The ingestion by normal subjects of 3 g of sodium iopodate, which is widely used in routine oral cholecystography, resulted in significant decreases of serum total and free T3 to a nadir on day 4 which averaged 43% and 40%, respectively, below initial mean values. Total and free rT3 increased markedly to a peak on day 3, 244% and 189%, respectively, above initial mean values. Total and free Ti and free T4 index rose to a maximum on day 4, but these changes were not statistically significant. A marked TSH increase was also seen, most evident on day 3. All these changes reverted to baseline values by day 14 at a time when serum total iodide was still markedly elevated. It is concluded that the changes observed after iopodate were not due to alterations in serum binding proteins nor to an effect on thyroid gland by the large iodine component of iopodate, but were consistent with an effect on the peripheral metabolism of T4. Difficulty in ipterpreting routine thyroid function tests may occur for up to 14 days after oral cholecystography with iopodate. Sodium iopodate is a contrast medium commonly used in oral cholecystography. Its chemical struc¬ ture bears some similarity to that of thyroxine (T4) and 61.4% of its weight consists of iodine. Wu et al. (1978) observed the effects of iopodate ingestion for a week and showed that serum 3, 5, 3' triiodothyronine (T3) decreased, 3, 3', 5' triiodothyronine (rT3) increased and T4 increased in euthyroid subjects. Similar changes were observed in thyrotoxic patients excepting that serum T4 decreased. They concluded that iopodate alters peripheral metabolism of T4 and, in thyrotoxicosis, it may decrease thyroid activity also.Because of its widespread use in clinical practice iopodate may commonly complicate the interpreta¬ tion of routine thyroid function tests. We therefore decided to document the magnitude and duration of such interference by observing the effects of oral iopodate on routine thyroid function tests. We also studied the effects on the serum concentrations of total and free rT3, free T3, free T4, thyroid stimu¬ lating hormone (TSH) and total iodide to help elucidate the mechanism of the interference. Subjects and MethodsSix healthy adult male volunteer subjects were studied whose average age was 25 years. Sodium iopodate was given in 3 separate 1 g oral doses between 09.00 and 12.00 h. Similar studies were conducted on two other healthy volunteers given an equivalent oral dose of iodine in the form of potassium iodide. Blood was sampled by venepuncture at 09.00 h on each day of observation namely 10 and 6 days before iopodate, on the day of taking iopodate and on days 1, 3, 4, 7, 14 and 21 after the doses. Samples were taken with minimal venostasis after the subjects had been sitting for 5 min. Serum was stored in aliquots and analyzed soon after the last sample was collected. All samples from each subject were analyzed in the same batch.Concentrations of total T4, total T3, rT» and the TSH were determined by specific radioimmunoassay (RIA) using second anti...
Serum biochemical tests were observed for about three weeks following oral cholecystography with fractionated high doses (6 g) of iopanoic acid (Telepaque) or sodium ipodate (Biloptin) in 24 and 29 patients, respectively. Both agents produced similar effects. No significant changes were seen in renal or hepatic function except for a mild increase in bilirubin on day 22. Serum urate decreased 10% on day 4, but the change was not significant. On days 4 and 11, there were significant increases in thyroid-stimulating hormone, thyroxine and free thyroxine index, and a moderate fall in triiodothyronine. Reverse triiodothyronine increased sharply on day 4. The pattern of changes observed suggests that these contrasts interfere with the extrathyroidal deiodination of iodothyronines. The temporary rise in thyroxine and free thyroxine index exceeded reference ranges in about half of all subjects, but they remained clinically euthyroid. Thyroid function tests should be interpreted with caution within three weeks of cholecystography.
Clinical and biochemical studies on a family in which 3 members have familial dysalbuminaemic hyperthyroxinaemia (FDH) are presented. They were clinically euthyroid with elevated serum thyroxine (T4) and free T4 indices but normal free T4 by equilibrium dialysis and normal serum triiodothyronine (total and free). All thyroid function tests on the remaining family members were normal. The inheritance is consistent with autosomal dominance. Also presented are data on 4 unrelated patients with FDH and two patients with T4 autoantibodies. The methods for detecting FDH, T4 antibodies and other causes of euthyroid hyperthyroxinaemia are now freely available. Since these anomalies may be more common than previously supposed, clinical awareness of the conditions is necessary to protect patients from the consequences of incorrect diagnosis of thyrotoxicosis.
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