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Urinary urgency and frequency and even enuresis may be manifestations of augmented adrenergic activity in hyperthyroidism, as are sweating, tremor, and tachycardia. Because patients rarely volunteer problems with urgency, frequency, and enuresis, it is worthwhile for the physician to inquire about such symptoms in patients with moderate to severe hyperthyroidism. Symptoms generally cease after treatment of the hyperthyroidism.
It is well established that bone turnover increases and bone resorption exceeds bone formation in patients with hyperthyroidism. Recently, urinary pyridinoline and deoxypyridinoline have been employed as indicators of bone resorption. In this study, urinary pyridinoline and deoxypyridinoline levels in fourteen female patients with untreated hyperthyroidism were measured and compared with levels in 134 healthy females. Values of urinary pyridinoline and deoxypyridinoline were significantly higher than in age-matched controls. Moreover, values of serum free triiodothyronine correlated with urinary pyridinoline (r = 0.769, p < 0.01), and urinary deoxypyridinoline (r = 0.799, p < 0.001) in patients with hyperthyroidism.
The effect of hypo- and hyperthyroidism on uterine and cervical collagen and glycosidases were studied in mature albino rats. Hypothyroidism significantly increased the salt-soluble, acid-soluble, insoluble and total collagen in the uterus and cervix. However, all of these collagens were significantly decreased in the hyperthyroid condition. The activities of alpha- and beta-galactosidases and glucosidases were significantly decreased in the uterus and cervix of hypothyroid rats, whereas, in hyperthyroid rats, all of these enzymes were significantly increased in the uterus and cervix. The data obtained in the present study suggested that the increase in lysosomal enzymes increased the degradation of uterine and cervical collagen. In contrast, the decrease in lysosomal enzymes in hypothyroid condition increased uterine and cervical collagen by decreasing degradation.
Thyroid disorders are associated to a number of vascular diseases that involve processes such as platelet aggregation and vascular tone control. Since, these processes can be also affected by ATP, ADP and adenosine levels, we investigate the hydrolysis of these nucleotides in platelets from hyperthyroid, hypothyroid, and hypothyroid with hormonal replacement rats. Hyperthyroidism was induced by daily injections of L-thyroxine (T4) 25 microg/100 g body weight for 14 days. Hypothyroidism was induced by thyroidectomy and methimazole (0.05%) for 14 days. In the hormonal replacement group, hypothyroid rats were injected with T4 (5 microg/100 g body weight, i.p.) for 5 days. The AMP hydrolysis by platelets was increased 49% in hyperthyroid rats and decreased 50% in response to hypothyroidism, while the ATP and ADP hydrolysis was not altered in both groups. Besides, the T4 replacement significantly reversed the inhibition of the AMP hydrolysis observed in hypothyroid rats. Our findings indicate that the thyroid disorders affect the 5'-nucleotidase activity and consequently can alter the adenosine levels in a reversible manner in platelet fraction. Since, adenosine is able to inhibit platelet aggregation and acts as a potent vasodilator, these results can contribute to a better comprehension of the vascular events described in thyroid disorders.
Liver microsomal functions related to xenobiotic biotransformation and free radical production were studied in control rats and in animals subjected to L-3,3',5-triiodothyronine (T3) and/or lindane administration as possible mechanisms contributing to oxidative stress, in relation to the activity of enzymes (superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G-6PDH)) and content of lipid-soluble vitamins (alpha-tocopherol, beta-carotene, and lycopene) affording antioxidant protection. Lindane treatment in euthyroid rats at a dosage of 20mg/kg did not modify the content of liver microsomal cytochromes P450 and b5, the activity of NADPH-cytochrome P450 reductase and NADH-cytochrome b5 reductase, and the production of superoxide radical (O2.-), as well as antioxidant systems, except for the reduction in lycopene levels. Hyperthyroidism elicited a calorigenic response and increased specific and molecular activities of NADPH-cytochrome P450 reductase, O2.- generation, and G-6PDH activity, concomitantly with diminution in liver SOD and catalase activities and in alpha-tocopherol, beta-carotene, and lycopene levels. The administration of lindane to hyperthyroid animals led to a further increase in the molecular activity of NADPH-cytochrome P450 reductase and in the O2.- production/SOD activity ratio, and decrease of hepatic alpha-tocopherol content, in a magnitude exceeding the sum of effects elicited by the separate treatments, as previously reported for reduced glutathione depletion. Collectively, these data support the contention that the increased susceptibility of the liver to the toxic effects of acute lindane treatment in hyperthyroid state is conditioned by potentiation of the hepatic oxidative stress status.
