In vivo assessment about the effects of a diet containing iodine-enriched foodstuffs. A pilot study in 30 volunteers.

BACKGROUND: Iodine deficiency (ID) still now represents one of the major worldwide health problems. ID is the result of insufficient dietary iodine intake. Iodine is an essential micronutrient but scarcely present in nature. The main strategy for the correction of ID is the fortification of table salt with iodide/iodine but Italy is far from reaching an iodized salt use higher 90% of population. Also because of the evidence for the risk on blood pressure, it is recommended to decrease the daily salt intake to less than 5 g/d. An opportunity to increase the iodine intake is the possibility to introduce iodine fortification in the industrial processing of foods. AIM: The aim was to evaluate the effectiveness of a diet containing iodized foods enriched during industry processing with protected iodized salt (Presal®). SUBJECTS AND METHODS: The evaluation of increasing of iodine intake was assessed by measuring the urinary iodine excretion (UIE) in 30 healthy volunteers who added to their alimentary habits a basket of iodine-enriched foodstuffs. RESULTS: Median UIE at baseline was 105 µg/l, 156 µg/l during the enriched diet and 90.5 µg/l a week after withdrawal of enriched diet. CONCLUSIONS: Stable iodized salt (Presal®) represents a good way to introduce iodine with the normal diet without increasing the normal consumption of salt for the healthy problems related to the blood pressure. The availability of stable iodized salt (Presal®) allows the preservation of iodine after cooking.

The size of the community rather than its geographical location better defines the risk of iodine deficiency: results of an extensive survey in Southern Italy.

AIM: The objective of this study was to establish the status of iodine nutrition in Southern Italy. MATERIAL AND METHODS: The survey was carried out on 11-14 yr old children attending primary school and living in urban and non urban areas of 8 regions of Southern Italy. Urinary iodine excretion (UIE) was measured in 23,103 urinary samples randomly collected. RESULTS: Median UIE in the whole studied population was 74 µg/l [interquartile range (IR) 34-139 µg/l]. UIE was significantly higher in chief towns compared to non chief towns (81 µg/l, IR 39-145 µg/l vs 73 µg/l, IR 33-138 µg/l, p<0.0001) and in areas with >500 inhabitants per km² (median 87 µg/l, IR 43-154 µg/l) compared to areas with 100-500 per km² (median 66 µg/l, IR 29-126 µg/l, p<0.0001) and with <100 per km² (median 61 µg/l, IR 25-121 µg/l, p<0.0001). Median UIE was significantly lower in inland mountainous/hilly areas (68 µg/l, IR 30-129 µg/l) compared to coastal mountainous/hilly areas (79 µg/l, IR 37-144 µg/l, p<0.0001) and lowland (79 µg/l, IR 37-146 µg/l, p<0.0001). According to a binary logistic regression model, population density was the only independent parameter significantly associated with UIE ≥ 100 µg/l. CONCLUSION: The results of the present survey indicate that: 1) in Southern Italy mild to moderate iodine deficiency is still present; 2) median UIE in non urban areas is lower than in urban areas and is related to the size of the community rather than to its geographical location, being higher in a larger community. This may be due to better diversification of dietary habits and the easier availability of iodized salt and processed food through commercial facilities, more common in larger communities. Future monitoring surveys should take into account these observations.

Amiodarone and the thyroid: a 2012 update.

