THE INFLUENCE OF THE PLASMA INORGANIC IODINE CONCENTRATION ON THYROID FUNCTION IN DEHALOGENASE DEFICIENCY

1967 ◽  
Vol 55 (2) ◽  
pp. 361-368 ◽  
Author(s):  
R. McG. Harden ◽  
W. D. Alexander ◽  
S. Papadopoulos ◽  
M. T. Harrison ◽  
S. Macfarlane

ABSTRACT Iodine metabolism and thyroid function were studied in a patient with hypothyroidism and goitre due to dehalogenase deficiency. Initially the plasma inorganic iodine (PII) level was within the normal range but circulating levels of hormone were low and the thyroid clearance and absolute uptake of iodine (AIU) by the thyroid were high. Administration of iodide supplements resulted in a rapid rise in the plasma thyroxine concentration and restoration of the euthyroid state. Thyroid hormone synthesis appeared to proceed normally when the PII exceeded 1.0 μg/100 ml. This was achieved by increasing the intake of iodide by 612 μg per day. At PII levels around 10 μg/100 ml there was evidence of increased levels of circulating thyroid hormone.

1972 ◽  
Vol 69 (2) ◽  
pp. 321-328
Author(s):  
K. Liewendahl ◽  
E. Niskanen ◽  
A. Gordin

ABSTRACT The effects of excess iodide on the histology and function of the thyroid were studied in rats. A slight increase in thyroid weight and minimal histological alterations were observed. The thyroid function of rats was studied by measuring the serum total and free thyroxine. Excess iodide did not significantly change the concentration of thyroid hormone in the serum and signs of hypothyroidism were not seen. Thus, rats were capable of adaptation to chronic administration of large amounts of iodide. A slight increase in the serum thyrotrophin after prolonged ingestion of excess iodide was measured with both bioassay and radioimmunoassay techniques. The possible role of thyrotrophin in the mechanism of escape from the transient inhibition of iodide on thyroid hormone synthesis is discussed.


1963 ◽  
Vol 19 (2) ◽  
pp. 103-104 ◽  
Author(s):  
Vera Dolgova ◽  
N. Serafimow ◽  
G. Sestakov

1980 ◽  
Vol 112 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Alain VIRION ◽  
Daniele DEME ◽  
Jacques POMMIER ◽  
Jacques NUNEZ

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Starry H. Rampengan

Abstract: Amiodarone is a highly effective anti-arrhythmic agent used in certain arrhythmias from supraventricular tachycardia to life-threatening ventricular tachycardia. Its use is associated with numerous side-effects that could deteriorate a patient’s condition. Consequently, a clinician should consider the risks and benefits of amiodarone before initiating the treatment.The thyroid gland is one of the organs affected by amiodarone. Amiodarone and its metabolite desethyl amiodaron induce alterations in thyroid hormone metabolism in the thyroid gland, peripheral tissues, and probably also in the pituitary gland. These actions result in elevations of serum T4 and rT3 concentrations, transient increases in TSH concentrations, and decreases in T3 concentrations. Both hypothyroidism and hyperthyroidism are prone to occur in patients receiving amiodarone. Amiodarone-induced hypothyroidism (AIH) results from the inability of the thyroid to escape from the Wolff-Chaikoff effect and is readily managed by either discontinuation of amiodarone or thyroid hormone replacement. Amiodarone-induced thyrotoxicosis (AIT) may arise from either iodine-induced excessive thyroid hormone synthesis (type I, usually with underlying thyroid abnormality), or destructive thyroiditis with release of preformed hormones (type II, commonly with apparently normal thyroid glands). Therefore, monitoring of thyroid function should be performed in all amiodarone-treated patients to facilitate early diagnosis and treatment of amiodarone-induced thyroid dysfunction. Key words: Amiodarone, thyroid function, side effect, management, monitoring.     Abstrak: Amiodaron adalah obat antiaritmia yang cukup efektif dalam menangani beberapa keadaaan aritmia mulai dari supraventrikuler takikardia sampai takikardia ventrikuler yang mengancam kehidupan. Namun penggunaan obat ini ternyata menimbulkan efek samping pada organ lain yang dapat menimbulkan perburukan keadaan pasien. Sehingga, dalam penggunaan amiodaron, klinisi juga harus menimbang keuntungan dan kerugian yang ditimbulkan oleh obat ini. Salah satu organ yang dipengaruhi oleh amiodaron adalah kelenjar tiroid. Amiodaron dan metabolitnya desetil amiodaron memengaruhi hormon tiroid pada kelenjar tiroid, jaringan perifer, dan mungkin pada pituitari. Aksi amiodaron ini menyebabkan peningkatan T4, rT3 dan TSH, namun menurunkan kadar T3. Hipotiroidisme dan tirotoksikosis dapat terjadi pada pasien yang diberi amiodaron. Amiodarone-induced hypothyroidism (AIH) terjadi karena ketidakmampuan tiroid melepaskan diri dari efek Wolff Chaikof, dan dapat ditangani dengan pemberian  hormon substitusi T4 atau penghentian amiodaron. Amiodarone-induced thyrotoxicosis (AIT) terjadi karena sintesis hormon tiroid yang berlebihan yang diinduksi oleh iodium (tipe I, biasanya sudah mempunyai kelainan tiroid sebelumnya) atau karena tiroiditis destruktif yang disertai pelepasan hormon tiroid yang telah terbentuk (tipe II, biasanya dengan kelenjar yang normal). Pemantauan fungsi tiroid seharusnya dilakukan pada semua pasien yang diberi amiodaron untuk memfasilitasi diagnosis dan terapi yang dini terjadinya  disfungsi tiroid yang diinduksi amiodaron. Kata Kunci: Amiodaron, fungsi tiroid, efek samping, penanganan, pemantauan.


2015 ◽  
Vol 72 (4) ◽  
pp. 311-316 ◽  
Author(s):  
Ceylan Bal ◽  
Murat Büyükşekerci ◽  
Müjgan Ercan ◽  
Asım Hocaoğlu ◽  
Hüseyin Tuğrul Çelik ◽  
...  

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