Thyroidal 131I Uptake Research Articles

Thyroid dysfunction in patients with amyloid goitre.

Widespread amyloid deposition in the thyroid gland causes diffuse, clinically apparent enlargement of the thyroid (amyloid goitre: AG). The aim of this study was to clarify the abnormalities of thyroid function in patients with AG. Thirty patients with secondary amyloidosis were retrospectively analysed. Their thyroid status was evaluated using the results of routine thyroid function tests and measurement of thyroid autoantibodies. Thyroid needle biopsy was carried out to identify amyloid deposition in the thyroid gland. Thyroid enlargement was observed in 19 (63%) of 30 patients with amyloidosis. Eleven of these 19 patients had a thyroid biopsy and/or autopsy and amyloid deposition was histologically revealed in 10 (defined as AG) of these 11 patients. Nine of 10 patients (90%) with AG had abnormalities of thyroid function, including five patients with hypothyroidism, one with hyperthyroidism, one with transient hypothyroidism, and two with low T3 syndrome. Five had thyroid autoantibodies. The patient with hyperthyroidism had positive thyroid stimulating antibody (TSAb) and high 131I thyroidal uptake, suggesting the coexistence of Graves' disease. Another patient suffered from thyroidal pain and showed transient hypothyroidism, high level of serum thyroglobulin and low thyroidal uptake of 123I, the clinical course being compatible with subacute thyroiditis. The incidence of thyroid abnormalities accompanied by AG, although asymptomatic, is unexpectedly high. Thyroid function should therefore be regularly assessed during follow-up of patients with systemic amyloidosis.

Longitudinal study on goiter prevalence and goitrogen factors in northeastern Sicily

A longitudinal study was carried out in an area of endemic goiter of north-eastern Sicily. Three different surveys (in 1977, 1983 and 1994) evaluated the epidemiological prevalence of goiter in schoolchildren of the endemic area (towns of Bronte, Troina and Maniaci) in comparison to an iodine sufficient control area (Catania). Biochemical studies were also performed on urinary iodine and thiocyanate (SCN) excretion and 131I thyroid uptake. In the town of Troina an experimental program of active iodine prophylaxis was carried out from 1979 to 1987 by iodinating the municipal water supply. The aim of this study was to evaluate the effect of an active iodine prophylaxis program in comparison to the "silent iodoprophylaxis" due to improved economic conditions and widespread introduction of industrially produced food. In the 1977-94 period a significant decrease of goiter prevalence in schoolchildren was observed in all areas where no active iodoprophylaxis had been introduced. An abnormal prevalence of goiter, however, was still present in Bronte (12.1%) and Maniaci (25.9%) schoolchildren in respect to Catania (0.7%). In Troina, goiter prevalence decreased from 52.2 to 6.1% after only five years of active iodine prophylaxis (1983). It increased to 8.4% seven years after the program was discontinued (1994). In all areas studied average urinary iodine excretion increased by 70-100 micrograms/day except in the more rural area at Maniaci. During the same period urinary SCN values decreased by 30-40% and were lower in Troina (non volcanic soil) than in other towns studied. The balance between iodine and SCN intake appears a relevant factor in the etiology of endemic goiter in these areas and the iodine/SCN ratio inversely correlated with goiter prevalence. The persistence of endemic goiter in spite of the important changes in life style and socio-economic conditions if compared to the dramatic amelioration obtained by an active iodine prophylaxis program, confirms the inadequacy of the silent iodine prophylaxis, and further supports the need of an immediate introduction of active iodine prophylaxis in the areas of endemic goiter in Sicily.

Laboratory Tests Necessary at the First Examination of Patients with Suspected Thyroid Disorders.

