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Maitreyee Bhattacharyya

Researcher at All India Institute of Medical Sciences

Publications -  42
Citations -  392

Maitreyee Bhattacharyya is an academic researcher from All India Institute of Medical Sciences. The author has contributed to research in topics: Thalassemia & Medicine. The author has an hindex of 9, co-authored 33 publications receiving 345 citations.

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Inherited prothrombotic defects in Budd-Chiari syndrome and portal vein thrombosis: a study from North India.

TL;DR: Genetic mutations for factor V Leiden, prothrombin gene 20210A, and methyltetrahydrofolate reductase (MTHFR) C677T were studied in Budd-Chiari syndrome and portal vein thrombosis patients for underlying inherited prothROMbotic defects such as protein C, protein S, and antithrombin III deficiencies.
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Inherited Prothrombotic Defects in Budd-Chiari Syndrome and Portal Vein Thrombosis

TL;DR: Genetic mutations for factor V Leiden, prothrombin gene 20210A, and methyltetrahydrofolate reductase (MTHFR) C677T were studied in Budd-Chiari syndrome and portal vein thrombosis patients for underlying inherited prothROMbotic defects such as protein C, protein S, and antithrombin III deficiencies.
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Hypercoagulable state in five thalassemia intermedia patients.

TL;DR: It is suggested that expression of a procoagulant surface by thalassemia intermedia red blood cells may be the major underlying factor giving rise to platelet and coagulation inhibitor abnormalities in these patients, not related to iron overload or hepatic dysfunction.
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Intracellular iron overload leading to DNA damage of lymphocytes and immune dysfunction in thalassemia major patients.

TL;DR: To investigate the cause and effects of intracellular iron overload in lymphocytes of thalassemia major patients, a large number of patients with this condition have suffered from iron overload.
Journal Article

Venous thrombosis: prevalence of prothrombotic defects in north Indian population.

TL;DR: 431 patients with thrombosis of different venous system were evaluated for underlying acquired and inherited prothrombotic states and deficiency of protein C, protein S and AT III were attributed to inherited factors as no associated acquired risk factor was present.