Amiodarone-induced thyroid dysfunction occurs in 15-20% of amiodarone-treated patients. Amiodarone-induced hypothyroidism (AIH) does not pose relevant problems, is easily controlled by L-thyroxine replacement, and does not require amiodarone withdrawal. Most frequently AIH develops in patients with chronic autoimmune thyroiditis. Amiodarone- induced thyrotoxicosis (AIT) is most frequently due to destructive thyroiditis (type 2 AIT) causing discharge of thyroid hormones from the damaged, but otherwise substantially normal gland. Less frequently AIT is a form of hyperthyroidism (type 1 AIT) caused by the iodine load in a diseased gland (nodular goiter, Graves' disease). A clearcut differentiation between the two main forms is not always possible, despite recent diagnostic advances. As a matter of fact, mixed or indefinite forms do exist, contributed to by both thyroid damage and increased thyroid hormone synthesis. Treatment of type 1 (and mixed forms) AIT is based on the use of thionamides, a short course of potassium perchlorate and, if treatment is not rapidly effective, oral glucocorticoids. Glucocorticoids are the first-line treatment for type 2 AIT. Amiodarone should be discontinued, if feasible from a cardiac standpoint. Continuation of amiodarone has recently been associated with a delayed restoration of euthyroidism and a higher chance of recurrence after glucocorticoid withdrawal. Whether amiodarone treatment can be safely reinstituted after restoration of euthyroidism is still unknown. In rare cases of AIT resistance to standard treatments, or when a rapid restoration of euthyroidism is advisable, total thyroidectomy represents a valid alternative. Radioiodine treatment is usually not feasible due to the low thyroidal iodine uptake.

The effect of dietary iodine supplementation in dairy goats on milk production traits and milk iodine content.

Dairy products offer an important source of iodine for humans, particularly infants and children. An adequate iodine content in the diet of lactating animals must guarantee a suitable milk iodine concentration. In this experiment, the effects of iodine supplementation of dairy goat diets on the iodine concentration, milk yield, and milk composition of goat milk were studied. Thirty crossbred dairy goats of the Sarda population were divided into 3 groups supplemented with 0 (control group), 0.45 (group 1), or 0.90 (group 2) mg of KI/d per goat. The dose of KI (76.5% of iodine) was dissolved in water and orally administered with a syringe every day for 10 wk. Mean milk iodine concentrations were 60.1 +/- 50.5, 78.8 +/- 55.4, and 130.2 +/- 62.0 microg/L (mean +/- SD) in the control group, group 1, and group 2, respectively. The extent of iodine enrichment in milk was approximately 31% in group 1 and 117% in group 2 compared with the control group. Milk yield was not influenced by KI supplementation and averaged 1,229, 1,227, and 1,179 g/d in groups 0, 1, and 2, respectively. Milk urea nitrogen concentration was significantly lower in the KI-supplemented groups (32 and 33 mg/dL in groups 1 and 2, respectively) than in the control group (37 mg/dL). Iodine supplementation of dairy goat diets can increase milk iodine content without adverse effects on milk production traits.

Potassium perchlorate only temporarily restores euthyroidism in patients with amiodarone-induced hypothyroidism who continue amiodarone therapy.

CONTEXT: Amiodarone-induced hypothyroidism (AIH) may occur in patients with or without underlying thyroid disorders. In the latter, restoration of euthyroidism, after amiodarone discontinuation, can be facilitated and accelerated by a short course of potassium perchlorate (KClO4). However, it is unknown whether KClO4 may exert similar effects on thyroid function of AIH patients if amiodarone treatment is continued. OBJECTIVE: To evaluate the effects of KClO4 on thyroid function in AIH patients (without underlying thyroid disease) while continuing amiodarone treatment. DESIGN AND PATIENTS: An open, prospective study of 10 consecutive AIH patients without underlying thyroid abnormalities referred to a tertiary referral center, and treated with KClO4 (600 mg/day) for a period of 26+/-13 days (range, 15-45 days). An additional, historical group of 12 consecutive patients with subclinical AIH left untreated while continuing or after withdrawing amiodarone was retrospectively evaluated as to the outcome of thyroid function. MEASUREMENT: Serum free T4, free T3, and TSH concentrations were measured at booking, during KClO4 treatment and after withdrawing the drug. RESULTS: In the prospective study, KClO4 treatment restored euthyroidism in all patients within 28+/-11 days (range, 15-45 days). After KClO4 withdrawal, however, all patients became hypothyroid again after 45+/-15 days (range, 30-60 days). Two patients developed mild leukopenia (1 case) or a slight increase in serum creatinine levels (1 case), which promptly normalized after KClO4 withdrawal. In the historical group, followed for at least 12 months, euthyroidism was spontaneously and stably achieved after an average of 6 months in 5 patients in whom amiodarone could be discontinued, while subclinical hypothyroidism persisted in 7 patients in whom amiodarone had to be continued. CONCLUSIONS: KClO4 very effectively restores normal thyroid function in AIH patients without underlying thyroid abnormalities, despite the fact that amiodarone therapy is continued. However, euthyroidism does not persist after KClO4 is withdrawn; in addition, spontaneous recovery of euthyroidism does not seem to occur in this subset of AIH patients, unless amiodarone is discontinued. Therefore, also in view of its potential side-effects, KClO4 cannot be recommended as a first-line treatment for AIH if amiodarone needs to be continued, while LT4 replacement is recommended under these circumstances, with periodical reassessment of thyroid function.

