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Related Concept Videos

Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
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Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
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Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
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Pharmacokinetics: Drug–Drug Interactions

Drug interactions occur when the pharmacological effect of one drug is altered by another substance, either enhancing or diminishing its activity. The drug whose activity is altered is known as the object drug, and the substance causing the alteration is called the agent drug or the precipitant. The net effects of these interactions are mostly undesirable, leading to decreased effectiveness or increased adverse effects. In rare cases, interactions can be beneficial, such as the enhanced...

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Colchicine toxicity precipitated by interaction with sunitinib.

Oladapo A Abodunde1, Raghava Reddy LevakaVeera, Ravi Desai

  • 1Department of Internal Medicine, Abington Memorial Hospital, Abington, PA 19001, USA. oabodunde@amh.org

Journal of Clinical Pharmacy and Therapeutics
|March 2, 2013
PubMed
Summary

Colchicine toxicity occurred in an elderly patient due to interaction with sunitinib, a tyrosine kinase inhibitor. This highlights the importance of understanding P-glycoprotein interactions to prevent adverse drug events.

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Area of Science:

  • Pharmacology
  • Nephrology
  • Oncology

Background:

  • Colchicine is an anti-inflammatory drug used for gout and familial Mediterranean fever.
  • Toxicity is rare but can be increased by drug interactions, especially with P-glycoprotein inhibitors.
  • The maximum recommended dose of colchicine is 0.3 mg/day when co-administered with P-glycoprotein inhibitors.

Observation:

  • An 82-year-old male with gout and chronic kidney disease developed colchicine toxicity.
  • The patient experienced severe diarrhea, metabolic acidosis, pneumonia, and cardiovascular collapse.
  • Symptoms began after starting sunitinib, a tyrosine kinase inhibitor, while on high-dose colchicine.

Findings:

  • The patient's cumulative colchicine dose was 41.4 mg over ten days.
  • Sunitinib likely inhibited P-glycoprotein, leading to increased colchicine levels and toxicity.
  • The patient presented with multi-organ dysfunction, including acute systolic heart failure.

Implications:

  • This is the first reported case of colchicine toxicity precipitated by interaction with a tyrosine kinase inhibitor.
  • Clinicians need greater awareness of P-glycoprotein's role in drug interactions and potential toxicity.
  • Understanding these interactions is crucial for safe colchicine and tyrosine kinase inhibitor co-administration.