Clinical Pharmacokinetics of Probenecid

Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uri...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Cunningham, R. F. [verfasserIn] Israili, Z. H. [verfasserIn] Dayton, P. G. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	1981

Schlagwörter:	Gout Allopurinol Probenecid Oxypurinol Cinoxacin

Übergeordnetes Werk:	Enthalten in: Clinical pharmacokinetics - Berlin [u.a.] : Springer, 1976, 6(1981), 2 vom: Apr., Seite 135-151
Übergeordnetes Werk:	volume:6 ; year:1981 ; number:2 ; month:04 ; pages:135-151

Links:	Volltext

DOI / URN:	10.2165/00003088-198106020-00004

Katalog-ID:	SPR033032858

Internformat


LEADER	01000caa a22002652 4500
001	SPR033032858
003	DE-627
005	20230519074216.0
007	cr uuu---uuuuu
008	201007s1981 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.2165/00003088-198106020-00004 \|2 doi
035			\|a (DE-627)SPR033032858
035			\|a (SPR)00003088-198106020-00004-e
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
082	0	4	\|a 610 \|q ASE
084			\|a 44.00 \|2 bkl
084			\|a 44.40 \|2 bkl
100	1		\|a Cunningham, R. F. \|e verfasserin \|4 aut
245	1	0	\|a Clinical Pharmacokinetics of Probenecid
264		1	\|c 1981
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
520			\|a Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.
650		4	\|a Gout \|7 (dpeaa)DE-He213
650		4	\|a Allopurinol \|7 (dpeaa)DE-He213
650		4	\|a Probenecid \|7 (dpeaa)DE-He213
650		4	\|a Oxypurinol \|7 (dpeaa)DE-He213
650		4	\|a Cinoxacin \|7 (dpeaa)DE-He213
700	1		\|a Israili, Z. H. \|e verfasserin \|4 aut
700	1		\|a Dayton, P. G. \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Clinical pharmacokinetics \|d Berlin [u.a.] : Springer, 1976 \|g 6(1981), 2 vom: Apr., Seite 135-151 \|w (DE-627)327644974 \|w (DE-600)2043781-X \|x 1179-1926 \|7 nnns
773	1	8	\|g volume:6 \|g year:1981 \|g number:2 \|g month:04 \|g pages:135-151
856	4	0	\|u https://dx.doi.org/10.2165/00003088-198106020-00004 \|z lizenzpflichtig \|3 Volltext
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_SPRINGER
912			\|a SSG-OLC-PHA
912			\|a SSG-OPC-PHA
912			\|a SSG-OPC-ASE
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2190
936	b	k	\|a 44.00 \|q ASE
936	b	k	\|a 44.40 \|q ASE
951			\|a AR
952			\|d 6 \|j 1981 \|e 2 \|c 04 \|h 135-151

