Because of lack of well-documented laboratory criteria, we assessed the usefulness of measuring free thyroxine (FT4) levels for monitoring levothyroxine replacement therapy in patients with central hypothyroidism. This consisted of a retrospective review from 1991-1997 of patient profiles extracted into a Macintosh 4th Dimension data base from the medical information system at a tertiary care biomedical research facility. Information was also retrieved from medical records of 135 ambulatory patients treated by 42 endocrinology practitioners, and 52 ambulatory patients treated by 20 endocrinology practitioners for central and primary hypothyroidism, respectively. Patient profiles were reviewed for most recent thyroid function test results and levothyroxine dosing information. Of 112 (83%) patients with central hypothyroidism who had FT4 levels within the laboratory's reference interval, only 2 had a dosage change. The FT4 concentration was concordant with physician-assessed thyroid status in 65 (82%) of 79 patients (95% CI 72-90, p<0.02) for whom clinical assessment was available in medical records. Thyrotropin, total thyroxine, and triiodothyronine levels were not significantly associated with clinical status (p>0.12) in patients with central hypothyroidism. Despite similar demographic and levothyroxine dosing profiles, patients with central hypothyroidism had significantly lower serum FT4 and thyrotropin concentrations than those with primary hypothyroidism. The appropriateness of levothyroxine replacement therapy in most patients with central hypothyroidism is reflected by a normal FT4 concentration measured with a valid assay. Whether midnormal or upper normal values are necessary for optimal therapy, and whether the therapeutic goal should be different in children than in adults, require prospective studies with independent, objective assessment of thyroid status.

The purposes of this study were to examine (a) the effects of acute exercise on metabolic rate 24 and 48 h postexercise and (b) the interaction of acute exercise and the thermic effect of caffeine on metabolic rate and hormonal changes during the late postexercise recovery period. In six young males, who were regular consumers of caffeine, resting energy expenditure was measured before and after caffeine (5 mg.kg-1) and placebo ingestion under the following conditions: (i) control (e.g., no prior exercise), (ii) 24 h postexercise, and (iii) 48 h postexercise. Blood samples were drawn for plasma glucose, insulin, glycerol, free fatty acids, catecholamines, and thyroid hormones (triiodothyronine, thyroxine, and free thyroxine). Results showed that acute exercise did not exert a detectable effect on resting metabolic rate in the late postexercise recovery period, that is, resting metabolic rate was similar among the conditions of control (1.17 +/- 0.12 kcal.min-1), 24 h postexercise (1.16 +/- 0.12), and 48 h postexercise (1.16 +/- 0.11). Caffeine ingestion increased metabolic rate (approximately 7%), but the thermic effect was not different among the experimental conditions. Plasma insulin and norepinephrine were lower after caffeine ingestion, whereas an increase in plasma free fatty acids was noted. Other hormones and substrates did not change significantly in response to caffeine ingestion. Furthermore, the hormonal and substrate milieu was not significantly different 24 and 48 h postexercise when compared with the control condition. Our results support the view that acute exercise does not alter the resting metabolic rate in the late postexercise recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)

This study investigated the effects of different stocking densities on growth and serum concentrations of thyroid hormones and cortisol in Amur sturgeon, Acipenser schrenckii. Fish were reared at low, medium, and high stocking densities (initial experimental densities were 0.30, 0.75, and 1.78 kg m(-2), respectively) for 70 days. The results showed that high stocking density had negative effects on growth and feeding efficiency, and altered serum levels of thyroid hormones and cortisol in Amur sturgeon. A significant decrease in specific growth rate was observed as stocking density was increased. The feeding rate decreased significantly in the medium and high density groups, indicating that high stocking density reduced the food consumption of sturgeon. Food conversion ratio increased with increasing stocking density, suggesting that high stocking density might inhibit fish growth through decreasing food conversion efficiency. Serum concentrations of total triiodothyronine, free thyroxine, and free triiodothyronine were inversely related to stocking densities, whereas serum total thyroxine level of sturgeon stocked at different densities remained stable. Also, higher stocking density resulted in an elevation of serum cortisol level, indicating that the sturgeon stocked at the higher density experienced density-dependent physiological stress. These results suggest growth suppression caused by high stocking density might be related to both crowding stress and the declines in peripheral circulating levels of thyroid hormones, as well as associated with the reductions in both food consumption and food conversion efficiency.

