Multifocal avascular necrosis in a patient with refractory immune thrombocytopenia and antiphospholipid antibodies; case report and review of literature

El-Gendy, Hala; Elgohary, Rasmia; Mahfouz, Safaa; Ahmed, Hamdy; Demerdash, Doaa El; Ragab, Gaafar

doi:10.1080/09537104.2018.1535701

Cited by 3 publications

(4 citation statements)

References 45 publications

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“…Antiphospholipid bodies have a strong acquired risk for arterial and venous thrombosis, being the most common form of acquired thrombophilia. Some publications have shown the coexistence of APA and ITP [115,116]. According to the current guidelines, when APA are detected in an ITP patient without a history of thrombosis or obstetric complications, this finding will not change the diagnosis of primary ITP [117,118].…”

Section: Thrombosis Related To Itp As a Diseasementioning

confidence: 98%

Immune Thrombocytopenic Purpura as a Hemorrhagic Versus Thrombotic Disease: An Updated Insight into Pathophysiological Mechanisms

et al. 2022

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Immune thrombocytopenic purpura (ITP) is a blood disorder characterized by a low platelet count of (less than 100 × 109/L). ITP is an organ-specific autoimmune disease in which the platelets and their precursors become targets of a dysfunctional immune system. This interaction leads to a decrease in platelet number and, subsequently, to a bleeding disorder that can become clinically significant with hemorrhages in skin, on the mucous membrane, or even intracranial hemorrhagic events. If ITP was initially considered a hemorrhagic disease, more recent studies suggest that ITP has an increased risk of thrombosis. In this review, we provide current insights into the primary ITP physiopathology and their consequences, with special consideration on hemorrhagic and thrombotic events. The autoimmune response in ITP involves both the innate and adaptive immune systems, comprising both humoral and cell-mediated immune responses. Thrombosis in ITP is related to the pathophysiology of the disease (young hyperactive platelets, platelets microparticles, rebalanced hemostasis, complement activation, endothelial activation, antiphospholipid antibodies, and inhibition of natural anticoagulants), ITP treatment, and other comorbidities that altogether contribute to the occurrence of thrombosis. Physicians need to be vigilant in the early diagnosis of thrombotic events and then institute proper treatment (antiaggregant, anticoagulant) along with ITP-targeted therapy. In this review, we provide current insights into the primary ITP physiopathology and their consequences, with special consideration on hemorrhagic and thrombotic events. The accumulated evidence has identified multiple pathophysiological mechanisms with specific genetic predispositions, particularly associated with environmental conditions.

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Section: Thrombosis Related To Itp As a Diseasementioning

confidence: 98%

Immune Thrombocytopenic Purpura as a Hemorrhagic Versus Thrombotic Disease: An Updated Insight into Pathophysiological Mechanisms

et al. 2022

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“…Имеются данные о развитии ОН у пациентов с первичным антифосфолипидным синдромом, не получавших ГК [52], и у пациентов с мультифокальным ОН на фоне гиперпродукции антифосфолипидных антител (аФЛ) и других нарушений, ассоциирующихся с развитием тромбофилии [53][54][55][56]. Это свидетельствует о потенциальном значении аФЛ, индуцирующих развитие микротромбозов сосудов, кровоснабжающих головку бедренной кости, в генезе этой патологии.…”

Section: Hip Arthroplasty In Patients With Systemic Lupus Erythematosusunclassified

Hip Arthroplasty in Patients With Systemic Lupus Erythematosus

Mukhanov

Рыбников

Попкова³

et al. 2020

Naučno-praktičeskaâ revmatologiâ

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“…Platelet micro-particles (PMP) produced during immune-mediated platelet destruction are pro-thrombotic, and contribute to the TEE in ITP. Possible mechanisms underlying the TEE in ITP have been summarized in Table 1 [3][4][5][6][7]. Certain questions from the index case needs discussion.…”

mentioning

confidence: 99%

“…This could be achieved by (a) immunosuppressive drugs like corticosteroids/IVIG which block platelet destruction, and consequent PMP production, or (b) calcium-channel blockers like amlodipine, which inhibit the calcium-dependent PMP release [5]. To this Table 1 Review of the proposed mechanisms contributing to thrombosis in ITP [3][4][5][6][7] Host factors 1. Age, co-morbidities (diabetes, hypertension, dyslipidaemia), infection Disease factors 1.…”

mentioning

confidence: 99%

Recurrent Arterial and Venous Thrombosis in Chronic Immune Thrombocytopenia: Clinical Paradox and Therapeutic Challenges

Jain

Saluja

Chaudhry

et al. 2019

Indian J Hematol Blood Transfus

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Multifocal avascular necrosis in a patient with refractory immune thrombocytopenia and antiphospholipid antibodies; case report and review of literature

Cited by 3 publications

References 45 publications

Immune Thrombocytopenic Purpura as a Hemorrhagic Versus Thrombotic Disease: An Updated Insight into Pathophysiological Mechanisms

Immune Thrombocytopenic Purpura as a Hemorrhagic Versus Thrombotic Disease: An Updated Insight into Pathophysiological Mechanisms

Hip Arthroplasty in Patients With Systemic Lupus Erythematosus

Recurrent Arterial and Venous Thrombosis in Chronic Immune Thrombocytopenia: Clinical Paradox and Therapeutic Challenges

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