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PubMed1983

Uptake of iopanoic acid and its glucuronide conjugate by rat hepatocytes in primary culture.

Uptake of iopanoic acid (IOP) and iopanoate glucuronide (IOP-G) was studied in 3-day primary cultures of rat hepatocytes isolated by the collagenase perfusion method. 125I activity of cells after incubation with 125I-IOP (10-100 microM) and 125I-IOP-G (10-100 microM) was used as a measure of uptake. At each concentration, uptake was linear for the first 45 sec. In the absence of albumin, the initial uptake velocity was directly proportional to the concentration or IOP or IOP-G and was nonsaturable up to 100 microM. The calculated uptake rate constants for IOP and for IOP-G were 0.059 and 0.048 nmole/(mg protein X min X microM), respectively. IOP uptake was not inhibited by sodium taurocholate nor by the contrast agents iodipamide, ipodate, and iopronic acid. The data indicate that the enhancement of IOP excretion by bile salts noted in vivo does not occur at the uptake step and that the hepatic uptake of both IOP and IOP-G in the absence of albumin is limited by diffusion.

Adsorption↗
PubMed1990

The therapeutic efficacy of oral cholecystographic agent (iopanoic acid) in the management of hyperthyroidism.

Five randomly chosen patients with thyrotoxicosis were administered 1 gm of the oral cholecystographic agent iopanoic acid daily for 21 days. There was a marked fall in T3 levels by 75% of the pretherapy value by 96 hr; values remained normal over the 21-day period. T4 values fell significantly by seven days of therapy, and the decreased values were sustained. FT3 and FT4I also showed corresponding decreases in value. All subjects showed clinical improvement by both subjective and objective criteria. During therapy, escape from the effect of iopanoic acid was not encountered. However, after stopping the drug for 2-4 wk, the patients' iodine-131 uptake become as high as the pretherapy level, enabling them to undergo radioiodine treatment for thyrotoxicosis. The treatment strategy can be aimed at achieving quick euthyroidism and in planning radioiodine treatment as early as possible in high risk patients. This treatment may also be useful in preoperative control of thyrotoxicosis.

Administration, Oral↗
PubMed1977

Thrombocytopenic purpura following iopanoic acid ingestion.

A 48-year-old woman had severe symptomatic thrombocytopenia three times in 13 months. Each episode followed ingestion of iopanoic acid. The interval between drug ingestion and onset of symptoms was 40, 12, and 8 hours. Resolution to normal platelet counts occurred in 6, 5, and 8 days. The third thrombocytopenic crisis occurred while the patient was receiving maintenance steroid therapy, given because the initial diagnosis was idiopathic thrombocytopenic purpura. Incubation of platelet-rich plasma with the patient's serum caused platelet lysis if either the patient or the donor serum obtained after ingestion of iopanoic acid was present in the mixture.

Blood Platelets↗
PubMed1983

Uptake of iopanoic acid by isolated rat hepatocytes in primary culture.

Uptake of iopanoic acid (IOP) was studied in 3-day primary cultures of rat hepatocytes isolated by the collagenase perfusion method. 125I activity of cells after incubation with 125I-IOP (1.0-100 microM) was used as a measure of uptake. At each IOP concentration uptake was linear for the first 45 s. The initial uptake velocity was directly proportional to IOP concentration and was nonsaturable up to 100 microM. The calculated uptake rate constant was 0.67 nmol . mg prot-1 . min-1 . microM-1. Uptake was only slightly reduced when the incubation was performed at 4 degrees C and was independent of sodium concentration. Albumin in the medium reduced IOP uptake. Uptake, however, was always greater than that predicted from the unbound IOP concentration alone. The data indicate that the hepatocyte uptake of IOP occurs by both a passive process and a saturable process. The saturable uptake component depends on an albumin-IOP-hepatocyte interaction. The influence of albumin on uptake occurs possibly by an undefined specific cell surface phenomenon of albumin that promotes uptake of IOP or by enhancement of the diffusibility of IOP across the unstirred layer.

Animals↗
PubMed1979

Persistent gallbladder opacification after iopanoic acid cholecystography: diagnostic implications for acalculous cholecystitis.

