Why there is thrombocythopenia in Endocarditis ?

#1- rare causes -one type is Nonbacterial thrombotic endocarditis (Marantic endocarditis) - if this can be seen with thrombocytopenia then called -Para-neoplastic syndrome. Cancer may affect cellular elements of the blood as well as coagulation system , resulting in a wide range of para neoplastic syndrome . In this cases thrombocytopenia is rare but thrombocytosis which results from IL-6 and thrombopoietin release which may play a role in hypercoagulable state and may present as non-bacterial endocarditis in either cases.

#2- is more common : Infective endocarditis (IE) is a life threatening disease caused by a bacterial infection of the endocardial surfaces of the heart. It is typified by the formation of septic thrombi or vegetative growth on the heart valve. Typically, both platelets and fibrin are deposited on exposed extracellular matrix proteins as part of the normal response to damage of the endocardium . However, this sterile platelet-fibrin nidus facilitates colonisation of the endocardium by bacteria in the bloodstream . Following attachment, bacteria can recruit platelets from the circulation inducing platelet activation and platelet aggregation. !! S aureus adheres to platelets, leading to platelet activation and aggregation,platelet consumption, and eventually thrombocytopenia.

#3- Initial studies focused on secreted mediators of platelet activation such as alpha-toxin, which accelerates thrombin generation. Later studies focused on Clf A and fibronectin-binding protein A as the dominant surface proteins mediating platelet activation.Also, Clf A has been shown to be a virulence factor for endocarditis.This platelet activation process requires 2 mechanisms of S aureus binding to platelets: by a fibrinogen or fibronectin bridge to the platelet integrin GPIIb/IIIa and an immunoglobulin bridge to the Fc-γ-RIIa receptor.

 

For Further Reading Please Click Here !

Platelets play an important role in the local host defense against endovascular infections, and experimentally induced thrombocytopenia is associated with more severe disease in animal models . Consistent with this, it has been found thrombocytopenia to be an independent predictor of mortality at both day 1 and 8.

In contrast, acute phase reactants such as C-reactive protein and white cell count were univariate predictors of mortality but were not independently predictive on multivariate analysis. In addition, there was no association between erythrocyte sedimentation rate and mortality.

The finding of thrombocytopenia in patients with endocarditis has clinical implications. First, patients presenting with thrombocytopenia should receive empirical antistaphylococcal therapy because of the strong association between baseline thrombocytopenia and Staphylococcus aureus infection. Second, if antiplatelet agents are being considered as adjunctive therapy , clinicians should exclude coexistent thrombocytopenia because of its potential to increase the risk of bleeding. Third, thrombocytopenia at day 8 indicates an impaired host response to sepsis and predicts increased mortality. In this setting, patients with thrombocytopenia may warrant more intensive monitoring, alterations to treatment, and, where relevant, consideration of surgery.

Thrombocytopenia was significantly and independently associated with higher mortality, increasing the odds for death by 2.8 in the main analysis and sensitivity analyses.
Cohort studies shown, patients with thrombocytopenia were diagnosed as having endocarditis at presentation significantly more frequently than patients without thrombocytopenia (8.9% vs 4.5%, respectively). However, we could not assess the association between thrombocytopenia at baseline with thrombotic complications because the outcomes of bacteremia persistence, relapse, development of endocarditis, and metastatic complications are confounded by the fact that patients with thrombocytopenia died more frequently and sooner than did those without thrombocytopenia, and postmortem studies were not performed.