Early abnormalities of left ventricular myocardial characteristics associated with subclinical hyperthyroidism.

The aim of the present study was to analyze heart function in subclinical hyperthyroidism (sHT) in otherwise healthy subjects by new methods using intramyocardial ultrasonic techniques. Twenty-four newly diagnosed and untreated sHT patients (20 women, 4 men; mean age: 42+/-4 yr) and 24 sex- and age-matched healthy volunteers were studied. All subjects were submitted to conventional 2D color-Doppler echocardiography, pulsed wave tissue Doppler imaging (PWTDI) for the analysis of diastolic function, color Doppler myocardial imaging (CDMI) for the analysis of regional strain and strain rate (SR) expression of regional myocardial deformability, and to integrated backscatter (IBS) for the evaluation of intrinsic contractility and tissue characterization. Regional myocardial systolic strain findings were significantly higher in sHT patients when compared with controls (p<0.001). Considering diastolic SR, the early phase of diastolic SR was compromised in sHT subjects as compared with controls (p<0.001). Cyclic variation index (CVI), expression of intrinsic contractility, was significantly higher in sHT subjects in comparison with controls (p<0.0001). IBS values were comparable between the 2 study groups. In conclusion, the present study suggests that in patients with sHT early systolic hyperdeformability and hypercontractility are present, together with impairment of both active and passive phases of diastole. On the contrary, no left ventricular hypertrophy or other structural alterations are documented.

Long-term outcome of thyroid function after amiodarone-induced thyrotoxicosis, as compared to subacute thyroiditis.

BACKGROUND: Two main forms of amiodarone- induced thyrotoxicosis (AIT) exist: type 1 AIT is a condition of true hyperthyroidism developing in patients with pre-existing thyroid disorders, and usually requires thyroid ablative treatment. On the other hand, type 2 AIT is a form of destructive thyroiditis occurring in normal thyroids, the management of which usually consists in glucocorticoid treatment. AIM: To assess the long-term outcome of thyroid function in a prospective study of type 2 AIT patients, as compared to patients with De Quervain's subacute thyroiditis (SAT). PATIENTS AND METHODS: Sixty consecutive patients with type 2 AIT were evaluated during oral glucocorticoid treatment (oral prednisone 30 mg/day, gradually tapered and withdrawn over a 3-month period) and followed for 38+/-4 months (range 6-72) thereafter. Sixty consecutive patients with SAT, referred to our Institutes during the same period and treated with the same therapeutic schedule, served as controls. RESULTS: Type 2 AIT patients were older (p<0.0001) and showed a larger male preponderance (M:F 3.6:1 vs 0.5:1, p<0.0001) than SAT patients. Mean serum free T4 (FT4) and free T3 (FT3) concentrations at diagnosis were increased in both conditions, but higher in type 2 AIT than in SAT (FT4 47.6+/-18.8 and 29.6+/-8.3 pmol/l, respectively, p<0.0001; FT3 15.4+/-7.0 and 11.2+/-3.0 pmol/l, respectively, p<0.001). Correction of thyrotoxicosis was obtained in all patients in both groups, but restoration of euthyroidism occurred earlier in SAT than in type 2 AIT (p=0.006). Ten type 2 AIT patients (17%) and 3 SAT patients (5%, p<0.03) became permanently hypothyroid after glucocorticoid withdrawal and required levothyroxine replacement. CONCLUSIONS: A relevant proportion of type 2 AIT patients develop permanent hypothyroidism after correction of thyrotoxicosis. Thus, periodic surveillance of thyroid status is required after type 2 AIT.

