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Sirak Petros - One of the best experts on this subject based on the ideXlab platform.

  • Intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Purpose Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. Methods We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Results Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Conclusion Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • Metamizole inhibits arachidonic acid induced platelet aggregation after surgery and impairs the effect of aspirin in hospitalized patients
    European Journal of Clinical Pharmacology, 2019
    Co-Authors: Christian Pfrepper, Ines Gockel, S Deters, Michael Metze, R Siegemund, Sirak Petros
    Abstract:

    The inhibitory effect of Metamizole on platelet aggregation is known for several years, but most studies were conducted in healthy volunteers with contradictory results. Recent studies have shown an inhibitory effect of Metamizole on acetylsalicylic acid (ASA)-induced platelet aggregation. We aimed to investigate the effect of Metamizole on platelet aggregation after an elective surgery and the effect of Metamizole on ASA-induced platelet aggregation in hospitalized patients. We performed platelet aggregation analysis after induction with ADP, arachidonic acid (AA), epinephrine, and collagen in 37 patients prior to an elective visceral or thoracic surgery and on postoperative day (POD) 1 and POD 3 1–2 h and 5–6 h after Metamizole. In another cohort of 10 hospitalized patients receiving the combination of Metamizole and ASA for more than 7 days, AA-induced platelet aggregation was analyzed in the morning prior to the intake of both drugs. Metamizole induced a strong inhibitory effect on AA-induced platelet aggregation at all time points being detectable up to 41 h in some patients. Besides a less pronounced effect on collagen-induced platelet aggregation on POD 3 1–2 h after Metamizole, all other inductors showed no effect. In 4 out of 10 hospitalized patients, no ASA-induced inhibition of platelet aggregation was detectable without correlation to sequence of administration. The reason why some patients have a long-lasting inhibitory effect of Metamizole on COX-induced platelet aggregation that might interfere with ASA should be investigated in a larger cohort of patients.

Joanna Mika - One of the best experts on this subject based on the ideXlab platform.

  • Metamizole relieves pain by influencing cytokine levels in dorsal root ganglia in a rat model of neuropathic pain
    Pharmacological Reports, 2020
    Co-Authors: Renata Zajaczkowska, Klaudia Kwiatkowski, Katarzyna Pawlik, Anna Piotrowska, Ewelina Rojewska, Wioletta Makuch, Jerzy Wordliczek, Joanna Mika
    Abstract:

    Background Treatment of neuropathic pain is still challenging. Recent studies have suggested that dorsal root ganglia (DRG), which carry sensory neural signals from the peripheral nervous system to the central nervous system, are important for pathological nociception. A proper understanding of the significance and function of DRG and their role in pharmacotherapy can help to improve the treatment of neuropathic pain. Metamizole, also known as sulpyrine or dipyrone, is a non-opioid analgesic commonly used in clinical practice, but it is not used for neuropathic pain treatment. Methods Chronic constriction injury (CCI) of the sciatic nerve was induced in Wistar rats. Metamizole was administered intraperitoneally (ip) preemptively at 16 and 1 h before CCI and then twice a day for 7 days. To evaluate tactile and thermal hypersensitivity, von Frey and cold plate tests were conducted, respectively. Results Our behavioral results provide evidence that repeated intraperitoneal administration of Metamizole diminishes the development of neuropathic pain symptoms in rats. Simultaneously, our findings provide evidence that Metamizole diminishes the expression of pronociceptive interleukins ( IL - 1beta , IL - 6 , and IL - 18 ) and chemokines ( CCL2 , CCL4 , and CCL7 ) in DRG measured 7 days after sciatic nerve injury. These assays indicate, for the first time, that Metamizole exerts antinociceptive effects on nerve injury-induced neuropathic pain at the DRG level. Conclusions Finally, we indicate that Metamizole-induced analgesia in neuropathy is associated with silencing of a broad spectrum of cytokines in DRG. Our results also suggest that Metamizole is likely to be an effective medication for neuropathic pain. Graphic abstract