Recent reports in the surgical literature state that persistent dense visualization of an otherwise normal-appearing gallbladder 36 hr after the administration of iopanoic acid is highly suggestive of acalculous cholecystitis. To determine the incidence and significance of persistent gallbladder visualization, 324 patients and 66 asymptomatic controls were evaluated. An equal percentage (about 10%) of both groups showed persistent dense gallbladder opacification 36 hr after iopanoic acid ingestion. The results do not support the contention that patients with acalculous cholecystitis can be identified by simply obtaining an additional abdominal radiograph the day after oral cholecystography.

Cholecystitis↗
PubMed2003

Treatment of type II amiodarone-induced thyrotoxicosis by either iopanoic acid or glucocorticoids: a prospective, randomized study.

Amiodarone-induced thyrotoxicosis (AIT) may occur either in the presence of underlying thyroid disease (type I AIT) or in apparently normal thyroid glands (type II AIT). Type II AIT, a destructive thyroiditis, often favorably responds to glucocorticoids. Iopanoic acid (IopAc) is an iodinated cholecystographic agent that inhibits deiodinase activity and reduces the conversion of T(4) toT(3). It has recently been reported that cholecystographic agents restore euthyroidism in patients with type II AIT. We describe the results of a prospective randomized study conducted in 12 patients with type II AIT treated with either iopanoic acid (group A, n = 6) or glucocorticoids (group B, n = 6). Serum free T(3) levels normalized rapidly in both groups after 7 d, from 0.75 +/- 0.20 ng/dl (11.5 +/- 3.1 pmol/liter) to 0.46 +/- 0.10 ng/d (7.1 +/- 1.7 pmol/liter), P < 0.01, and from 0.58 +/- 0.10 ng/dl (9.0 +/- 1.2 pmol/liter) to 0.34 +/- 0.03 ng/dl (5.2 +/- 0.5 pmol/liter), P < 0.003, in groups A and B, respectively (P = NS). Serum free T(4) levels reduced at 6 months in group B [from 2.70 +/- 0.32 ng/dl (35.1 +/- 4.1 pmol/liter) to 1.0 +/- 0.04 ng/dl (13.4 +/- 0.6 pmol/liter), P < 0.0001] but not in group A (from 2.90 +/- 0.6 ng/dl (38.0 +/- 7.5 pmol/liter) to 2.30 +/- 0.4 ng/dl (35.6 +/- 6.1 pmol/liter, P = 0.39; P = 0.005 group B vs. group A). All patients in both groups became euthyroid and had their amiodarone-induced destructive thyroiditis cured as defined by normalization of both serum free T(4) and free T(3) levels, during both drugs therapy. However, patients in group B were cured more rapidly than patients in group A (43 +/- 34 d vs. 221 +/- 111 d, respectively, P < 0.002). This study shows that, albeit both drugs are effective, glucocorticoids are probably the drug of choice for more rapidly curing type II AIT.

Aged↗
PubMed2002

Preparation with iopanoic acid rapidly controls thyrotoxicosis in patients with amiodarone-induced thyrotoxicosis before thyroidectomy.

BACKGROUND: Amiodarone-induced thyrotoxicosis (AIT) may develop either in apparently normal glands (type II AIT) or in the presence of thyroid abnormalities (type I AIT). Sometimes AIT is resistant to conventional treatment. Thyroidectomy was used in patients with AIT, but in patients who are thyrotoxic it may be hazardous. METHODS; Seven patients with AIT (6 type I and 1 type II, 5 men, 2 women, mean age 70 years [range, 60-82 years]) were prepared for total thyroidectomy with a short course of iopanoic acid (1 g/day orally for a mean of 13 days), an oral iodinated cholecystographic agent inhibiting 5'-deiodinase and causing a reduction in the peripheral conversion of thyroxine to triiodothyronine. Mean thyroid volume was 64 mL (range, 10-145 mL). RESULTS: Mean serum-free triiodothyronine levels decreased from 20 +/- 16.7 pmol/L to 6 +/- 2 pmol/L (P =.0004), whereas serum-free thyroxine values remained unchanged. Euthyroidism was rapidly (7-20 days) restored, allowing an uncomplicated total thyroidectomy in all patients and the ability to continue amiodarone therapy in 6 patients. None had increased surgical bleeding, recurrent nerve palsy, or hypoparathyroidism. No cardiovascular complications occurred. CONCLUSIONS: Iopanoic acid is an effective drug allowing rapid control of hyperthyroidism in AIT.