Enhanced susceptibility to amiodarone-induced hypothyroidism in patients with thyroid autoimmune disease.

BACKGROUND: The iodine-rich antiarrhythmic drug, amiodarone, can induce both thyrotoxicosis and hypothyroidism, the former being more frequent in iodine-deficient areas, the latter in iodine-sufficient areas. In this study we evaluated prospectively thyroid function in amiodarone-treated patients with positive or negative baseline thyroid autoantibody test results who resided in a moderately iodine-deficient area of Italy. SUBJECTS: Two groups of patients received long-term amiodarone treatment: Group 1 included 13 patients with negative thyroid autoantibody test results. Group 2 consisted of seven patients with positive thyroid autoantibody test results and thyroid ultrasound patterns compatible with Hashimoto's thyroiditis. The control group (group 3) included 16 untreated euthyroid patients with Hashimoto's thyroiditis. All subjects resided in a mildly iodine-deficient area of Italy (Southern Sardinia) and had low urinary iodine values. Patients in groups 1 and 2 had markedly elevated urinary iodine excretion during treatment. The follow-up period ranged from 6 to 29 months in group 1, from 4 to 9 months in group 2, and from 12 to 55 months in group 3. RESULTS: Two (15%) of 13 patients in group 1 with nodular goiter developed thyrotoxicosis. No patient in this group developed circulating thyroid autoantibodies. Five (71%) of seven patients in group 2 became hypothyroid after 4 to 9 months of amiodarone treatment associated with a rise in serum thyroid autoantibody levels. No patient in group 3 became hypothyroid. CONCLUSIONS: (1) Amiodarone administration can cause both thyrotoxicosis and hypothyroidism. (2) Hypothyroidism is far more frequent in patients with preexisting thyroid autoimmune disease. (3) Amiodarone can modify the natural history of Hashimoto's thyroiditis. (4) Circulating thyroid autoantibodies do not appear in amiodarone-treated patients who have negative test results prior to therapy.

Serum sex hormone-binding globulin in amiodarone-treated patients. A marker for tissue thyrotoxicosis.

The lodinated antiarrhythmic drug amiodarone frequently causes an elevation of the serum thyroxine (T4) level in patients who remain clinically euthyroid. Less frequently, true iodine-induced hyperthyroidism may occur. The clinical and laboratory distinction between these two conditions is often difficult. Since the serum sex hormone-binding globulin (SHBG) concentration is elevated in hyperthyroidism, this study was carried out to evaluate the serum SHBG concentration as a possible marker of hyperthyroidism in patients receiving amiodarone. Patients treated with amiodarone were divided into three groups: clinically euthyroid with normal serum T4 and triiodothyronine (T3) concentrations, clinically euthyroid with elevated serum T4 and normal T3 concentrations, and clinically hyperthyroid with elevated serum T4 and T3 concentrations. The mean serum SHBG concentration was significantly elevated in amiodarone-induced hyperthyroid patients, while it was normal in euthyroid patients treated with amiodarone who had normal or elevated serum T4 concentrations. The results suggest that the hyperthyroxinemia induced by amiodarone is not associated with excess thyroid hormone action in the liver unless the serum T3 concentration is also elevated.

Ontogeny of nyctohemeral variations of thyrotropin-releasing hormone in rat hypothalamus.