  • Metamizole relieves pain by influencing cytokine levels in dorsal root ganglia in a rat model of neuropathic pain
    Pharmacological Reports, 2020
    Co-Authors: Renata Zajaczkowska, Klaudia Kwiatkowski, Katarzyna Pawlik, Anna Piotrowska, Ewelina Rojewska, Wioletta Makuch, Jerzy Wordliczek, Joanna Mika
    Abstract:

    Treatment of neuropathic pain is still challenging. Recent studies have suggested that dorsal root ganglia (DRG), which carry sensory neural signals from the peripheral nervous system to the central nervous system, are important for pathological nociception. A proper understanding of the significance and function of DRG and their role in pharmacotherapy can help to improve the treatment of neuropathic pain. Metamizole, also known as sulpyrine or dipyrone, is a non-opioid analgesic commonly used in clinical practice, but it is not used for neuropathic pain treatment. Chronic constriction injury (CCI) of the sciatic nerve was induced in Wistar rats. Metamizole was administered intraperitoneally (ip) preemptively at 16 and 1 h before CCI and then twice a day for 7 days. To evaluate tactile and thermal hypersensitivity, von Frey and cold plate tests were conducted, respectively. Our behavioral results provide evidence that repeated intraperitoneal administration of Metamizole diminishes the development of neuropathic pain symptoms in rats. Simultaneously, our findings provide evidence that Metamizole diminishes the expression of pronociceptive interleukins (IL-1beta, IL-6, and IL-18) and chemokines (CCL2, CCL4, and CCL7) in DRG measured 7 days after sciatic nerve injury. These assays indicate, for the first time, that Metamizole exerts antinociceptive effects on nerve injury-induced neuropathic pain at the DRG level. Finally, we indicate that Metamizole-induced analgesia in neuropathy is associated with silencing of a broad spectrum of cytokines in DRG. Our results also suggest that Metamizole is likely to be an effective medication for neuropathic pain.

Christian Pfrepper - One of the best experts on this subject based on the ideXlab platform.

  • Intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Purpose Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. Methods We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Results Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Conclusion Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • Metamizole inhibits arachidonic acid induced platelet aggregation after surgery and impairs the effect of aspirin in hospitalized patients
    European Journal of Clinical Pharmacology, 2019
    Co-Authors: Christian Pfrepper, Ines Gockel, S Deters, Michael Metze, R Siegemund, Sirak Petros
    Abstract:

    The inhibitory effect of Metamizole on platelet aggregation is known for several years, but most studies were conducted in healthy volunteers with contradictory results. Recent studies have shown an inhibitory effect of Metamizole on acetylsalicylic acid (ASA)-induced platelet aggregation. We aimed to investigate the effect of Metamizole on platelet aggregation after an elective surgery and the effect of Metamizole on ASA-induced platelet aggregation in hospitalized patients. We performed platelet aggregation analysis after induction with ADP, arachidonic acid (AA), epinephrine, and collagen in 37 patients prior to an elective visceral or thoracic surgery and on postoperative day (POD) 1 and POD 3 1–2 h and 5–6 h after Metamizole. In another cohort of 10 hospitalized patients receiving the combination of Metamizole and ASA for more than 7 days, AA-induced platelet aggregation was analyzed in the morning prior to the intake of both drugs. Metamizole induced a strong inhibitory effect on AA-induced platelet aggregation at all time points being detectable up to 41 h in some patients. Besides a less pronounced effect on collagen-induced platelet aggregation on POD 3 1–2 h after Metamizole, all other inductors showed no effect. In 4 out of 10 hospitalized patients, no ASA-induced inhibition of platelet aggregation was detectable without correlation to sequence of administration. The reason why some patients have a long-lasting inhibitory effect of Metamizole on COX-induced platelet aggregation that might interfere with ASA should be investigated in a larger cohort of patients.

