scholarly journals Recurrent thrombosis in a lady: Is there a missed connection?

2021 ◽  
Vol 73 ◽  
pp. S52
Author(s):  
Deepanjan Bhattacharya ◽  
Kurup K.N. Harikrishnan ◽  
Bijulal Sasidharan ◽  
V.K. Ajitkumar
Keyword(s):  
1997 ◽  
Vol 77 (03) ◽  
pp. 444-451 ◽  
Author(s):  
José Mateo ◽  
Artur Oliver ◽  
Montserrat Borrell ◽  
Núria Sala ◽  
Jordi Fontcuberta ◽  
...  

SummaryPrevious studies on the prevalence of biological abnormalities causing venous thrombosis and the clinical characteristics of thrombotic patients are conflicting. We conducted a prospective study on 2,132 consecutive evaluable patients with venous thromboembolism to determine the prevalence of biological causes. Antithrombin, protein C, protein S, plasminogen and heparin cofactor-II deficiencies, dysfibrinoge-nemia, lupus anticoagulant and antiphospholipid antibodies were investigated. The risk of any of these alterations in patients with familial, recurrent, spontaneous or juvenile venous thrombosis was assessed. The overall prevalence of protein deficiencies was 12.85% (274/2,132) and antiphospholipid antibodies were found in 4.08% (87/2,132). Ten patients (0.47%) had antithrombin deficiency, 68 (3.19%) protein C deficiency, 155 (7.27%) protein S deficiency, 16 (0.75%) plasminogen deficiency, 8 (0.38%) heparin cofactor-II deficiency and 1 had dysfib-rinogenemia. Combined deficiencies were found in 16 cases (0.75%). A protein deficiency was found in 69 of 303 (22.8%) patients with a family history of thrombosis and in 205/1,829 (11.2%) without a history (crude odds ratio 2.34, 95% Cl 1.72-3.17); in 119/665 (17.9%) patients with thrombosis before the age of 45 and in 153/1,425 (10.7%) after the age of 45 (crude odds ratio 1.81, 95% Cl 1.40-2.35); in 103/616 (16.7%) with spontaneous thrombosis and in 171/1,516 (11.3%) with secondary thrombosis (crude odds ratio 1.58, 95% Cl 1.21-2.06); in 68/358 (19.0%) with recurrent thrombosis and in 206/1,774 (11.6%) with a single episode (crude odds ratio 1.78,95% Cl 1.32-2.41). Patients with combined clinical factors had a higher risk of carrying some deficiency. Biological causes of venous thrombosis can be identified in 16.93% of unselected patients. Family history of thrombosis, juvenile, spontaneous and recurrent thrombosis are the main clinical factors which enhance the risk of a deficiency. Laboratory evaluation of thrombotic patients is advisable, especially if some of these clinical factors are present.


2002 ◽  
Vol 27 (7) ◽  
pp. 48-49 ◽  
Author(s):  
Cheryl Cummings Stegbauer
Keyword(s):  

2021 ◽  
Author(s):  
Thomas M. O'Gorman ◽  
Rukhmi V. Bhat ◽  
Shankar Rajeswaran ◽  
Sherif M. Badawy
Keyword(s):  

Author(s):  
П.А. Жарков ◽  
Д.С. Морозова ◽  
Д.А. Евстратов ◽  
Д.В. Федорова ◽  
Ю.А. Шифрин ◽  
...  