1. Iodothyronine 5'-deiodinase, which is mainly responsible for peripheral triiodothyronine (T3) production, has recently been demonstrated to be a selenium-containing enzyme. In the elderly, reduced peripheral conversion of thyroxine (T4) to T3 and overt hypothyroidism are frequently observed. 2. We measured serum selenium and erythrocyte glutathione peroxidase (as indices of selenium status), thyroid hormones and thyroid-stimulating hormone in 109 healthy euthyroid subjects (52 women, 57 men), carefully selected to exclude abnormally low thyroid hormone levels induced by acute or chronic diseases or calorie restriction. The subjects were subdivided into three age groups. To avoid conditions of under-nutrition or malnutrition, dietary records were obtained for a sample of 24 subjects, randomly selected and representative of the whole population for age and sex. 3. In order to properly assess the influence of selenium status on iodothyronine 5'-deiodinase type I activity, a double-blind placebo-controlled trial was also carried out on 36 elderly subjects, resident at a privately owned nursing home. 4. In the free-living population, a progressive reduction of the T3/T4 ratio (due to increased T4 levels) and of selenium and erythrocyte glutathione peroxidase activity was observed with advancing age. A highly significant linear correlation between T4, T3/T4 and selenium was observed in the population as a whole (for T4, R = -0.312, P < 0.002; for T3/T4 ratio, R = 0.32, P < 0.01) and in older subjects (for T4, R = -0.40, P < 0.05; for T3/T4 ratio, R = 0.54, P < 0.002). 5. The main result of the double-blind placebo-controlled trial was a significant improvement of selenium indices and a decrease in the T4 level in selenium-treated subjects; serum selenium, erythrocyte glutathione peroxidase activity and thyroid hormones did not change in placebo-treated subjects. 6. We concluded that selenium status influences thyroid hormones in the elderly, mainly modulating T4 levels.

Further examination of rat pituitary cell line GH3/C14 showed that at least the physiologic concentration of L-thyroxine was required for estrogen-dependent growth in vivo. Two L-thyroxine synthesis inhibitors, 6-n-propyl-2-thiouracil (propylthiouracil) and 1-methylimidazole-2-thiol (methimazole), were administered concurrently with estrogen to GH3/C14-inoculated hosts. Propylthiouracil administration to estrogen-treated males, intact females, and estrogen-treated ovariectomized females inhibited tumor formation by 93, greater than 95, and 68%, respectively, as compared to tumor formation in controls not treated with propylthiouracil. Methimazole treatment of estrogen-primed males and intact females inhibited tumor formation by 78 and 95%, respectively. Concentrations of total L-thyroxine and free L-thyroixine in sera from normal and inhibitor-treated hosts were depressed 70-80% by propylthiouracil and 60-70% by methimazole. Administration of either drug caused greater inhibition of tumor growth than of total body weight gain. In addition, the administration of a combination of L-thyroxine and L-triiodothyronine to male rats promoted tumor formation even in the absence of exogenous estrogen.

The prevalence of abnormal thyroid hormone levels in diabetes mellitus in Nigeria is not well described. To determine the incidence of abnormal thyroid hormone levels in diabetics in Calabar, Nigeria, fasting blood samples from 161 diabetic subjects and 105 non-diabetic controls were analysed. Free thyroxine (FT), thyroid stimulating hormone (TSH), total triiodothyronine (T(3)) and total thyroxine (T(4)) kits obtained from Biomerica Inc. of USA were used for the analysis. TSH levels (1.80±1.62) in diabetics were significantly lower (p=0.016) than the level in non-diabetic controls (2.34±1.24). Male diabetics had lower (p<0.05) levels of TSH (1.192±0.68 miu/ml) than diabetic females (1.90±1.70 mlu/mt). The level of T(3) in diabetic males (125±97ng/ml) was higher than the level in females (98±75ng/dl). TSH (F=2.74, p=0.049), T(4)(F=56.87, p=0.001), T(3)(F=56.44, P=0.001) in diabetics and FT(4) (F=5.74, p=0.002) in controls showed significant variation with the ages of the subjects. Out of 161 diabetics subjects studies 26.6% had low plasma thyroid hormone levels (FT(4)>2.01 ng/dl). This study has shown a high incidence (46.5%) of abnormal thyroid hormone levels among the diabetics in Nigeria (hypothyroidism 26.6%, hyperthyroidism, 19.9%). The prevalence of hypothyroidism was higher in women (16.8%) than in men (9.9%), while hyperthyroidism was higher in males (11%) than in females (8%). This study has defined thyroid function status of diabetics in Calabar, Nigeria probably the first of such work in Africa.

