A case of hypothyroidism with simultaneous presence of stimulating type anti-thyrotropin (TSH) receptor antibodies and anti-thyroxine (T4) autoantibodies.

We have examined a hypothyroid patient with stimulating type anti-thyrotropin (TSH) receptor antibodies and without blocking type anti-TSH receptor antibodies. Although she had high serum TSH (240 microU/ml) and low free triiodothyronine (FT3, 0.49 pg/ml) concentrations, which agree with physical findings of hypothyroidism, she had an unusually high free thyroxine (FT4) concentration (3.56 ng/dl). Incubation of her serum with 125I-T4, followed by precipitation with 12.5% polyethylene glycol (PEG) disclosed a higher binding of 125I-T4 (34.4%) than in normal controls, being 5-7%. In addition, binding of 125I-T4 to her serum gamma-globulin was completely displaced by the addition of unlabelled T4. From these results it was concluded that her serum contained anti-T4 autoantibodies. Treatment with synthetic T4 was begun and her thyroid function was monitored by sensitive TSH radioimmunoassay (RIA) and RIA of FT4 after PEG treatment. Since both sensitive TSH RIA and FT4 RIA results after PEG treatment give results concordant with the physical findings, it was concluded that both of the RIA results are useful for the evaluation of thyroid function in patients with thyroid hormone autoantibodies.     

Iodide-induced hypothyroidism in a patient with anorexia nervosa

A 39-year-old woman who had been suffering from anorexia nervosa was found to have hypothyroidism. Serum T4, free T4, T3, free T3 and TSH were 3.19 micrograms/dl, 0.5 ng/dl, 15.3 ng/dl, 1.2 pg/ml and 162.1 microU/ml, respectively. On careful questioning, she was found to have taken an iodine-rich diet. The serum iodine concentration was 122 micrograms/dl (normal: 4-9 micrograms/dl) and urinary iodide excretion was 13.05 mg/day (normal: less than 2 mg). After withdrawal of the iodine-rich diet, her serum T4 gradually increased and TSH returned to the normal range. She was diagnosed as having iodide-induced hypothyroidism. However, no significant elevation of serum T3 or free T3 was observed. Serum T4, free T4, T3, free T3 and TSH were 7.85 micrograms/dl, 0.8 ng/dl, 13.6 ng/dl, 4.3 pg/ml and 6.02 microU/ml, respectively. The iodide-perchlorate discharge test result was negative. These findings suggest that there exists some unknown mechanism by which a patient with anorexia nervosa may be sensitive to excess iodide. Furthermore, it is of interest to note that in a recovery phase from the hypothyroid state, normalization of serum T4 rather than T3 is well-correlated to TSH secretion.     

Thyroid dysfunction in adult long-term survivors after hemapoeitic stem-cell transplantation (HSCT).

Thyroid function was evaluated in 72 adult survivors (41 females and 31 males) at 16 to 56 years of age, 1.5 years mean time (range 0.2 - 9.8) after hemapoeitic stem cell transplantation (HSCT) with no known prior history of thyroid dysfunction. Thyroid stimulating hormone (TSH) and free thyroxin levels (FT4) were determined before and after stimulation with thyrotropin releasing hormone (TRH). Conditioning regimens for HSCT did not include TBI. Overt hypothyroidism (basal TSH > 8 microIU/ml, FT4 < 0.8 ng/dl) was observed in 6% of male patients and 5% of female patients; subclinical hypothyroidism (basal TSH 4 - 8 microIU/ml, low normal FT4 0.8 - 1.9 ng/dl) was observed in 13% of males and 5% of females. A significant number of euthyroid patients (40% males and 54% females) with normal basal TSH and FT4 levels overresponded to TRH stimulation; the finding being statistically significant (p < 0.005). A heavy TSH response after TRH stimulation indicates compensated subclinical dysfunction of the thyroid gland. Chemotherapy-only conditioning regimens may have an adverse effect on thyroid gland function not always detected by determination of basal TSH and FT4 levels. This finding warrants long-term evaluation of thyroid function in HSCT patients.     

