This interventional prospective multicenter nonrandomized clinical and epidemiological study is the first Russian study aimed at evaluating the effectiveness of a single-lead electrocardiography device (CardioQVARK) in screening for atrial fibrillation in primary health care.

NCT04204330

Conditions

1. Atrial Fibrillation

Interventions

1. Device: CardioQvark cardiac monitor and software, single-lead ECG

MeSH:Atrial Fibrillation

HPO:Atrial fibrillation Paroxysmal atrial fibrillation

For new oral anticoagulants - rs2244613 of the gene CES1, rs1045642 (C3435T), rs1128503 (C1236T), rs2032582 (G2677T / А) of the gene ABCB1, rs2231142 (С421А, Q141K) of the gene ABCG2, rs776746 (A6986G * 399 CYP3 CYP3) CYP3A4.. Inclusion Criteria: Men and women aged 18 to 96 years who have one or more of the following risk factors: - hypertonic disease - history of ischemic stroke or transient ischemic attacks - type 1 and type 2 diabetes - 1-3 degrees obesity - heart failure or the presence of a clinic to reduce exercise tolerance associated with shortness of breath - coronary heart disease or the presence of symptoms of chest pain, in the absence of an established diagnosis of coronary heart disease - the presence of peripheral arterial atherosclerosis - the presence of a clinic of interruptions in the work of the heart (bouts of rapid, irregular heartbeats, pauses in work of heart) Non-inclusion criteria: - Acute coronary syndrome - Acute ischemic or hemorrhagic stroke - Acute psychosis - The presence of severe concomitant diseases with an expected life expectancy of less than 2 years Exclusion Criteria: Refusal of further participation in the study Inclusion Criteria: Men and women aged 18 to 96 years who have one or more of the following risk factors: - hypertonic disease - history of ischemic stroke or transient ischemic attacks - type 1 and type 2 diabetes - 1-3 degrees obesity - heart failure or the presence of a clinic to reduce exercise tolerance associated with shortness of breath - coronary heart disease or the presence of symptoms of chest pain, in the absence of an established diagnosis of coronary heart disease - the presence of peripheral arterial atherosclerosis - the presence of a clinic of interruptions in the work of the heart (bouts of rapid, irregular heartbeats, pauses in work of heart) Non-inclusion criteria: - Acute coronary syndrome - Acute ischemic or hemorrhagic stroke - Acute psychosis - The presence of severe concomitant diseases with an expected life expectancy of less than 2 years Exclusion Criteria: Refusal of further participation in the study Atrial Fibrillation Atrial Fibrillation This is an interventional, prospective, multicenter, nonrandomized clinical and epidemiological study. --- C3435T --- --- C1236T ---

This study tested the hypothesis that response to digoxin is modulated by single Nucleotid Polymorphism (SNP): - Multi Drug Resistance (MDR1) gene haplotypes and Solute carrier organic anion transporter family member 1B3 (SLCO1B3) gene Polymorphism and their role in the response to treatement. - Aldosterone synthase (CYP11B2) gene and sodium channel, voltage-gated, type V alpha subunit gene (SCN5A) correlated with atrial fibrillation and their roles in response to digoxin.

NCT02167165

Conditions

1. Atrial Fibrillation

Interventions

1. Drug: Digoxin Injection

MeSH:Atrial Fibrillation

HPO:Atrial fibrillation Paroxysmal atrial fibrillation

The aim of the current study is to analyze the ABCB1: C1236T (Gly412Gly), G2677>T⁄A (Ala893Ser/ Thr) and C3435T (Il1145Ile) polymorphisms. --- C1236T ---

Dabigatran (Pradaxa ®) is a new oral anticoagulant. It is used to prevent venous thromboembolism in orthopedic surgery and has recently demonstrated efficacy and safety at least as good as anticoagulants in the prevention of thromboembolism in atrial fibrillation and the treatment of venous thromboembolism. It is administered with fixed dose and does not require laboratory monitoring because of the low inter and intra individual pharmacokinetic (PK) and pharmacodynamics (PD) of dabigatran. However, the bioavailability of dabigatran is very low (6.5%) and is controlled by an efflux protein, P-GP. This molecule has a genetic polymorphism. The inhibition of this protein can cause a significant increase in intestinal absorption of dabigatran and expose patients to a risk of bleeding by overdose. Two major drug interactions have been identified : quinidine (cons-indication) and amiodarone (precautions). It is likely that other interactions exist and can be clinically significant in patients not selected such as testing. The development of tools to study the influence of P-GP on the PK and PD of dabigatran is therefore interesting. As the P-GP has a genetic polymorphism, the study of the latter is an important element in the detection of drug interactions. In this sense, clarithromycin, a potent inhibitor of P-GP is a good model to evaluate the primary mechanism of drug interaction of dabigatran and optimize the experimental design of studies to be conducted.

NCT01385683

Conditions

1. Healthy

Interventions

1. Drug: Dabigatran then dabigatran and clarithromycin
2. Drug: Clarithromycin and dabigatran then dabigatran

Genotyping of MDR-1 (gene for P-GP): C3435T SNP of exon 26, SNP G2677T / A of exon 21 and C1236T SNP of exon 12. Inclusion Criteria: - affiliated or beneficiary of a social security category - having signed the inform consent form - having signed the genetic consent form - weight between 60 and 85 kg - normal clinical exam - normal biological exam Exclusion Criteria: - contra-indication to dabigatran - contra-indication to clarithromycin - previous history of psychiatric disease, or antidepressant treatment, or convulsion, or hemorrhagic disease - smoker - peptic ulcer - severe liver disease - severe kidney failure - previous surgery within one month Inclusion Criteria: - affiliated or beneficiary of a social security category - having signed the inform consent form - having signed the genetic consent form - weight between 60 and 85 kg - normal clinical exam - normal biological exam Exclusion Criteria: - contra-indication to dabigatran - contra-indication to clarithromycin - previous history of psychiatric disease, or antidepressant treatment, or convulsion, or hemorrhagic disease - smoker - peptic ulcer - severe liver disease - severe kidney failure - previous surgery within one month Healthy null --- C3435T --- --- G2677T --- --- C1236T ---