Aged↗
PubMed2004

Rapid preparation of severe uncontrolled thyrotoxicosis due to Graves' disease with Iopanoic acid--a case report.

PURPOSE: To report the rapid preoperative preparation of a case of thyrotoxicosis due to Graves' disease resistant to medical treatment. CLINICAL FEATURES: A 14-yr-old boy presented with a history of progressive swelling in the neck. Signs and symptoms were compatible with hyperthyroidism. Thyroid function tests revealed: serum T4 296.5 nmol.L(-1), serum T3 6.06 nmol.L(-1) and serum thyroid-stimulating hormone < 0.15 mIU.L(-1). The diagnosis of thyrotoxicosis due to Graves' disease was made. Therapy was instituted with carbimazole 30 mg.day(-1) and propranolol 80 mg.day(-1), which were gradually increased to carbimazole 80 mg.day(-1) and propranolol 120 mg.day(-1), without response. Preparation was attempted by adding Iopanoic acid 500 mg four times a day and dexamethasone 0.5 mg four times a day in addition to the above drugs for five days. T3 levels declined to 1.8 nmol.L(-1), but the serum T4 remained elevated. Symptoms of hyperthyroidism persisted but with decreased intensity. As the patient could not be made euthyroid, surgery was planned to relieve the symptoms. Anesthesia was uneventful except for intraoperative and postoperative tachycardia, which was managed successfully with esmolol. CONCLUSION: In life threatening thyrotoxicosis refractory to medical treatment, Iopanoic acid may be used as an adjuvant to antithyroid drugs for rapid preparation of the patient prior to surgery.

Adolescent↗
PubMedDate not supplied

The biliary and urinary excretion of sodium tyropanoate and sodium ipodate in dogs: pharmacokinetics, influence of bile salts and choleretic effects with comparison to iopanoic acid.

The biliary and urinary excretion of sodium tyropanoate (Bilopaque) and sodium ipodate (Oragrafin) were studied in unanesthetized bile-fistula dogs using stepwise, increasing, intravenous infusions of the contrast materials. A constant intravenous infusion of sodium taurocholate was administered at the rate of either 0.5 or 2.0 mu moles per min per kg throughout each experiment. The biliary excretion of sodium tyropanoate or sodium ipodate was not effected by the rate of sodium taurocholate infusion. The maximum rate of biliary excretion of sodium ipodate was significantly greater than that of sodium tyropanoate with the low taurocholate infusion, but there was no significant difference between the two with the high taurocholate infusion. With the low taurocholate infusion the maximum biliary excretion rate of sodium tyropanoate (0.956 mu moles per min per kg) and sodium ipodate (1.472 mu moles per min per kg) were significantly greater than the maximum biliary excretion of iopanoic acid (Telepaque) (0.671 mu moles per min per kg). With the high taurocholate infusion the maximum biliary excretion rates of the three contrast agents were not statistically different. Both sodium tyropanoate and sodium ipodate produced an increase in canalicular bile flow (8-11 ml per millimole). These data suggest that in clinical cholecystography sodium tyropanoate and sodium ipodate are not excreted in bile more rapidly than iopanoic acid, except when the rate of biliary excretion of bile salts is low; that is, except in patients who are fasting or those who are on a fat-free diet.

Animals↗
PubMedDate not supplied

Rapid assay of iopanoic acid in dog plasma using a Hisep column.

A rapid method for the determination of iopanoic acid (IOP) in dog plasma utilizing a Hisep column was developed. A mobile phase of 12% methanol, 88% 0.05 M phosphate buffer pH 3.4 yielded a k' of 8.5 with no interference from proteins present in plasma. Recoveries of IOP from spiked plasma ranged from 97% to 103% at 270 mumol/L and 1.75 mmol/L respectively. Replication was +/- 2.8% at 1.75 mmol/L and +/- 6% at 21 mumol/L. A method utilizing 2,4,6-triiodobenzoic acid as internal standard was also developed for comparison.