A case of hypokalemic myopathy associated with transient hypothyroidism

A case of transient hypothyroidism in the course of hypokalemic myopathy is reported. A 69-year-old woman had severe muscle weakness and marked potassium deficiency associated with alkalosis during treatment with thiazide diuretics. The cause of muscle weakness proved to be hypokalemic myopathy confirmed by clinical findings and muscle biopsy. After the episode of hypokalemic myopathy, serum levels of thyroid hormone were lowered (T4; 3.8 micrograms/dl, T3; 54 ng/dl) and that of TSH was elevated (25.1 microU/ml). Antithyroid microsomal antibody was positive (1:25600) and anti-thyroglobulin antibody was negative. About one month after potassium supplement, her thyroid functions returned to normal, along with normalization of serum potassium level. This is the first documented case report of hypokalemic myopathy accompanied by transient hypothyroidism in a patient with autoimmune thyroiditis. We suggest that this transient hypothyroidism might be induced by hypokalemia during the course of autoimmune thyroiditis.     

Response of thyrotropin, prolactin and free thyroid hormones to graded exercise in normal male subjects

Serum levels of thyrotrophin (TSH), prolactin (PRL), free thyroxine (FT4) and free triiodothyronine (FT3) were determined before and after physical exercise in 21 normal male subjects. The subjects were divided into 3 groups as follows: group I--light exercise (exercise on the Mijnhardt bicycle ergometer at 100 Watts for 15 min); group II--moderate exercise (a 5 km marathon); group III--heavy exercise (a 10 km marathon). In group I, TSH level rose from 1.96 +/- 0.42 mu u/ml (mean +/- SEM) to 2.52 +/- 0.30 mu u/ml (p less than 0.01), and PRL levels rose from 11.0 +/- 2.0 ng/ml to 19.0 +/- 5.2 ng/ml (p less than 0.01). In group II, TSH rose from 2.11 +/- 0.51 mu u/ml to 2.62 +/- 0.56 mu u/ml (p less than 0.05), and PRL rose from 11.2 +/- 1.6 ng/ml to 24.0 +/- 5.2 ng/ml (p less than 0.01). In group III, TSH rose from 2.01 +/- 0.41 mu u/ml to 2.36 +/- 0.45 mu u/ml (p less than 0.02), and PRL rose from 12.1 +/- 2.0 ng/ml to 47.7 +/- 9.3 ng/ml (p less than 0.01). The serum levels of FT4 showed different results among the three groups: Group I showed an increased response from 1.60 +/- 0.12 ng/dl to 1.72 +/- 0.12 ng/dl (p less than 0.01); Group II showed no significant difference; and group III demonstrated a diminished response from 1.61 +/- 0.14 ng/dl to 1.45 +/- 0.16 ng/dl (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cold-induced changes in thyroid function in a poikilothermic mammal, the naked mole-rat

Cold acclimation induces very divergent responses in thyroid function in reptiles and mammals reflective of their different thermoregulatory modes. Naked mole-rats, unlike other small mammals, are unable to effectively employ endothermy and are operatively poikilotherms. We therefore investigated changes in their thyroid status with chronic cold exposure. Under simulated burrow conditions, free thyroxine (T(4); 0.39 +/- 0.09 ng/dl) and thyroid stimulating hormone (TSH; 1.12 +/- 0.56 microIU/ml) levels fell within the reptilian range, one order of magnitude lower than mammalian levels. However, cold induced typical mammalian responses: free T(4) levels (0.55 +/- 0.09 ng/dl) and thyroid follicular cell height were significantly greater. Although TSH levels (1.28 +/- 0.83 microIU/ml) were not significantly elevated, thyrotrophs exhibited ultrastructural signs of increased secretory activity. Low thyroid hormone concentrations may contribute substantially to the unusual thermoregulatory mode exhibited by naked mole-rats.     