Oral administration has many advantages above intravenously administrated drugs for patients. Up to now, oral administration of docetaxel as single agent has not been feasible due to low and variable bioavailability. This low systematic exposure to docetaxel can effectively be increased after co-administration of ritonavir. The department of pharmacy of the Slotervaart Hospital and Netherlands Cancer Institute developed a solid oral dosage form for docetaxel, ModraDoc001 10 mg capsules. Two other novel dosage forms of docetaxel with improved pharmaceutical characteristics, have been developed: ModraDoc003 10 mg tablets and ModraDoc004 10/50 mg tablets. The systemic exposure after administration of those forms is now being investigated.

NCT01173913

Conditions

1. Cancer

Interventions

1. Drug: ModraDoc001 10mg capsules
2. Drug: ModraDoc003 10mg tablets and ModraDoc004 10/50 mg
3. Drug: ModraDoc006 10 mg tablet

To establish the effect of functional genetic polymorphisms, C1236T (for MDR1) and CYP3A4*1B, on pharmacokinetics of orally administered docetaxel.. Inclusion Criteria: 1. Histological or cytological proof of cancer 2. Patients for whom no standard therapy of proven benefit exist 3. Patients who might benefit from treatment with docetaxel, e.g. --- C1236T ---

Another part of this study is the screening for 2 different polymorphism, C1236T (for MDR1)and CYP3A4*1B. --- C1236T ---

Ciclosporin inhibits P-glycoprotein should increase colchicine bioavailability whereas tacrolimus should not influence colchicine disposition. This is a prospective, controlled, open labeled study performed in renal graft recipients comparing colchicine single dose (1mg) pharmacokinetics in 14 patients treated with tacrolimus and 14 patients treated with cyclosporin.

NCT01160276

Conditions

1. Renal Replacement Therapies

Interventions

1. Drug: cyclosporine+colchicine
2. Drug: tacrolimus

ABCB1 Haplotypes composed of 3 SNPs: C3435T, G2677T / A and C1236T.. null. --- C3435T --- --- G2677T --- --- C1236T ---

Dosing methods for digoxin, a drug used to treat heart failure, have not been updated in decades despite evidence in recent years suggesting that blood levels of digoxin achieved with traditional dosing practices may increase the risk of adverse events. We developed a simple dosing tool that targets lower blood levels of digoxin that have been associated with improved outcomes compared to higher blood levels. The aim of this study is to determine if this simplified dosing tool is more effective than standard digoxin dosing practices at achieving lower blood levels and also to determine if digoxin dosing may be further optimized by incorporating patients' genetic information believed to influence the drug's properties.

NCT01005602

Conditions

1. Heart Failure

Interventions

1. Other: Digoxin Dosing per Nomogram
2. Drug: Digoxin

MeSH:Heart Failure

HPO:Abnormal left ventricular function Congestive heart failure Right ventricular failure

Serum Digoxin Concentration by ABCB1 Single Nucleotide Polymorphism (SNP) C1236T. --- C1236T ---

Solid organ transplant recipients would greatly benefit from pharmacogenetic evaluation since immunosuppressive drug regimens consist of multiple medications with narrow therapeutic ranges and toxic adverse event profiles. Tacrolimus is a potent immunosuppressive agent utilized for rejection prophylaxis. Intensive pharmacokinetic monitoring must be performed following organ transplantation to ensure therapeutic drug concentrations due to its highly variable pharmacokinetics profile and narrow therapeutic index. Tacrolimus is a substrate for CYP450 3A and for the membrane transporter p-glycoprotein (Pgp). Polymorphisms in the gene encoding for CYP3A5 have been extensively studied and have been found to influence the dosing of tacrolimus. The effect of ABCB1 gene polymorphisms (which encodes for Pgp) upon tacrolimus pharmacokinetics has been more difficult to establish. This study will determine if haplotypes derived from three frequent polymorphisms in the ABCB1 gene (C1236T, G2677T, C3435T) can predict the degree of drug interaction between tacrolimus (CYP3A5/Pgp substrate) and ketoconazole (CYP3A5/Pgp inhibitor) in patients who are CYP3A5 nonexpressors. This prospective pharmacokinetic and pharmacogenomic study will enroll 20 stable renal transplant recipients with the CYP3A5 *3/*3 genotype and grouped by ABCB1 haplotype (CGC vs TTT). Pharmacokinetics of tacrolimus will be assessed on 2 occasions with and without ketoconazole coadministration separated by 1 week. The order of study occasions will be randomized in a crossover design. The results of this study may identify a genomic marker for predicting drug-drug interactions. Knowing this information a priori will aid clinicians in modifying drug dosing and alleviate patients of the burden of significant drug toxicities.

NCT01288521

Conditions

1. Kidney Transplantation

Interventions

1. Drug: Tacrolimus + Ketoconazole, Then Tacrolimus alone
2. Drug: Tacrolimus alone, Then Tacrolimus + Ketoconazole

This study will determine if haplotypes derived from three frequent polymorphisms in the ABCB1 gene (C1236T, G2677T, C3435T) can predict the degree of drug interaction between tacrolimus (CYP3A5/Pgp substrate) and ketoconazole (CYP3A5/Pgp inhibitor) in patients who are CYP3A5 nonexpressors. --- C1236T ---