OBJECTIVE

It is known that thyroid hormones alter the bile acid metabolism in humans, however the effect on individual enzymes has been difficult to elucidate. This is mainly due to the lack of human liver cell lines producing bile acids. We used cultures of primary human hepatocytes to study the effects of triiodothyronine (T(3)) on bile acid synthesis.

METHODS

Primary hepatocytes were isolated from liver tissue obtained from three different patients undergoing liver resection due to underlying malignancy. The hepatocytes were cultured under serum-free conditions and treated from d 1 to d 5 with culture containing 0.1 - 1000 nmol/L of T(3). Bile acid formation and mRNA levels of key enzymes were analysed.

RESULTS

The lowest concentration of T(3) decreased cholic acid (CA) formation to 43%-53% of controls and chenodeoxycholic acid (CDCA) to 52%-75% of controls on d 5. The highest dose further decreased CA formation to 16%-48% of controls while CDCA formation remained at 50%-117% of controls. Expression of mRNA levels of cholesterol 7alpha-hydroxylase (CYP7A1) and sterol 12alpha-hydroxylase (CYP8B1) dose-dependently decreased. Sterol 27-hydroxylase (CYP27A1) levels also decreased, but not to the same extent.

CONCLUSIONS

T(3) dose-dependently decreased total bile acid formation in parallel with decreased expression of CYP7A1 and CYP8B1. CA formation is inhibited to a higher degree than CDCA, resulting in a marked decrease in the CA /CDCA ratio.

BACKGROUND

Hyperthyroidism is a common hormonal disorder in women that may cause female sexual dysfunction (FSD).

OBJECTIVE

To assess sexual function in women with hyperthyroidism.

METHODS

A total of 40 women with clinical hyperthyroidism and 40 age-matched voluntary healthy women controls were included in the study. All the subjects were evaluated with a detailed medical and sexual history, including a Female Sexual Function Index (FSFI) questionnaire for sexual status and the Beck Depression Inventory (BDI) for psychiatric assessment.

METHODS

The levels of serum thyroid-stimulating hormone (TSH), thyroid hormones, sex hormone binding globulin (SHBG), total testosterone (tT), free testosterone (fT), prolactin, estradiol, follicle-stimulating hormone, and luteinizing hormone were measured.

RESULTS

The mean total FSFI scores were 24.2 ± 9.96 in the hyperthyroidic group and 29 ± 10.4 in the control group (P < 0.0001). Desire (P < 0.040), arousal (P < 0.0001), lubrication (P < 0.0001), orgasm (P < 0.0001), satisfaction (P < 0.0001), and pain (P < 0.007) domain scores were also significantly lower in women with hyperthyroidism. The mean BDI score for hyperthyroidic patients was significantly greater than the score for the control group (P < 0.0001). The mean SHBG level in the hyperthyroidic group was found to be significantly higher than the level in the controls (P < 0.0001), whereas the mean fT level in the hyperthyroidic group was lower than in the control group (P < 0.0001). The FSFI score showed a significant negative correlation with the serum SHBG (r = -0.309, P = 0.005), free triiodothyronine (r = -0.353, P = 0.006) and free tetraiodothyronine (r = -0.305, P = 0.018) levels, BDI scores (r = -0.802, P = 0.0001) and positive correlation with tT (r = 0.284, P = 0.011), fT (r = 0.407, P = 0.001), and TSH (r = 0.615, P = 0.0001) levels.