Animals↗
PubMed1994

Inhibition of iodothyronine 5'-deiodinase by iopanoic acid does not block nuclear T3 accumulation during rat fetal development.

We studied the effect of iopanoic acid (IOP), an iodinated contrast medium, on iodothyronine 5'-deiodinase (5'D) and nuclear T3 content (nT3) in fetal tissues. In 18- and 20 day-old fetuses from control dams, nT3 was higher in interscapular brown adipose tissue (IBAT, 69 +/- 5 and 281 +/- 8 fmol/mg of DNA) than in brain (16 +/- 2 and 42 +/- 3 fmol/mg of DNA) or liver (5.6 +/- 1 and 27 +/- 2 fmol/mg of DNA). IOP administration (10 mg, twice daily) to pregnant rats on days 18 and 19 postconception significantly blocked 5'D activity in fetal IBAT and brain at day 20. Liver 5'D was not affected. The rise in nT3 was not modified by IOP treatment in IBAT, but it was enhanced in brain and liver of IOP-treated fetuses on day 20. In contrast, in adult rats, IOP treatment reduced IBAT nT3. Prolongation of IOP treatment until day 21 decreased fetal body weight on day 22 and inhibited IBAT 5'D. No change was produced in mitochondrial oxidative capacity, the subunit II of cytochrome oxidase, or uncoupling protein mRNA expression in IBAT from IOP-treated fetuses. Thus, the finding that IOP does not decrease the nT3 of fetal IBAT explains the lack of effect of IOP on uncoupling protein expression in fetuses, in contrast with the known decrease in adults. Present results also show that IOP increases nT3 in brain and liver, indicating a general incapacity of IOP to decrease nT3 in fetal tissues. It is concluded that the effects of IOP during fetal life differ from those in adults.

Adipose Tissue, Brown↗
PubMed2005

Effect of iopanoic acid on radioiodine therapy of hyperthyroidism: long-term outcome of a randomized controlled trial.

CONTEXT: Telepaque [iopanoic acid (IA)] is believed to rapidly ameliorate hyperthyroidism; however, it may preclude subsequent 131I therapy, possibly delaying it for several months. OBJECTIVE: Our objective was to see how early patients, made euthyroid with Telepaque, can be treated with 131I and to compare their short- and long-term outcome with patients treated with 131I, after making them euthyroid with carbimazole and beta-blockers. DESIGN: We conducted a randomized controlled trial. SETTING AND PATIENTS: We studied 200 hyperthyroid patients at a tertiary care teaching institute. INTERVENTIONS: The IA group received Telepaque, 500 mg/d orally, for 7 d and then no medication for 1 wk followed by 131I therapy if radioiodine neck uptake had recovered. The control group received 30-40 mg oral carbimazole daily until patients became euthyroid followed by 131I. MAIN OUTCOME: After 1 wk of Telepaque therapy and 6 wk of carbimazole, almost all patients became clinically and biochemically euthyroid, and 86 and 94% of patients were ready for 131I therapy after 1 and 2 wk off Telepaque, respectively. The cure rate, defined as euthyroid plus hypothyroid, after the first dose of 131I in controls and the IA group was 80 and 76.2%, respectively (P = 0.54). Thirty-two percent among controls and 25% in the IA group became hypothyroid within 1 yr (P = 0.33); thereafter, the annual rate of hypothyroidism was about 2% in both groups. After a mean follow-up duration of 11 yr, 58% of patients in the control group and 51% in the IA group were hypothyroid. CONCLUSIONS: Telepaque rapidly ameliorates hyperthyroidism without jeopardizing the subsequent radioiodine therapy, and the outcome of radioiodine therapy in this subset of patients is in no way different compared with those prepared by carbimazole.

Adult↗
PubMed1989

Iopanoic acid prevents spring premigratory increase in body weight of redheaded bunting Emberiza bruniceps.

Effects of long term administration of iopanoic acid (IOP), a potent inhibitor of peripheral conversion of thyroxine (T4) into triiodothyronine (T3), on body weight and gonad development in intact and in thyroidectomized (Thx) redheaded bunting that received replacement therapy with T4 were studied. IOP prevented the premigratory increase in body weight observed in intact bunting (during March/April). In contrast to the Thx birds receiving T4 only, IOP administration in combination with T4 caused a significant decrease in body weight of Thx birds. The gonad development in intact and Thx birds that received IOP was significantly inhibited. Results suggest that IOP through an effective inhibition of peripheral T4-monodeiodination may prevent the spring premigratory fattening. Emphasis is given for an important role of T3 in the physiological preparations associated with migration.

