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Related Concept Videos

Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

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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...
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Pharmacokinetics: Drug–Drug Interactions01:25

Pharmacokinetics: Drug–Drug Interactions

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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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Bioequivalence of Drugs: Drugs with Multiple Indications01:09

Bioequivalence of Drugs: Drugs with Multiple Indications

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The concept of therapeutic equivalence (TE) in drugs with multiple indications is complex. A generic drug may be therapeutically equivalent to a brand-name product for one specific indication, but this doesn't necessarily mean it's equivalent for all other indications. Evidence of TE in one patient group and bioequivalence shown in healthy volunteers can support—but not confirm—TE for other indications. However, definitive proof requires individual clinical studies for each...
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FDA Approved Drugs: Changes to Approved Drugs01:26

FDA Approved Drugs: Changes to Approved Drugs

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Post-approval, manufacturers may modify an approved new or generic drug product. Such modifications can encompass alterations in the Active Pharmaceutical Ingredient (API), manufacturing process, formulation, batch size, manufacturing site, and container closure system (FDA Guidance for Industry, April 2004). Often, a drug product may undergo multiple changes.These modifications require careful evaluation to determine their potential impact on the drug product's identity, strength, quality,...
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Induced-fit Model01:13

Induced-fit Model

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Most chemical reactions in cells require enzymes—biological catalysts that speed up the reaction without being consumed or permanently changed. They reduce the activation energy needed to convert the reactants into products. Enzymes are proteins, that usually work by binding to a substrate—a reactant molecule that they act upon.
Enzymes exhibit substrate specificity, meaning that they can only bind to certain substrates. This is mainly determined by the shape and chemical...
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Tissue-Drug Binding: Localization of Drugs and its Significance01:24

Tissue-Drug Binding: Localization of Drugs and its Significance

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Body tissues, comprising approximately 40% of the body weight, are crucial in drug distribution and localization. These tissues can serve as drug storage sites, competing with plasma binding sites for drug molecules.
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Drug induced pseudolymphoma.

Cynthia M Magro1, Brianne H Daniels1, A Neil Crowson2

  • 1Weill Cornell Medicine, Department of Pathology & Laboratory Medicine, 1300 York Avenue, F-309, New York, NY 10065, United States.

Seminars in Diagnostic Pathology
|January 24, 2018
PubMed
Summary
This summary is machine-generated.

Drug-associated pseudolymphoma can mimic cutaneous lymphoma, presenting as atypical lymphocytic infiltrates. Careful evaluation is crucial for distinguishing these reactive conditions from true lymphoma.

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Area of Science:

  • Dermatopathology
  • Immunology
  • Oncology

Background:

  • Atypical lymphocytic infiltrates of the skin encompass a range of conditions, from benign to malignant.
  • Many are reactive lymphomatoid processes linked to drug therapy, termed drug-associated pseudolymphoma.
  • These can mimic low-grade lymphomas, T-cell dyscrasias, and lymphomatoid papulosis.

Purpose of the Study:

  • To review the spectrum of drug-associated pseudolymphoma.
  • To highlight the diverse drug classes implicated.
  • To emphasize the diagnostic challenges in differentiating pseudolymphoma from lymphoma.

Main Methods:

  • Review of literature on atypical cutaneous lymphoid infiltrates and drug associations.
  • Analysis of morphologic and phenotypic features of pseudolymphoma subtypes.
  • Discussion of pathomechanisms involving drug-induced immune responses.

Main Results:

  • Implicated drug classes include antidepressants, antihistamines, calcium channel blockers, statins, anticonvulsants, and biologics.
  • Drugs can cause overzealous immune responses or immune dysregulation (e.g., DRESS syndrome).
  • A temporal link between drug initiation and skin lesions may be absent due to cumulative effects or drug interactions.

Conclusions:

  • Distinguishing drug-associated pseudolymphoma from cutaneous lymphoma requires close collaboration between pathologists and clinicians.
  • Pathologic analysis alone may not be sufficient for definitive diagnosis.
  • Recognition of these reactive conditions is vital to avoid misdiagnosis and inappropriate treatment.