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  • Key words Imidapril  (2)
  • Pharmacokinetics  (2)
  • 17-OHCS  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of imidapril and its active metabolite imidaprilat following single dose and during steady state in patients with impaired liver function (1997)
    Springer
    European journal of clinical pharmacology 51 (1997), S. 489-491 
    Details
    ISSN: 1432-1041
    Keywords: Key words Imidapril ; Liver dysfunction; pharmacokinetics ; angiotensin-converting enzyme inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: The possible influence of impaired liver function on the pharmacokinetic disposition of imidapril, a novel prodrug type angiotensin-converting enzyme (ACE) inhibitor, and its active metabolite, imidaprilat, was investigated. Methods: Eight subjects with normal liver function and eight patients with liver dysfunction received an oral dose of 10 mg imidapril once daily for 7 days. Results: Plasma imidapril concentrations after single and, although less pronounced, after repeated dosing were higher in the liver disease patients, whereas imidaprilat concentrations were lower. This suggests that the conversion of imidapril into imidaprilat in the liver is delayed in patients with impaired liver function. However, the slower biotransformation did not result in statistically significant differences in Cmax and AUC for either imidapril or its active metabolite following repeated administration. Moreover, no relevant accumulation of either imidapril or imidaprilat occurred after repeated dosing. Conclusions: Imidapril is regarded as an ACE inhibitor of which the pharmacokinetic disposition is only slightly affected in patients with impaired liver function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050236
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of rifampicin and cimetidine on pharmacokinetics and pharmacodynamics of lamotrigine in healthy subjects (2000)
    Springer
    European journal of clinical pharmacology 56 (2000), S. 299-304 
    Details
    ISSN: 1432-1041
    Keywords: Key words Lamotrigine ; Pharmacokinetics ; Electroencephalogram
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: To study the effects of rifampicin, a potent inducer of the microsomal P 450 enzyme system and of specific isoforms of the uridine 5′-diphosphate(UDP)-glucuronyl-transferase enzyme system, and cimetidine, a known inhibitor of the hepatic microsomal cytochrome P 450 enzyme system, on pharmacokinetics and pharmacodynamics of lamotrigine in healthy subjects. Methods: Ten healthy male subjects received a single oral dose of 25 mg lamotrigine after a 5-day pretreatment with (1) cimetidine 800 mg divided into two equal doses, (2) rifampicin 600 mg, or (3) placebo. Serum and urine samples were analyzed using high-performance liquid chromatography. Changes in electroencephalographic (EEG) power were determined up to 48 h after lamotrigine administration. Results: The values of the pharmacokinetic parameters of lamotrigine were: clearance over bioavailability (CL/F) 2.60 ± 0.40 l/h, renal clearance (CLR) 0.10 ± 0.03 l/h, terminal half-life (t 1/2) 23.8 ± 2.1 h, mean peak serum concentration (Cmax) 0.29 ± 0.02 μg/l, time to reach Cmax (tmax) 1.6 ± 0.28 h, and total area under the serum concentration-time curve (AUC0–∞) 703.99 ± 82.31 μg/ml/min (mean ± SEM). The amount of lamotrigine excreted as glucuronide was 8.90 ± 0.77 mg. Rifampicin significantly increased CL/F (5.13 ± 1.05 l/h) and the amount of lamotrigine excreted as glucuronide (12.12 ± 0.94 mg), whereas both t 1/2 (14.1 ± 1.7 h) and AUC0–∞ (396.24 ± 60.18 μg/ml/min) were decreased (P 〈 0.05). Cimetidine failed to affect pharmacokinetics of lamotrigine. Lamotrigine did not change EEG power. Conclusion: Rifampicin altered pharmacokinetics of lamotrigine due to induction of the hepatic enzymes responsible for glucuronidation, while coadministration of cimetidine to ongoing lamotrigine therapy has negligible effects on lamotrigine pharmacokinetics. Lamotrigine administered as a single dose of 25 mg has no effect on EEG power in healthy subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280000146
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  • 3
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of imidapril and its active metabolite imidaprilat following single dose and during steady state in patients with chronic renal failure (1998)
    Springer
    European journal of clinical pharmacology 54 (1998), S. 59-61 
    Details
    ISSN: 1432-1041
