PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “IOPANOIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1987

The effect of iopanoic acid on thyrotropin secretion in patients with cirrhosis of the liver.

Ten patients with liver cirrhosis and six normal subjects were studied to evaluate the effect of iopanoic acid (IA) on thyrotropin secretion. A thyrotropin-releasing-hormone (TRH) test was performed before and 5 days after IA administration (single oral dose of 3 g). After IA administration, a significant increase in TSH response to TRH was observed in normal subjects. In cirrhotics, however, it did not significantly increase after IA administration. The serum T3 and T3/TBG ratio were significantly decreased and the serum T4 and T4/TBG ratio were increased after IA administration in normal subjects and cirrhotics. There was no significant difference in the % decrease in serum T3, % increase in serum T4 or other thyroid hormone parameters including TSH in IA induced TSH responders (R) and non-responders (NR). However, r-T3 before and after IA in R was higher than those in NR. The values for hepatic function tests such as serum albumin, prothrombin time, 45 minutes retention rate of bromsulphalein (BSP 45 min) and the cholinesterase (ChE) level in R were not different from those of NR. These results suggested that in cirrhotics, abnormal regulation of the hypothalamo-pituitary system might exist.

Adult↗
PubMed2002

Effect of iodine or iopanoic acid on thyroid Ca2+/NADPH-dependent H2O2-generating activity and thyroperoxidase in toxic diffuse goiters.

OBJECTIVE: The aim of the present study was to compare the effects of iopanoic acid (IOP) or a saturated solution of potassium iodide (SSKI) administration to patients with toxic diffuse goiters (TDG). DESIGN: Patients with TDG are treated with thionamides and high doses of iodine preoperatively. In this study, two types of preoperative drug regimens were used: propylthiouracil or methimazole plus SSKI for 10-15 days (n=8) or IOP for 7 days (n=6). METHODS: Serum thyroid hormones (total and free thyroxine (T(4)), total tri-iodothyronine (T(3)) and reverse T(3) (rT(3)), were evaluated after 7 days of either SSKI or IOP treatment, and after 10-15 days of SSKI administration. During thyroidectomy, samples of thyroid gland were obtained to evaluate thyroperoxidase and thyroid H(2)O(2)-generating activities. RESULTS: Serum total T(3) was significantly decreased after 7 days of either treatment, and serum rT(3) was significantly increased in IOP-treated patients. Serum total and free T(4) were unaffected by 7 days of IOP treatment, but decreased after 7 days of SSKI treatment, although significantly diminished levels were only reached after a further 3-8 days of SSKI administration. During both drug regimens, serum TSH remained low (SSKI: 0.159+/-0.122; IOP: 0.400+/-0.109 microU/ml). Thyroperoxidase activity was significantly lower in thyroid samples from patients treated with SSKI for 10-15 days than in the thyroid glands from IOP-treated patients. However, thyroid H(2)O(2) generation was inhibited in samples from patients treated with either IOP or SSKI. CONCLUSIONS: We show herein that IOP treatment can be effective in the management of hyperthyroidism and that this drug inhibits thyroid NADPH oxidase activity, just as previously described for SSKI, probably due to its iodine content.

Adolescent↗
PubMed1980

Evidence against a major role of L-thyroxine at the pituitary level: studies in rats treated with iopanoic acid (telepaque).

To determine whether T4 has an intrinsic effect at the pituitary level, it would be important to block conversion of T4 to T3 completely. We have attempted to achieve this with iopanoic acid (IOP), a radiographic contrast agent. We have then measured in the same animals the effects of such treatment on the conversion of T4 to T3 or on the deiodination of T3 and on the pituitary response to a dose of T4 or T3. Plasma TSH levels and pituitary GH content were measured as biological end points. Thyroidectomized rats were injected with a single dose of T4 (1.7 micrograms/100 g BW) labeled with [125I]T4 (Exp A) or with a single dose of T3 (0.33 microgram/100 g BW) labeled with [125I]T3 (Exp B) and treated with IOP or solvent. Animals of Exp A were killed 24 h after iodothyronine injection and those of Exp B were killed 4, 12, and 24 h after injection of the iodothyronine. The concentrations of [125I]T4 and [125I]T3 were measured in several tissues, including the anterior pituitary, after extraction and paper chromatography and quantified with the aid of 131I-labeled markers added in vitro. Plasma and pituitary T3 and T4 plasma TSH, and pituitary GH were measured by specific RIAs. Results show that treatment with IOP markedly inhibits the conversion of T4 to T3 and the deiodination of T3. In IOP-treated thyroidectomized rats, the injection of T4 results in little, if any, effect at the pituitary level, despite an almost 3-fold increase in the percentage of injected T4 found in the gland. Treatment with IOP does not inhibit the effects of a T3 dose; if anything, they appear to be enhanced. It is concluded that, as assessed from biological responses involving the anterior pituitary, a dose of T4 has little if any effect other than that which can be attributed to the T3 generated from it.

Animals↗
PubMed1990

Effect of iopanoic acid on basal and thyrotropin-stimulated thyroid hormone levels in suckling rat pups.

