Lack of association between thyroid function and mitral valve prolapse in Graves' disease.
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1. To determine whether the association between mitral valve prolapse and Graves' disease is related to thyroid function, three groups of individuals were studied: 16 patients with Graves' disease and hyperthyroidism (hyperthyroid: T4 greater than 11.5 micrograms/100 ml), 16 patients with Graves' disease without hyperthyroidism (euthyroid: T4 less than 11.5 micrograms/100 ml), and 40 healthy individuals. The three groups were similar in age, sex distribution, and anthropometrical characteristics. 2. All patients were evaluated clinically and by M-mode and two-dimensional echocardiography to determine the presence of mitral valve prolapse. 3. The frequency of mitral valve prolapse was similar in the hyperthyroid (31%) and euthyroid patients (25%), but was higher than in the normal individuals (5%). The frequency of systolic murmur was higher in the hyperthyroid patients (75%) than the euthyroid patients (19%) or the normal subjects (0%); however, the presence of a murmur was not associated with mitral valve prolapse. Hyperthyroid (13%) and euthyroid (13%) patients had a higher frequency of clicks than the normal individuals (0%), and the presence of click was associated with mitral valve prolapse. 4. Although patients with Graves' disease have a higher frequency of mitral valve prolapse, this is not associated with thyroid function. The presence of a click but not the presence of a systolic murmur may be a clinical indicator of mitral valve prolapse in Graves' disease.Keywords:
Mitral valve prolapse
Thyroid disease
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The status of thyroid function during the course of subacute thyroiditis has been assessed in 56 cases, 21 of which received no specific therapy to modify the natural course of the disease. In 11 very severe cases the initial extensive inflammatory necrosis presumably led to flooding of the body with thyroid hormone, thus producing symptoms of hyperthyroidism with a high level of serum protein-bound iodine (PBI), an increased basal metabolic rate and a profound depression of thyroidal I131 uptake to virtually zero. Following the acute phase the patient passed through a euthyroid interval into a phase characterized by symptoms of hypothyroidism with a low level of serum PBI. During the later part of this phase the ability of the gland to concentrate iodine began to increase. During the recovery phase, the thyroidal I131 uptake rose to levels above normal in a rebound phenomenon, whereas the serum PBI gradually rose to levels that did not exceed the normal range. In 15 moderately severe cases, the acute phase was similar in character but usually less severe. The thyroid glands of patients in this group were not sufficiently damaged to cause a hypothyroid phase. After the serum PBI level fell to a normal range, the ability of the gland to take up radioiodine also returned to normal, without the rebound phenomenon. In the 30 milder cases, there was neither a hyperthyroid nor a hypothyroid phase, but the thyroidal uptake of I131 was usually depressed for several weeks. In all cases there appeared to be complete recovery with no permanent sequelae. Roentgen-ray or cortisone therapy modified the symptoms greatly. However, the phase of temporary hypothyroidism was not averted by therapy in very severe cases, and it is difficult to be certain (because of individual variations) whether or not the total duration of the thyroiditis was shortened.
Subacute thyroiditis
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We investigated the interrelationship and the influence of thyroid-stimulating antibodies (TSAb), TSH-blocking antibodies (TSHBAb), and of radioiodine (131I)-induced thyroid damage in the early (within 1 yr) outcome of thyroid function in hyperthyroid patients with Graves’ disease (GD) treated with 131I. TSAb, TSHBAb, and ultrasound thyroid volume (as an index of thyroid damage) were simultaneously measured before and at 1, 3, 6, and 12 months after 131I in 31 GD patients. One year after radioiodine, 9.7% of patients were hyperthyroid (Hyper-group), requiring methimazole; 12.9% were euthyroid (Eu-group); and 77.4% were hypothyroid (Hypo-group). Pretreatment thyroid volume in the Eu-group and Hyper-group was significantly greater (P = 0.009) than in the Hypo-group. Pre-131I TSAb levels were higher in the Hyper-group vs. the Hypo-group (P = 0.01) or the Eu-group (P = 0.03). A significant post-131I increase in TSAb levels occurred in 66% of patients developing hypothyroidism but not in those remaining hyperthyroid. After 131I, TSHBAb appeared in 7 patients, in all but one associated with high levels of TSAb. One year after radioiodine: 1) the mean percent reduction in thyroid volume was greater in the Hypo-group (80.7%) or the Eu-group (83.5%) than in the Hyper-group (35.7%) (P = 0.007 and 0.033, respectively); 2) hypothyroid patients had smaller (P = 0.0058) post-131I thyroids than hyperthyroid patients; and 3) TSAb were still elevated in 75% hypothyroid patients, but all of them had a thyroid volume ≤8 mL, indicating major postradioiodine gland damage. In conclusion: 1) the early outcome of thyroid function after 131I for GD is mainly related to pretreatment thyroid volume and to the degree of its reduction after therapy; 2) high TSAb levels before 131I are associated with a relative resistance to therapy; 3) a postradioiodine increase in TSAb levels is related to the development of hypothyroidism; and 4) the concomitant appearance of TSHBAb and disappearance of TSAb are not frequent after 131I and play a role in the development of early postradioiodine hypothyroidism only in a minority of patients.