In vitro study on release of thyroid hormone in solitary autonomously functioning thyroid nodules using cell culture method

In vitro release of thyroid hormone was investigated under basal and TSH-stimulated conditions in the solitary autonomously functioning thyroid nodules (AFTN). A small portion (0.5 g of wet weight) of the nodules and adjacent thyroid tissues removed surgically from five patients with solitary AFTN were prepared for the dispersed cell culture. In the experiment on non TSH-stimulated (basal) conditions, those culture media which were totally replaced on the 5th day after primary culture were utilized for the determination of thyroxine (T4) and triiodothyronine (T3) by radioimmunoassay. T4 and T3 levels in culture media of the functioning nodules were 1.15 +/- 0.33 microgram/dl (mean +/- SEM) and 2.72 +/- 0.68 ng/ml, contrasted with levels of 0.67 +/- 0.09 microgram/dl and 1.24 +/- 0.22 ng/ml in the paranodular tissues. The mean ratios of T3/T4 of the nodules and paranodular tissues were 0.25 +/- 0.02 and 0.19 +/- 0.02, respectively (p less than 0.05). Meanwhile, in another experiment under TSH stimulatory conditions employing 40 and 80 microU/ml of human TSH, there were no significant differences in T4 and T3 releases when the two groups were compared.     

Highly sensitive immunoradiometric assay for TSH and thyroid radioiodine uptake as predictors of thyroid suppression test

Suppression of TSH and thyroid radioiodine uptake by doses of either T4 or T3 were compared in 33 patients in whom Graves' thyrotoxicosis had been treated with thioamide drugs and the medication was discontinued for at least 4 months. Thyroidal radiodine uptake was suppressed in 19 patients and was not suppressed in the remaining 14 patients. Basal TSH levels before suppression were 2.07 microU/ml in the former, significantly exceeding those of the latter (0.91 microU/ml). A TSH level of at least 1.2 microU/ml before suppression is a good predictor of positive thyroid radioiodine suppression with a predictive value of 76%. A level lower than 0.7 microU/ml before suppression is a good predictor of negative thyroid radioiodine uptake suppression with a predictive value of 89%. The determination of TSH levels before the thyroid suppression test was helpful in predicting the result, but there were limitations. In the thyroid suppression test positive group, circulating T4 was depressed by doses of T3. In them, the magnitude of T4 depression correlated with the levels of thyroid radioiodine uptake before suppression. The levels of TSH correlated neither to changes in T4 nor to those in thyroid radioiodine uptake. This indicates that the thyroid glands which show high radioiodine uptake are sensitive to TSH and are also sensitive to suppression. The elevated sensitivity to TSH probably warrants the disappearance of abnormal thyroid stimulation more precisely.     

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familial thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3.4 +/- 0.9 microgram/dl, mean +/- SD. vs. 9.0 +/- 1.5 microgram/dl, p less than 0.01 and 87 +/- 27 ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs. 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 muU/ml) and the maximum TSH increments following TRH 500 microgram iv were 8.9 +/- 2.0 muU/ml and of no significant difference from the normal control (10.2 +/- 4.5 muU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.     

Hypothyroid myopathy with unusually high serum creatine kinase values

Depending on the degree of hormone deficiency, skeletal muscle involvement may occur in hypothyroidism. Usually, hypothyroid myopathy is associated with creatine kinase values <5,000 U/l. We report a 54-year-old man suffering from increasing fatigability, hoarseness, gait disturbances and a creatine kinase of 9,000 (normal: <80 U/l). He presented with bradyphrenia, macroglossia, dysarthria, myxedema, monoparesis, reduced deep tendon reflexes and stocking-type sensory disturbances. Free triiodthyronine was 0.25 pg/ml (normal: 0.6-1.9 pg/ml), free thyroxine <0.1 ng/dl (normal: 0. 6-1.8 ng/dl) and the thyroid-stimulating hormone >48.0 (normal: 0. 1-4.0 IU). Clinical neurologic examination and electromyography were compatible with myopathy and polyneuropathy. Other causes of myopathy, except hypothyroidism, were excluded. After L-thyroxine therapy (1.7 microg/kg BW/day) during 3 months, the patient's symptoms and signs vanished, except for sensory disturbances, and creatine kinase values and electromyography became normal. Severe hypothyroidism may be associated with highly elevated creatine kinase and myopathy. Adequate therapy leads to complete recovery, including myopathy.     

