Platelet haemostatic function in psychiatric disorders: Effects of antidepressants and antipsychotic drugs

Abstract

Objectives Platelets, the smallest anucleated blood cells, play an essential role in the first step of complex haemostatic process. This review presents the haemostatic function of blood platelets related to their activation in psychiatric disorders (schizophrenia, depression), the role of antipsychotic and antidepressant medication, and introduces the mechanisms by which activated platelets may be involved in the pathophysiology of these disorders. Methods Platelets are interesting and easily accessible blood cells to study biochemical pathways related to schizophrenia and other psychiatric disorders, and their complex activation process might be useful as a diagnostic peripheral marker for studying psychiatric disorders and haemostatic complications. Results The excessive activation of platelets observed in patients with depression and schizophrenia is involved in cardiovascular diseases, stroke and increased risk of thrombotic complications that may be major causes of morbidity and mortality of patients. The use of antidepressants or antipsychotic drugs in depression and schizophrenia treatment is often associated with haematological side effects such as bleeding, venous thromboembolism and impaired platelet function. Conclusions Understanding the role of platelet activation in psychiatric disorders such as schizophrenia or depression and medication may improve therapies in the future.

Elevated neutrophil‑to‑lymphocyte and platelet‑to‑lymphocyte ratios predict post‑stroke depression with acute ischemic stroke

“…Activated platelets play an important role in psychiatric disorders, including depression (43,44), and high levels are considered to be a risk factor for an increased incidence of cardiovascular and cerebrovascular diseases (45). The activation of platelets, mediated by a number of inflammatory factors, including cytokines, serotonin, glutamate, dopamine and P-selectin, serves an important role in psychiatric disorders (46). In particular, serotonin has been previously reported to be involved in the activation of plasma platelets and accelerate aggregation (47).…”

Psychopharmacologic treatment and blood transfusion in fast‐track total hip and knee arthroplasty

“…We also found that patients treated with APs alone had an increased transfusion rate (OR, 2.37; 95% CI, 1.04‐2.41). The underlying mechanisms are unclear, although a potential association linking AP drugs to altered PLT function and abnormal bleeding has been reported . Psychiatric disease may also be a risk factor for several other adverse outcomes in THA and TKA …”

Venous Thromboembolism Risk With Antidepressants: Driven by Disease or Drugs?

“…Risk‐factor associations like the ones discussed in the present study are important to ascertain, but the authors wisely stopped short of suggesting a causative relationship. It difficult to determine whether depression or antidepressant use drove the increased VTE risk or even if another related factor (eg, thrombophilia traits, use of other recreational or illicit drugs, presence of BDNF Val66met polymorphism leading to combined prothrombotic and depressive traits) was the major impetus and caused some women to develop VTE, especially because—as the authors point out—the increased VTE risk was seen across several classes of antidepressants, including selective serotonin reuptake inhibitors, which have been reported to inhibit platelet function . This likely relates to the fact that serotonin is a weak platelet agonist but also potentiates stimulation from ADP or thrombin .…”

“…It difficult to determine whether depression or antidepressant use drove the increased VTE risk or even if another related factor (eg, thrombophilia traits, use of other recreational or illicit drugs, presence of BDNF Val66met polymorphism leading to combined prothrombotic and depressive traits) was the major impetus and caused some women to develop VTE, especially because—as the authors point out—the increased VTE risk was seen across several classes of antidepressants, including selective serotonin reuptake inhibitors, which have been reported to inhibit platelet function . This likely relates to the fact that serotonin is a weak platelet agonist but also potentiates stimulation from ADP or thrombin . When the reuptake of serotonin is blocked, it cannot be replaced within the dense granules of the platelet and thus is not available to augment the activation response or to help retain procoagulant proteins (fibrinogen, von Willebrand factor, thrombospondin, fibronectin, and α2‐antiplasmin) on their surface …”

“…Similar to the screening questions about personal or family history of VTE recommended before estrogen‐containing hormone‐modulating therapy, providers may want to ask about VTE before prescribing antidepressants. Answers to these questions, and also ones hopefully being asked about bleeding history, given the previous studies on this topic, may help providers determine which class of antidepressant may be best for a particular patient (consistent with the general trend toward more personalized medication regimens) . Nevertheless, more studies of the thrombotic and hemorrhagic potential of these drugs in various patient populations are needed before specific recommendations can be confidently expressed.…”