Risk of Upper Gastrointestinal Bleeding When Taking SSRIs With NSAIDs or Aspirin

Kuo, Chun-Ya; Liao, Yin-To; Chen, Vincent Chin‐Hung

doi:10.1176/appi.ajp.2014.14010108

Cited by 1 publication

(1 citation statement)

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“…Although there are still a few studies, SSRIs would appear the safest and the most efficient antidepressants to reduce platelet activation status in depression, although a debate is still open on their potentially increased risk for major bleeding (especially in combination with platelet inhibitor drugs or oral anticoagulants). [258][259][260][261][262][263][264] Platelet hyper-responsivity Platelet hyper-reactivity is not merely an unavoidable adverse effect of conditions ranging from infections to diabetes, it is a strong factor exacerbating most aging-related human pathologies. 265 Taken together, recent studies indicate that platelet reactivity is not just a biomarker of adverse effects, but it is by itself a condition that requires management, not limited to cardiovascular disease and stroke.…”

Section: Biomarkers Of Platelet Activationmentioning

confidence: 99%

Is there a relationship between morphological and functional platelet changes and depressive disorder?

et al. 2020

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Background Blood platelets, due to shared biochemical and functional properties with presynaptic serotonergic neurons, constituted, over the years, an attractive peripheral biomarker of neuronal activity. Therefore, the literature strongly focused on the investigation of eventual structural and functional platelet abnormalities in neuropsychiatric disorders, particularly in depressive disorder. Given their impact in biological psychiatry, the goal of the present paper was to review and critically analyze studies exploring platelet activity, functionality, and morpho-structure in subjects with depressive disorder. Methods According to the PRISMA guidelines, we performed a systematic review through the PubMed database up to March 2020 with the search terms: (1) platelets in depression [Title/Abstract]”; (2) “(platelets[Title]) AND depressive disorder[Title/Abstract]”; (3) “(Platelet[Title]) AND major depressive disorder[Title]”; (4) (platelets[Title]) AND depressed[Title]”; (5) (platelets[Title]) AND depressive episode[Title]”; (6) (platelets[Title]) AND major depression[Title]”; (7) platelet activation in depression[All fields]”; and (8) platelet reactivity in depression[All fields].” Results After a detailed screening analysis and the application of specific selection criteria, we included in our review a total of 106 for qualitative synthesis. The studies were classified into various subparagraphs according to platelet characteristics analyzed: serotonergic system (5-HT2A receptors, SERT activity, and 5-HT content), adrenergic system, MAO activity, biomarkers of activation, responsivity, morphological changes, and other molecular pathways. Conclusions Despite the large amount of the literature examined, nonunivocal and, occasionally, conflicting results emerged. However, the findings on structural and metabolic alterations, modifications in the expression of specific proteins, changes in the aggregability, or in the responsivity to different pro-activating stimuli, may be suggestive of potential platelet dysfunctions in depressed subjects, which would result in a kind of hyperreactive state. This condition could potentially lead to an increased cardiovascular risk. In line with this hypothesis, we speculated that antidepressant treatments would seem to reduce this hyperreactivity while representing a potential tool for reducing cardiovascular risk in depressed patients and, maybe, in other neuropsychiatric conditions. However, the problem of the specificity of platelet biomarkers is still at issue and would deserve to be deepened in future studies.

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