In order to determine what and how many test items are necessary for the initial tests when examining patients with thyroid disorders, a questionnaire was sent to the council members of the Japan Thyroid Association. Thyroid disorders were divided into 4 categories; hyperthyroidism, hypothyroidism, diffuse goiter, and nodular goiter. The questionnaire was designed to assess: 1) tests routinely ordered at the initial examination; 2) minimum test battery necessary; 3) the 5 most important tests in order; and 4) selection of only 2 tests at most. The data on 112 completed questionnaires were collected and analyzed. When the choice was limited to only 2 tests, TSH and fT4 were commonly selected for hyperthyroidism hypothyroidism and diffuse goiter, but these 2 tests would be insufficient for the differentiation of disorders. In the case of nodular goiter, ultrasonogram and fine needle aspiration biopsy (FNA) were selected. The mean number of routinely ordered tests was 6.62 +/- 2.00 (S.D.) for hypothyroidism and 8.06 +/- 2.48 for nodular goiter, but many fewer tests were cited as absolutely necessary. In hyperthyroidism, 4.56 +/- 1.92 tests were required, in hypothyroidism 4.39 +/- 1.92, in diffuse goiter 4.93 +/- 1.75, and in nodular goiter 5.15 +/- 2.13. Most of the function-related tests, ultrasonogram and autoantibodies were commonly selected, while TBII and thyroid 123I or 99mTcO4 uptake in hyperthyroidism, and FNA, Tg and scintigram in nodular goiter were considered to be for specific purposes. Summarizing all these, the authors propose 5 or 6 tests to be necessary as the initial tests when examining patients with 4 individual thyroid disorders.

Antithyroid effects in vivo and in vitro of vitexin: a C-glucosylflavone in millet.

Millet diets rich in C-glycosylflavones (C-GF) are goitrogenic, and its three most abundant C-GF inhibit in vitro thyroid peroxidase, suggesting that these compounds are the goitrogens in millet. However, proof of a cause and effect relationship between C-GF and goitrogenesis requires a demonstration of in vivo antithyroid activity by the purified isolated compounds. Vitexin, one of the three major C-GF in millet, was used to test this hypothesis. Twenty-four female Wistar rats, divided into groups of six rats each and fed Purina iodine-rich diet (12 micrograms I-/day.rat), were administered acutely by gastrointestinal tube goitrogen-free water (controls), methimazole (0.5 mumol), and vitexin (20 and 80 mumol). 125I (1 microCi) was injected ip 1 h later, and the rats were killed 2 h after the injection. The thyroid glands were removed and analyzed for their content of total 125I and 125I-labeled compounds. Rats given vitexin, in contrast to those receiving methimazole, did not show suppressed thyroid 125I uptake. However, significant inhibition of the coupling mechanism (high 125I-labeled monoiodotyrosine plus diiodotyrosine/125T3 plus T4 ratio and low 125T3 and T4 concentrations) did occur with the highest dose of vitexin. These results provide direct evidence in vivo of C-GF antithyroid activity, strongly supporting the concept that C-GF are the goitrogens in millet.

Effect of humic acids on thyroidal function

Humic substances (HS) have been implicated as environmental goitrogens. Increased prevalence of goiter has been recently noticed in the blackfoot disease endemic area on the southwest coast of Taiwan, where well water is rich in HS. This study investigated the in vivo effects of humic acids (HA) on the thyroid gland of rats and mice. Groups of mice and rats were fed regular or moderately iodine deficient (approximately 167 vs 700 micrograms l- per kg) chow and distilled water or HA water (1mg/ml) for 3 or 4 months. Serum T4, T3, reverse T3, and/or TSH were measured by radioimmunoassay. Thyroidal 125I uptake was measured in mice at 2 h after injection of 1 microCi125I ip. Treatment of the rat with HA was associated with a significantly (p < 0.05) reduced serum T4 without a change in other parameters of study. Treatment with low iodine diet was associated with a clear increase in serum T3 and a decrease in serum rT3. Rats treated with both HA and low iodine diet showed a significantly reduced serum T4, increased serum T3 and decreased serum rT3. In mice, treatment with low iodine diet significantly increased thyroidal 125I uptake and additional treatment with HA significantly enhanced the effect of low iodine diet. Treatment with HA did not influence thyroid weight of rats or mice given normal or iodine deficient diets. We conclude that HA per se do not induce goiter, but they may enhance the goitrogenic effect of low iodine.