The ontogeny of nyctohemeral variations of hypothalamic TRH content was determined in male rats from 7-45 days after birth, exposed to a daily 12-h light, 12-h dark cycle (0600-1800 h light; 1800-0600 h dark) or maintained in complete darkness until 45 days. TRH was extracted from whole hypothalami with 90% methanol and assayed by specific RIA. Hypothalamic TRH extracted from rats at different ages showed immunological, chromatographic, and biological properties identical to those of synthetic TRH. No significant variations in hypothalamic TRH content during the day were observed in 7-, 10-, and 17-day-old rats; a significant change, with a maximal value at 1800 h, was observed in 23-day-old rats, while an adult pattern with a maximal value at 1200 h and a minimal value at 2400 h was found in rats of 31 days of age and became more evident in 45-day-old rats. In animals maintained in complete darkness for 45 days after birth, no significant changes in hypothalamic TRH content at 1200 and 2400 h were observed. These findings indicate that environmental cyclic light-dark exposure is required for the development of diurnal changes in hypothalamic TRH content. Furthermore, any study involving hypothalamic TRH determination should take into account the age of animals and the diurnal variations of TRH.

Serum interleukin-6 in amiodarone-induced thyrotoxicosis.

Amiodarone, an iodine-rich cardiac drug, may induce thyrotoxicosis (AIT), which can occur in patients with preexisting thyroid abnormalities and in subjects with apparently normal thyroid glands. The pathogenesis of AIT is often due to iodine-induced excessive thyroid hormone synthesis, especially in patients with underlying thyroid disease. In some instances, however, AIT may be related to a destructive process due to amiodarone-induced thyroiditis, resulting in thyroid cell damage and thyroid hormone release into the circulation. Another thyroid inflammatory process, subacute thyroiditis, has been recently reported to be associated with markedly increased serum interleukin-6 (IL-6) levels. To investigate the significance of serum IL-6 levels in AIT, we evaluated in a cross-sectional study the following subjects: 27 AIT patients, 15 with no apparent thyroid abnormalities (AIT-) and 12 with nodular goiter and/or thyroid autoimmune disease (AIT+); 14 euthyroid patients receiving chronic amiodarone therapy; 10 patients with amiodarone-induced hypothyroidism; 56 patients with spontaneous hyperthyroidism due to Graves' disease (n = 35) or toxic adenoma/nodular goiter (n = 21); 20 subjects with nontoxic goiter; and 50 healthy controls. Serum free thyroid hormone concentrations did not differ in patients with amiodarone-induced or spontaneous hyperthyroidism. Mean (+/- SE) serum IL-6 values were as follows: AIT-, 573.5 +/- 78.7 fmol/L (range, 149.4-1145.1); AIT+, 152.7 +/- 46.3 fmol/L (range, < 25-505.6); euthyroid patients receiving chronic amiodarone therapy, 51.4 +/- 10.0 fmol/L (range, < 25-122.5); amiodarone-induced hypothyroidism, 43.8 +/- 8.4 fmol/L (range, < 25-84.3); Graves' disease, 108.2 +/- 18.2 fmol/L (range, < 25-250); toxic adenoma/nodular goiter, 97.6 +/- 10.3 fmol/L (range, < 25-168.9); nontoxic goiter, 47.3 +/- 7.1 fmol/L (range, < 25-106.6); and controls, 37.8 +/- 6.2 fmol/L (range, < 25-99.4). Serum IL-6 values in AIT- patients were markedly higher (P < 0.0001) than those in all other groups. Values in AIT+, although slightly higher, did not significantly differ from those in patients with spontaneous hyperthyroidism. AIT- patients had low 24-h thyroidal radioiodine uptake (RAIU), whereas AIT+ had inappropriately low normal to high (9-58%) RAIU values in the presence of excess iodine. The presence of markedly elevated serum IL-6 concentrations and low thyroidal RAIU values in patients with AIT without underlying thyroid disease suggests the presence of amiodarone-induced thyroiditis as the etiology of thyrotoxicosis. Treatment of 2 such patients with prednisone was associated with a dramatic reduction and prompt normalization of IL-6 and thyroid hormone values.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of iodized salt on thyroid volume of children living in an area previously characterized by moderate iodine deficiency.

