The Experts below are selected from a list of 246 Experts worldwide ranked by ideXlab platform
Lionel D Lewis - One of the best experts on this subject based on the ideXlab platform.
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Olsalazine and 6 mercaptopurine related bone marrow suppression a possible drug drug interaction
Clinical Pharmacology & Therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M OtternessAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
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Olsalazine and 6‐mercaptopurine‐related bone marrow suppression: A possible drug‐drug interaction
Clinical pharmacology and therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M Otterness, L. Lennard, Richard M. Weinshilboum, David W. NierenbergAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
Andrea Benin - One of the best experts on this subject based on the ideXlab platform.
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Olsalazine and 6 mercaptopurine related bone marrow suppression a possible drug drug interaction
Clinical Pharmacology & Therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M OtternessAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
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Olsalazine and 6‐mercaptopurine‐related bone marrow suppression: A possible drug‐drug interaction
Clinical pharmacology and therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M Otterness, L. Lennard, Richard M. Weinshilboum, David W. NierenbergAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
Carol L Szumlanski - One of the best experts on this subject based on the ideXlab platform.
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Olsalazine and 6 mercaptopurine related bone marrow suppression a possible drug drug interaction
Clinical Pharmacology & Therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M OtternessAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
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Olsalazine and 6‐mercaptopurine‐related bone marrow suppression: A possible drug‐drug interaction
Clinical pharmacology and therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M Otterness, L. Lennard, Richard M. Weinshilboum, David W. NierenbergAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
Diane M Otterness - One of the best experts on this subject based on the ideXlab platform.
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Olsalazine and 6 mercaptopurine related bone marrow suppression a possible drug drug interaction
Clinical Pharmacology & Therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M OtternessAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
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Olsalazine and 6‐mercaptopurine‐related bone marrow suppression: A possible drug‐drug interaction
Clinical pharmacology and therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M Otterness, L. Lennard, Richard M. Weinshilboum, David W. NierenbergAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
David W. Nierenberg - One of the best experts on this subject based on the ideXlab platform.
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Olsalazine and 6‐mercaptopurine‐related bone marrow suppression: A possible drug‐drug interaction
Clinical pharmacology and therapeutics, 1997Co-Authors: Lionel D Lewis, Andrea Benin, Carol L Szumlanski, Diane M Otterness, L. Lennard, Richard M. Weinshilboum, David W. NierenbergAbstract:A patient with refractory Crohn's disease had two separate episodes of bone marrow suppression while receiving 50 to 75 mg 6-mercaptopurine a day and 1000 to 1750 mg Olsalazine a day. This adverse reaction necessitated dose reduction of 6-mercaptopurine on the first occasion and withdrawal of 6-mercaptopurine and Olsalazine on the second occasion. The patient's red blood cell thiopurine methyltransferase (TPMT) activity was 12.2 U per milliliter red blood cells (low normal range) and her TPMT genotype was wild-type sequence for all known alleles of TPMT that result in low TPMT enzyme activity. In vitro enzyme kinetic studies confirmed the hypothesis that Olsalazine and Olsalazine-O-sulfate are potent noncompetitive inhibitors of recombinant human TPMT. We suggest that the patient's relatively low baseline level of TPMT activity was inhibited by Olsalazine and Olsalazine-O-sulfate, leading to decreased clearance of 6-mercaptopurine and its accumulation. This ultimately increased intracellular 6-thiopurine nucleotide levels to toxic concentrations, which caused bone marrow suppression. Clinical Pharmacology & Therapeutics (1997) 62, 464–475; doi:
