Earlier diagnosis and international registries may improve outcomes in pulmonary tumour thrombotic microangiopathy

Price, Laura; Wort, Stephen J.

doi:10.1183/13993003.01736-2015

Cited by 2 publications

(3 citation statements)

References 11 publications

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“…У онкологических пациентов концентрация vWF выше и ниже концентрация ADAMTS-13, чем в целом в популяции, при этом имеется зависимость данных изменений от стадии заболевания. Выявлена взаимосвязь между концентрацией vWF, активностью ADAMTS-13 и риском развития тромбозов у онкологических пациентов [66]. Концентрация vWF выше у тех пациентов, у которых в течение 6 мес развивался тромбоз.…”

Section: • Vol 18 • № 1 Obstetrics Gynecology and Reproductionunclassified

The role of the microenvironment in tumor growth and spreading

Bitsadze,

Slukhanchuk,

Solopova

et al. 2024

Akušerstvo, ginekologiâ i reprodukciâ

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Introduction. The tumor microenvironment (TME) consisting of non-tumor cells and other components plays a crucial role in cancer development by promoting uncontrolled tumor growth.Aim: to detail all the components in TME and their contribution to carcinogenesis by analyzing available publications.Results. Currently, TME study is of great interest in the medical field. Its crucial role in the tumor initiation, progression, and spreading is emphasized. Several constituents have been identified in TME including cancer-associated fibroblasts, neutrophils, adipocytes, tumor vasculature, lymphocytes, extracellular matrix, dendritic cells, neutrophil extracellular traps, etc. Thromboinflammatory reactions are also considered an important TME element.Conclusion. TME constituents can serve as new targets for both diagnostics and antitumor therapy.

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Section: • Vol 18 • № 1 Obstetrics Gynecology and Reproductionunclassified

The role of the microenvironment in tumor growth and spreading

Bitsadze,

Slukhanchuk,

Solopova

et al. 2024

Akušerstvo, ginekologiâ i reprodukciâ

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show abstract

“…эндотелиального фактора роста может привести к вазоконстрикции. Возникновению или ухудшению системной гипертензии может предшествовать возникновение ТМА, связанной с химиотерапией [37,41,75]. Ингибирование сосудисто-эндотелиального фактора роста в гломерулярном микроциркуляторном русле может таким образом препятствоватьформированию и поддержанию здорового, фенестрированного эндотелия, и это может нарушать барьер клубочковой фильтрации, что приведет к возникновению гипертензии и почечной недостаточности [73,74].…”

Section: A R T I C L E I N P R E S Sunclassified

“…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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Earlier diagnosis and international registries may improve outcomes in pulmonary tumour thrombotic microangiopathy

Abstract: Earlier diagnosis and international registries may improve outcomes in pulmonary tumour thrombotic microangiopathy http://ow.ly/V74E

Cited by 2 publications

References 11 publications

The role of the microenvironment in tumor growth and spreading

The role of the microenvironment in tumor growth and spreading

Thrombotic microangiopathy in cancer patients

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