It is well established that an adequate iodine intake prevents iodine deficiency disorders. Prophylaxis through iodized salt is able to correct urinary iodine deficiency and to prevent goiter endemia, but scanty data are available about its effect on decreasing the thyroid size in goitrous children born before prophylaxis. The prevalence of goiter was evaluated by ultrasound in the school-children population of an area of Eastern Tuscany (Tiberina Valley) characterized by moderate iodine deficiency in 1985. At present, after the implementation of voluntary iodized salt consumption, iodine urinary excretion was borderline sufficient (median, 98 micrograms/L). Goiter prevalence was higher at ultrasound (17%) than by palpation (10%). The median thyroid volume ranged from 3.1 mL in 7-yr-old children to 9.2 mL in 14-yr-old children. In the 7-10 yr age class (i.e. in children born after iodine prophylaxis), no statistical difference in thyroid volume was found with respect to controls. In older children (11-14 yr) born before the institution of iodine prophylaxis, the median thyroid volume was significantly higher than that in age-matched controls. Moreover, in this cluster of subjects, the median thyroid volume in nongoitrous children was higher than that in controls. In conclusion, the data of the present study indicate that the iodized salt prophylaxis is able to prevent the development of goiter in children born after the implementation of iodized salt consumption and to further control thyroid enlargement in older children, but is less effective (or rapid) in reducing goiter size in children exposed to iodine deficiency in the first years of life.

Thyroid volume measurement by ultrasound in children as a tool for the assessment of mild iodine deficiency.

Thyroid ultrasound was used to measure thyroid volume in children and compared with thyroid palpation for the assessment of the prevalence of goiter in an area of mild iodine deficiency. School children, 6-14 yr old, were from control areas (n = 2693; urinary iodine excretion, 110 micrograms/L) or from an area of mild iodine deficiency (IDA; n = 278; urinary iodine excretion, 72 micrograms/L). Thyroid volume determined by ultrasound in control children increased with age (r = 0.62; P < 0.0001) and was significantly correlated with height (r = 0.51; P < 0.0001) and body weight (r = 0.126; P < 0.0001). Both median and mean thyroid volumes were greater in IDA children than in controls. The prevalence of goiter determined by ultrasound was 68 of 268 children (25.3%) in IDA and 105 of 2693 children (3.9%) in the control area (chi 2 = 204; P < 0.0001). Thyroid enlargement, as assessed by palpation, was found in 59 of 268 children (22%) in the IDA group and in 165 of 2693 (6.1%) subjects in the control area (chi 2 = 88; P < 0.0001). Some subjects of the IDA who were judged goitrous by palpation (11.2%) had a normal thyroid volume at ultrasound, and 12.7% of subjects with an abnormal thyroid volume at ultrasound were judged nongoitrous by palpation. In conclusion, 1) thyroid volume in children, as assessed by ultrasound, increases with age and is closely related to the parameters of body growth; 2) in every age group, thyroid ultrasound shows greater thyroid volume in an IDA group than in controls; and 3) a discrepancy between palpation and ultrasound is found in 23.9% of children living in an IDA, confirming that palpation is relatively inaccurate for assessing the prevalence of goiter in mild iodine deficiency. These data indicate that thyroid volume measurement by ultrasound in children provides a useful tool for the assessment of goiter in mild iodine deficiency.

Factors affecting suppression of endogenous thyrotropin secretion by thyroxine treatment: retrospective analysis in athyreotic and goitrous patients.