CONCLUSIONS

A significant percentage of women with clinical hyperthyroidism had sexual dysfunction. Increased depressive symptoms, increased SHBG level, and decreased fT levels were all found to be associated with FSD in clinical hyperthyroidism.

The derangement of neuro-endocrine control of circulation influences both disease evolution and response to treatment in patients with heart failure, but little data are available about the complex relationships between the degree of neuro-hormonal activation and clinical severity. We studied the relationships between cardiac natriuretic hormones (CNHs) and several neuro-hormones and immunological markers in a prospective cohort of 105 consecutive patients with cardiomyopathy (77 men and 28 women, mean age 66.7+/-12.4 years, range 33-89 years). We assayed the circulating levels of CNHs (atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)), plasma renin activity (PRA), aldosterone, cortisol, adrenaline, noradrenaline, thyroid hormones and thyroid stimulating hormone (TSH), tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). The concentrations of all CNHs and neurohormones were higher in patients with heart failure compared to normal subjects, except for free triiodothyronine (FT3), which was below normal values. ANP was positively related to NYHA class, IL-6, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. BNP was positively related to age, NYHA class, IL-6, TNF-alpha, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. A stepwise multiple linear regression indicated that plasma ANP depended only on ejection fraction, adrenaline and noradrenaline values, while for plasma BNP variation NYHA class contributed too. Our data confirm a progressive activation of hormonal and immunological systems in patients with heart failure. Furthermore, CNH circulating levels in heart failure are affected not only by cardiac function and disease severity, but also by activation of neuro-hormonal and stress-related cytokine systems, as well as by the thyroid hormones, even on usual medical treatment.

To define metabolic influences on cardiac myosin expression and sarcoplasmic reticulum (SR) Ca(2+)-stimulated ATPase streptozotocin-diabetic rats were treated for 9-10 wk with etomoxir, an inhibitor of carnitine palmitoyl transferase I (CPT-1) and fatty acid synthesis, or an antilipolytic drug, acipimox. Etomoxir reduced myosin V3 of diabetic rats but did not normalize it. However, the high serum triglyceride, free-fatty acid and cholesterol concentrations in diabetic animals were greatly reduced. After bypassing the CPT-1 inhibition with a medium-chain fatty acid (miglyol) diet, the V3 contents and serum lipids were still reduced in the etomoxir-treated diabetic rats; V3 was also reduced in diabetic rats fed miglyol or treated with acipimox. Since low serum insulin or triiodothyronine concentrations in diabetic rats were not improved by these interventions but changes in V3 were correlated with those in triglyceride, free-fatty acid and cholesterol concentrations, it is likely that myosin may be influenced by some metabolic factors. To assess the role of adrenergic influences, diabetic rats (7-8 wk) were treated with an antisympathotonic drug, moxonidine, a beta-adrenoceptor blocking drug, propranolol, and a bradycardic drug, tedisamil. Myosin V3 was not reduced significantly in moxonidine-treated or propranolol-treated rats in comparison to untreated diabetic rats. Serum thyroid hormones and insulin were not altered, whereas triglycerides were reduced but not significantly by these antiadrenergic agents. Lowering serum lipids in diabetic rats by treatment with etomoxir, miglyol and acipimox increased the depressed SR Ca(2+)-stimulated ATPase activity. On the other hand, in diabetic rats treated with moxonidine, propranolol or tedisamil, the ATPase activity was not increased significantly. These results suggest that normalization of blood lipids is important for improving subcellular organelle function in diabetic hearts with impaired glucose utilization.

