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Published on: November 8, 2024
Enhanced platelet reactivity in pediatric depression: an observational study
Mehmet M Can1, Gamze Guler, Ekrem Guler
1aMalatya State Hospital, Malatya bDüzce State Hospital, Düzce cYeditepe Unıversıty Hospital, İstanbul, Turkey dDepartment of Preventive Cardiology, Saint Luke's Mid America Heart Institute, Kansas City, Missouri eJohns Hopkins University, Baltimore, Maryland, USA.
Insights
Children with depression show increased platelet activity, a key factor potentially linking mental health and cardiovascular disease. Further research into platelet function in pediatric depression is warranted.
Area of Science:
- Cardiovascular Medicine
- Pediatric Psychiatry
- Hematology
Background:
- Depression is linked to poorer cardiovascular disease (CVD) outcomes, including mortality.
- Platelet reactivity is a proposed mechanism connecting depression and CVD, but data in children are scarce.
- Understanding these links in pediatric populations is crucial for early intervention.
Purpose of the Study:
- To investigate hemostatic indices, specifically platelet aggregation, in children with major depression.
- To compare platelet function and other hemostatic markers between depressed children and healthy controls.
- To explore the relationship between depression severity and platelet activity in pediatric patients.
Main Methods:
- Sixty-seven children diagnosed with major depression (Beck Depression Inventory score ≥19) were compared to 78 healthy controls.
- Measurements included plasma fibrinogen, D-dimer, platelet count, mean platelet volume, and platelet aggregation induced by ADP and collagen.
- Beck Depression Inventory scores were used to assess depression severity.
Main Results:
- Depressed children exhibited significantly higher platelet aggregation induced by both ADP and collagen compared to controls.
- Beck Depression Inventory scores correlated positively with platelet aggregation.
- Platelet counts, fibrinogen, D-dimer, and mean platelet volume were similar between depressed children and healthy controls.
Conclusions:
- Pediatric depression is associated with heightened platelet activity, independent of other hemostatic parameters.
- These findings support the role of platelets in the pathophysiology of depression, aligning with adult studies.
- Further research is needed to explore serotonin content and cell receptor changes in pediatric depression to justify future clinical trials.
Abstract:
Depression is associated with poor prognosis for cardiovascular disease (CVD) including mortality. Among multiple mechanisms linking depression and CVD, changes in platelet reactivity are known to be one of the major confounders of such adverse association. However, there are very limited data in children. Thus, we evaluated some conventional hemostatic indices including whole blood platelet aggregation in patients with documented pediatric depression and compared these data with those obtained from healthy children. The pediatric patients fulfilled criteria for major depression with a minimum score of 19 on the 21-item Beck Depression Inventory Scale. Plasma fibrinogen, D-dimer, platelet count, mean platelet volume, and platelet aggregation induced by ADP and collagen were measured in 67 pediatric patients with depression and matched by age and sex with 78 healthy controls. As expected, the depressed children had significantly higher BECK scales (P = 0.001) compared with the normal subjects. Platelet aggregation induced by ADP and collagen (P = 0.0001 for both) was significantly higher in depressed children. BECK scale scores correlated significantly with platelet aggregation induced by ADP (r = 0.3, P = 0.001) and collagen (r = 0.4, P = 0.01). In contrast, platelet counts, fibrinogen, D-dimer, mean platelet volume, and antithrombin-III levels were almost identical between both groups. Children with depression exhibit mostly intact hemostatic parameters, with the exception of significantly higher platelet activity when compared with healthy controls. These data match well with prior evidence from depressed adults supporting the hypothesis that platelets participate in the pathogenesis of depression. However, beyond pure assessment of platelet activity, other elements including serotonin content and cell receptor changes in pediatric depression should be elucidated before randomized trial(s) can be justified.
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