Renata Zajaczkowska - One of the best experts on this subject based on the ideXlab platform.

  • Metamizole relieves pain by influencing cytokine levels in dorsal root ganglia in a rat model of neuropathic pain
    Pharmacological Reports, 2020
    Co-Authors: Renata Zajaczkowska, Klaudia Kwiatkowski, Katarzyna Pawlik, Anna Piotrowska, Ewelina Rojewska, Wioletta Makuch, Jerzy Wordliczek, Joanna Mika
    Abstract:

    Background Treatment of neuropathic pain is still challenging. Recent studies have suggested that dorsal root ganglia (DRG), which carry sensory neural signals from the peripheral nervous system to the central nervous system, are important for pathological nociception. A proper understanding of the significance and function of DRG and their role in pharmacotherapy can help to improve the treatment of neuropathic pain. Metamizole, also known as sulpyrine or dipyrone, is a non-opioid analgesic commonly used in clinical practice, but it is not used for neuropathic pain treatment. Methods Chronic constriction injury (CCI) of the sciatic nerve was induced in Wistar rats. Metamizole was administered intraperitoneally (ip) preemptively at 16 and 1 h before CCI and then twice a day for 7 days. To evaluate tactile and thermal hypersensitivity, von Frey and cold plate tests were conducted, respectively. Results Our behavioral results provide evidence that repeated intraperitoneal administration of Metamizole diminishes the development of neuropathic pain symptoms in rats. Simultaneously, our findings provide evidence that Metamizole diminishes the expression of pronociceptive interleukins ( IL - 1beta , IL - 6 , and IL - 18 ) and chemokines ( CCL2 , CCL4 , and CCL7 ) in DRG measured 7 days after sciatic nerve injury. These assays indicate, for the first time, that Metamizole exerts antinociceptive effects on nerve injury-induced neuropathic pain at the DRG level. Conclusions Finally, we indicate that Metamizole-induced analgesia in neuropathy is associated with silencing of a broad spectrum of cytokines in DRG. Our results also suggest that Metamizole is likely to be an effective medication for neuropathic pain. Graphic abstract

  • Metamizole relieves pain by influencing cytokine levels in dorsal root ganglia in a rat model of neuropathic pain
    Pharmacological Reports, 2020
    Co-Authors: Renata Zajaczkowska, Klaudia Kwiatkowski, Katarzyna Pawlik, Anna Piotrowska, Ewelina Rojewska, Wioletta Makuch, Jerzy Wordliczek, Joanna Mika
    Abstract:

    Treatment of neuropathic pain is still challenging. Recent studies have suggested that dorsal root ganglia (DRG), which carry sensory neural signals from the peripheral nervous system to the central nervous system, are important for pathological nociception. A proper understanding of the significance and function of DRG and their role in pharmacotherapy can help to improve the treatment of neuropathic pain. Metamizole, also known as sulpyrine or dipyrone, is a non-opioid analgesic commonly used in clinical practice, but it is not used for neuropathic pain treatment. Chronic constriction injury (CCI) of the sciatic nerve was induced in Wistar rats. Metamizole was administered intraperitoneally (ip) preemptively at 16 and 1 h before CCI and then twice a day for 7 days. To evaluate tactile and thermal hypersensitivity, von Frey and cold plate tests were conducted, respectively. Our behavioral results provide evidence that repeated intraperitoneal administration of Metamizole diminishes the development of neuropathic pain symptoms in rats. Simultaneously, our findings provide evidence that Metamizole diminishes the expression of pronociceptive interleukins (IL-1beta, IL-6, and IL-18) and chemokines (CCL2, CCL4, and CCL7) in DRG measured 7 days after sciatic nerve injury. These assays indicate, for the first time, that Metamizole exerts antinociceptive effects on nerve injury-induced neuropathic pain at the DRG level. Finally, we indicate that Metamizole-induced analgesia in neuropathy is associated with silencing of a broad spectrum of cytokines in DRG. Our results also suggest that Metamizole is likely to be an effective medication for neuropathic pain.