Although the thyroid gland can become overactive at any age, the syndrome of hyperthyroidism changes considerably in elderly persons. The principal reason is comorbidity. The patient over age 65 is much more likely than a young adult of 20 or 25 to have one or more preexisting disorders when the thyroid becomes overactive. In the elderly, therefore, the classic picture of hyperthyroidism--the constellation of irritability, sweating, palpitations without heart disease, weight loss despite good appetite, goiter, and warm, fine skin, familiar to all physicians--may never develop. Well before it might have appeared, a milder degree of thyroid hyperfunction may become manifest because of worsening of an underlying disease. Accordingly, the recognition of the thyroid disorder is often delayed. The purpose of this article is not so much to review hyperthyroidism as to delineate the special features found in geriatric patients and to describe a simple but effective scheme of evaluation.
This investigation was designed to compare in vitro dissolution profiles from sodium iodide capsules with radioiodide thyroid uptake in hyperthyroid cats using sodium iodide capsules prepared with a formulation exhibiting a complete release of radioiodide (I-123) in vitro and a formulation with an incomplete release of radioiodide. In vitro dissolution profiles for I-123 sodium iodide capsules with two different formulations were determined using the USP XXIII dissolution test. The two formulations studied in vitro were sodium phosphate dibasic powder with 1% magnesium stearate and calcium phosphate dibasic powder with 3% magnesium stearate. By 20 min after initiation of the dissolution test, over 95% of the I-123 was released from capsules of sodium phosphate dibasic powder. The capsules of calcium phosphate dibasic powder reached 75% at 65 min, with no further release occurring thereafter. There was a statistically significant difference in the dissolution profiles of the two formulations. The thyroid uptake of I-123 from capsules exhibiting complete release and incomplete release of radioiodide was determined in hyperthyroid cats. At 4 hr, the mean percentage thyroid uptake value for sodium phosphate dibasic powder with 1% magnesium stearate (complete release formulation) was 12.0% compared to 9.4% for calcium phosphate dibasic powder with 3% magnesium stearate (incomplete release formulation); at 24 hr, the values were 34.4% compared to 23.7%. The data suggest that the incomplete dissolution profile observed in vitro may correlate with a reduction in the bioavailability of the radioiodide in vivo. However, using the Wilcoxon signed rank test, statistically significant differences did not occur between the complete release formulation and incomplete release formulation at either 4 hr or 24 hr (p > .05). The results of the in vivo study with five hyperthyroid cats were not conclusive due to the variability in response between individual cats.
OBJECTIVE: To evaluate the role of lithium (Li) as an adjuvant in radioiodine therapy of hyperthyroidism. METHODS: A randomized controlled trial was carried out on 350 hyperthyroid patients with a mean follow-up period of 32.3 +/- 9.8 months (range, 12-60 months). The patients were randomized into two groups with 175 patients in each group: (1) radioiodine group (controls)-no lithium was given to these patients at any stage of their treatment and (2) radioiodine and lithium group (Li group)-lithium carbonate, 300 mg three times a day, for 3 weeks starting on the day of radioiodine administration. All patients were made euthyroid with antithyroid drugs prior to radioiodine therapy. RESULTS: Mean age was 41.8 +/- 11.5 years (range, 18-71) in the control group and 41.8 +/- 12.2 years (range, 19-73) in the Li group. Mean first dose and cumulative dose of (131)I were 229 +/- 85 MBq and 326 +/- 204 MBq in controls and 233 +/- 110 MBq and 344 +/- 281 MBq in the Li group. Average number of radioiodine therapy administered was the same (1.4) in both groups. The cure rate (euthyroid plus hypothyroid) after the first dose of radioiodine in the control and the lithium groups was 68.4% and 68.9%, respectively (p = ns). The overall cure rate at the end of the study was also the same in both groups (96.7% and 96.3%, respectively). Even in patients with a rapidly discharging gland or in patients with a large goiter, no significant statistical difference was observed in radioiodine therapy outcome between the two groups. Ten percent of the patients complained of mild to moderate side effects of lithium. CONCLUSION: The role of lithium as an adjuvant in radioiodine therapy of hyperthyroidism is insignificant.