Reduction of Thyroid Hormone Levels and Alteration of Thyroid Function by Four Representative UDP-Glucuronosyltransferase Inducers in Rats

Male Sprague-Dawley rats (250-275 g) were fed diets containing four representative UDP-glucuronosyltransferase (UDP-GT) inducers, phenobarbital (PB), 3-methylcholanthrene (3MC), and pregnenolone-16α-carbonitrile (PCN), as well as a polychlorinated biphenyl (PCB) mixture for 21 days to determine their effect on thyroid hormone levels and thyroid gland function. On Days 3, 7, 14, and 20, blood was collected and serum levels of free and total thyroxine (T 4), free and total triiodothyronine (T 3), and thyroid-stimulating hormone (TSH) were determined by radioimmunoassay. On Day 21, following treatment with (Na 131I), the thyroid glands were removed and weighed, and the amount of 131I incorporated was determined. The livers were removed and microsomes were isolated for determination of T-4 UDP-GT activity. UDP-GT activity toward T 4 was increased by PB, 3MC, PCN, and PCB approximately 190, 290, 260, and 550%, respectively, per kilogram of body weight. PB, 3MC, and PCN reduced serum total and free T 4 30-40%, whereas PCB produced a 80-90% reduction. Total T 4 levels were slightly reduced by treatment with PB, PCN, and PCB, but none of the treatments decreased free T 3 levels. Serum T 4 levels (total and free) were found to correlate with UDP-GT activity toward T 4. The reductions in thyroid hormone levels led to an increase in TSH levels by PB, 3MC, PCN, and PCB (approximately 50, 50, 210, and 40%, respectively) on Day 20. The elevation of TSH led to an increase in thyroid gland weight by PCN (60%) and PCB (30%) and an increase in thyroidal 131I uptake by PB (60%), PCN (160%), and PCB (100%). Thus, while reasonable correlations between T 4 glucuronidation and reduction of serum T 4 can be made, only qualified correlations between reduction of T 4 and increase in TSH and increase in TSH and stimulation of the thyroid can be made. In conclusion, three classes of microsomal enzyme inducers, represented by PB, 3MC, PCN, as well as PCB, increase UDP-GT activity toward T 4 and decrease T 4 levels. It appears that induction of UDP-GT plays a role in the effect of these chemicals on the thyroid gland.

Iodide induced lymphocytic thyroiditis in the BB/W rat: evidence of direct toxic effects of iodide on thyroid subcellular structure.

A high dietary iodine intake accelerates the development of lymphocytic thyroiditis (LT) in the BB/W rat. Our previous studies have defined the temporal sequence of the immunological events triggered by excess iodide intake in these animals. It was still not clear, however, whether these observed immunological changes were a direct effect on immune effector cells, or whether they represented a secondary response to a toxic effect of iodine on thyroid tissue. In the present study, the effect of excessive iodine intake on the subcellular structure of the BB/W rat thyroid gland, particularly, whether iodide had a toxic effect independent of its immune response has been examined. BB/W rats were exposed, prenatally through maternal drinking water, to excessive iodide at two doses (Moderate 3 x 10(-6) M iodide/l; High 3 x 10(-3) M iodide/l); a third group of BB/W rats was given tap water; till 12 weeks postnatal age. Two groups of Wistar rats received high dose iodide water or tap water for the same period of time and served as controls. Thyroid gland ultrastructure was determined by electron microscopic (EM) examination. Thyroid 125I uptake and perchlorate discharge tests were also performed in separate experiments. We found that thyroid glands of non-iodine supplemented Wistar rats were morphlogically normal under EM. There were no overt changes in the iodide treated Wistar rats. By contrast, iodide treated BB/W rats exhibited marked accumulation of secondary lysosomes and lipid droplets; markedly swollen and disrupted mitochondria and extreme dilatation of rough endoplasmic reticulum (RER).(ABSTRACT TRUNCATED AT 250 WORDS)

The thyroid status of the Yanomamö Indians of southern Venezuela: 1992 update.