Animals↗
PubMed1984

Esters of iopanoic acid as liver-specific CT contrast agents: biodistribution and CT evaluation.

The synthesis and preliminary biodistribution data for a series of sterol-like esters of iopanoic acid having potential value as liver-specific CT contrast agents are described. Structural modification of the sterol portion of the iopanoate ester afforded a group of compounds that displayed tissue specificity similar to cholesteryl iopanoate, the prototype ester of this series, but were rapidly cleared from the target tissues after hydrolysis. From the biodistribution data, the most promising of these agents, pregnenolone iopanoate (PI), was evaluated by CT in rabbits receiving a radiologic dose equivalent to 30 mg I/kg. The hepatic parenchyma was enhanced within 2 h of infusion to a maximal level of 31 HU above precontrast values. Hepatic CT attenuation returned to normal within 24 h. However, CT performed after PI infusion into Vx2 tumor-bearing rabbits failed to provide superior images compared with those acquired following bolus administration of urographic contrast.

Adenocarcinoma↗
PubMed1990

Influence of chronic treatment with iopanoic acid on thyroxine metabolism in the newborn rat.

Parameters of the peripheral metabolism of thyroxine (T4) were studied in the early postnatal period. Iopanoic acid (IOP) was administered to newborn rats that were either euthyroid or rendered hypothyroid in utero by propylthiouracil (PTU) or methimazole (MMI) administration to the mothers during gestation and injected with thyroxine on postnatal days 6 and 7. In euthyroid newborn rats given IOP from postnatal day 6, the plasma T4 level increased (+50%) while the plasma 3,3',5'-triiodothyronine (T3) level slightly decreased (-18%). Peripheral deiodination of T4 was also reduced (about -50%) as estimated by thyroid 125I uptake after injection of 125I (3'-5')L-T4. In the newborn rats rendered hypothyroid in utero and given T4 on postnatal days 6 and 7, IOP treatment started on day 4 decreased the constant rate of elimination (-50%), the distribution volume (-43%) and the metabolic clearance (-74%) of plasma T4. The results were the same in PTU- and MMI-treated newborn rats. The differences between newborn and adult animals under IOP treatment are discussed.

Animals↗
PubMed1987

Effects of iopanoic acid on thyroid hormone receptor, growth hormone production, and triiodothyronine generation from thyroxine in pituitary GH1 cells.

We have studied the effect of iopanoic acid (IOP), a radiographic contrast agent which inhibits T4 to T3 conversion, on thyroid hormone nuclear receptors, GH response to T4 and T3, and T4 5'-monodeiodination in GH1 cells, a rat pituitary cell line. IOP at concentrations higher than 10 microM inhibits iodothyronine binding to the nuclear receptor without changing the dissociation constant (Kd) (0.1 nM for T3 and 1 nM for T4), and reduces the GH response to 50 nM T4, 5 nM T3, or the combined effect of T4 and glucocorticoids. These results could be explained by an inhibition of protein synthesis which was reduced by more than 50% by 50 microM IOP. By contrast, nontoxic concentrations of IOP did not change the GH response to different doses of T4 ranging from 1 nM to 50 nM. We also examined T3 generation from T4 and found that the intracellular T3 levels of cells incubated with 50 nM T4 were almost as high as those of cells incubated with 5 nM T3 which induces a full GH response. Intracellular T3 levels were markedly reduced in the cells incubated with T4 and IOP, but GH production was not reduced despite these differences in T3 levels. Additionally, more than 40% of the nuclear receptor was occupied by T3 in cells incubated with T4, whereas more than 90% was occupied by T4 in cells receiving the same amount of T4 with 5 microM IOP. Our results suggest that the effect of T4 on GH production by GH1 cells could be attributed to an important extent to the T3 generated from it, whereas when T4 monodeiodination is strongly inhibited, most of the biological activity is a result of intrinsic T4 activity.

Animals↗