Assessment of the relationship between serum thyroid hormone levels and peripheral metabolism in patients with anorexia nervosa

It has been observed that basal and/or TRH-stimulated serum TSH levels occasionally conflict with the actual values of circulating thyroid hormones in patients with anorexia nervosa. In the present study sixteen female patients with anorexia nervosa during self-induced starvation displayed clinical findings suggesting hypothyroidism, e.g., cold intolerance, constipation, bradycardia, hypothermia and hypercholesterolemia in association with decreased serum total T3 (62.8 +/- 5.2 ng/dl) and T4 (6.6 +/- 0.3 micrograms/dl). Markedly decreased T3 correlated positively with average heart rate (r = 0.5655, P less than 0.025) and negatively with total cholesterol (r = -0.7413, P less than 0.005). This result may suggest that peripheral metabolic state of the underweight anorexics depends considerably upon the serum T3 concentration. Despite decreased total thyroid hormones, free T4 assayed by radioimmunoassay was normal in all five cases examined (1.4 +/- 0.2 ng/dl) and the free T4 index in fifteen cases was normal except in one case. Basal TSH was not increased and TSH response to exogenous TRH was not exaggerated in any. These results may be compatible with a theory that free T4 has a dominant influence on pituitary TSH secretion. Furthermore, glucocorticoids may also have some influence on depressed TSH response, because an inverse correlation between increased plasma cortisol and the sum of net TSH increase after TRH was observed in twelve cases examined. In conclusion, it is suggested that normal sensitivity of peripheral tissues and pituitary thyrotroph to different circulating thyroid hormones is maintained in anorexia nervosa patients even during severe self-induced starvation, and that the metabolic state in these patients is considerably under the influence of circulating T3.     

Valores de referencia y estudio de la variabilidad de hormonas tiroideas en gestantes de El Bierzo

Background and objectivesEl Bierzo area is characterized by low urinary iodine levels in the pregnant population. Guidelines recommend that local reference values are established for the diagnosis of thyroid dysfunction in pregnancy. Our objectives were to establish reference values for thyroid-stimulating hormone (TSH), free thyroxine (FT4) and free triiodothyronine (FT3) in women in the first trimester of pregnancy and to explore the factors influencing variability in these hormones.Patients and methodsA retrospective study of 412 women in the first trimester of pregnancy who were measured serum levels of TSH, FT4, and FT3; 163 women with conditions with a potential influence on thyroid function were excluded. Thirty smoking pregnant women were also excluded from the study of reference values. Factors examined in the variability study included age, body mass index (BMI), and smoking. A multifactorial analysis of covariance was performed.ResultsReference values in first-trimester pregnant women were: TSH: 0.497-3.595 mIU/L; FT4: 0.90–1.42 ng/dL; FT3: 2.49–3.56 pg/mL. TSH levels depended on mother age and on interaction between age and smoking. FT3 levels depended on the mother's BMI and smoking, and there was also an interaction between both factors.ConclusionThe reference values found may be used to assess thyroid dysfunction in pregnant women from El Bierzo. TSH and FT3 levels are influenced by age and BMI of the mother and by smoking, in addition to the interaction of these factors.     

