Influence of antidepressants on hemostasis

Halpérin, Daniel; Reber, Guido

doi:10.31887/dcns.2007.9.1/dhalperin

Cited by 192 publications

(79 citation statements)

References 74 publications

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“…Upon initiation of platelet aggregation, 5-HT is released into the blood and activates 5-HT2A receptors on the platelet membrane, which enhances the aggregation process. 5-HT per se is a weak activator, but dose-dependently enhances platelet activation induced by adenosine diphosphate [35] . Since Fluoxetine may inhibit platelet uptake of 5-HT and cause platelet depletion, this can inhibit 5-HT-induced platelet aggregation amplification, and therefore explain why we did not observe a drop in platelet count after decompression in the treated group.…”

Section: Discussionmentioning

confidence: 95%

Protective Effects of Fluoxetine on Decompression Sickness in Mice

Blatteau¹,

Barre²,

Pascual³

et al. 2012

PLoS ONE

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Massive bubble formation after diving can lead to decompression sickness (DCS) that can result in central nervous system disorders or even death. Bubbles alter the vascular endothelium and activate blood cells and inflammatory pathways, leading to a systemic pathophysiological process that promotes ischemic damage. Fluoxetine, a well-known antidepressant, is recognized as having anti-inflammatory properties at the systemic level, as well as in the setting of cerebral ischemia. We report a beneficial clinical effect associated with fluoxetine in experimental DCS. 91 mice were subjected to a simulated dive at 90 msw for 45 min before rapid decompression. The experimental group received 50 mg/kg of fluoxetine 18 hours before hyperbaric exposure (n = 46) while controls were not treated (n = 45). Clinical assessment took place over a period of 30 min after surfacing. At the end, blood samples were collected for blood cells counts and cytokine IL-6 detection. There were significantly fewer manifestations of DCS in the fluoxetine group than in the controls (43.5% versus 75.5%, respectively; p = 0.004). Survivors showed a better and significant neurological recovery with fluoxetine. Platelets and red cells were significantly decreased after decompression in controls but not in the treated mice. Fluoxetine reduced circulating IL-6, a relevant marker of systemic inflammation in DCS. We concluded that fluoxetine decreased the incidence of DCS and improved motor recovery, by limiting inflammation processes.

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Section: Discussionmentioning

confidence: 95%

Protective Effects of Fluoxetine on Decompression Sickness in Mice

Blatteau¹,

Barre²,

Pascual³

et al. 2012

PLoS ONE

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“…It was shown that there is a weak link between SSRI and upper GIB at a population level in patients who are not taking warfarin [23][24][25][26][27] as SSRI impair platelet aggregation [26]. This is most significant in patients who were using SSRI and NSAID concomitantly.…”

Section: Discussionmentioning

confidence: 99%

A Study of Proton Pump Inhibitors and Other Risk Factors in Warfarin-Associated Gastrointestinal Bleeding

Tang¹,

Sharma²,

Desai³

et al. 2021

Cureus

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Background Warfarin users are at increased risk for gastrointestinal bleeding (GIB). History of GIB, stroke, cardiovascular or chronic kidney disease, age greater than 65 years, and drug interaction with proton pump inhibitors (PPI) have previously been identified as risk factors for GIB in warfarin users. We hypothesized that concomitant use of warfarin and PPI would increase the incidence of GIB relative to warfarin use alone. Methods We did a retrospective review of medical records of 626 patients taking warfarin for at least two weeks. Parameters including age, concomitant medication use (non-steroidal anti-inflammatory drugs (NSAID), aspirin, selective serotonin reuptake inhibitors (SSRIs), PPI, and anti-platelet drug), history of GIB, chronic renal failure (CRF), and peptic ulcer disease (PUD) prior to warfarin use were analyzed. Results Variables that increase the likelihood of bleeding in warfarin users included aspirin, PPI, history of PUD, history of previous GIB, CRF, and elevated prothrombin time (PT)/international normalized ratio (INR) values. Concomitant antiplatelet use showed a slight increase in GIB but this was not statistically significant (p=0.082). NSAID use and SSRI use were not associated with a higher risk of GIB among warfarin users. Patients who are on PPI and warfarin simultaneously are more likely to be on acetylsalicylic acid (ASA) or have a history of PUD, GIB, or CRF, all of which are associated with increased incidences of GIB. Conclusions Although concomitant use of warfarin and PPI appears to be associated with an increased incidence of GIB, these patients are more likely to have other risk factors that also increase the risk of a GIB outcome. Therefore, the interaction between PPI and warfarin is clinically insignificant.

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“…As stated earlier, COX-2-inhibitors do not affect platelet aggregation, as shown by impedance aggregometry, thromboelastometry, and platelet function analyzer (PFA-100) assays [ 34 , 35 ]. Nevertheless, COX-2 inhibitors may increase blood loss via drug interactions [ 36 , 37 ]. Parecoxib and its metabolite valdecoxib are suspected to potentiate warfarin’s effects since both COX-2 inhibitors exert inhibitory effects on CYP2C9 [ 38 ], an enzyme that also metabolizes warfarin.…”

Section: Discussionmentioning

confidence: 99%

Effects of parecoxib on analgesia benefit and blood loss following open prostatectomy: a multicentre randomized trial

et al. 2015

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BackgroundThis multi-centre, prospective, randomized, double-blind, placebo-controlled study was designed to test the hypotheses that parecoxib improves patients’ postoperative analgesia without increasing surgical blood loss following radical open prostatectomy.Methods105 patients (64 ± 7 years old) were randomized to receive either parecoxib or placebo with concurrent morphine patient controlled analgesia. Cumulative opioid consumption (primary objective) and the overall benefit of analgesia score (OBAS), the modified brief pain inventory short form (m-BPI-sf), the opioid-related symptom distress scale (OR-SDS), and perioperative blood loss (secondary objectives) were assessed.ResultsIn each group 48 patients received the study medication for 48 hours postoperatively. Parecoxib significantly reduced cumulative opioid consumption by 24% (43 ± 24.1 mg versus 57 ± 28 mg, mean ± SD, p=0.02), translating into improved benefit of analgesia (OBAS: 2(0/4) versus 3(1/5.25), p=0.01), pain severity (m-BPI-sf: 1(1/2) versus 2(2/3), p < 0.01) and pain interference (m-BPI-sf: 1(0/1) versus 1(1/3), p=0.001), as well as reduced opioid-related side effects (OR-SDS score: 0.3(0.075/0.51) versus 0.4(0.2/0.83), p=0.03). Blood loss was significantly higher at 24 hours following surgery in the parecoxib group (4.3 g⋅dL−1 (3.6/4.9) versus (3.2 g⋅dL−1 (2.4/4.95), p=0.02).ConclusionsFollowing major abdominal surgery, parecoxib significantly improves patients’ perceived analgesia. Parecoxib may however increase perioperative blood loss. Further trials are needed to evaluate the effects of selective cyclooxygenase-2 inhibitors on blood loss.Trial registrationClinicalTrials.gov Identifier: NCT00346268

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Influence of antidepressants on hemostasis

Cited by 192 publications

References 74 publications

Protective Effects of Fluoxetine on Decompression Sickness in Mice

Protective Effects of Fluoxetine on Decompression Sickness in Mice

A Study of Proton Pump Inhibitors and Other Risk Factors in Warfarin-Associated Gastrointestinal Bleeding

Effects of parecoxib on analgesia benefit and blood loss following open prostatectomy: a multicentre randomized trial

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