Disturbances of thyroid function tests by drugs.

K W Wenzel

Home/Archive/PubMed

PubMed · 8767516

Disturbances of thyroid function tests by drugs.

K W Wenzel

View original source ↗Export metadata ↓

Abstract

Commonly prescribed drugs can variously cause changes in measuring serum T3 and T4 concentrations. Thus spuriously normal thyroid hormone levels may result in moderate hypo- or hyperthyroidism, or the influence of pharmacological substances may lead to a false diagnosis of thyroid disease in euthyroid subjects. On the other hand numerous pharmacological agents, especially those interacting with neurotransmitters, may influence TSH secretion, too. While generally such drug-induced abnormal thyroid tests do not correspond to clinical features of thyroid dysfunction, iodine containing drugs, especially amiodarone, may result in overt thyroid disease.

Explore related subjects

Amiodarone Diagnosis, Differential Drug-Related Side Effects and Adverse Reactions Humans Predictive Value of Tests Thyroid Diseases Thyroid Function Tests Thyrotropin Thyroxine Triiodothyronine Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

K W Wenzel. 1996. Disturbances of thyroid function tests by drugs.. https://pubmed.ncbi.nlm.nih.gov/8767516/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Novel quinolizidinyl derivatives as antiarrhythmic agents.

Eighteen analogues of lidocaine, mexiletine, and procainamide were synthesized, replacing their aminoalkyl chains with the rigid and cumbersome quinolizidine nucleus. The target compounds were tested for antiarrhythmic, inotropic, and chronotropic effects on isolated guinea pig (gp) heart tissues and to assess calcium antagonist activity. Most compounds exhibited from moderate to high antiarrhythmic activity, and compounds 7, 9, and 19 were more active and potent than quinidine and lidocaine, while producing only modest inotropic, chronotropic, and vasorelaxant effects. These compounds were studied on spontaneously beating Langendorff-perfused gp heart. While quinidine and amiodarone produced a dose-dependent prolongation of all the ECG intervals, compounds 7, 9, and 19, even at concentrations 10-20 times higher than EC50 for the antiarrhythmic activity, only moderately prolonged the PR and QT intervals, leaving unchanged the QRS complex. Ether 7 deserves further investigations due to its interesting cardiovascular profile.

Amiodarone↗

PubMed2007

A liquid chromatography-mass spectrometry assay method for simultaneous determination of amiodarone and desethylamiodarone in rat specimens.

A liquid chromatographic-mass spectrometry (LC/MS) assay method was developed for the determination of amiodarone and desethylamiodarone in rat specimens. Analytes were extracted using liquid-liquid extraction in hexane. The LC/MS system consisted of a Waters Micromass ZQtrade mark 4000 spectrometer with an autosampler and pump. A C(18) 3.5 microm (2.1 x 50 mm) column heated to 45 degrees C was used for separation. The mobile phase consisted of methanol and 0.2% aqueous formic acid pumped at 0.2 mL/min as a linear gradient. Components eluted within 12 min. The concentrations of ethopropazine (internal standard), desethylamiodarone and amiodarone were monitored for m/z of 313.10, combination of 546.9 and 617.73, and 645.83, respectively. In plasma (0.1 mL), linearity was achieved between the peak area ratios and concentrations over the range of 2.5-1000 ng/mL for both amiodarone and desethylamiodarone (r(2) > 0.999). The intraday and interday CV were equal or less than 18%, and mean error was <12%. Similarly, in homogenates containing 0.1 g of rat tissue, linearity was observed in standards ranging from 5 to 5000 ng/g. The method was successfully used to measure tissue and plasma concentrations of drug. The validated lower limit of quantitation was 2.5 ng/mL for drug and metabolite, based on 0.1 mL of plasma.

Amiodarone↗

PubMed2007

Prophylactic therapy to prevent atrial arrhythmia after cardiac surgery.

PURPOSE OF REVIEW: Atrial fibrillation after cardiac surgery is associated with adverse outcomes and increased costs. Accordingly, therapy should be provided to prevent postoperative atrial fibrillation. The evaluation of therapies to do so is an area of active investigation with significant recent advances. The purpose of this review is to summarize these recent advances in the context of our previous knowledge base regarding the prevention of postoperative atrial fibrillation. RECENT FINDINGS: Recent evaluations of therapy to prevent postoperative atrial fibrillation have raised the prominence of prophylactic amiodarone, redefined the efficacy of prophylactic standard beta-blockers in contemporary cardiac surgical populations, provided further evidence for the use of prophylactic sotalol, magnesium, and atrial pacing, and identified new approaches, including the use of combination therapy, for the prevention of postoperative atrial fibrillation. SUMMARY: According to newly released ACC/AHA/ESC guidelines, use of standard beta-blockers or amiodarone to prevent postoperative atrial fibrillation have a level of evidence of A. Use of prophylactic sotalol has a level of evidence of B, while the use of prophylactic intravenous magnesium or atrial pacing has a lower level of evidence. The use of novel and combination therapies continues to be an area of active investigation.

Amiodarone↗