We proposed that basal and thyrotropin (TSH)-stimulated thyroid hormone levels of rat pups would be altered in the presence of iopanoic acid (IA), a radiographic contrast agent which competitively inhibits T4-to-T3 conversion, and that the nature of these changes would further depend upon the route of TSH administration in a manner distinct from that reported in adults. To test this hypothesis, litters from 24 Sprague-Dawley female rats were adjusted to 8 pups each. On day 5, 80 pups received IA (2.5 mg/100 g body weight) injections. On day 8, control and IA pups were further subdivided, and given bovine TSH (bTSH) either by subcutaneous injection or by intragastric gavage (to simulate milk-borne TSH intake), and then sacrificed 0, 1.5, or 3 hours later. We found significantly higher T4 and reverse-T3 (rT3) levels in IA-treated pups, but IA had no effect on basal or TSH-stimulated T3 levels attained, regardless of route of bTSH administration or time post-treatment. Our data demonstrate that the effects of IA on T4 and rT3 levels in the immature rat are comparable to those observed in adult rats and humans, but that the marked depression of T3 levels found in IA-treated adults does not occur in the 8-day old rat pup. We speculate that the IA-treated suckling pup's ability to sustain normal basal T3 levels and generate elevated T3 concentrations in response to TSH stimulation may reflect the activity during development of a T4-5'-deiodinase relatively resistant to competitive inhibition by this drug.

Animals↗
PubMed1987

Inhibition of the response of thyrotrophin to thyrotrophin-releasing hormone by thyroxine in hypothyroid rats treated with iopanoic acid: evidence suggesting an intrinsic biological activity of thyroxine without prior conversion to 3,5,3'-tri-iodothyronine.

The effects of a physiological replacement dose of thyroxine (T4) on the response of plasma TSH to TRH in hypothyroid rats were studied. Animals were treated with iopanoic acid (IOP; 5 mg/100 g body weight) or vehicle 24, 12 and 1.5 h before the experiment. Thereafter, 800 ng T4/100 g body weight were administered i.v. and 20 min later 1 microgram TRH/100 g body weight was injected i.v. In control rats the basal concentration of TSH was 1450 +/- 300 (S.E.M.) mu./1. The plasma concentration of TSH 10 min after injection of TRH increased to 167 +/- 14% of the mean basal value (P less than 0.001). The injection of T4 significantly (P less than 0.005) reduced the TSH response to TRH in both IOP-treated (118 +/- 15%) and vehicle-treated (108 +/- 15%) rats compared with untreated controls. Tri-iodothyronine (T3) was undetectable in the plasma of all rats, whereas the plasma concentration of T4 was 121 +/- 19 nmol/l in IOP-treated and 139 +/- 23 nmol/l in vehicle-treated rats 30 min after injection of 800 ng T4/100 g body weight. In pituitary cells of control rats, cytoplasmic radioactivity 30 min after injection of [125I]T4 was 1.28 +/- 0.13 X 10(-2)% (76 +/- 6% T4 and 17 +/- 3% T3), whereas that in nuclei reached 0.42 +/- 0.36 X 10(-2)% (51 +/- 4% T4 and 28 +/- 3% T3) of the injected dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

The activity of antioxidant enzymes and the content of uncoupling protein-1 in the brown adipose tissue of hypothyroid rats: comparison with effects of iopanoic acid.

The activity of antioxidant enzymes, copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD) and catalase (CAT), as well as that of the mitochondrial FAD-dependent alpha-glycerophosphate dehydrogenase (alpha-GPD) in the rat interscapular brown adipose tissue (IBAT) were studied after the treatment with methimazole (MMI) for three weeks or with iopanoic acid (IOP) for five days. Besides, the mitochondrial concentration of uncoupling protein-1 (UCP-1) and the activity of catecholamine degrading enzyme monoamine oxidase (MAO) in the IBAT as well as the activity of the catecholamine synthesizing enzyme, dopamine beta-hydroxylase (DBH) in rat serum were examined. Judging by the significantly enhanced level of serum DBH, which is an index of sympathetic activity, and that of IBAT MAO, the increase in MnSOD and CAT activities in the IBAT of hypothyroid (MMI-treated) rats seems to be due to elevated activity of sympathetic nervous system (SNS). However, CuZnSOD activity is not affected by SNS. On the contrary, IOP, which is a potent inhibitor of T4 deiodination into T3 producing "local" hypothyroidism, did not change either SNS activity or activities of IBAT antioxidant enzyme. However, both treatments significantly decreased IBAT UCP-1 content and alpha-GPD activity suggesting that the optimal T3 concentration in the IBAT is necessary for maintaining basal levels of these key mitochondrial parameters.

Adipose Tissue, Brown↗
PubMed1980

The effect of iopanoic acid on the regulation of thyrotropin secretion in euthyroid subjects.