Indexfelder

author_variant	r f c rf rfc z h i zh zhi p g d pg pgd
matchkey_str	article:11791926:1981----::lnclhraoieisf
hierarchy_sort_str	1981
bklnumber	44.00 44.40
publishDate	1981
allfields	10.2165/00003088-198106020-00004 doi (DE-627)SPR033032858 (SPR)00003088-198106020-00004-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl 44.40 bkl Cunningham, R. F. verfasserin aut Clinical Pharmacokinetics of Probenecid 1981 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay. Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213 Israili, Z. H. verfasserin aut Dayton, P. G. verfasserin aut Enthalten in Clinical pharmacokinetics Berlin [u.a.] : Springer, 1976 6(1981), 2 vom: Apr., Seite 135-151 (DE-627)327644974 (DE-600)2043781-X 1179-1926 nnns volume:6 year:1981 number:2 month:04 pages:135-151 https://dx.doi.org/10.2165/00003088-198106020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 44.00 ASE 44.40 ASE AR 6 1981 2 04 135-151
spelling	10.2165/00003088-198106020-00004 doi (DE-627)SPR033032858 (SPR)00003088-198106020-00004-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl 44.40 bkl Cunningham, R. F. verfasserin aut Clinical Pharmacokinetics of Probenecid 1981 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay. Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213 Israili, Z. H. verfasserin aut Dayton, P. G. verfasserin aut Enthalten in Clinical pharmacokinetics Berlin [u.a.] : Springer, 1976 6(1981), 2 vom: Apr., Seite 135-151 (DE-627)327644974 (DE-600)2043781-X 1179-1926 nnns volume:6 year:1981 number:2 month:04 pages:135-151 https://dx.doi.org/10.2165/00003088-198106020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 44.00 ASE 44.40 ASE AR 6 1981 2 04 135-151
allfields_unstemmed	10.2165/00003088-198106020-00004 doi (DE-627)SPR033032858 (SPR)00003088-198106020-00004-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl 44.40 bkl Cunningham, R. F. verfasserin aut Clinical Pharmacokinetics of Probenecid 1981 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay. Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213 Israili, Z. H. verfasserin aut Dayton, P. G. verfasserin aut Enthalten in Clinical pharmacokinetics Berlin [u.a.] : Springer, 1976 6(1981), 2 vom: Apr., Seite 135-151 (DE-627)327644974 (DE-600)2043781-X 1179-1926 nnns volume:6 year:1981 number:2 month:04 pages:135-151 https://dx.doi.org/10.2165/00003088-198106020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 44.00 ASE 44.40 ASE AR 6 1981 2 04 135-151
allfieldsGer	10.2165/00003088-198106020-00004 doi (DE-627)SPR033032858 (SPR)00003088-198106020-00004-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl 44.40 bkl Cunningham, R. F. verfasserin aut Clinical Pharmacokinetics of Probenecid 1981 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay. Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213 Israili, Z. H. verfasserin aut Dayton, P. G. verfasserin aut Enthalten in Clinical pharmacokinetics Berlin [u.a.] : Springer, 1976 6(1981), 2 vom: Apr., Seite 135-151 (DE-627)327644974 (DE-600)2043781-X 1179-1926 nnns volume:6 year:1981 number:2 month:04 pages:135-151 https://dx.doi.org/10.2165/00003088-198106020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 44.00 ASE 44.40 ASE AR 6 1981 2 04 135-151
allfieldsSound	10.2165/00003088-198106020-00004 doi (DE-627)SPR033032858 (SPR)00003088-198106020-00004-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl 44.40 bkl Cunningham, R. F. verfasserin aut Clinical Pharmacokinetics of Probenecid 1981 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay. Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213 Israili, Z. H. verfasserin aut Dayton, P. G. verfasserin aut Enthalten in Clinical pharmacokinetics Berlin [u.a.] : Springer, 1976 6(1981), 2 vom: Apr., Seite 135-151 (DE-627)327644974 (DE-600)2043781-X 1179-1926 nnns volume:6 year:1981 number:2 month:04 pages:135-151 https://dx.doi.org/10.2165/00003088-198106020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 44.00 ASE 44.40 ASE AR 6 1981 2 04 135-151
language	English
source	Enthalten in Clinical pharmacokinetics 6(1981), 2 vom: Apr., Seite 135-151 volume:6 year:1981 number:2 month:04 pages:135-151
sourceStr	Enthalten in Clinical pharmacokinetics 6(1981), 2 vom: Apr., Seite 135-151 volume:6 year:1981 number:2 month:04 pages:135-151
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Gout Allopurinol Probenecid Oxypurinol Cinoxacin
dewey-raw	610
isfreeaccess_bool	false
container_title	Clinical pharmacokinetics
authorswithroles_txt_mv	Cunningham, R. F. @@aut@@ Israili, Z. H. @@aut@@ Dayton, P. G. @@aut@@
publishDateDaySort_date	1981-04-01T00:00:00Z
hierarchy_top_id	327644974
dewey-sort	3610
id	SPR033032858
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR033032858</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519074216.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s1981 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/00003088-198106020-00004</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR033032858</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)00003088-198106020-00004-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.40</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Cunningham, R. F.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Clinical Pharmacokinetics of Probenecid</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1981</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gout</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Allopurinol</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Probenecid</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Oxypurinol</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cinoxacin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Israili, Z. H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dayton, P. G.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Clinical pharmacokinetics</subfield><subfield code="d">Berlin [u.a.] : Springer, 1976</subfield><subfield code="g">6(1981), 2 vom: Apr., Seite 135-151</subfield><subfield code="w">(DE-627)327644974</subfield><subfield code="w">(DE-600)2043781-X</subfield><subfield code="x">1179-1926</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:6</subfield><subfield code="g">year:1981</subfield><subfield code="g">number:2</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:135-151</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.2165/00003088-198106020-00004</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-ASE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_702</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2190</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.00</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.40</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">6</subfield><subfield code="j">1981</subfield><subfield code="e">2</subfield><subfield code="c">04</subfield><subfield code="h">135-151</subfield></datafield></record></collection>