Previous reports described an apparent paradox in the clinical expression of endemic iodine deficiency in Amazonian Indians, who were severely iodine deficient but had no goiter and were clinically euthyroid. To confirm and explain this unique observation, we estimated the iodine intake and evaluated the functional and structural thyroid status of an isolated population of Yanomamö Indians (n = 104) in southern Venezuela. Twenty-six children, 32 adolescents, and 46 adults were studied with serum thyroid function tests, spot urinary iodide concentration determinations, and sonographic measurement of thyroid gland volume. A subset of adolescents and adults (n = 35) had 24-h fractional thyroidal 131I uptake determinations. No individual with goiter, clinical hypothyroidism, or cretinism was observed. Children had higher mean serum T4 (114.5 vs. 102.9 nmol/L; P < 0.02) and serum T3 (2.96 vs. 2.46 nmol/L; P < 0.02) concentrations than adults, with 2% and 50%, respectively, of children having levels more than 2 SD above the mean for a North American reference population. Serum TSH concentrations were also higher in children than adults (3.3 vs. 2.3 mU/L; P < 0.02), with 25% of the subjects above the reference range. Mean urinary iodide was 61 +/- 29 micrograms/L (range, 10-178 micrograms/L), reflecting borderline iodine sufficiency. Thyroidal 131I uptake values were 28 +/- 7%, with 33% above the upper limit of normal (30%). Compared to an iodine-replete Swedish population, the thyroid gland volume was above normal (> mean + 2 SD) in 71% of the study children. We conclude that the Yanomamö have borderline iodine deficiency, associated in children with predictably higher serum T3 and TSH concentrations and a high prevalence of small goiters. The basis for the apparent change in their dietary iodide intake over the past 30 yr is unclear, as is the explanation for their previously postulated resistance to goitrogenesis with more profound iodine deficiency.

The effects of hyperthyroidism on MIBG uptakes in the human heart--preliminary report.

Twelve cases of hyperthyroidism with cardiac manifestations (4 males, 8 females, ages: 20 to 70 years) and 12 normal controls of euthyroidism (6 males, 6 females, ages: 27 to 70 years) were included in our study. Each case accepted an I.V. injection of I-131 MIBG (I.R.E., Belgium) with 0.5mCi/1.7m2 of body surface area. The 24 and 48 hr imagings of the anterior chest, including total heart and lungs, were used to estimate cardiac sympathetic nerve innervation by the following formula: H/L = (the mean counts of pixels in the regions of interest (ROI) over the heart)/(the mean counts of pixels in the ROI over the lungs). The results showed that the 24 and 48 hr H/L values in euthyroidism were a little higher than those in hyperthyroidism, but the differences were not significant by a Wilcoxon rank sum test. The correlation between H/L and 24 hr I-131 thyroid uptake in patients with hyperthyroidism were also evaluated and the results showed no significant correlation between the H/L and uptake. In conclusion, we consider that the clinical manifestations concerning the heart in hyperthyroidism may not totally depend on the effects of increased cardiac sympathetic nerve innervation.

'Early' thyroid 123I uptake: correction for extrathyroidal neck radioactivity.

Should one correct for extrathyroidal neck radioactivity ('neck background') when interpreting perchlorate discharge test results? A new background correction method was developed using a linear probe. 123I produces photon peaks at two energy levels: 159 keV (gamma-rays) and 28 keV (X-rays), with an attenuation of 15 and 35% per cm water, respectively. If one fixes the position of the subject's neck, radiation from thyroid 123I produces an X/gamma detection ratio (alpha) which is constant and, due to the anterior localization of the thyroid, higher than the ratio (beta) produced by extrathyroidal 123I. These two ratios can be determined in vivo and used to calculate background-corrected and depth-corrected thyroid uptake. In simulation experiments our method was effective so long as the 'gland' was situated close enough to the 'neck' surface for the difference (alpha-beta) to be less than 0.19. Perchlorate discharge tests were performed in five euthyroid subjects who were pretreated with methimazole. The difference (alpha-beta) ranged from 0.27 to 0.36. Uncorrected, the mean discharge was 57% (range 47-66); corrected, it was 92% (range 88-94). In 15 hyperthyroid Graves' patients, with goitres varying from 13 to 63 ml, alpha-beta ranged from 0.22 to 0.40 and was unrelated to goitre size. The contribution of neck background is quantitatively important, especially when thyroid uptake is low; our new method corrects for it, even with large goitres.