Oral cholecystographic agents induce a decrease in serum T3 and an increase in serum T4 and rT3 concentrations in normal subjects. However, their effect on TSH secretion in man is unclear. In the present study, the serum TSH concentration was increased above baseline values 5 days after the administration of 3 g iopanoic acid (IA) in five of six euthyroid volunteers (an increase of borderline significance), and the TSH response to TRH was significantly augmented after IA administration. In four other euthyroid subjects who had received IA 3 days earlier, the administration of T3 (5 microgram, five times daily) for the next 2 days restored the serum T3 concentration toward baseline values and prevented the IA-induced increase in TRH-stimulated serum TSH concentrations. It is concluded from the present study that IA enhances pituitary thyrotroph sensitivity to TRH and that this effect may be related, at least in part, to the IA-induced decrease in circulating T3 as well as the previously demonstrated inhibitory effect of IA on the pituitary conversion of T4 to T3. This decrease in the serum T3 concentration after IA administration is due primarily to inhibition of peripheral 5-monodeiodination of T4 and, possibly, to a direct inhibitoy effect of excess iodide on the release of T3 from the thyroid.

Adult↗
PubMed1981

Effect of Iopanoic acid on the pituitary-thyroid axis: time sequence of changes in serum iodothyronines, thyrotropin, and prolactin concentrations and responses to thyroid hormones.

We have previously shown that some oral cholecystographic agents induce marked increase in basal and TRH-stimulated TSH concentrations in normal subjects. To define the relationship between circulating iodothyronines and pituitary secretion after oral cholecystography, temporal changes in the responses of serum TSH and PRL to a fixed dose of TRH (500 micrograms iv) and in serum T4, T3, and rT3 concentrations were assessed before, immediately after, and then at weekly intervals after the three daily doses of iopanoic acid (Ip). Both basal and TRH-stimulated TSH concentrations were significantly increased at the end of the period of Ip administration when the serum T3 concentration was decreased, were still above the pretreatment level 1 week after the course of Ip when the serum T3 had returned to pre-Ip levels, and returned toward normal 2 weeks after the course of Ip. The changes in serum T3 concentration were accompanied by reciprocal changes in rT3 concentration. PRL secretion was not significantly changed. To evaluate further the relationship between the enhanced TSH secretion and the changes in serum iodothyronine concentrations, subjects were given oral doses of T3 (5 micrograms every 4 h) or T4 (50 micrograms every 8 h) during the administration of Ip. In the subjects given Ip plus T3, serum T3 concentrations were maintained at pre-Ip levels, and both basal and TRH-stimulated TSH concentrations were not different from the control. Administration of T4 did not completely prevent the Ip-induced increment of TSH secretion. It is suggested that in subjects given Ip, 1) the serum T3 level is, at least partly, a determining factor for TSH secretion; and 2) the set-point of TSH secretion is appropriately tuned to either reduction or elevation of serum T3 concentration by a mechanism that is different from that in fasting subjects.

Adult↗
PubMed2002

Iopanoic acid rapidly controls type I amiodarone-induced thyrotoxicosis prior to thyroidectomy.

Amiodarone-induced thyrotoxicosis (AIT) may develop either in apparently normal thyroid glands (Type II AIT) or in the presence of sub-clinical thyroid abnormalities (either autonomous goiter or latent Graves' disease; Type I AIT). Mixed forms also occur. While Type I AIT is due to iodine-induced excess thyroid hormone synthesis, Type II AIT is a form of amiodarone (possibly iodine) -induced destructive thyroiditis. Type I AIT is usually treated by combined thionamide and potassium perchlorate therapy, but may be resistant to therapy. On the other hand, Type II AIT often responds favorably to glucocorticoids and may not require further therapy once euthyroidism has been restored. Not infrequently, however, AIT (especially Type I) is resistant to conventional treatment, and several weeks or months may elapse before euthyroidism is restored. Thyroidectomy has been carried out in Type I AIT patients, but thyroid surgery in thyrotoxic patients, especially those with underlying cardiac problems, carries a high surgical risk. In this study we describe 3 patients with Type I AIT, who were successfully treated with a short course of iopanoic acid (IOP), an oral cholecystographic agent, which is rich in iodine and is a potent inhibitor of 5'-deiodinase, resulting in a marked decrease in the peripheral tissue conversion of T4 to T3, in preparation for thyroid surgery. Euthyroidism was rapidly restored in 7-12 days, allowing a subsequent safe and uneventful thyroidectomy in all cases. These patients were then treated with L-T4 for their hypothyroidism and amiodarone was safely re-instituted. We suggest that IOP is the drug of choice in the rapid restoration of euthyroidism prior to definitive thyroidectomy in patients with drug resistant Type I AIT.

Aged↗
PubMed1959

Iopanoic acid.

Explore the source record for details and available documents.

Cholecystography↗
PubMed1992

Management of neonatal Graves disease with iopanoic acid.

An infant with thyrotoxicosis whose mother had Graves disease was treated with sodium iopanoate. Euthyroid status was achieved rapidly and maintained with minimal effort in comparison with the conventional multidrug regimen. There were no toxic effects, and hypothyroidism did not occur.

Graves Disease↗