The anti-platelet effect of niceritrol in patients with arteriosclerosis and the relationship of the lipid-lowering effect to the anti-platelet effect

Nagakawa, Yuzo; Orimo, Hajime; Harasawa, M

doi:10.1016/0049-3848(85)90291-9

Cited by 10 publications

(8 citation statements)

References 17 publications

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“…While laropiprant at 1 µmol/L had no effect on thrombus formation, it caused a pronounced inhibition at 10 µmol/L, comparable to the inhibition of thrombogenesis by acetylsalicylic acid (1 mmol/L) (Figure 6). It has been shown that niacin and its metabolite niceritrol inhibit platelet aggregation in vitro [40], [41] and cause the release of TXA 2 , PGD 2 and PGE 2 at a clinically relevant concentration of 3 mmol/L [41]. Therefore, we investigated the effect of niacin on thrombus formation.…”

Section: Resultsmentioning

confidence: 99%

“…It has been shown that niacin and its metabolite niceritrol inhibit platelet aggregation in vitro [40], [41] and incubation of whole blood with niacin at a clinically relevant concentration increases the concentrations of PGD 2 , PGE 2 and TXA 2 [41]. Our results show that niacin causes a profound inhibition of thrombus formation in vitro ; however, prostaglandins such as PGD 2 do not seem to be involved in this process, since pre-treatment of blood with acetylsalicylic acid as well as laropiprant did not counteract this effect.…”

Section: Discussionmentioning

confidence: 99%

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Laropiprant Attenuates EP3 and TP Prostanoid Receptor-Mediated Thrombus Formation

et al. 2012

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The use of the lipid lowering agent niacin is hampered by a frequent flush response which is largely mediated by prostaglandin (PG) D2. Therefore, concomitant administration of the D-type prostanoid (DP) receptor antagonist laropiprant has been proposed to be a useful approach in preventing niacin-induced flush. However, antagonizing PGD2, which is a potent inhibitor of platelet aggregation, might pose the risk of atherothrombotic events in cardiovascular disease. In fact, we found that in vitro treatment of platelets with laropiprant prevented the inhibitory effects of PGD2 on platelet function, i.e. platelet aggregation, Ca2+ flux, P-selectin expression, activation of glycoprotein IIb/IIIa and thrombus formation. In contrast, laropiprant did not prevent the inhibitory effects of acetylsalicylic acid or niacin on thrombus formation. At higher concentrations, laropiprant by itself attenuated platelet activation induced by thromboxane (TP) and E-type prostanoid (EP)-3 receptor stimulation, as demonstrated in assays of platelet aggregation, Ca2+ flux, P-selectin expression, and activation of glycoprotein IIb/IIIa. Inhibition of platelet function exerted by EP4 or I-type prostanoid (IP) receptors was not affected by laropiprant. These in vitro data suggest that niacin/laropiprant for the treatment of dyslipidemias might have a beneficial profile with respect to platelet function and thrombotic events in vascular disease.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Laropiprant Attenuates EP3 and TP Prostanoid Receptor-Mediated Thrombus Formation

et al. 2012

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“…Because the HPS2‐THRIVE trial could not determine whether the higher incidence of adverse events was due to the niacin or to the laropiprant component, concerns were also raised about the safety of niacin. Niacin is known to reduce platelet counts and affect clotting . In vitro studies have found that niacin inhibits platelet aggregation and stimulates prostaglandin release, and clinical studies have found reductions in fibrinogen and prothrombin F1.2 with niacin treatment …”

Section: Introductionmentioning

confidence: 99%

“…Niacin is known to reduce platelet counts and affect clotting. 7,8 In vitro studies have found that niacin inhibits platelet aggregation and stimulates prostaglandin release, and clinical studies have found reductions in fibrinogen and prothrombin F1.2 with niacin treatment. [9][10][11] To better understand the bleeding safety of niacin, the FDA conducted an assessment within the Mini-Sentinel program.…”

mentioning

confidence: 99%

Safety assessment of niacin in the US Food and Drug Administration's mini‐sentinel system

Gagne

Houstoun

Reichman

et al. 2017

Pharmacoepidemiology and Drug

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“…The flushing response is due to the prostaglandins [51,52]. Niacin reduces platelet counts [53] and affects clotting [54][55][56][57].…”

Section: Vitamin Bmentioning

confidence: 99%

Adverse Effects and Side Effects on Vitamin Therapy: A Review

Korah

Pv²,

Rajeswari³

et al. 2017

Asian J Pharm Clin Res

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Vitamins are essential for our daily life. Its shortage in our body can cause many disorders, decreased enzyme activities also affect the genetic factors. Vitamins should be supplied through the diet in the required amount. If it is not supplied properly, vitamin tablets will be prescribed. And also vitamin tablets are the co-medication for therapies such as anticancer, antitubercular, antiviral and anti-HIV treatments. Many newspapers reported that vitamin therapies are causing major health problems like nephro/urolithiasis, it can increase mortality rates in smokers by increasing the risk of lung cancer, it can cause abortion when it is taken during pregnancy. Thus here, we reviewed the adverse effects of vitamin therapy from various reported cases, books, instructions provided from various health organizations and also newspapers, and magazines. It can help health professionals to control and monitor the vitamin therapies and make awareness about the adverse effects and possible side effects of regular vitamin uptake to society.

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The anti-platelet effect of niceritrol in patients with arteriosclerosis and the relationship of the lipid-lowering effect to the anti-platelet effect

Cited by 10 publications

References 17 publications

Laropiprant Attenuates EP3 and TP Prostanoid Receptor-Mediated Thrombus Formation

Laropiprant Attenuates EP3 and TP Prostanoid Receptor-Mediated Thrombus Formation

Safety assessment of niacin in the US Food and Drug Administration's mini‐sentinel system

Adverse Effects and Side Effects on Vitamin Therapy: A Review

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