GLC Determination of Phenylbutazone in Human Plasma

Sioufi, A.; Caudal, F.; Marfil, F.

doi:10.1002/jps.2600670230

Cited by 22 publications

(2 citation statements)

References 14 publications

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“…Consequently, plasma and urinary concentrations of salicylate are usually more meaningful than blood and urine concentrations of the parent compound. Salicylic acid is distributed throughout most body tissues and most transcellular fluids such as synovial, spinal and peritoneal fluids, and in saliva and milk (Findlay et aI., 1981;Levy et aI., 1980; Sample Reference 0.5ml S Wahiin-Boll et al (1981) 0.2ml P Rumble and Roberts (1981) 0.5ml P Van Loenhout et al (1980) 0.5ml P Balali-Mood et al (1982) 1.0ml P Marunaka et al (1980) O.lml P Sioufi et al (1978) 1.0ml P Marunaka et al (1980) 0.5ml P Gikalov et al (1982) 0.5ml P Shimek et al (1981a) lml P Bayne et al (1981) O.lml P Evans (1980) 0.5ml P Shimek et al (1981a) 0.25ml P Shimek et al (1981a) 0.2ml P Nielsen-Kudsk (1980) O.lml P Upton et al (1980a) lmlP Bopp et al (1981) lmlP Upton et al (1980a) 1ml P Kaye et al (1981) lml P Fleitman et al (1982) 1ml P Cuisinaud et al (1978) lml S Snider et al (1981) 0.5ml P Ali et al (1981) 1.0ml P Shimek et al (1981b) 0.2ml S Whitlam andVine (1980) 0.5ml P Ikeda et al (1980) lml P Geiger et al (1975 2ml P Sennello et al (1978) lml P Lin et al (1980) 1ml P Lin et al (1980) 0.2-2ml P Pentikainen et al (1981) O.lml P Twomey et al (1980) Soren , 1979). Salicylate readily crosses the placental barrier (Levy and Garrettson, 1974).…”

Section: Distributionmentioning

confidence: 97%

Clinical Pharmacokinetics of Non-steroidal Anti-inflammatory Drugs

Verbeeck

Blackburn

Loewen

1983

Clinical Pharmacokinetics

214

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The number of non-steroidal anti-inflammatory drugs (NSAIDs) available for clinical use has dramatically increased during the last decade. As a general rule, NSAIDs are well absorbed from the gastrointestinal tract, with the exception of aspirin (and possibly diclofenac, tolfenamic acid and fenbufen) which undergoes presystemic hydrolysis to form salicylic acid. Concomitant administration of NSAIDs with food or antacids may in some cases lead to delayed or even reduced absorption. The NSAIDs are highly bound to plasma proteins (mainly albumin), which limits their body distribution to the extracellular spaces. Apparent volumes of distribution of NSAIDs are, therefore, very low and usually less than 0.2 L/kg. The elimination of these drugs depends largely on hepatic biotransformation; renal excretion of unchanged drugs is usually small (less than 5% of the dose). Total body clearance is low and for most NSAIDs is less than 200 ml/min. The effect of age and disease on the disposition of NSAIDs has not been extensively studied. Due to the central role of the liver in the overall elimination of the majority of these compounds, hepatic disease will most likely lead to a significant alteration in their pharmacokinetic behaviour. NSAIDs have been reported to be involved in numerous pharmacokinetic drug interactions. Aspirin decreases the plasma concentrations of many other NSAIDs, although the clinical significance of this is uncertain. Due to the extremely high plasma protein binding of NSAIDs (around 99% in many cases), competition for the same binding sites on plasma proteins may be at least partly responsible for some interactions of NSAIDs with other highly bound drugs; however, another mechanism such as decreased metabolism or decreased urinary elimination is usually involved as well. The most important interactions with NSAIDs are those involving the oral anticoagulants and oral hypoglycaemic agents, though not all NSAIDs have been found to interact with these drugs. In clinical practice, there appear to be no clear-cut guidelines to assist the clinician in the selection of the most appropriate drug for an individual patient. The selection of an anti-inflammatory drug should be based on clinical experience, patient convenience (e.g. once or twice daily dosage schedule), side effects and cost. Since a marked interindividual variability exists in the clinical response to a given NSAID, clinicians prescribing these agents may try several of them sequentially until an adequate response is obtained.

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Section: Distributionmentioning

confidence: 97%

Clinical Pharmacokinetics of Non-steroidal Anti-inflammatory Drugs

Verbeeck

Blackburn

Loewen

1983

Clinical Pharmacokinetics

214

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“…However, this test is non-specific and many other drugs and metabolites (for example, salicylate) will also react. For quantitative analysis several procedures are suitable (Clarke, 1969;Sioufi & Marfil, 1978 Clarke, 1969), whereas a 21-month-old child survived 2.2 g but developed toxic hepatitis (v. Muhlendahl et al, 1979). Similar toxicity can be assumed for oxyphenbutazone.…”

Section: Chemical Analysismentioning

confidence: 99%

Intoxication with pyrazolones.

Okonek¹

1980

Brit J Clinical Pharma

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1 About 50 severe or fatal (mostly accidental) cases of intoxication in children by pyrazolones have been reported in the German literature of the past 59 years. 2 Characteristic symptoms are impaired consciousness progressing to coma and convulsions. In addition, sudden apnoea and cardiac arrest may occur. Hepatic lesions may develop after a latent period of 12‐24 hours. 3 Haemoperfusion seems to be the only therapeutic measure which is able to reduce the total body load of all pyrazolones to a toxicologically relevant extent. Actual clinico‐ toxicological data from poisoned patients are not available as yet; however, distribution volumes, plasma half‐lives and endogenous plasma clearances as well as removal kinetics in vitro of aminophenazone (aminopyrine), propyphenazone, metamizole (dipyrone), phenylbutazone and oxyphenbutazone as point to the efficacy of haemoperfusion with amberlite XAD‐4 resin.

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Bioavailability of phenylbutazone from a new enteric‐coated formulation with superior dissolution characteristics

John¹,

Goldsborough²,

Morrison

et al. 1982

Biopharm & Drug Disp

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The bioavailability of an improved formulation of enteric-coated phenylbutazone with faster dissolution, more consistent in vitro rate of drug release and improved stability was compared in 8 normal subjects at doses of 100 and 200 mg with commercially available Butacote. Phenylbutazone was more rapidly absorbed from the new formulation and higher plasma concentrations were achieved at shorter intervals after dosing. Drug elimination rate was unaffected by reformulation and despite faster absorption the total amounts of drug reaching the circulation from the new and commercial products were similar. It was concluded that replacing Butacote by the new formulation would provide the same therapeutic benefit.

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GLC Determination of Phenylbutazone in Human Plasma

Cited by 22 publications

References 14 publications

Clinical Pharmacokinetics of Non-steroidal Anti-inflammatory Drugs

Clinical Pharmacokinetics of Non-steroidal Anti-inflammatory Drugs

Intoxication with pyrazolones.

Bioavailability of phenylbutazone from a new enteric‐coated formulation with superior dissolution characteristics

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