Objective: The purpose of this study was to develop a LC-MS method to determine amiodarone (AMI) and its major metabolite desethylamiodarone (DEA) from rat plasma released from the adipose tissue of AMI treated rats subjected to a weight gain/weight loss cycle.
Methods: Separation of the compounds was performed on a Kinetex 2.6 μm C18 100 x 4.6 mm column under isocratic conditions using a mixture of acetonitrile: 0.1% formic acid 65:35 at a flow rate of 0.5 ml/min. Detection of the analyte was performed by electrospray positive ionization, the monitored ions being 135 m/z from 646 for AMI and 135 m/z of 618 for DEA. Analytes were extracted after plasma protein precipitation with methanol.
Results: The developed method presented specificity and linearity on the concentration range of 25-2500 ng/ml plasma for AMI and 2.5-1250 ng/ml plasma for DEA and the precision and accuracy of the method at all of quality control concentration levels including LLOQ were according to official guidelines for validating analytical methods.
Conclusions: A sensitive and accurate LC-MS method has been developed with a much lower LLOQ than literature data to detect the plasma concentration differences of the studied analytes that result from forced lipolysis and mobilization from the adipose tissue.
Tag Archives: amiodarone
The Incidence and Risk of Inducing Hyperthyroidism Following Amiodarone Treatment
Introduction: Amiodarone, a frequently used antiarrhythmic drug in cardiology, is very efficient in the treatment of ventricular and supraventricular tachiarrithmyas. The iodine content of amiodarone is 39%. Its chemical structure is similar to tyrosine. It is estimated that 1–23% of patients treated with amiodarone can develop hyperthyroidism. The purpose of this study is to assess and monitor the incidence of hyperthyroidism induced by amiodarone in patients admitted for various types of cardiac dysrhythmias, considering that most of the patients included in the study came from an endemic goitre area.
Material and method: One-hundred patients chosen systematically (62 men, 38 women) from 560 patients treated with amiodarone in the January 1st, 2009 – December 31, 2009 period were assessed (clinically, laboratory findings and imaging studies); their mean age was 64 years (range 50–70 years). In order to identify and diagnose hyperthyroidism, a questionnaire (Newcastle index) was used, also urinary iodine dosage, hormonal dosages (T3, T4, TSH) and thyroid imaging (ultrasound, radioactive iodine uptake test) were used.
Results: The incidence of hyperthyroidism induced by amiodarone in this study was 8%. Hyperthyroidism was more frequent in women (6 women vs. 2 men).
Conclusions: Thyroid hormonal levels have to be determined and a clinical or thyroid ultrasound examination should be made prior to initiating a treatment with amiodarone. At the end of the study, 8 patients, most of them female, were diagnosed with hyperthyroidism.
The Characteristics of Amiodarone-induced Thyrotoxicosis in a Moderate Iodine Deficit Area
Introduction: Amiodarone (AMI), a class III anti-arrhythmic drug, is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism), which is due to amiodarone’s high iodine content and its direct toxic effect on the thyroid.
Objective: To evaluate the incidence of Amiodarone induced thyrotoxicosis (AIT) (type, rate of occurrence) and to identify the risk factors involved in its occurrence.
Material and method: We examined patients treated with amiodarone, between January 2002 and December 2011, who presented to our Department of Endocrinology Târgu Mures for thyroid dysfunctions.
Results: The retrospective study included 87 patients with thyroid dysfunctions; 58 (66.7%) patients had AIT and 29 (33.3%) had Amiodarone induced hypothyroidism (AIH). In the AIT group: 35 were women (60.3%), 23 were men (39.7%); the average age was 61.60 ± 12.39 years. Risk factors identified for the AIT group were male gender (RR = OR = 3.8; Chi-squer = 5.7, p = 0.004) and pre-existing thyroid abnormalities (RR = 2.5, Chi-square = 4.1, p = 0.005). The thyroid dysfunction occurrence was heterogeneous (0.2–183 months). The patients with previous thyroid abnormalities developed earlier thyroid dysfunction compared to those with an apparently normal thyroid gland (22.25 ± 4.14 months versus 32.09 ± 7.69 months, p = 0.02, T test).
Conclusion: In the context of the specific iodine geoclimatic intake and the area of origin, amiodarone – induced thyroid dysfunction spectrum is dominated by thyrotoxicosis. Screening and monitoring of thyroid function for patiens under chronic amiodarone treatment is necessary.