Endocrine Toxicity of Drinking Water Disinfectants. I. In Vivo Dehalogenation and Clearance of Iodinated Nutrients

Ingestion of aqueous chlorine-based disinfectants has been shown earlier to cause decreased serum thyroxine levels and increased 131-I thyroid uptake in nonhuman primates. Disinfectants also were shown to immobilize iodine on gastric mucosa and cause covalent binding of dietary iodide to gastrointestinal contents in laboratory rodents. It has been demonstrated that nutrients in the presence of chlorine oxides, under conditions simulating the alimentary tract, effectively organify I- in vitro. A logical consequence of these is that traces of iodinated organics are absorbed after ingestion of drinking water disinfectants. Since over 100 million consumers receive a daily dose of about 0.4 mM of free chlorine, the pharmacotoxicology of such modified nutrient molecules is of public health interest. Therefore, we examined the in vivo deiodination of randomly in vitro iodinated organic mixtures prepared from different nutrients. Using adult female rats, we determined the 24-hour thyroid uptake of 125-I liberated from nutrients administered by gavage, relative to simultaneously ip-injected I131-. Also, 24-hour fecal and urinary clearances of the iodinated organics as well as tissue distributions were determined. The results showed that although various iodinated nutrient classes widely differed in their in vivo fate, most were dehalogenated effectively. Thus, their iodine content was returned as inorganic I- for thyroid uptake. It was also shown that tissue (blood, liver, intestinal, adipose, and muscle) distribution of the two isotopes did not differ significantly, suggesting that at 24 hours, the originally organic iodine existed in the tissues as inorganic I-. It is likely that oral exposure to chlorine-based disinfectants did not disturb the bioavailability of I-, and any thyroid effects caused were due to mechanisms other than I- deficiency.

Long‐term follow‐up of treatment of thyrotoxicosis by three different methods

In view of continuing debate regarding the best definitive therapy for thyrotoxicosis, we examined the long-term outcome of radioiodine (131I) or surgical treatment of 1918 thyrotoxic patients divided into three groups: those given 131I at a dose calculated from thyroid size, 131I uptake and effective half-life to administer a fixed radioactivity dose to the thyroid; those treated with a dose of 131I (110, 185 or 370 MBq) chosen empirically; and those treated by partial thyroidectomy. A minimum 10-year follow-up was achieved for 1119 patients treated with a calculated 131I dose; a single dose resulted in control of disease in 90.5%. At 5 years, 18% were hypothyroid, the prevalence rising to 42% at 20 years. Of 504 patients treated with an empirical 131I dose and followed for at least 5 years, thyrotoxicosis was controlled by a single dose in 89.7%. The rate of hypothyroidism at 5 years (38.5%) was higher than that found in the calculated dose group. A minimum 10-year follow-up was achieved for 295 surgically treated patients; thyrotoxicosis was controlled in 89.2%. The prevalence of hypothyroidism (2% at 5 years, 27.5% at 20 years) was lower than that found after 131I, whether given by calculated or empirical dose. Each of the treatments employed resulted in an acceptable rate of cure of thyrotoxicosis. If maintenance of euthyroidism is the major objective, our findings suggest that surgery represents the treatment of choice. Furthermore, calculated dose 131I administration has advantages in terms of risk of hypothyroidism over empirical dose treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Susceptibility to Subacute Thyroiditis Is Genetically Influenced: Familial Occurrence in Identical Twins