UNLABELLED: Factors affecting TSH suppression by L-T4 administration were retrospectively evaluated in 452 patients: 180 who were athyreotic after total thyroidectomy and remnant radioiodine ablation for differentiated thyroid carcinoma and 272 with nontoxic diffuse or nodular goiter. All patients were considered clinically euthyroid. TSH secretion was assessed by iv TRH stimulation testing. The T4 dose associated with an undetectable basal serum TSH level and no increase in serum TSH after TRH administration (suppressive dose) averaged 2.7 +/- 0.4 (SD) micrograms/kg body weight (BW)/day in athyreotic patients and 2.1 +/- 0.3 micrograms/kg BW/day in goitrous patients (P less than 0.001). The 25th-75th percentile intervals were 2.5-2.9 micrograms/kg BW/day for athyreotic patients and 1.9-2.3 micrograms/kg BW/day for goitrous patients. The suppressive dose of T4 was dependent in both groups on patient age, younger patients needing higher doses than older patients. The duration of treatment also proved to be an important parameter, since in both groups the percentage of patients with suppressed TSH secretion increased if TRH testing was carried out after at least 6 months after the initiation of therapy. Serum total T4, total T3, free T3 (FT3), free T4 (FT4) index, and FT3 index values did not differ in the two groups and were significantly higher (P less than 0.001) than in normal subjects. Mean serum FT4 was significantly higher in athyreotic patients than in goitrous patients with suppressed TSH secretion. Among athyreotic patients with suppressed TSH secretion, 24% had elevated serum FT4 and FT3, and 47% had elevated serum FT4 alone. Of goitrous patients with suppressed TSH secretion, 20% had elevated serum FT4 and FT3, and 27% had elevated serum FT4 alone. On the other hand, 35% of athyreotic patients and 14% of goitrous patients whose TSH secretion was not suppressed had elevated serum FT4. Serum sex hormone-binding globulin concentrations were measured in 3 groups of goitrous women. Values above normal limits were found in 13/26 patients (50%) with high serum FT4 and FT3, in 4/30 patients (13%) with elevated serum FT4 alone, and in 1/25 patients (4%) with normal FT4 and FT3. IN CONCLUSION: TSH suppression requires daily doses of T4 between 2.5 and 2.9 micrograms/kg BW in athyreotic patients and between 1.9 and 2.3 micrograms/kg BW in goitrous patients, with appropriate adjustments in relation to the age of the patient; Assessment of the adequacy of treatment should not be carried out before 6 months after the institution of therapy.

Evaluation of the nocturnal serum thyrotropin (TSH) surge, as assessed by TSH ultrasensitive assay, in patients receiving long term L-thyroxine suppression therapy and in patients with various thyroid disorders.

Circadian variations of serum TSH concentrations have been reported, with higher values occurring in the late evening or early morning. In patients receiving long term L-T4 suppression therapy, it may be important to achieve suppression of TSH secretion throughout the day. To investigate whether undetectable serum TSH values in the morning are associated with undetectable serum TSH levels at night, serum TSH concentrations were measured by an ultrasensitive immunoradiometric assay in 16 normal subjects, 20 hyperthyroid patients, 10 patients with primary hypothyroidism (either untreated or inadequately treated with L-T4), 1 patient with central hypothyroidism, 10 patients with nontoxic nodular goiter, 5 patients with functioning thyroid adenoma, 20 patients receiving L-T4 replacement therapy, and 30 patients receiving L-T4 suppression. In 6 subjects blood was drawn at hourly intervals for 24 h; in 2 normal subjects a major TSH surge occurred between 2300-0100 h, with other minor peaks, and the same pattern was found in two patients receiving L-T4 replacement, whereas in 2 patients receiving L-T4 suppression, serum TSH was constantly below the limit of detection of the assay (i.e. less than 0.07 mU/L). In the remaining patients blood was drawn at hourly intervals between 2300-0200 h and on the next morning before (0830-0900 h) and 30 min after iv TRH administration. In normal subjects, in patients receiving L-T4 replacement therapy, and in hypothyroid patients, serum TSH values at night were higher than in the morning, with normal responses to TRH in the first 2 groups and exaggerated responses in the latter. The patient with central hypothyroidism had no nocturnal TSH surge and no TSH response to TRH. In all hyperthyroid patients, serum TSH was undetectable both at night and during the day, and none had a serum TSH response to TRH. Among patients with nontoxic goiter, 7 had detectable serum TSH in the morning, with higher values at night, and a normal response to TRH; the remainder had undetectable serum TSH both at night and in the morning, and subnormal or absent TSH responses to TRH. All 5 patients with a functioning thyroid adenoma had undetectable serum TSH levels in the morning and during the night, and subnormal or absent TSH responses to TRH. Of the 30 patients receiving long term (greater than 6 months) L-T4 suppression therapy, 28 had undetectable serum TSH both during the night and in the morning and unresponsiveness to TRH.(ABSTRACT TRUNCATED AT 400 WORDS)

