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[Interference in the conversion of T4 to T3 and rT3 by medications in man].

Several drugs are known to interfere in thyroid hormone metabolism: 1) They can affect directly and specifically T4 to T3 conversion. This can be observed in vivo and in vitro. In vivo serum T3 concentrations will decrease and rT3 concentrations increase. Amiodarone, other iodinated compounds (cholecystographic agents: ipodate and iopanoic acid), propylthiouracil and propranolol are known to act in this way. 2) Other drugs which induce the hepatic capacity to catabolize drugs will also affect thyroid hormone metabolism, e.g. diphenylhydantoine. Clinically, inhibitors of conversion will increase serum total and free T4, however this finding per se does not proof hyperthyroidism as in some cases serum TSH will increase after i.v. injection of 400 micrograms TRH. Furthermore the increase in serum T4 can be explained in part by a low metabolic clearance rate, T4 production being barely increased.

Amiodarone↗

PubMed1994

[Thyrotoxic crisis].

A thyrotoxic Crisis is an acute or subacute metabolic explosion caused by uncontrolled release of tyronines from the thyroid gland (more frequently a diffuse thyroid gland) following its injury: strumectomy, administration of a therapeutic dose of I131, inflammations, or excessive stimulation (massive release of TSIg by stress lympholysis, low iodine doses). Concurrently a massive conversion of T4 to T3 in tissues must occur which is enhanced by discontinuation of beta-blockers, thyrostatics, synthetic glucocorticoids and administration of drugs replacing T4 from the bond to plasma carries (salicylates, sodantone, furosemide, barbiturates etc.) during stress. The trigger mechanism of the crisis is any severe stress (surgery, accidents, infection, childbirth) and the administration of iodine preparations. Their effect depends, however, on the dose, period of administration and the functional and morphological state of the thyroid gland. Small doses of iodine administered for a short period stimulate hormonogenesis, large doses (more than 10 mg/day), on the other hand, block the iodine pump, T4 and T3 secretion by the thyroid gland and conversion of T4 to T3 in tissues. In therapy specific procedures are involved: I. Block of T4, T3 synthesis and secretion a) ipodate, ioipanoic acid, Lugol's solution i.v. b) propycil, methimasol c) in iodine-basedowized goitres perchlorate and lithium II. Block of T4 to T3 conversion (iodine preparations, incl. amiodarone, beta-blockers, propycil, dexamethasone). III. Reduction of hypermetabolism (beta-blockers, Ca inhibitors) IV. Reduction of free T4 and T3 in blood stream (by plasmapheresis, haemoperfusion, haemodialysis) V. General provisions in intensive therapy (control of hyperpyrexia, dehydration, hypoxia, supraventricular arrhythmia and circulatory decompensation).

Humans↗

PubMed1977

Uptake of uric acid by separated renal tubules of the rabbit. II. Effects of drugs.

The effect of various drugs on the rate of uptake of uric acid by separated renal tubules of the rabbit was investigated. Determinations were made of 150 values and slopes of the inhibition curves. The most potent inhibitor of uric acid uptake was sulfinpyrazone, with an 150 of 0.02 mM. Calcium ipodate and benzbromarone were also potent inhibitors. Uricosuric drugs, with the exception of benzbromarone, had shallow inhibition slopes. Diuretic drugs had steep inhibition slopes. More than one mechanism of action is probably involved in the inhibition of uric acid uptake in separated renal tubules by drugs.

Animals↗

PubMed1965