Atrial fibrillation is often induced in patients with hyperthyroidism and may trigger heart failure. Its prevalence and outcome were examined to obtain up-to-date information. Persistent atrial fibrillation was observed in approximately 1.7% of new hyperthyroid patients. It occurs more frequently in males (2.86%) than in females (1.36%), even though the number of male hyperthyroid patients is only one fifth of female patients. The rate increased with age, being 8% in the patients older than 70 years old. The initial treatment is to control the heart rate with routine pharmacologic therapy and to start antithyroid therapy as quickly as possible. Attempted cardioversion should be deferred until approximately the fourth month of maintaining a euthyroid state, because more than 56% of atrial fibrillation spontaneously reverts to sinus rhythm when the thyroid hormone levels start to decline. Elective cardioversion for those whose atrial fibrillation persists is highly effective and sinus rhythm maintenance rates were 56.7% and 47.6% at the 10th and the 14th year, respectively, even though the duration of atrial fibrillation prior to cardioversion was extremely long (35.0 +/- 29.0 months).
Using noninvasive imaging, we have previously demonstrated that myocardial efficiency is impaired in hypothyroidism and improves after establishing euthyroid conditions. Little is known about the effects of abnormally elevated thyroid hormone exposure on cardiac metabolic performance. We studied 10 patients without evidence of heart disease in mild hyperthyroidism, and after therapy under euthyroid conditions. Cardiac oxidative metabolism was quantified by positron emission tomography with [(11)C]acetate. Left ventricular geometry was determined by cine magnetic resonance imaging. Myocardial efficiency, defined by the relation between work and oxygen consumption, was estimated using the work metabolic index [WMI = stroke volume * systolic blood pressure * heart rate/(oxidative metabolism * ventricular mass)]. In hyperthyroidism, heart rate and cardiac output were expectedly higher. Peripheral vascular resistance was reduced. Differences of blood pressure, stroke volume, and ventricular mass were not observed. Oxidative metabolism was significantly higher, but WMI was not different from the euthyroid state. In summary, while improvement of efficiency through thyroid hormone substitution was observed previously in hypothyroidism, our data in mild hyperthyroidism suggest an increase of oxygen consumption, paralleled by an increase of work. Thus, moderately elevated thyroid hormone levels neither result in further increase nor in reduction of cardiac metabolic performance.
Subclinical hyperthyroidism is a relatively common condition for which prospectively derived evidenced-based management guidelines do not exist. We have conducted a case-based mail survey to solicit opinions from members of the American Thyroid Association (ATA) about various issues that arise in the management of patients with this disorder. The survey was completed and returned by 185 of 300 (62%) of the original survey recipients. Four hypothetical cases varying in age, thyrotropin (TSH) level and underlying etiology were presented. The majority of respondents recommended further evaluation of all cases, most commonly choosing a radioactive iodine uptake (42%-71%), thyroid scan (39%-68%) and antithyroid (TPO/Tg) antibodies (49%-55%) as the additional tests to be ordered. The large majority (84%) recommended observation rather than active treatment for a young patient with a low but detectable serum TSH level. A small majority also recommended observation alone for a young woman with an undetectable serum TSH level (58%) and for an older woman with a low but detectable serum TSH value (63%). However, the majority (66%) favored treating an older woman with an undetectable serum TSH. When treatment was advised in the patients with subclinical hyperthyroidism, the respondents strongly favored anti-thyroid drugs when the etiology was Graves' disease and radioactive iodine when the etiology was toxic nodular thyroid disease. In the absence of adequate evidence-based guidelines, it is hoped that this survey of expert opinions may provide useful guidance for physicians providing care for patients with subclinical hyperthyroidism.
Severe hyperthyroidism is not included in the traditional differential diagnosis of ketoacidosis. However, thyroid hormone has well-documented lipolytic effects on adipocytes and may also promote hepatic beta-oxidation. We present a case in which a woman with severe hyperthyroidism developed otherwise unexplained ketoacidosis during the acute phase of her illness. We propose that thyrotoxicosis was a significant contributor to ketoacidosis in this patient and that severe hyperthyroidism should be added to the differential diagnosis of ketoacidosis.