Transient subclinical hypothyroidism in early pregnancy

In the present study, a new clinical state of transient subclinical hypothyroidism in 12 early pregnant women is documented. The incidence of transient subclinical hypothyroidism was 18 (0.19%) among 9,453 pregnant women examined in this series in Sapporo. The characteristics of transient subclinical early gestational hypothyroidism in our study may be summarized as follows: temporarily increased TSH in the blood (11.7 +/- 6.3 microU/ml; mean +/- S.D.) in early pregnant women at 8.5 +/- 2.4 weeks of gestation, accompanied with or without reduced FT4 which spontaneously return to normal at 17.9 +/- 7.1 weeks; no subjective complaints and no previous history of thyroid disease; small struma; positive titers of antimicrosome antibody and antithyroglobulin antibody; normal serum hCG; negative results for TSH receptor antibody. None of the infants show any physical abnormality such as struma and none of the patients had neck pain or fever suggesting subacute thyroiditis. The presence of autoantibody to the thyroid gland and echographical findings strongly suggest the existence of Hashimoto's thyroiditis in early pregnant women with transient subclinical hypothyroidism, although the cause of transient subclinical early gestational hypothyroidism remains obscure.     

Visfatin Levels in Subclinical Hypothyroidism

Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation abnormal thyroid function may be associated with disturbances in the production of adipokines also. Although there have been studies showing changes in visfatin levels in thyroid dysfunction, exact relationship between them was still unclear. Our aim was to evaluate serum concentrations of visfatin in patients with subclinical thyroid dysfunction before and after normalization of thyroid function tests. The study included 43 patients (mean age 50.1 ± 10.6 years) with subclinical hypothyroidism. Serum insulin, visfatin, TSH, free T4 (FT4) and free T3 (FT3) levels of subjects were analyzed. Visfatin levels were measured in all patients before starting therapy and after normalization of thyroid function. Serum visfatin levels of subclinical hypothyroid patients were 0.99 ± 0.45 and they were similar after normalization of thyroid function (p = 0.394). Serum visfatin levels were negatively correlated with FT4 levels before treatment (r = ?0.329 p < 0.05). There was no significant correlation between serum levels of visfatin and the serum levels of TSH and FT3. Serum visfatin levels did not correlate with insulin, fasting blood glucose, total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride levels. In this study, it was shown visfatin levels did not change after replacement therapy in patients with subclinical hypothyroidism. Subclinical hypothyroid state may be an earlier stage regarding the changes of adipocytokines specifically the visfatin secretion as seen in overt hypothyroidism.     

Thyroid hormone levels in the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex.

Hypothalamic-pituitary dysfunction and thyroid gland cytomegalovirus inclusions have been described in patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC). We evaluated 80 patients with AIDS or ARC for the frequency of hypothalamic-pituitary or thyroid gland failure and altered serum thyroid hormone levels due to nonthyroidal disorders. One patient had subclinical hypothyroidism. Of these patients, 60% had low free triiodothyronine (T3) index values and 4% had low free thyroxine (T4) indexes; none of the latter had hypothalamic-pituitary or thyroid gland failure, since all serum cortisol values were greater than or equal to 552 nmol per liter (greater than or equal to 20 micrograms per dl) and all thyrotropin levels were less than or equal to 3 mU per liter (less than or equal to 3 microU per ml), respectively. Those who died had lower total T4 and T3, free T3 index, and albumin levels than those discharged from hospital. Serum total T4 and T3 levels correlated with albumin levels and total T3 with serum sodium levels. Serum total T3 levels best predicted the outcome of the hospital stay (accuracy = 82%). Thus, abnormal serum thyroid hormone levels in AIDS or ARC patients are most frequently due to nonthyroidal disorders, but hypothalamic-pituitary or thyroid gland failure may occur.     

Thyroid function and antimicrosomal antibody during the course of silent thyroiditis