Thyroid Dysfunction
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In order to determine whether there are any predictive factors, other than the amount of remnant thyroid tissue, for subsequent thyroid function after subtotal thyroidectomy for Graves' disease, thyroid function was assessed in 329 patients 3 years after surgery, and a case control study was carried out in euthyroid, hyperthyroid, and hypothyroid groups by remnant-weight matched-pair analysis. Factors that affected thyroid function 3 years after surgery were thyroid gland infiltration by lymphocytes and the thyrotropin binding inhibiting immunoglobulin (TBII) value in the hyperthyroid and euthyroid groups, and the free triiodothyronine (FT3) value at the time of surgery and lymph follicle formation in the thyroid gland in the hypothyroid and euthyroid groups. It is concluded that no single factor studied at surgery, other than the amount of remnant tissue, can predict thyroid function after subtotal thyroidectomy for Graves' disease.
Wolff–Chaikoff effect
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Anti-thyroid autoantibodies
Wolff–Chaikoff effect
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This study investigated 1) the relationship between thyroid volume and thyroid function in radioactive iodine (RAI) treatment for Graves' disease, and 2) the activity of thyroid-related Ig in serum on the responsiveness of thyroid tissue to RAI. The changes in thyroid volume per megabecquerel (MBq) of 131I retained in thyroid tissue was calculated by ultrasonography as a quantitative indicator of the effect of RAI on thyroid volume. Of the 52 patients treated with 131I (3.7 MBq retained/g thyroid tissue), 26 patients showed thyrotoxicosis, 20 patients became euthyroid, and 6 patients developed hypothyroidism 6 months after therapy. The change in thyroid volume per MBq 131I was lower (P < 0.01) in the hyperthyroid patients than in the euthyroid or hypothyroid patients. The activity of thyroid-stimulating antibody in serum immediately before the therapy was greater (P < 0.01) in the hyperthyroid patients than in the euthyroid patients and was greater (P < 0.05) in the euthyroid patients than in the hypothyroid patients; it was inversely correlated with the changes in thyroid volume per MBq 131I (r = -0.667; P < 0.01). Accurate measurement of changes in thyroid volume during the course of RAI treatment provides evidence of the responsiveness of Graves' disease thyroid tissue to RAI, which is related to the outcome of thyroid function. Thyroid-stimulating antibody determination may be useful in deciding the appropriate dose of RAI to obtain euthyroidism instead of hyperthyroidism.
Wolff–Chaikoff effect
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Central congenital hypothyroidism (CH-C) in neonates born to mothers with inadequately treated Graves' disease usually needs T(4) supplementation. The thyroid and its regulatory system have not yet been extensively studied after T(4) withdrawal, until we observed disintegrated thyroid glands in some patients.The aim was to study the occurrence and pathogenesis of disintegrated thyroid glands in CH-C patients. DESIGN, SETTING, PATIENTS, PARTICIPANTS: Thyroid function was measured and thyroid ultrasound imaging was performed in 13 children with CH-C due to inadequately treated maternal Graves' disease after T(4)-supplementation withdrawal (group Aa). In addition, thyroid ultrasound imaging was performed in six children with CH-C born to inadequately treated mothers with Graves' disease, in whom T(4) supplementation was not withdrawn yet (group Ab) or never initiated (group Ac), in six euthyroid children born to adequately treated mothers with Graves' disease (group B), and in 10 T(4)-supplemented children with CH-C as part of multiple pituitary hormone deficiency (group C).Thyroid function and aspect (volume, echogenicity, echotexture) were measured.In group A, five children had developed thyroidal hypothyroidism characterized by persistently elevated TSH concentrations and exaggerated TSH responses after TRH stimulation. In the majority of patients in groups A and C, thyroid echogenicity and volume were decreased, and echotexture was inhomogeneous. Thyroid ultrasound imaging was normal in group B children.Inadequately treated maternal Graves' disease not only may lead to CH-C but also carries an, until now, unrecognized risk of thyroid disintegration in the offspring as well. We speculate that insufficient TSH secretion due to excessive maternal-fetal thyroid hormone transfer inhibits physiological growth and development of the child's thyroid.