Введение. Тромбозы глубоких вен (ТГВ) являются нередким осложнением течения и лечения у детей с заболеваниями крови и требуют проведения антитромботической терапии и профилактики для снижения количества повторных тромботических эпизодов. Цель исследования: анализ частоты и определение факторов риска повторных ТГВ у детей, госпитализированных для лечения заболеваний крови. Материалы и методы. Проведен ретроспективный анализ электронной базы данных пациентов в возрасте от 0 до 17 лет включительно, которым проводили стационарное лечение гемобластозов и синдромов костномозговой недостаточности в период 01.0.2012 по 31.12.2017. В анализ вошли только те пациенты, у которых было зарегистрировано более 1 случая тромбоза. Результаты. Рецидивы тромбозов наблюдали у 13,3 детей с асимптоматическими (аТГВ) и у 5,4 с симптоматическими (сТГВ) ТГВ. Рецидивы аТГВ при остром лимфобластном лейкозе (ОЛЛ) выявлены у 14,5, при остром миелобластном лейкозе (ОМЛ) у 8,9, при лимфоме у 11,9. У детей с сТГВ рецидивы тромбоза выявлены при ОЛЛ у 8,2, при ОМЛ у 8,3, при лимфоме у 2,8 пациентов. Медиана возраста пациентов с единственным эпизодом сТГВ составила 10 лет, с рецидивом сТГВ 9 лет, при аТГВ 7 лет для пациентов с единственным эпизодом и 6 лет с рецидивом аТГВ. Некорректно проведенная терапия была зарегистрирована у 50 детей. Заключение. Рецидивирующее течение тромбоза у детей, госпитализированных для лечения заболеваний крови, уста новлено у 5,4 детей с сТГВ и у 13,3 детей с аТГВ, причем 1/3 часть сТГВ является потенциально жизнеугрожающей. Полученные данные подчеркивают необходимость проведения вторичной антитромботической профилактики у детей с ТГВ и ставят вопрос о необходимости и целесообразности проведения таковой у пациентов с аТГВ. Introduction. Deep vein thrombosis (DVT) remains a common complication of hematological diseases in children and requires antithrombotic therapy and prophylaxis of recurrent thrombotic events. Aim: to determine incidence and risk factors of recurrent DVT for hospitalized children with blood diseases. Materials and methods. Medical records of patients hospitalized with oncohematological diseases and bone marrow aplasia, aged from 0 to 17 years, were analyzed retrospectively. Only patients with more than one DVT were taken into this analysis. Results. Recurrent DVT was diagnosed in 13.27 children with asymptomatic DVT (aDVT) and in 5.41 with symptomatic DVT (sDVT). Recurrent DVT was found in 14.49 children with acute lymphoblastic leukemia (ALL), in 8.89 with acute myeloblastic leukaemia (AML), in 11.86 with lymphomas. Incidence of recurrent thrombosis in children with sDVT was 8.16 for ALL, 8.33 for AML, 2.78 for lymphomas. Age analysis of patients with the single episode and recurrent thrombosis showed that age median with single sDVT was 10 years, recurrent DVT 9 years, in case of single asymptomatic or incidental (aDVT) episode 7 years, recurrent DVT 6 years. Incorrect therapy was registered for 50 of children with recurrent sDVT. Conclusion. Recurrent DVT in hospitalized children with blood diseases occurred in 5.41 children with sDVT and in children 13.33 with aDVT 1/3 episodes of sDVT was lifethreatening. In conclusion, secondary prophylaxis is needed for children with DVT and future research should be done for prophylaxis in those with aDVT.


2018 ◽  
Vol 67 (6) ◽  
pp. 50-59 ◽  
Author(s):  
Maria G. Nikolayeva ◽  
Andrey P. Momot ◽  
Marina S. Zaynulina ◽  
Ksenia A. Momot ◽  
Natalia N. Yasafova