We present the case of a 24-year-old woman with thymic enlargement accompanied by hyperthyroidism. An x-ray incidentally detected her thymic enlargement and the size was estimated to be 226 cm(3) by computed tomography (CT) using three-dimensional analysis. Physical examination revealed a soft diffuse goiter, increased sweating and restlessness; thyroid function tests showed hyperthyroidism. Because the possibility of a thymoma could not be completely excluded, a mediastinal biopsy via a supracervical approach was done that determined the specimen was composed of normal thymic tissue. Together with these findings, the patient's thymic enlargement was likely to be consistent with true thymic hyperplasia. Moreover, we have demonstrated the presence of the thyrotropin (TSH) receptor in her thymus using reverse transcription-polymerase chain reaction (RT-PCR). She was treated with methimazole, resulting in the resolution of not only the thyroid dysfunction but also thymic enlargement. Thymic enlargement has often been recognized as a complication of hyperthyroidism. However, the pathophysiologic mechanisms underlying these conditions remain obscure. Our result raises the speculation that the thymus is also a target organ of autoimmune attack as are the orbital and fibroblasts, which lead to Graves' ophthalmopathy and pretibial dermopathy, respectively.
Despite vast worldwide experience in the use of 131I for treating Graves' disease (GD), no consensus of opinion exists concerning the optimal method of dose calculation. In one of the most popular equations, the administered (131)I dose is directly proportional to the estimated thyroid gland volume and inversely proportional to the measured 24-hour radioiodine uptake. In this study, we compared the efficiency of different tissue-absorbed doses to induce euthyroidism or hypothyroidism within 1 year after radioiodine therapy in GD patients. The study was carried out in 134 GD patients (age, 53 +/- 14 year; range, 16-82 year; thyroid volume, 28 +/- 18 mL; range, 6-95 mL; average 24-hour thyroid uptake, 72%) treated with (131)I therapy. The average radioiodine activity administered to patients was 518 +/- 226 MBq (range, 111-1110). The corresponding average thyroid absorbed dose, calculated by a modified Medical Internal Radiation Dose (MIRD) equation was 376 +/- 258 Gy (range, 99-1683). One year after treatment, 58 patients (43%) were hypothyroid, 57 patients (43%) were euthyroid, and 19 patients (14%) remained hyperthyroid. The patients were divided into 3 groups: 150 Gy (n = 32), 300 Gy (n = 58) and >300 Gy (n = 44). No significant difference in the rate of recurrent hyperthyroidism was found among the 3 groups (150 Gy: 15%; 300 Gy: 14%; and > or =300 Gy: 14%; chi-square test, p = 0.72). Whereas, the rate of hypothyroidism in the 3 groups was significantly correlated with the dose (150 Gy: 30%; 300 Gy: 46%; >300 Gy: 71%; chi-square test, p = 0.0003). The results obtained in this study show no correlation between dose and outcome of radioiodine therapy (in terms of persistent hyperthyroidism) for thyroid absorbed doses > or =150 Gy, while confirming the relation between the thyroid absorbed dose and the incidence of hypothyroidism in GD patients.
We have previously described that sodium ipodate (500 mg/day, p.o.) is effective in normalizing serum T3 and T4 levels in most patients with Graves' hyperthyroidism. In this study, we examined serum T3, T4, and rT3 levels in 14 hyperthyroid patients with Graves' disease during treatment with a lower dose (500 mg, every other day, p.o.) of sodium ipodate for a period of 3-30 weeks (mean 15.5 weeks). Three types of responses were observed. In group I (4 patients), both serum T3 and T4 were in the normal range at the end of treatment [baseline: mean +/- SEM T3, 6.8 +/- 0.96 nmol/L (normal 0.92-3.0)] and T4 [256 +/- 44 nmol/L (normal 62-167); post-ipodate: T3, 2.0 +/- 0.46 nmol/L and T4 107 +/- 28 nmol/L]. In group II (n = 5), either serum T3 (3 patients) or serum T4 (2 patients) did not become normal (baseline: T3 7.7 +/- 1.1 and T4 228 +/- 3.9; post-ipodate: T3 2.9 +/- 0.57 and T4 188 +/- 27 nmol/L). In group III (5 patients), neither serum T3 nor serum T4 returned to normal following ipodate treatment (baseline: T3 11.9 +/- 1.8 and T4 260 +/- 23; post-ipodate: T3 7.5 +/- 0.49 and T4 322 +/- 17 nmol/L). The mean serum rT3 concentration increased during ipodate treatment to a peak value of 100% above baseline and remained elevated (20-75% above baseline) throughout the study. Some improvement in hyperthyroidism was suggested by increase in body weight during