The thyroid function and antithyroidal antibody were studied in 17 patients with silent thyroiditis unrelated to pregnancy. The antimicrosomal hemagglutination antibody (MCHA) was negative in ten of them (group I) and was positive in seven (group II). At one month after the thyrotoxicosis, thyroid function became normal in both groups. At two months after the onset of thyrotoxicosis, in group I T4 (8.1 +/- 1.8 micrograms/dl, Mean +/- SD), T3 (113 +/- 25 ng/dl) and TSH were normal. At that time T4 (2.8 +/- 2.2 micrograms/dl) was significantly decreased (p less than 0.001) compared with those of group I and the levels of TSH were strikingly increased in 6 patients in group II. The level of T3 (96 +/- 29 ng/dl) in group II was not different from that of group I. Therefore MCHA was negative in patients who did not develop hypothyroidism and MCHA was positive in patients who developed hypothyroidism. The development of hypothyroidism two months after thyrotoxicosis and positive MCHA are correlated. The Tg was elevated in 7 out of 13 patients (54%) with negative antithyroglobulin hemagglutination antibody and in the remainder was normal during thyrotoxicosis. The discrepancy between the level of Tg and thyroid hormones was discussed.     

Blood-spotted filter paper measurements of thyroxine and thyroid-stimulating hormone in the follow-up of children with congenital hypothyroidism

Neonatal screening for congenital hypothyroidism using T4 and TSH measurements from blood-spotted filter paper is a well-established method. However, it has not been used to monitor T4 and TSH concentrations in the follow-up of these children. In 22 treated children with congenital hypothyroidism whom we follow up in our Clinic, T4 and TSH concentrations were concomitantly measured from venous blood and blood-spotted filter paper. There was a significant positive correlation between both T4 and TSH measurements from venous blood versus blood-spotted filter paper (r = 0.7, p = 0.001; r = 0.78, p less than 0.05). Filter paper T4 values above 7 micrograms/dl could exclude hypothyroxinemia in 98% of the specimens. When TSH values were above 10 microU/ml, it was confirmed in 94% of the specimens, and when they were above 20 microU/ml, it was confirmed in 97% of the specimens. Measurements of both filter paper T4 and filter paper TSH did not increase the reliability of the results obtained by examining the two hormones separately. We therefore suggest that filter paper T4 and/or TSH measurements have distinct advantages in monitoring the treatment of children with congenital hypothyroidism. It can be performed in the community, enabling assistance in the follow-up of children in remote areas who are unable to show up for serum tests. The results are obtained quickly and allow improved follow-up by providing useful information such as excluding hypothyroxinemia or suggesting the possibility of noncompliance, and by a psychological effect on parents. However, they cannot replace serum T4 and TSH measurements altogether.     

The pituitary-thyroid axis in patients with pituitary disorders

The pituitary-thyroid axis of 12 patients, exposed to transsphenoidal pituitary microsurgery because of nonfunctioning adenomas (6), prolactinomas (3) and craniopharyngioma (1), or to major pituitary injury (1 apoplexy, 1 accidental injury), was controlled more than 6 months following the incidents. The patients did not receive thyroid replacement therapy and were evaluated by measurement of the serum concentration of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), T3-resin uptake test and thyrotropin (TSH, IRMA method) before and after 200 micrograms thyrotropin releasing hormone (TRH) iv. The examination also included measurement of prolactin (PRL) and cortisol (C) in serum. Apart from 1 patient with pituitary apoplexy all had normal basal TSH levels and 9 showed a significant TSH response to TRH. Compared to 40 normal control subjects the 12 patients had significantly decreased levels of T4, T3 and rT3 (expressed in free indices), while the TSH levels showed no change. Five of the patients, studied before and following surgery, had all decreased and subnormal FT4I (free T4 index) after surgery, but unchanged FT3I and TSH. The levels of FT4I were positively correlated to both those of FT3I and FrT3I, but not to TSH. The TSH and thyroid hormone values showed no relationship to the levels of PRL or C of the patients exposed to surgery. It is concluded that the risk of hypothyroidism in patients exposed to pituitary microsurgery is not appearing from the TSH response to TRH, but from the thyroid hormone levels.     