Subacute thyroiditis is thought to be virally induced in genetically predisposed individuals because a strong association has been suggested recently between HLA-B35 and patients in whom subacute thyroiditis has developed. Two identical twin brothers were seen at our clinic with the same symptoms and date of onset of hyperthyroidism and enlargement and tenderness of the thyroid, which gave us a unique opportunity to study the genetic predisposition and treatment of this thyroid disease. Diagnostic criteria for subacute thyroiditis were met in both twins, including hyperthyroxinemia, suppression of thyroidal 123I uptake, increased erythrocyte sedimentation rate, transient painful goiter, and absence of antimicrosomal antibodies. Twin B was treated with corticosteroids, and a nonsteroidal anti-inflammatory agent was prescribed for Twin A. The mode of treatment used did not make a difference in affecting the course of the disease. The erythrocyte sedimentation rate was normal after 2 months from onset of symptoms. Results of viral studies were inconclusive. The same HLA typing was found in each twin: A3, B18, B35, Cw4, DR2, DRw10, DQw1. Thus, each was heterozygous for HLA-B35. We reviewed the literature and found a strong association between HLA-B35 and subacute thyroiditis in various ethnic groups tested. Our experience with these identical twins provides additional evidence to suggest that HLA-35 and perhaps Cw4 confer genetic susceptibility in acquiring subacute painful thyroiditis in a possible dominant mode of inheritance.

A Case of Graves' Disease with False Hyperthyrotropinemia Who Developed Silent Thyroiditis.

We encountered a patient who developed silent thyroiditis during the course of Graves' disease. The diagnosis of silent thyroiditis was made on the basis of a low thyroidal 131I uptake, no response to the thyrotropin releasing hormone (TRH) test, and subsequent hypothyroidism despite the presence of high titers of thyrotropin (TSH) receptor antibody (TRAb) and thyroid stimulating antibody (TSAb). The patient, in addition, had a discrepancy between serum TSH and thyroid hormone values. This was due to the presence of interfering substances that react to mouse IgG in the sera since serum TSH levels were decreased in a dose dependent manner by the addition of increasing amounts of mouse IgG to the sera. It should therefore be noted that silent thyroiditis can develop in patients with Graves' disease. Furthermore, clinicians should be aware that two-site immunoassay kits that use mouse monoclonal antibodies are subject to interference by some substances, possibly antibodies which react to mouse IgG.

A Case of Progressive Systemic Sclerosis(PSS) with Silent Thyroiditis and Anti-Bovine Thyrotropin Antibodies.

We have examined a patient with progressive systemic sclerosis (PSS) who had increased serum T3 (235 ng/dl) and T4 (13.2 micrograms/dl) and low 24-h thyroidal 123I-uptake (1.2%). A diagnosis of silent thyroiditis was made on the basis of the clinical course and laboratory and histopathologic findings. Simultaneous measurement of serum anti-thyrotropin receptor antibody (TRAb) showed a negative value (-49.0%) which suggested the presence of anti-TSH antibody. Further examination by immune precipitation with 125I-bovine TSH (bTSH) and also with 125I-human TSH (hTSH) revealed the presence of anti-bTSH antibody but not anti-hTSH antibody in his serum gamma-globulin. The significance of the association of PSS, silent thyroiditis, and anti-bTSH in one individual is discussed.

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.

THYROID FUNCTION IN PATIENTS WITH MYOTONIC DYSTROPHY

In order to investigate endocrine disturbances in patients with myotonic dystrophy (MD), 12 patients and 20 normal controls were studied. All patients were clinically euthyroid and there were no significant differences between circulating levels (mean +/- SD) of T4 (114.7 +/- 26.8 vs 129.9 +/- 28.3 nmol/l), FT4 (16.6 +/- 4.5 vs 18.4 +/- 3.8 pmol/l), T3 (1.61 +/- 0.29 vs 1.86 +/- 0.33 pmol/l), TSH (2.7 +/- 1.3 vs 2.4 +/- 1.4 mU/l), TBG (26.7 +/- 5.5 vs 27.6 +/- 4.9 mg/l), T4/T3 (84.3 +/- 18.4 vs 82.1 +/- 15.3), and FT4/FT3 (0.28 +/- 0.05 vs 0.33 +/- 0.08). Serum FT3 (4.3 +/- 1.4 pmol/l) in patients were significantly lower than those (5.3 +/- 0.9 pmol/l) in normal controls (P less than 0.02). Thyroidal 131I-uptakes (8.7 +/- 4.3%) in patients were significantly lower than those (25.8 +/- 7.4%) in controls (P less than 0.01). The mean maximal TSH responses following TRH stimulation were significantly less in patients with MD (11.4 +/- 4.5 vs 17.0 +/- 6.2 mU/l; P less than 0.02). Neither circulating thyroid microsomal nor thyroglobulin antibodies were detectable in the 11 patients tested. Serum thyroglobulin concentrations were within the normal range in all patients but one. In conclusion, it is suggested that normal levels of serum T4, T3, FT4, TSH, TBG, T4/T3 and FT4/FT3, slight but significant decrease of serum FT3, reduced TSH response to TRH and a decrease of thyroidal radioiodine uptake might be due to a slight functional failure of TSH secretion in patients with myotonic dystrophy.