ipodate treatment in most cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Amiodarone (Cordarone) has been proven to be useful in the management of atrial fibrillation. However, because of a large iodine content, this drug is not used in this complication of thyrotoxicosis. We previously have observed a greater fall in serum T3 and T4 concentrations in hyperthyroid patients treated with amiodarone and methimazole than with methimazole alone. In the present study, we determined whether the addition of amiodarone to propylthiouracil (PTU) could improve the levels of circulating thyroid hormones in hyperthyroid patients, and we assessed the release of iodide from amiodarone by measuring the 24 h urinary iodine excretion. Twelve hyperthyroid patients were treated either with PTU, 600 mg daily for 10 days (group PTU), or with amiodarone (A), 1200 mg daily for 3 days in addition to PTU (group A-PTU). Basal serum T4, T3, and rT3 concentrations (mean +/- SEM) were respectively 206 +/- 13 nmol/L, 5.13 +/- 0.8 nmol/L, and 81 +/- 7 ng/dL for group PTU and 238 +/- 39 nmol/L, 4.73 +/- 1.06 nmol/L, and 84 +/- 12 ng/dL for group A-PTU (NS). In group A-PTU, plasma amiodarone peaked on day 3 (mean +/- SEM: 0.48 +/- 0.11 mg/L), and urinary iodine reached 5.27 +/- 1.28 mg/day on day 5. The fall in serum T3 and the increase in serum rT3 concentrations were significantly greater in group A-PTU than in group PTU (ANOVA, p less than 0.05). In group A-PTU, the minimal serum T3 concentration was observed on day 5 of treatment (28 +/- 6% of the pretreatment values).(ABSTRACT TRUNCATED AT 250 WORDS)
A recent article in the New England Journal of Medicine reported the successful diagnosis and treatment of fetal goitrous hypothyroidism in a mother with Graves' disease. The fetus is being recognized as an important patient in its own right in terms of thyroid disease. The fetal thyroid system develops independently of the normal maternal thyroid axis. Presence of feedback suppression of TSH by T4 has been demonstrated in a 35-week fetus. Information learned from congenital hypothyroidism suggests that lack of fetal thyroid hormones may have a negative impact on the developing fetal brain with lack of normal myelination. It is uncertain at what gestational age the fetus and the developing central nervous system become adversely affected by thyroid hormone deficiency. Since congenital hypothyroidism is sporadic and since there is no current method for easily screening all pregnancies for hypothyroidism, the thrust in fetal diagnosis and therapy has been in those pregnancies suspected of having a hypothyroid fetus when a fetal goiter is detected by ultrasonography or in a hyperthyroid mother who may be on antithyroid therapy. Intraamniotic injections of L-thyroxine have proven successful for fetal therapy. Amniotic fluid TSH may prove useful in the diagnosis and treatment of a hypothyroid fetus. Previous studies have suggested that the period of thyroxine dependency of the fetal central nervous system is limited predominantly to the last 4-8 weeks of gestation. Fetal hyperthyroidism due to transplacental transmission of thyroid-stimulating immunoglobulins may occur in a mother with a history of hyperthyroidism due to Graves' disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinically symptomatic osteoporosis and fractures from thyrotoxicosis have been rare since the availability of antithyroid drugs and radioiodine for the treatment of hyperthyroidism. However, the widespread use of bone density measurements and sensitive TSH assays in the past decade has demonstrated that women taking levothyroxine with subclinical hyperthyroidism have reduced bone density. Cortical bone is affected more than trabecular bone, and postmenopausal women are at a greater risk than premenopausal women. However, it is uncertain whether subclinical hyperthyroidism is associated with an increased risk of fracture. Hypothyroidism is associated with an increase in cortical bone width. The initiation of levothyroxine treatment in hypothyroid women results in a reduction in cortical bone width to levels seen in euthyroid controls after 6-12 months. There is no reduction in bone density when women with subclinical hypothyroidism are treated with levothyroxine for a year. A single study showing reduced bone density in patients receiving chronic levothyroxine replacement therapy requires confirmation and raises an important question: Does levothyroxine replacement therapy, which results in higher serum thyroxine concentrations than those seen in euthyroid controls, accurately mimic physiology?