Serum concentrations of total and free thyroxine (T4 and FT4) and total and free triiodothyronine (T3 and FT3) were measured in normal pregnant women, in patients with toxemia of pregnancy, and in patients with gestational trophoblastic disease (GTD). In normal pregnancy, FT4 and FT3 levels remained normal while T4 and T3 levels were elevated. In patients with pre-eclampsia, the mean serum T3 concentration was significantly lower than that of normal pregnancy and the serum FT3 concentrations in three out of nine patients were below the normal pregnancy range. The mean serum T4 and FT4 concentrations in patients with pre-eclampsia were, however, significantly higher than those in normal pregnant women. In patients with GTD without signs of hyperthyroidism, the mean serum total and free T4 concentrations were 43 and 92% higher than those in normal pregnancy (P less than 0.02), and many patients had levels above the range of values observed in normal pregnant women. The mean serum total and free T3 concentrations in GTD patients without signs of hyperthyroidism were not different from those of normal pregnancy (P less than 0.05). In the single GTD patient with hyperthyroid crisis, the s. erum FT4 concentration was within the range seen in GTD patients without signs of hyperthyroidism. Her serum FT3 concentration was, however, much higher than the ranges in normal pregnancy or in GTD patients without clinical hyperthyroidism. Higher than normal FT4 levels were found in patients with and without elevated hCG levels.

OBJECTIVE

Apart from the effects of a dysfunctional thyroid gland on the cardiovascular system, thyroid function within the reference range may have an impact on the vasculature. The present study aimed to evaluate the association between thyroid function and markers of arterial structure and function in euthyroid postmenopausal women.

METHODS

The present cross-sectional study recruited 106 healthy postmenopausal women with a mean age of 55.0 years and thyroid-stimulating hormone (TSH) levels within the laboratory reference range (0.4-4.5 μIU/ml). Anthropometric and biochemical measures as well as blood pressure were determined in each individual. Vascular structure and function were assessed by intima-media thickness, pulse wave velocity (PWV), augmentation index and flow-mediated dilation, respectively. We evaluated the associations between arterial markers and serum TSH, free triiodothyronine, free thyroxin, as well as serum thyroid peroxidase and thyroglobulin autoantibodies.

RESULTS

Mean levels of PWV increased linearly across increasing TSH quartiles (P value = 0.014). Individuals with serum TSH greater than 2.5 μIU/ml had significantly higher values of PWV when compared with individuals with TSH levels below 2.5 μIU/ml (9.68 ± 1.97 vs. 8.54 ± 1.83 m/s; P = 0.030). In multivariate analysis, age, insulin resistance and TSH above 2.5 μIU/ml were the only significant predictors of PWV (TSH, β-coefficient = 0.222; P = 0.014). No associations were found between the remaining markers and levels of thyroid hormones, whereas thyroid antibodies were not associated with any of the arterial markers.

CONCLUSIONS

Women with TSH levels in the upper reference range have increased arterial stiffness compared to women with lower TSH. The upper limit of normal TSH in postmenopausal women may need re-evaluation with respect to the effects on the vasculature.

Thyroid function was studied in 176 male workers occupationally exposed to lead. The mean blood lead concentration of the workers was 2.70 (SD 1.15, range 0.70-6.45) mumol/l. The mean duration of lead exposure was 7.6 (range 0.1-20) years. The total thyroxine (T4), free thyroxine (FT4), total triiodothyronine (T3), and thyrotropin concentrations in serum were similar in the workers in the low and high blood lead categories. In regression equations the duration of lead exposure had a weak but significant negative association with T4 and FT4, and this association was particularly pronounced when the analyses were restricted to workers with the most intense lead exposure over time. Thus, the results suggest that thyroid function might be depressed as a result of intense long-term lead exposure.

Current understanding of the thyroid disruptive properties of perfluoroalkyl substances (PFASs), particularly in aging populations, is limited. The objectives of this study were to (i) assess associations between thyroid function, as measured by serum thyrotropin (thyroid stimulating hormone, TSH), free thyroxine (fT4), total thyroxine (T4), and total triiodothyronine (T3), and serum perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) in an aging population and (ii) determine if other persistent organic pollutants with thyroid disruptive properties including polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) modify such associations. We conducted a cross-sectional study of 87 men and women 55 to 74years of age, without clinically-diagnosed thyroid disease, who resided in upper Hudson River communities in New York. Geometric means (standard deviations) of serum PFOS and PFOA were 31.6 (1.7) ng/mL and 9.17 (1.72) ng/mL, respectively. Multivariable linear regression analyses indicated that one interquartile range difference in PFOS corresponded to 4% and 9% increases in fT4 and T4 respectively. We detected statistical interactions between PFOA and age for effects on fT4 and T4; joint increases in PFOA and age were associated with increases in fT4 and T4, of 3% and 7%, respectively. We also detected statistical interactions between PFOS and total PCBs for the effect on T3 and between PFOA and total PBDEs for the effect on TSH. Our results suggest that PFASs are associated with subtle alterations in thyroid hormone levels in this population, and that these associations are likely to vary by age, and levels of PCBs and PBDEs.