Hypothesis/aims of study. The current analysis was undertaken to elucidate the role of Factor Va resistance to proteolytic cleavage by activated protein C in FVL(1691)GA female carriers in the development of acute and recurrent thromboses. Study design, materials and methods. A prospective clinical cohort study of 1100 women of reproductive age was conducted, with the course and outcomes of 2,707 pregnancies analyzed. Two cohorts were specified: the main group consisted of 500 patients with FV(1691)GA genotype, and the control group consisted of 600 patients with FVL(1691)GG genotype. Results. FVL(1691)GA genotype was significantly associated with the development of venous thromboembolic complications (VTEC) compared to FVL(1691)GG genotype (OR 9.3; p < 0.0001). Episodes of recurrent thrombosis during and outside of pregnancy were registered only in FVL(1691)GA patients (OR 5.7, p = 0.2). In all cases, at the time of the thrombotic event and during the period before the episode of acute or recurrent thrombosis, an APC resistance normalized ratio (NR) value was ≤ 0.49, with no episodes of VTEC registered with an APC resistance NR value ≥ 0.5. Conclusion. Venous thromboses occur under the condition of expressed APC resistance with underlying FVL(1691)GA carriage. The APC resistance index can serve as an objective biochemical marker to determine the feasibility of thromboprophylaxis within the framework of personalized medicine.


1981 ◽  
Author(s):  
S Kondo ◽  
T Matsuo ◽  
Y Ohoki ◽  
O Matsuo

In the familial AT III deficiency of a Japanese family, the propositus (a-39-yr old female) and her mother had episodes of recurrent thrombosis and their AT III levels as measured immunologically and biologically were below the normal value. In the plasma of her brother, the AT III concentration as measured immunologically was half of the normal value, but his biological antithrombin activity was within the normal range. The progressive antithrombin activity and antifactor Xa activity of plasma samples in this familial AT III deficiency were within the normal range. Measurements of the rate of thrombin neutralization activity revealed that the brother’s plasma was in the normal range, but the plasma of the propositus and of her mother showed rates of thrombin neutralization activity which were somewhat below the normal value. The rate of thrombin neutralization activity per mg protein of AT III was highest in the plasma of the brother, and became slower in the mother, propositus, and pooled normal plasma in that order. In the plasma of this familial AT III deficiency, the rate of Xa neutralization activity was much slower than the normal value. It is postulated that since the antithrombin of the brother of the propositus was found to react as normal in the neutralization of thrombin, he does not have episodes of thrombosis. Such characteristic hyperfunction of antithrombin in the plasma of the brother may be due to some molecular abnormality of AT III within this hereditary deficient family.


2020 ◽  
Vol 18 (5) ◽  
pp. 1141-1153 ◽  
Author(s):  
Yeling Lu ◽  
Hemant Giri ◽  
Bruno O. Villoutreix ◽  
Qiulan Ding ◽  
Xuefeng Wang ◽  
...  

2020 ◽  
Vol 106 (6) ◽  
pp. NP41-NP45
Author(s):  
Teresa Beninato ◽  
Giuseppe Lo Russo ◽  
Marina Chiara Garassino ◽  
Filippo De Braud ◽  
Marco Platania

Introduction: Patients with cancer have higher risk of thrombosis compared to the general population and particularly lung adenocarcinoma is considered at high risk for venous thromboembolism. Some targetable oncogenic drivers are supposed to further increase this risk. Case description: A 35-year-old man who had developed a recurrent venous thromboembolism and pulmonary embolism (PE) was diagnosed with ROS1 rearranged non-small cell lung cancer (NSCLC). While molecular examinations were ongoing, he developed progressive respiratory failure. For PE and thrombosis worsening with detection of right heart thrombus, he underwent therapy with unfractionated heparin. Despite initial good radiologic results, only with the start of crizotinib did the patient’s clinical condition significantly improve to configure a Lazarus response. Conclusions: Cancer diagnosis should always be considered in patients with unprovoked thrombosis and, if NSCLC is diagnosed, genetic alterations should be always sought after. A possible relation between venous thromboembolism and oncogenic drivers, particularly for ALK translocations, has been hypothesized. Similarly to ALK-positive NSCLC, ROS1 rearranged disease has been associated with an increased thromboembolic risk. Further studies are needed to better evaluate this relation and to evaluate the potential benefit of a prophylactic anticoagulating treatment in this subset of patients.


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