Thrombotic Microangiopathy in Cancer

Weitz, Ilene C.

doi:10.1055/s-0039-1687893

Cited by 32 publications

(23 citation statements)

References 75 publications

(171 reference statements)

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“…Поскольку патогенез различных форм злокачественных новообразований, механизмов роста и метастазирования опухоли имеет множество взаимодействующих между собой факторов, то и в случае развития опухольассоциированной ТМА невозможно выделить какой-то ведущий или первичный механизм [77].…”

Section: Discussionunclassified

“…Многие случаи ТМА регистрируются через 6−12 мес после курсов химиотерапии. Пациенты могут находиться на стадии ремиссии, но затем умирать из-за её осложнений[41], смертность при этом составляет до 72%[77].Случаиострого некардиогенного отека легких, синдрома дыхательной недостаточности у взрослых могут быть результатом развития ТМА на фоне применения митомицина С [65]. Механизм развития отека легких неясен, но наиболее вероятно, что он является результатом токсического действия на эндотелий микрососудов легких.…”

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Thrombotic microangiopathy in cancer patients

et al. 2019

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Thrombotic microangiopathy (TMA) is a rare phenomenon, which is severe pathology based on systemic microvascular thrombosis. TMA is characterized by thrombocytopenia and signs of microangiopathic hemolytic anemia. The review presents a modern data on the pathogenesis of tumor-associated thrombotic microangiopathy, considers the interaction of various effectors related to both tumor growth and metastasis process ― immune system activation, endotheliopathy formation, use of chemotherapeutic agents and targeted therapy in the pathogenesis of various forms of TMA. The interaction between the tumor tissue, hemostasis and immune systems are of the type of cascade of mutual activation, thus leading to the formation of a vicious circle, resulting in damage to endothelium and thrombosis in the microcirculatory channel, that is, the development of TMA. The formation of thromboembolism, which includes tumor tissue in the microvessels of the lungs, contributes to the development of pulmonary tumor thrombotic microangiopathy (PTTM). Сancer patients have higher vWF levels and lower ADAMTS13 levels or/and activity than the general population, often also depending on the stage of cancer: vWF and ADAMTS13 have been shown to be associated with thrombotic complications in cancer patients, and ADAMTS13 shows prognostic potential. Increased expression of complement proteins and/or activation of complement during chemotherapy, infectious and inflammatory complications may also cause TMA development. Pathogenesis of thrombotic microangiopathy also is associated with numerous chemotherapeutic agents, such as mitomycin C, gemcitabine, cisplatin, carboplatin and Bevacizumab, an inhibitor of VEGF. This may be the result of both the direct toxic effect of the drug on endothelium and damage of it by immune complexes caused by expression of the VEGF-antibodies. Usage of number of chemotherapeutic agents, especially anti-VEGF and tyrosine kinase inhibitors, which have a direct toxic effect on endothelium, are associated with the development of TMA. Mechanisms causing the development of TMA are considered as components of the hemostasis system, leading to the development of chronic, long-lasting disorders of the hemostasis system (chronic DIC syndrome) and are associated with high incidence of thrombotic complications.

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Thrombotic microangiopathy in cancer patients

et al. 2019

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“…Differential diagnosis includes several pathologies that can be grouped according to TMA trigger (Fig. 3) [40-56]. TTP arises from an acquired or congenital severe deficiency of a disintegrin-like and metalloproteinase with thrombospondin type 1 motif, 13 (ADAMTS13), a specific cleaving protease of von Willebrand factor (VWF).…”

Section: Diagnosis and Differential Diagnosis Of Ahusmentioning

confidence: 99%

“…Pregnancy-associated HUS (P-HUS) develops in postpartum period (73–79%) [42, 52, 53] although its appearance during pregnancy is feasible. Cancer-related HUS is associated with metastatic cancer in up to 90% of cases [40, 41], being able to relapse after complete remission with cancer recurrence. Lots of drugs have been associated with HUS, mainly drugs used in immunosuppressive therapy – solid organ transplant or hematopoietic stem cell transplantation – or antineoplastic therapies – gemcitabine, cisplatin, anti-VEGF therapy, proteasome inhibitors, and so forth [41].…”

Section: Diagnosis and Differential Diagnosis Of Ahusmentioning

confidence: 99%

Atypical Hemolytic Uremic Syndrome: New Challenges in the Complement Blockage Era

Bernabeu

Escribano

Vilariño

2020

Nephron

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Atypical hemolytic uremic syndrome (aHUS) is a rare cause of thrombotic microangiopathy (TMA), characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and multisystem end organ involvement, most commonly affecting the kidney. Diagnosis is clinical, after exclusion of other TMA causes. Primary aHUS arises from genetic abnormalities, resulting in uncontrolled complement activity, while a variety of clinical scenarios cause secondary aHUS, including infection, pregnancy, malignancy, autoimmune disease, and medications. They can also induce a temporary complement deregulation with an overlap between both scenarios, which can make differential diagnosis difficult. Primary aHUS can be sporadic or familial and is associated with a high rate of progression to ESRD. Many aHUS patients relapse in the native or transplanted kidneys, leading to kidney failure. The introduction of eculizumab has changed the prognosis of aHUS, by inducing hematologic remission, improving or stabilizing kidney functions, and preventing graft failure. The early institution of appropriate therapy can prevent multiorgan damage, so is essential to recognize and differentiate the TMA syndromes. Eculizumab is considered now the first-line treatment, and it is recommended lifelong therapy. However, the high cost of therapy has led to make efforts to develop precise complement functional and genetic studies that help physicians to determine the appropriate duration of eculizumab therapy. Nowadays, more studies are needed to select candidates to adjustment of therapy.

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“…6 Another significant manifestation of the coagulopathy seen in cancer is "cancerassociated thrombotic microangiopathy" as discussed by Weitz. 7 The diagnostic characteristics of cancer-associated thrombosis can be assessed by a variety of means, including viscoelastography. This new diagnostic approach is championed by Walsh et al 8 They point out the similarity and differences between the coagulopathies seen in acute trauma and malignancy-associated coagulopathy, using this particular technique.…”

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confidence: 99%