Ines Gockel - One of the best experts on this subject based on the ideXlab platform.

  • Intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Purpose Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. Methods We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Results Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Conclusion Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • intake of aspirin prior to Metamizole does not completely prevent high on treatment platelet reactivity
    European Journal of Clinical Pharmacology, 2020
    Co-Authors: Christian Pfrepper, Carolin Dietze, Yvonne Remane, Thilo Bertsche, Susanne Schiek, Thorsten Kaiser, Ines Gockel, Christoph Josten, Sirak Petros
    Abstract:

    Metamizole can sterically inhibit aspirin (ASA) from binding to cyclooxygenase 1 (COX1). It is recommended that ASA should be taken 30 min prior to Metamizole to maintain the irreversible inhibition of arachidonic acid (AA)–induced platelet aggregation. We aimed to analyse the inhibitory effect of ASA and Metamizole on AA-induced platelet aggregation over the course of the day. We analysed hospitalized patients who ingested ASA at least 30 min prior to Metamizole (recommended dosing group, n = 15), Metamizole prior or simultaneously with ASA (not recommended dosing group, n = 16) and patients with unknown or mixed intake (mixed dosing group, n = 5). AA-induced light transmission (LTA) and impedance aggregometry (IA) were measured before, 1–2 and 5–6 h after the intake of ASA ± Metamizole. Maximum AA-induced LTA prior to the intake of ASA was significantly lower and the rate of high on treatment platelet reactivity (HTPR) higher in the recommended compared with the not recommended dosing group (19.6% vs. 46.9%, p = 0.011 and 4/15 vs. 12/16 patients, p = 0.017). There was no difference when IA was used. Maximum AA-induced LTA after the intake of ASA ± Metamizole was lower in patients in the not recommended but not in the recommended dosing group. All patients with HTPR in the recommended dosing group had regular inhibition of AA-induced LTA after discontinuation of Metamizole. Co-medication of ASA and Metamizole significantly influences platelet inhibition with variations during the day and can cause HTPR in patients taking ASA prior to Metamizole or simultaneously.

  • Metamizole inhibits arachidonic acid induced platelet aggregation after surgery and impairs the effect of aspirin in hospitalized patients
    European Journal of Clinical Pharmacology, 2019
    Co-Authors: Christian Pfrepper, Ines Gockel, S Deters, Michael Metze, R Siegemund, Sirak Petros
    Abstract:

    The inhibitory effect of Metamizole on platelet aggregation is known for several years, but most studies were conducted in healthy volunteers with contradictory results. Recent studies have shown an inhibitory effect of Metamizole on acetylsalicylic acid (ASA)-induced platelet aggregation. We aimed to investigate the effect of Metamizole on platelet aggregation after an elective surgery and the effect of Metamizole on ASA-induced platelet aggregation in hospitalized patients. We performed platelet aggregation analysis after induction with ADP, arachidonic acid (AA), epinephrine, and collagen in 37 patients prior to an elective visceral or thoracic surgery and on postoperative day (POD) 1 and POD 3 1–2 h and 5–6 h after Metamizole. In another cohort of 10 hospitalized patients receiving the combination of Metamizole and ASA for more than 7 days, AA-induced platelet aggregation was analyzed in the morning prior to the intake of both drugs. Metamizole induced a strong inhibitory effect on AA-induced platelet aggregation at all time points being detectable up to 41 h in some patients. Besides a less pronounced effect on collagen-induced platelet aggregation on POD 3 1–2 h after Metamizole, all other inductors showed no effect. In 4 out of 10 hospitalized patients, no ASA-induced inhibition of platelet aggregation was detectable without correlation to sequence of administration. The reason why some patients have a long-lasting inhibitory effect of Metamizole on COX-induced platelet aggregation that might interfere with ASA should be investigated in a larger cohort of patients.