The spectrum of thyroid disorders in an iodine-deficient community: the Pescopagano survey.

We carefully assessed thyroid status and goiter by ultrasound in 1411 subjects virtually representing the entire resident population of Pescopagano, an iodine-deficient village of Southern Italy. Median urinary iodine excretion was 55 microg/L. The prevalence of goiter was 16.0% in children and 59.8% in adults. Thyroid nodularity was 0.5% in children and progressively increased with age to 28.5% in the 56- to 65-yr-old group. The prevalence of present or past hyperthyroidism was 2.9%, including 9 cases with toxic diffuse goiter and 20 with toxic nodular goiter. Functional autonomy was rare in children, progressively increased with age up to 15.4% in the elderly, and was related to nodular goiter. The prevalences of overt and subclinical hypothyroidism in the adults were 0.2% and 3.8%, respectively. Serum autoantibodies to thyroglobulin and thyroperoxidase were detected in 12.6% of the entire population. The prevalence of diffuse autoimmune thyroiditis was 3.5%, being very low in children. Thyroid cancer was found in only 1 case. In conclusion, in the present survey of an iodine-deficient community, a progressive increase with age of goiter prevalence, thyroid nodularity, and functional autonomy was observed. Hyperthyroidism was twice as high as that reported in iodine-sufficient areas, mainly due to an increased frequency of toxic nodular goiter. Although low titer serum thyroid antibodies were relatively frequent, the prevalences of both overt and subclinical autoimmune hypothyroidism were not different from those observed in iodine-sufficient areas.

Short term administration of potassium perchlorate restores euthyroidism in amiodarone iodine-induced hypothyroidism.

We studied the effect of potassium perchlorate (KClO4) in patients with hypothyroidism due to amiodarone. The short term administration of KClO4 to six such patients led to prompt restoration of euthyroidism, while the three untreated patients remained hypothyroid for 2-6 months. Since KClO4 inhibits thyroid iodide transport, thereby blocking further entrance of iodide into the thyroid and decreasing intrathyroidal iodide content, amiodarone-associated hypothyroidism is probably secondary to the inhibitory effect of excess intrathyroidal iodine on thyroid hormone synthesis.

Twenty-four hour radioactive iodine uptake in 35 patients with amiodarone associated thyrotoxicosis.

Amiodarone associated thyrotoxicosis (AAT) occurs in approximately 10% of patients treated with this iodine rich drug in areas of mild iodine deficiency. The thyroid radioactive iodine uptake (RAIU) is usually undetectable or very low in iodine-induced thyrotoxicosis. In the present study, 35 patients with AAT were evaluated. Twelve patients had no thyroid abnormalities by physical exam and all had 24-hr RAIU less than or equal to 4%. In contrast, nine of 11 patients with AAT and diffuse goiters and eight of 12 patients with AAT and nodular goiters had RAIU values greater than 8%. In patients with AAT and goiter it appears possible that the thyroid fails to adapt normally to the excess iodide load, resulting in an inappropriately high RAIU in the presence of excess plasma iodine.