Serum interleukin-18 levels as a predictor for patients with genetic dysfunction of cytochrome P450 2C19 in dual antiplatelet therapy with clopidogrel

Ishimatsu, Takashi; Sasaki, Ken-ichiro; Kakuma, Tatsuyuki; Harada, Atsushi; Hirakawa, Yuji; Ueno, Takayoshi

doi:10.1016/j.jjcc.2020.06.008

Cited by 2 publications

(2 citation statements)

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“…The results of this study concerning statins are in line with previous research findings. (Gulec et al, 2005;An et al, 2019;Takashi et al, 2020). Lau et al reported that atorvastatin could reduce clopidogrel activation by 90% and reduce the clopidogrel antiplatelet effect, attracting wide attention.…”

Section: Discussionmentioning

confidence: 99%

“…Clopidogrel is metabolized by CYP450 enzyme to form inactive intermediates 2-oxo-clopidogrel, and in the human body is further metabolized by CYP450 enzyme to form three sulfate metabolites, of which only H4 metabolites have antiplatelet effects. Some statins are similar to clopidogrel, metabolized by CYP3A4, while others do not by CYP3A4 (Gulec et al, 2005;An et al, 2019;Takashi et al, 2020), so clopidogrel-statatin interactions can be analyzed by H4 concentrations in the blood. This study used proven HPLC-mass spectrometry combination techniques to determine H4.…”

Section: Discussionmentioning

confidence: 99%

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The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction

Shi

Chen

et al. 2021

Front. Pharmacol.

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Objective: To explore the treatment effect of statins used together with clopidogrel on cerebral infarction (CI).Methods: One hundred and thirty non-clopidogrel resistant patients were divided into a dynamic clopidogrel resistant (DCR) group and a continuous Non clopidogrel resistance (NCR) group. Patients were randomly assigned to AC group (atorvastatin 40 mg/d + clopidogrel, 51 patients) and RC group (rosuvastatin 20 mg/d + clopidogrel, 47 patients). The patient’s platelet aggregation rate (PAR) was measured on visit 0 (baseline), visit 1 (1 week after clopidogrel alone treatment), and visits 2 to 4 (one, three, and 6 months after clopidogrel plus statins treatment). The platelet reactivity index (PRI) was assessed on visits 0, 2, and 4, and clopidogrel thiol metabolite (H4) levels was measured on visits 2 and 4. DNA sequencing was used to determine CYP3A4, CYP2C9, and CYP2C19 genotypes in all patients.Results: PAR, PRI, and H4 levels, DCR ratio, and the genotype frequencies of CYP2C9*3εC, CYP2C19*2εA, and CYP2C19*3εA of both groups were similar (p > 0.05). CYP2C19εA *2 and *3 were independent risk factors for DCR (p < 0.05).Conclusion: Clopidogrel combined with atorvastatin does not affect platelet inhibition and does not increase the incidence of DCR. The incidence of DCR in the Chinese population is high and is related to CYP2C19εA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction

Shi

Chen

et al. 2021

Front. Pharmacol.

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Clopidogrel protect against gentamicin-induced nephrotoxicity through targeting oxidative stress, apoptosis, and coagulation pathways

Akila,

Gad,

Ewees

et al. 2024

Preprint

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Gentamicin (Genta)-induced nephrotoxicity poses a significant clinical challenge due to its detrimental effects on kidney function. Clopidogrel (Clop), an antiplatelet drug known for its ability to prevent blood clots by inhibiting platelet aggregation, also has potential effects on oxidative stress and cell death. This study investigates Clop's protective role against Genta-induced nephrotoxicity, emphasizing the importance of the coagulation cascade. The 32 adult male albino rats were randomly assigned to four groups of eight (n = 8). The first group received only the vehicle. Genta was injected intraperitoneally at 100mg/kg/day for eight days in the second group. Groups 3 and 4 received oral Clop at 10 and 20 mg/kg/day for one week before Genta delivery and throughout the experiment. Renal tissue showed renal function tests, oxidative stress, pro-inflammatory cytokines, apoptotic markers, coagulation profile, and fibrin expression. Clop improved Genta-induced kidney function and histopathology. Clop substantially reduced pro-inflammatory cytokines, oxidative stress indicators, pro-apoptotic proteins, and fibrin protein. Clop also significantly boosted renal tissue anti-inflammatory and anti-apoptotic protein expression. Genta-induced nephrotoxicity involves oxidative stress, apoptosis, and coagulation system activation, according to studies. This study underscores that Genta-induced nephrotoxicity is associated with oxidative stress, apoptosis, and activation of the coagulation system. Clop's protective effects on nephrons are attributed to its anticoagulant, antioxidant, anti-inflammatory, and anti-apoptotic properties, presenting it as a promising therapeutic strategy against Genta-induced kidney damage.

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Serum interleukin-18 levels as a predictor for patients with genetic dysfunction of cytochrome P450 2C19 in dual antiplatelet therapy with clopidogrel

Cited by 2 publications

References 31 publications

The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction

The Dynamic Effect of Non-CYP3A4-Metabolized and CYP3A4-Metabolized Statins on Clopidogrel Resistance in Patients With Cerebral Infarction

Clopidogrel protect against gentamicin-induced nephrotoxicity through targeting oxidative stress, apoptosis, and coagulation pathways

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