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Biomedical subjects

K Nademanee

Publications and source records attributed to K Nademanee.

97 records · Page 6Linked to original sources
PubMed1981

Hyperthyroxinemia with bradycardia and normal thyrotropin secretion after chronic amiodarone administration.

Pituitary-thyroid function was tested in 15 euthyroid patients before, during, and after long term oral treatment with amiodarone (2-n-butyl-3,4'-diethylaminoethoxy-3',5'-diiodobenzoylbenzofurane; 600-1200 mg daily), an iodine-containing potent antiarrhythmic drug. The drug caused increases in serum total T4, free T4, and rT3, with a concomitant decrease in T3. Baseline serum TSH was significantly higher after 1 week of drug treatment and returned to normal levels after 12 weeks of treatment. All patients receiving amiodarone had a slowing of their heart rate (P less than 0.01), and heart rate gradually increased 6 weeks after drug withdrawal, concurrent with the slow fall in T4 and rT3 levels. Amiodarone did not cross-react in the iodothyronine RIAs. The results suggest that amiodarone inhibits the peripheral conversion of T4 to T3 and may block the metabolic action of thyroid hormone in man.

Aged↗
PubMedDate not supplied

Amiodarone and thyroid function.

Amiodarone blocks the action of thyroid hormone by the inhibition of 5'-deiodinase which reduces production of T3 in peripheral tissues and possibly by blocking nuclear binding of T3. Since the drug inhibits peripheral conversion of T4 to T3, many patients taking amiodarone have abnormal thyroid function studies (increased T4 and rT3; decreased T3) despite being euthyroid. Treatment of patients with amiodarone generates an iodine excess, which contributes greatly to the significant incidence of altered thyroid status in this population. The diagnosis of hyperthyroidism and hypothyroidism can be difficult. However, using the overall clinical picture and the tolerance limits of hormone levels determined for patients remaining euthyroid on amiodarone therapy, the accurate diagnosis of clinically significant thyroid dysfunction can almost always be made. To screen for thyroid disease, thyroid function should be assessed before initiating therapy, semiannually during therapy or whenever clinical features of thyroid dysfunction occur. Subclinical hypothyroidism as denoted by modest increases in TSH levels do not require treatment or the discontinuation of amiodarone therapy. An appreciation of the mechanism of the interaction between amiodarone and thyroid hormone metabolism allows the clinician to recognize thyroid dysfunction at an early stage and initiate appropriate therapy, thereby minimizing the morbidity associated with forms of amiodarone toxicity.

Amiodarone↗
PubMedDate not supplied

What is the sudden death syndrome in Southeast Asian males?

Sudden unexplained death syndrome describes the death of apparently healthy individuals--usually young men--in whom postmortem examination does not reveal the cause of death. The victims are in apparently good health and usually die at night while sleeping. They die within minutes after the onset of agonal respiration. Patients who have been resuscitated were found to have ventricular fibrillation and inducible polymorphic ventricular tachycardia in the electrophysiologic laboratory. This syndrome has been most frequently described in young Southeast Asian men. In this review, the epidemiology, clinical and electrophysiologic manifestations, pathology and risk factors, prognosis, and treatments for sudden unexplained death syndrome are described.

Adult↗
PubMedDate not supplied

Ventricular tachycardia-flutter associated with disopyramide therapy: a report of three cases.

Three patients developed episodes of ventricular tachycardia and/or flutter-fibrillation while receiving disopyramide (Norpace). Syncope was the presenting complaint in all of them. The arrhythmias did not recur after disopyramide was discontinued. The Q-T interval was markedly prolonged in all three patients. One patient developed syncope associated with both quinidine and Norpace therapy. It is postulated that disopyramide, like quinidine, may provoke ventricular flutter-fibrillation in sensitive patients by similar mechanisms.

Aged↗