

et al. 2016

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“…Some studies show cases of death as a complication of plasmapheresis, which makes it clear that, although it is a good treatment option, does not come without risks and new therapies need to be developed. [8,[19][20][21][22][23][24][25][26][27] …”

Section: Discussionmentioning

confidence: 99%

Thrombotic thrombocytopenic purpura and neurologic manifestations – Case report and integrative review

Mendes

Couto²,

Duarte³

et al. 2016

Int Arch Med

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Introduction: Thrombotic thrombocytopenic Purpura (TTP) is a rare and pontentially life-threatening condition caused by ADAMTS13 enzyme complex deficiency. It leads to microthrombi formation in the microvasculature, which may cause several organs manifestations. It mainly affects kidneys and nervous system leading to severe complications. The best treatment of TTP nowadays is Plasma Exchange (PEx). The most commom neurologic manifestation of TTP is headache, but stroke, mental confusion and others can also be present.Objective: To describe a case of atypical neurologic manifestation of TTP and to perform an integrative review.Case Report: Female patient, 32 years old was admitted to the emergency room with important dyspnea. She also presented hypotension, tachycardia and low oxygen-hemoglobin saturation. After these symptoms were stabilized, she was hospitalized for further investigation. During her hospitalization, she developed microangiopatic anemia, thrombocytopenia and renal failure, she also had a historic of neurologic manifestations such as strenght decrease in lower and upper limbs, gagging, dysphagia. She was diagnosed with TTP and we indicated a hospital transference for her to realize this procedure. Discussion:The Thrombotic thrombocytopenic purpura is a rare disease that mainly affects women. We present a case of atypical neurologic manifestations of TTP consisting with headache.

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“…This event was not associated with myeloma progression. TTP is rare in myeloma patients but has been reported as a complication of stem cell transplantation [3][4][5][6][7], treatment with the proteasome inhibitors [8][9][10][11][12][13][14], zoster infection [15], and as an initial disease manifestation [16]. Although thrombotic microangiopathy (TMA) is typically a feature of solid tumors with widespread metastatic disease progression [17], this may not be the case with myeloma.…”

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confidence: 99%

Thrombotic thrombocytopenic purpura in a patient with lenalidomide-responsive multiple myeloma

et al. 2015

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Dear Editor,We report a case of myeloma-associated thrombotic thrombocytopenic purpura (TTP). An 81-year-old female with multiple myeloma initially diagnosed 4 years prior was treated with 4 cycles of lenalidomide, bortezomib and dexamethasone, high-dose melphalan conditioned autologous stem cell transplant, followed by bortezomib maintenance. Subsequent biochemical progression was treated with lenalidomide 25 mg daily (days 1-21 in a 28-day cycle) and dexamethasone 20 mg weekly, complicated by venous thromboembolism, treated with enoxaparin for 6 months, then switched to aspirin. Lenalidomide was discontinued. She again experienced biochemical disease progression and was treated with lenalidomide and dexamethasone (LD), with prophylactic enoxaparin. Comorbidities included hypertension, hyperlipidemia, and well-controlled rheumatoid arthritis. She in addition took amlodipine, hydrochlorothiazide, valacyclovir, potassium, and vitamin D/calcium supplements.On cycle 5, day 15, she presented with dizziness, nausea, fatigue, petechiae and hematuria. Examination revealed widespread petechiae, normal neurologic examination, and mild dehydration. Laboratory studies revealed a platelet count of 2×10 3 /μL, hemoglobin 9.1 g/dL, white blood cell count 2.8× 10 3 /μL, reticulocyte 2.8 %, creatinine 1.77 mg/dL, total bilirubin 4.3 mg/dL, indirect bilirubin 3.2 mg/dL, prothrombin time 15.2 s, activated partial thromboplastin time 27.6 s, fibrinogen 422 mg/dL and serum lactate dehydrogenase of 3861 IU/L, haptoglobin <3 mg/dL, and negative DAT and elevated D-dimer 2.55 mcg/mL. The troponin I was elevated at 5.36 ng/mL. Electrocardiogram showed no ischemic changes. Enoxaparin was discontinued, and platelets were transfused without achieving platelet increment. Blood smear revealed schistocytes and thrombocytopenia (Fig. 1). The AD-AMTS13 activity was 7 % but ADAMTS13 inhibitor was not detected. The platelet count and serum lactate dehydrogenase over time are depicted in Fig. 2. Intravenous methylprednisolone 1 g was given for 3 days, with plasma exchange (1.5 times plasma volume) performed daily for 4 days. Myeloma restaging investigations were consistent with a partial Fig. 1 Peripheral blood smear (×100 magnification) showing many schistocytes and marked thrombocytopenia response: the difference between serum free lambda and kappa had decreased by >50 % and marrow plasma cell burden decreased from 60 to 14 %. She was re-challenged with lenalidomide 5 mg daily. Repeat ADAMTS13 activity 4 weeks later was 64 %.In summary, this patient with LD-treated relapsed myeloma appeared to develop tissue ischemia, intravascular hemolysis, schistocytosis, thrombocytopenia, and ADAMTS13 activity <10 % consistent with TTP [1]. ADAMTS13 inhibitor was not detected in this case presumably because the inhibitor was below the assay's detectable threshold or the pathological process may have involved some anti-ADAMTS13 non-inhibitory antibodies or circulating inhibitors not related to an immunoglobulin G or M [2]. This event was not associated with my...

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Bortezomib-induced thrombotic thrombocytopaenic purpura: Figure 1

Cited by 24 publications

References 11 publications

Proteasome inhibitor associated thrombotic microangiopathy

Proteasome inhibitor associated thrombotic microangiopathy

Thrombotic thrombocytopenic purpura and neurologic manifestations – Case report and integrative review

Thrombotic thrombocytopenic purpura in a patient with lenalidomide-responsive multiple myeloma

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