Effect of subclinical hypothyroidism and obesity on whole-body and regional bone mineral content

OBJECTIVE: The present investigation was aimed to evaluate the effect of subclinical hypothyroidism and obesity on bone mineral content (BMC) in different body segments. METHODS: Thirty-two premenopausal women (age: 37 +/- 9.9 years), with a wide range in body mass index (BMI), were studied. Subclinical hypothyroidism was defined by a basal TSH > or = 4 microU/l and/or a TRH-stimulated peak > or = 30 microU/l. For each subject, weight, height, BMI (weight/height(2)) and the waist/hip ratio were measured. Total BMC, total bone mineral density (BMD), leg BMC, leg BMD, trunk BMC, trunk BMD, arm BMC and arm BMD were determined using dual-energy X-ray absorptiometry. Thyroid function (basal and TRH-stimulated TSH, free T(3) and free T(4)) were determined from fasting blood samples for all subjects. RESULTS: Anova was conducted within all the groups to observe the effect of thyroid status and/or obesity on BMC and BMD. There was no statistical difference for age. Total BMC was affected by obesity (p < 0.05) but not by thyroid status, BMD of the legs was significantly influenced both by thyroid function and obesity (p < 0.01); total BMD was affected by hypothyroid status (p < 0.05). A direct relationship between leg BMD and TSH was demonstrated. CONCLUSION: Subclinical thyroid hypofunction and obesity seem to affect BMD differently in the body segments. An influence of gravitational force seems necessary in order to make evident the effect of subclinical hypothyroidism on bone. A condition of subclinical hypothyroidism should be considered when evaluating subjects for osteoporosis, since a BMD measured at the femoral neck may induce underestimation of initial osteoporosis.     

Goiter and impairment of thyroid function in acromegalic patients: basal evaluation and follow-up.

AIMS: We evaluated morphological, biochemical and cytological thyroid parameters in acromegalic patients, investigated before and after treatment for acromegaly. PATIENTS: 28 acromegalics were investigated before and, in 18 cases, after 2-7 years of therapy. Fourteen patients were from areas of moderate iodine deficiency in Southern Italy. One patient underwent thyroidectomy before entering this study. RESULTS: 19 patients were euthyroid (FT4: 17.7 +/- 0.8 pmol/l and FT3 4.6 +/- 0.2 pmol/l), but TSH was undetectable in 5/19. Among them, TRH-stimulated TSH increase was absent/impaired or exaggerated/delayed in 9 and one cases, respectively. Decreased FT3 and/or FT4 values with low/normal TSH values were detected in 7 cases; TRH-stimulated TSH response was absent/impaired in 2 patients and exaggerated/delayed in another two. Increased free T4 and free T3 concentrations with undetectable TSH levels were found in one. Two euthyroid patients had high TPOAb levels. Goiter was diagnosed in 21 cases and nodules were found in 14/21. 99Tc scintiscan showed "cold" areas in 13/14 cases and a "hot" nodule in the hyperthyroid patient. Acromegalics from iodine deficient areas showed a not significant increase of prevalence of goiter (86 vs. 71 %) and of mean thyroid volume (35 +/- 7 vs. 28 +/- 4 ml, NS), compared to others. Thyroid volume (TV) did not correlate with GH, IGF-1 and TSH levels, the area under the curve of insulin-increase during OGTT, the age of patients or the duration of acromegaly. Fine needle aspiration biopsy (FNAB), performed in 11/14 patients with nodular goiter, showed colloid nodules in 8 cases, hyperplastic nodules in 2 and an adenomatous nodule in one. Neurosurgery, radiotherapy or medical treatment for acromegaly induced a significant decrease of mean GH and IGF-1 levels (21.5 +/- 8.5 vs. 12.9 +/- 9.6 ng/ml, p< 0.005 and 747 +/- 94 vs. 503 +/- 88 ng/ml, p < 0.02, respectively), but both GH and IGF-1 values normalized only in 3 cases. No significant variation of mean TSH levels was found. Although TV normalized in 3 patients, ultrasound evaluation showed a not significant decrease of mean TV and no changes in the diameter and number of nodules. FNAB was unchanged. CONCLUSIONS: Our results suggest that, despite no correlation between serum GH and IGF-1 levels and thyroid volume being found, a decrease in serum GH and IGF-1 levels has favourable effects on thyroid status.