Studies on the T3 Suppression Test with Reference to the Thyrodial 123I Uptake in Graves' Disease: Comparison of 24-Hour and 3-Hour Uptake.

Eighty-three patients with Graves' disease had been treated with methylmercaptoimidazole (MMI). They were prescribed a maintenance dose of antithyroid drug (MMI, 5 mg/day) at the time of a T3 suppression test. The 3-hour and 24-hour thyroidal 123I uptake after T3 administration (75 micrograms/day, 2 weeks) were measured (post T3 uptake). In 38 patients whose post T3 uptake was below 35% in post T3 24-hour uptake, treatment was stopped. The T3 suppression test was then repeated 1 and 3 months later. During a one-year follow up, 26 remained well, while 12 relapsed within 6 to 12 months. We have observed a good correlation between 3-hour uptake and 24-hour uptake of 123I after T3 administration (r = 0.847, p less than 0.001). In 38 patients who showed positive T3 suppression, most patients with MMI withdrawal produced a marked overshoot of post T3 3-hour and 24-hour uptake at one month. Retrospective analysis indicated that there was no significant difference in circulating thyroid hormone levels between remission and relapse groups. The present study provides evidence that 3-hour uptake values are able to be substituted for 24-hour uptake values during a T3 suppression test. In addition, overshoot of thyroidal uptake after antithyroid drug withdrawal was observed in 3-hour values, similar to 24-hour values.

Hyperthyroidism and Thyroid Storm

Thyrotoxicosis and thyroid storm are disease states that result from thyroid hormone-induced hypermetabolism. The excess thyroid hormone is released from the thyroid gland as a result of excess thyroid hormone production, or by processes that disrupt the follicular structure of the gland with subsequent release of stored hormone. True hyperthyroidism results from increased synthesis and release of thyroid hormone and can be distinguished from other causes of thyrotoxicosis by the thyroid 131I uptake. Graves' disease is the most common cause of hyperthyroidism and occurs most often in women aged 30 to 50 years. The classic features of a patient with fully developed Graves' disease are difficult to overlook, but the clinical features of thyrotoxicosis vary with the etiology of the disease and the sensitivity of the patient's peripheral tissues. Thyroid storm presents with an exaggeration of the features of uncomplicated thyrotoxicosis and, in addition, an alteration in mental status. Thyroid storm may lead to irreversible cardiovascular collapse and death if proper treatment is not initiated in the Emergency Department. Specific therapy of hyperthyroidism follows several strategies, including inhibition of hormone synthesis and release, inhibition of peripheral conversion of T4 to T3, and blocking of the systemic effects of excess thyroid hormone. Treatments directed at these ends may be initiated rapidly in the emergency setting.

Studies on the effects of omeprazole on thyroid function in the rat.

The effects of omeprazole (an H+, K+ -ATPase inhibitor) on thyroid parameters in rats have been examined. SK&F Wistar rats were dosed orally with omeprazole (up to 500 mg kg-1) or vehicle. Treatment for 7 or 14 days resulted in generally decreased plasma T3 concentrations in males (with little change or slight increases in females) and increased serum TSH concentrations (22%-68% increases). No changes were detected in thyroid 125I uptake or organification. Liver 5'-deiodinase activity was decreased in male rats after 7 days treatment. Thyroxine clearance was not altered after a single dose of omeprazole. In-vitro studies showed omeprazole to be only a weak inhibitor of TSH-stimulated 125I organification in cultured porcine thyrocytes. It is concluded that omeprazole has weak effects on the pituitary-thyroid-liver axis, its main action being to inhibit the peripheral deiodination of thyroid hormones.