    Keywords: Key words Imidapril ; Chronic renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: An open study on the single dose and steady-state pharmacokinetics of imidapril, a novel prodrug-type angiotensin-converting enzyme (ACE) inhibitor, and its active metabolite imidaprilat was conducted in eight patients with moderate chronic renal failure [mean creatinine clearance (CLCR) 64 ml · min−1; range 42–77 ml · min−1], eight patients with severe chronic renal failure (mean CLCR, 18 ml · min−1; range 11–29 ml · min−1) and eight healthy volunteers with normal renal function. Subjects received an oral dose of 10 mg imidapril once per day for 7 days. Results: No statistical differences of either maximum concentration (Cmax) or the area under the curve (AUC) were found between patients with moderate renal failure and healthy subjects. However, Cmax and AUC for both imidapril and imidaprilat were significantly higher in patients with severe renal impairment than in healthy volunteers. There were no clinically relevant differences among the three subject groups with regard to total urinary excretion of both imidapril and imidaprilat. Conclusion: The smallest imidapril dose which is clinically effective should be used in patients with severe renal insufficiency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050421
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  • 4
    Electronic Resource
    Electronic Resource
    Pharmacokinetics and safety of propiverine in patients with fatty liver disease (1998)
    Springer
    European journal of clinical pharmacology 54 (1998), S. 767-771 
    Details
    ISSN: 1432-1041
    Keywords: Key words Propiverine ; Fatty liver disease ; Pharmacokinetics ; Adverse effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: The present study was designed to assess the pharmacokinetics of propiverine after single and multiple dosing in patients with and without fatty liver disease. Methods: The serum concentration-time curves of propiverine and its main metabolite propiverine-N-oxide were investigated in 12 patients with mild to moderate impairment of liver function (mean antipyrine clearance 26.0 ml · min−1) and in 12 controls (antipyrine clearance 42.8 ml · min−1). Subjects were treated orally with propiverine hydrochloride (Mictonorm) for 5 days (15 mg t. i. d.) to reach steady state. Results: No significant differences were observed for propiverine and its main metabolite with regard to peak serum concentration (Cmax), area under the serum concentration-time curve (AUC) and elimination half-life (t1/2). Adverse events were reported by 12 patients. Five patients with fatty liver disease and seven patients with normal liver function complained of dry mouth and/or blurred vision. All adverse events reported were transient and mild. Conclusion: No pharmacokinetic differences relevant for safety were observed, comparing patients with and without fatty liver disease following repeated oral administration of propiverine. Thus there seems to be no need to adjust the dose in patients with mild to moderate impairment of liver function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050549
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  • 5
    Electronic Resource
    Electronic Resource
    Divergent effects of different enzyme-inducing agents on endogenous and exogenous testosterone (1992)
    Springer
    European journal of clinical pharmacology 42 (1992), S. 641-644 
    Details
    ISSN: 1432-1041
    Keywords: Testosterone ; Enzyme Induction ; antipyrine ; phenobarbital ; rifampicin ; plasma testosterone ; urinary excretion ; FSH ; LH ; 6β-OH cortisol ; 17-OHCS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of three different enzyme-inducing drugs (antipyrine 1200 mg, phenobarbital 100 mg, rifampicin 600 mg per day for 7 days) on plasma and urinary testosterone concentrations, plasma gonadotropin levels, antipyrine kinetics, and urinary 6β-hydroxycortisol excretion were studied in 18 healthy volunteers. Changes in plasma and urinary testosterone concentrations following exogenous testosterone undecanoate (TU) were also investigated. Although both antipyrine and rifampicin increased antipyrine clearance by about 60%, they produced contrary effects on testosterone: antipyrine lowered the total morning plasma testosterone and plasma testosterone AUC following TU, while rifampicin led to increases of about 20% and 78%, respectively. By contrast, phenobarbital did not significantly alter the endogenous and exogenous plasma testosterone concentrations, but it increased the urinary excretion of testosterone by more than 60%. The other two enzyme inducers did not alter this parameter. Gonadotropin levels remained unchanged. The results indicate that different enzyme-inducing agents exert divergent effects on endogenous and exogenous testosterone concentrations and suggest that the effect of enzyme induction on endogenous testosterone depends on the type of microsomal enzyme-inducing drug used rather than on the extent of the induction achieved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265929
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