Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants.
Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1998 |
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| Umfang: |
8 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Pharmacy world & science - 1981, 20(1998) vom: März, Seite 123-130 |
| Übergeordnetes Werk: |
volume:20 ; year:1998 ; month:03 ; pages:123-130 ; extent:8 |
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NLEJ195426371 |
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| 520 | |a Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. | ||
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| 700 | 1 | |a Niewiarowski, W. |4 oth | |
| 700 | 1 | |a Rębowski, G. |4 oth | |
| 700 | 1 | |a Skrętkowicz, J. |4 oth | |
| 700 | 1 | |a Sekulska, M. |4 oth | |
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(DE-627)NLEJ195426371 DE-627 ger DE-627 rakwb eng Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. 1998 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. Springer Online Journal Archives 1860-2002 Zielińska, E. oth Bodalski, J. oth Mianowska, K. oth Niewiarowski, W. oth Rębowski, G. oth Skrętkowicz, J. oth Sekulska, M. oth in Pharmacy world & science 1981 20(1998) vom: März, Seite 123-130 (DE-627)NLEJ188983368 (DE-600)2008911-9 1573-739X nnns volume:20 year:1998 month:03 pages:123-130 extent:8 http://dx.doi.org/10.1023/A:1008664707825 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1998 3 123-130 8 |
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(DE-627)NLEJ195426371 DE-627 ger DE-627 rakwb eng Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. 1998 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. Springer Online Journal Archives 1860-2002 Zielińska, E. oth Bodalski, J. oth Mianowska, K. oth Niewiarowski, W. oth Rębowski, G. oth Skrętkowicz, J. oth Sekulska, M. oth in Pharmacy world & science 1981 20(1998) vom: März, Seite 123-130 (DE-627)NLEJ188983368 (DE-600)2008911-9 1573-739X nnns volume:20 year:1998 month:03 pages:123-130 extent:8 http://dx.doi.org/10.1023/A:1008664707825 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1998 3 123-130 8 |
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(DE-627)NLEJ195426371 DE-627 ger DE-627 rakwb eng Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. 1998 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. Springer Online Journal Archives 1860-2002 Zielińska, E. oth Bodalski, J. oth Mianowska, K. oth Niewiarowski, W. oth Rębowski, G. oth Skrętkowicz, J. oth Sekulska, M. oth in Pharmacy world & science 1981 20(1998) vom: März, Seite 123-130 (DE-627)NLEJ188983368 (DE-600)2008911-9 1573-739X nnns volume:20 year:1998 month:03 pages:123-130 extent:8 http://dx.doi.org/10.1023/A:1008664707825 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1998 3 123-130 8 |
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(DE-627)NLEJ195426371 DE-627 ger DE-627 rakwb eng Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. 1998 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. Springer Online Journal Archives 1860-2002 Zielińska, E. oth Bodalski, J. oth Mianowska, K. oth Niewiarowski, W. oth Rębowski, G. oth Skrętkowicz, J. oth Sekulska, M. oth in Pharmacy world & science 1981 20(1998) vom: März, Seite 123-130 (DE-627)NLEJ188983368 (DE-600)2008911-9 1573-739X nnns volume:20 year:1998 month:03 pages:123-130 extent:8 http://dx.doi.org/10.1023/A:1008664707825 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1998 3 123-130 8 |
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(DE-627)NLEJ195426371 DE-627 ger DE-627 rakwb eng Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. 1998 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. Springer Online Journal Archives 1860-2002 Zielińska, E. oth Bodalski, J. oth Mianowska, K. oth Niewiarowski, W. oth Rębowski, G. oth Skrętkowicz, J. oth Sekulska, M. oth in Pharmacy world & science 1981 20(1998) vom: März, Seite 123-130 (DE-627)NLEJ188983368 (DE-600)2008911-9 1573-739X nnns volume:20 year:1998 month:03 pages:123-130 extent:8 http://dx.doi.org/10.1023/A:1008664707825 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 20 1998 3 123-130 8 |
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genotyping of the arylamine n‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants |
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Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. |
| abstract |
Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. |
| abstractGer |
Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. |
| abstract_unstemmed |
Abstract The pathogenesis of hypersensitivity to trimethoprim‐sulfamethoxazole (TMP‐SMX) is supposed to be associated with the slow acetylation phenotype. This pharmacogenetic defect is associated with the mutations of the arylamine N‐acetyltransferase (NAT2) encoding gene. The aim of the study was to compare the usefulness of the acetylation phenotype and NAT2 coding genotype in the prediction of idiosyncratic reaction to Cotrimoxazole in infants. The study was carried out in the group of 20 infants, aged 2‐12 months (mean age 6.3 months) treated with Cotrimoxazole, administered at 100 mg/kg b.w./24 h doses. In seven children (35%) no adverse effects of the treatment have been observed, whereas in 13 (65%) children various adverse effects occurred as a result of the therapy, such as rash (4 children), granulocytopenia with anemization (5 children) or liver impairment (4 children). The acetylation phenotype of each child was determined on the basis of urine of N‐acetyl isoniazid/isoniazid ratio, after ingestion of isoniazid as a model drug. Furthermore we used polymerase chain reaction (PCR) followed by the analysis of restriction fragments length polymorphism (RFLP) technique to identify the known mutant alleles of the NAT2 gene. It has been presumed that the genotype determining fast acetylation contains at least one of wild‐type allele. No correlation has been found between the observed adverse effects of Cotrimoxazole and age, gender and acetylation phenotype. However, it has been demonstrated that the risk of adverse effects of Cotrimoxazole is considerably higher in children with mutations of the NAT2 encoding gene. The comparison of the results from PCR‐RFLP genotyping with phenotyping suggested that in infants, the NAT2 genotype rather than phenotype provides the basis for the detection of hypersensitivity to TMP‐SMX. |
| collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Genotyping of the arylamine N‐acetyltransferase polymorphism in the prediction of idiosyncratic reactions to trimethoprim‐sulfamethoxazole in infants. |
| url |
http://dx.doi.org/10.1023/A:1008664707825 |
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| author2 |
Zielińska, E. Bodalski, J. Mianowska, K. Niewiarowski, W. Rębowski, G. Skrętkowicz, J. Sekulska, M. |
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Zielińska, E. Bodalski, J. Mianowska, K. Niewiarowski, W. Rębowski, G. Skrętkowicz, J. Sekulska, M. |
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7.402767 |