BACKGROUND

Ovarian hyperstimulation syndrome, not related to ovulation induction, is rare. A MEDLINE search from 1987 to 1997 using the key words "spontaneous ovarian stimulation," "pregnancy," and "hypothyroidism" revealed only five cases: three associated with pregnancies and two with primary hypothyroidism.

METHODS

A 25-year-old white gravida 2, para 1, at 11-12 weeks' gestation presented with mild distension of a nontender abdomen, myxedematous facies, and large bilateral, multilobulated ovarian cysts. Conception had occurred spontaneously. Thyroid stimulating hormone was elevated, and free triiodothyronine and free thyroxine were low. Hypothyroidism, associated with spontaneous ovarian hyperstimulation syndrome, was diagnosed, and oral levothyroxine (0.10 mg/day) was started. With TSH still elevated at 21 weeks, levothyroxine was increased to 0.20 mg/day, and by 24 weeks, TSH and ovarian size were normal. Vaginal delivery of a 1120 g male infant occurred at 28 weeks.

CONCLUSIONS

A case of naturally conceived pregnancy associated with spontaneous ovarian hyperstimulation and primary hypothyroidism is reported.

Hypothyroidism is the most common endocrinopathy in the dog. Rather than being a comprehensive review of all possible thyroid function tests, the focus in this article is on the logical progression of test choice, highlighting total thyroxine, free thyroxine, triiodothyronine, thyrotropin (TSH), and antithyroid antibodies. This article includes extensive discussion of the current status of the canine TSH assay and the potential for improving this assay.

OBJECTIVE

Obesity and weight loss influence thyroid hormone physiology. The effects of weight loss by calorie restriction vs Roux-en-Y gastric bypass (RYGB) in obese subjects have not been studied in parallel. We hypothesized that differences in transient systemic inflammation and catabolic state between the intervention types could lead to differential effects on thyroid hormone physiology.

METHODS

We recruited 12 lean and 27 obese females with normal fasting glucose (normal glucose tolerant (NGT)) and 27 obese females with type 2 diabetes mellitus (T2DM) for this study. Weight loss was achieved by restrictive treatment (gastric banding or high-protein-low-calorie diet) or by RYGB. Fasting serum leptin, TSH, triiodothyronine (T₃), reverse T₃ (rT₃), and free thyroxine (fT₄) concentrations were measured at baseline and 3 weeks and 3 months after the start of the interventions.

RESULTS

Obesity was associated with higher TSH, T₃, and rT₃ levels and normal fT₄ levels in all the subjects when compared with the controls. After 3 weeks, calorie restriction and RYGB induced a decline in TSH levels and a rise in rT₃ and fT₄ levels. The increase in rT₃ levels correlated with serum interleukin 8 (IL8) and IL6 levels. After 3 months, fT₄ and rT₃ levels returned to baseline levels, whereas TSH and T₃ levels were persistently decreased when compared with baseline levels. No differences in the effects on thyroid hormone parameters between the interventions or between NGT and T2DM subjects were observed at any time point.

CONCLUSIONS

In summary, weight loss directly influences thyroid hormone regulation, independently of the weight loss strategy used. The effects may be explained by a combination of decreased leptin levels and transient changes in peripheral thyroid hormone metabolism.

BACKGROUND

Metabolic syndrome and thyroid dysfunction are two common disorders encountered in the metabolic clinic. Recently, there has been increased interest in the association between the two disorders because of the similarities between symptoms of hypothyroidism and components of the metabolic syndrome. While some reports suggest that metabolic syndrome is associated with subclinical hypothyroidism, this concept is largely under investigated in Nigerian adults with metabolic syndrome. The aim of this study is to determine the thyroid function status of adult Nigerians with metabolic syndrome and determine the association, if any, between metabolic syndrome and thyroid function.