Echogenicity
Congenital hypothyroidism
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The regulatory role of thyroid hormone on the adenyl cyclase-adenosine 3′,5′-monophosphate (cyclic AMP) system in human thyroid slices and plasma membranes from euthyroid subjects and thyrotoxic patients were studied by measuring the formation and accumulation of labeled and cold cyclic AMP. TSH stimulated adenyl cyclase-cyclic AMP system of the thyroid from euthyroid subjects and thyrotoxic patients, but the response was less in the thyroid from thyrotoxic patients. Small (10−9M) or large (10−4M) doses of thyroxin (T4) and triiodothyronine (T3) decreased the TSH-stimulated elevation of labeled and cold cyclic AMP level in the thyroid from euthyroid subjects. In contrast, graded doses of T4 (10−5 to 10−8M) and T3 (10−6 to 10−7M) failed to depress TSH-stimulated elevation of 3H cyclic AMP level in the thyroid from thyrotoxic patients. Large doses of T4 (10−4M) and T3 (10−4 and 10−5M) depressed TSH-stimulated adenyl cyclase activity, however. Since large doses of iodide and d-T4 have no effect on adenyl cyclase activity of the thyroid, and since T4 did not affect cyclic AMP accumulation of fat pads produced by catecholamine, it is suggested that thyroid hormones play an important role for the control of thyroid function through the depression of thyroidal adenyl cyclase-cyclic AMP system activated by TSH.
Thyroid-stimulating hormone
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Wolff–Chaikoff effect
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1. To determine whether the association between mitral valve prolapse and Graves' disease is related to thyroid function, three groups of individuals were studied: 16 patients with Graves' disease and hyperthyroidism (hyperthyroid: T4 greater than 11.5 micrograms/100 ml), 16 patients with Graves' disease without hyperthyroidism (euthyroid: T4 less than 11.5 micrograms/100 ml), and 40 healthy individuals. The three groups were similar in age, sex distribution, and anthropometrical characteristics. 2. All patients were evaluated clinically and by M-mode and two-dimensional echocardiography to determine the presence of mitral valve prolapse. 3. The frequency of mitral valve prolapse was similar in the hyperthyroid (31%) and euthyroid patients (25%), but was higher than in the normal individuals (5%). The frequency of systolic murmur was higher in the hyperthyroid patients (75%) than the euthyroid patients (19%) or the normal subjects (0%); however, the presence of a murmur was not associated with mitral valve prolapse. Hyperthyroid (13%) and euthyroid (13%) patients had a higher frequency of clicks than the normal individuals (0%), and the presence of click was associated with mitral valve prolapse. 4. Although patients with Graves' disease have a higher frequency of mitral valve prolapse, this is not associated with thyroid function. The presence of a click but not the presence of a systolic murmur may be a clinical indicator of mitral valve prolapse in Graves' disease.
Mitral valve prolapse
Thyroid disease
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SUMMARY To investigate further the relationship between thyroid hormones and thyroglobulin (TG) secretion, total and free thyroid hormone levels, TSH and its response to TRH and serum TG concentrations were determined in 61 patients with solitary autonomous thyroid nodules. Thyroid function varied widely from euthyroidism to clearcut thyrotoxicosis. Serum TG levels were significantly higher in patients than in normal controls. Individually they were above the normal range (> 50 ng/ml) in 95% of the patients, as well as in those with normal total and/or free thyroid hormone levels. Patients with high total and/or free thyroid hormone levels had higher TG concentrations than euthyroid patients. TG concentrations were significantly correlated with FT3 values. They were higher in patients in whom TSH was unresponsive to TRH than in the responsive groups. TG was also slightly higher in patients with hot nodules than in those with warm nodules. These data seem to indicate that TG is secreted along with thyroid hormones in the absence of any stimulatory action. It also is a sensitive index of thyroid hyperfunction. Twenty patients were controlled 6 months after nodulec‐tomy. TG levels, though significantly lower than in the preoperative state, were still higher than in normal subjects. This increase was attributed to persistent hyperthyroidism in two patients only. The observation that the increase in TSH after TRH stimulation in post‐operative patients was greater than that found in normal controls led us to believe that in most cases the high TG levels after surgery are due to stimulation of the normal thyroid tissue by rebound TSH secretion.
Thyroglobulin
Thyroid Nodules
Hypothalamic–pituitary–thyroid axis
Thyroid-stimulating hormone
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