author	Cunningham, R. F.
spellingShingle	Cunningham, R. F. ddc 610 bkl 44.00 bkl 44.40 misc Gout misc Allopurinol misc Probenecid misc Oxypurinol misc Cinoxacin Clinical Pharmacokinetics of Probenecid
authorStr	Cunningham, R. F.
ppnlink_with_tag_str_mv	@@773@@(DE-627)327644974
format	electronic Article
dewey-ones	610 - Medicine & health
delete_txt_mv	keep
author_role	aut aut aut
collection	springer
remote_str	true
illustrated	Not Illustrated
issn	1179-1926
topic_title	610 ASE 44.00 bkl 44.40 bkl Clinical Pharmacokinetics of Probenecid Gout (dpeaa)DE-He213 Allopurinol (dpeaa)DE-He213 Probenecid (dpeaa)DE-He213 Oxypurinol (dpeaa)DE-He213 Cinoxacin (dpeaa)DE-He213
topic	ddc 610 bkl 44.00 bkl 44.40 misc Gout misc Allopurinol misc Probenecid misc Oxypurinol misc Cinoxacin
topic_unstemmed	ddc 610 bkl 44.00 bkl 44.40 misc Gout misc Allopurinol misc Probenecid misc Oxypurinol misc Cinoxacin
topic_browse	ddc 610 bkl 44.00 bkl 44.40 misc Gout misc Allopurinol misc Probenecid misc Oxypurinol misc Cinoxacin
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	Clinical pharmacokinetics
hierarchy_parent_id	327644974
dewey-tens	610 - Medicine & health
hierarchy_top_title	Clinical pharmacokinetics
isfreeaccess_txt	false
familylinks_str_mv	(DE-627)327644974 (DE-600)2043781-X
title	Clinical Pharmacokinetics of Probenecid
ctrlnum	(DE-627)SPR033032858 (SPR)00003088-198106020-00004-e
title_full	Clinical Pharmacokinetics of Probenecid
author_sort	Cunningham, R. F.
journal	Clinical pharmacokinetics
journalStr	Clinical pharmacokinetics
lang_code	eng
isOA_bool	false
dewey-hundreds	600 - Technology
recordtype	marc
publishDateSort	1981
contenttype_str_mv	txt
container_start_page	135
author_browse	Cunningham, R. F. Israili, Z. H. Dayton, P. G.
container_volume	6
class	610 ASE 44.00 bkl 44.40 bkl
format_se	Elektronische Aufsätze
author-letter	Cunningham, R. F.
doi_str_mv	10.2165/00003088-198106020-00004
dewey-full	610
author2-role	verfasserin
title_sort	clinical pharmacokinetics of probenecid
title_auth	Clinical Pharmacokinetics of Probenecid
abstract	Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.
abstractGer	Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.
abstract_unstemmed	Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190
container_issue	2
title_short	Clinical Pharmacokinetics of Probenecid
url	https://dx.doi.org/10.2165/00003088-198106020-00004
remote_bool	true
author2	Israili, Z. H. Dayton, P. G.
author2Str	Israili, Z. H. Dayton, P. G.
ppnlink	327644974
mediatype_str_mv	c
isOA_txt	false
hochschulschrift_bool	false
doi_str	10.2165/00003088-198106020-00004
up_date	2024-07-03T16:11:21.844Z
_version_	1803574923069751296
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR033032858</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519074216.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s1981 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/00003088-198106020-00004</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR033032858</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)00003088-198106020-00004-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.40</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Cunningham, R. F.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Clinical Pharmacokinetics of Probenecid</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1981</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and Cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidneyblock of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gout</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Allopurinol</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Probenecid</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Oxypurinol</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cinoxacin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Israili, Z. H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dayton, P. G.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Clinical pharmacokinetics</subfield><subfield code="d">Berlin [u.a.] : Springer, 1976</subfield><subfield code="g">6(1981), 2 vom: Apr., Seite 135-151</subfield><subfield code="w">(DE-627)327644974</subfield><subfield code="w">(DE-600)2043781-X</subfield><subfield code="x">1179-1926</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:6</subfield><subfield code="g">year:1981</subfield><subfield code="g">number:2</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:135-151</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.2165/00003088-198106020-00004</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-ASE</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_702</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2190</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.00</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.40</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">6</subfield><subfield code="j">1981</subfield><subfield code="e">2</subfield><subfield code="c">04</subfield><subfield code="h">135-151</subfield></datafield></record></collection>
score	7.4021635

Nicht das Richtige dabei?

Schreiben Sie uns!

Clinical Pharmacokinetics of Probenecid

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?