METHODS

This was a cross sectional study of one hundred and fifty adults, members of staff of the College of Medicine of the University of Lagos. The participants were recruited using a cluster random sampling method. The Ethical Research & Review Committee of the institution approved the study protocol and signed informed consent was obtained from the participants. The statistics was analysed using the IBM SPSS Software of version 19.0. The Student's t test, Chi square test and multivariate regression analysis were employed for the analysis. Statistical significance was set at p < 0.05.

RESULTS

Thirty nine (twenty-six percent) of the study participants had metabolic syndrome and one hundred and eleven (seventy-four percent) of the study participants did not have metabolic syndrome, served as controls. Those who had metabolic syndrome group were significantly older (p = 0.03), metabolic syndrome was significantly associated with the female gender (p = 0.0002), higher systolic blood pressure (p = 0.0034), diastolic blood pressure (p = 0.0009), waist circumference (p < 0.0001), body mass index (p < 0.0001), waist-hip ratio (p = 0.003), fasting serum glucose (p = 0.0457) and free thyroxine (fT4) levels (p = 0.0496). Those with metabolic syndrome had significantly lower HDL (P = 0.004) and free triiodothyronine (fT3) levels (p = 0.037). There was no statistically significant difference in the thyroid stimulating hormone (TSH) levels between individuals with and without metabolic syndrome. Thirty-three percent of the metabolic syndrome cases had sick euthyroid syndrome (p= < 0.0001). In multivariate regression, waist circumference was significantly and inversely associated with the sick euthyroid syndrome (p = 0.011).

CONCLUSIONS

Metabolic syndrome is associated with the sick euthyroid syndrome in adult Nigerians. Abdominal obesity appears to be the link between metabolic syndrome and the sick euthyroid syndrome.

Thyroid hormone values and serum thyrotropin (thyroid-stimulating hormone [TSH]) responses to the intravenous administration of 400 micrograms of protirelin were determined in ten patients with Cushing's syndrome and in ten matched normal subjects. In patients with Cushing's syndrome, the serum thyroxine (T4) level was mildly depressed and free T4 level was normal. The mean (+/- SD) concentrations of serum triiodothyronine (T3) and free T3 were both reduced in patients compared with normal subjects (P less than .001). At 20 and 60 minutes after protirelin administration, serum TSH levels were, respectively, 3.3 +/- 2.7 microU/mL and 2.6 +/- 2.3 microU/mL in patients with Cushing's syndrome and 12.3 +/- 5.4 microU/mL and 10.7 +/- 5.4 microU/mL in normal subjects (P less than .001). The reduced serum T3 and free T3 levels are due to a glucocorticoid suppressive effect on the peripheral conversion of T4 to T3. The protirelin test is of limited value in assessing the thyroid status because the response of TSH is frequently blunted or absent due to glucocorticoid excess.

The effects of short-term administration of the antiprogestin and antiglucocorticoid, mifepristone, have been well characterized. However, little is known about the effects of prolonged administration of mifepristone. We analyzed hormonal parameters in four female and three male patients with unresectable meningioma who were treated with mifepristone (200 mg/d) for 20 to 40 months. Serum samples were collected at monthly intervals approximately 24 hours following mifepristone ingestion. Serum thyrotropin (TSH), thyroxine (T4), free T4 (fT4), 3,5,3-triiodothyronine (T3), prolactin, and cortisol were analyzed by fluoroimmunoassay, and androstenedione by radioimmunoassay (RIA). Levels of mifepristone and its three most proximal metabolites were measured by high-performance liquid chromatography. TSH values increased significantly (P < .005, one-way ANOVA), with the most pronounced increase evident during the first 3 months of mifepristone treatment. Despite these changes, concentrations of TSH remained within the normal range throughout the treatment period. There were no significant changes in serum T4, fT4, T3 or prolactin; however, a transient decrease in serum T4 was noted at 2 to 3 months. Cortisol and androstenedione values increased significantly and in parallel (P < .05), suggesting an adrenal origin also for androstenedione. As during short-term administration, levels of mifepristone and its metabolites remained stable in the micromolar range. Individual levels of mifepristone were significantly correlated with those of TSH and cortisol. This suggests that the alterations in the pituitary-thyroid and -adrenal axes occurred in a concentration-dependent manner. It is concluded that long-term mifepristone treatment results in resetting of the pituitary-thyroid balance. As in the case with cortisol and androstenedione, it is likely that the alterations in serum TSH are due to the antiglucocorticoid properties of mifepristone. The clinical significance of these biochemical alterations in thyroid homeostasis remains to be determined. However, monitoring thyroid function during long-term mifepristone treatment appears to be warranted.

Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating hormone (TSH) concentrations. The most common cause of subclinical hyperthyroidism is the use of suppressive doses of L-thyroxine for treatment of hypothyroidism or, less commonly, diffuse nontoxic goiter or thyroid carcinoma (exogenous subclinical hyperthyroidism). Endogenous subclinical hyperthyroidism may be caused by a variety of thyroid disorders that result in overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake or by inflammation in the thyroid resulting in release of excess thyroid hormones and low 24-hour thyroid radioiodine uptake. Several groups have investigated whether persistent endogenous or exogenous subclinical hyperthyroidism, like overt hyperthyroidism, causes symptoms, adverse effects on the cardiovascular and the skeletal systems, and increased mortality, whether endogenous subclinical hyperthyroidism evolves to overt thyrotoxicosis, and whether or not it should be treated. The present report reviews the most important and recent studies of subclinical hyperthyroidism and attempts to draw conclusions based upon the literature and the authors' experience.

In 29 women with anorexia nervosa, on a blood sample withdrawn at 0900 h before and during weight gain, the binding parameters of serum sex hormone binding globulin (SHBG) were measured by a solid phase method and the levels of testosterone, oestradiol and thyroid hormones were measured by radioimmunoassay. The binding capacity of SHBG was higher than the upper limit for normally menstruating women in 23 patients whilst its affinity for binding testosterone at 37 degrees C was normal (0.32-0.53 X 10(-9) mol/l). The mean levels of testosterone, oestradiol and free thyroxine were normal and the mean level of triiodothyronine was significantly (P less than 0.005) decreased. The binding capacity of SHBG did not correlate significantly with body mass index, percent weight lost, thyroid hormone or sex hormone levels. In 9 patients, an i.v. infusion providing 1200-1400 calories daily was given for 1 week. In these patients a significant decrease (P less than 0.005) in the binding capacity of SHBG (from 74.7 +/- 26.7 to 52.9 +/- 21.8 nmol/l) and a significant increase (P less than 0.001) in T3 levels (from 0.69 +/- 0.21 to 0.95 +/- 0.13 nmol/l) was observed. In 14 patients, when a weight gain of at least 5% was obtained, the binding capacity of SHBG fell into the normal range (25.6-62.9 nmol/l) while T3 levels rose to normal (0.85-2.30 nmol/l). These findings suggested that variations of calorie intake and/or body weight may influence the binding capacity of SHBG in the human.

Insulin-like growth factor I (IGF-I) is considered to mediate some of the growth-promoting and metabolic effects of growth hormone (GH). Growth hormone treatment of healthy and GH-deficient subjects is accompanied by increased conversion of thyroxine (T4) to triiodothyronine (T3) in peripheral tissues. Whether these effects are mediated by IGF-I is unknown. To assess the respective roles of these hormones on thyroid hormone metabolism we have treated two groups of subjects. The first group consisted of eight healthy subjects who were treated with IGF-I (10 micrograms.kg-1.h-1 sc for 5 days). The second group consisted of eight subjects with combined GH and thyrotropin (TSH) deficiency due to acquired pituitary disease. They were treated with IGF-I (10 micrograms.kg-1.h-1 sc for 7 days), GH (2 IU m-2 sc q.i.d.) or both hormones together. The IGF-I treatment in healthy subjects led to an increase in free T3 (FT3) and a reduction in TSH levels, whereas FT4 and total T4 (TT4) levels remained unchanged. In the second group-in which all subjects were substituted with oral L-thyroxine-treatment with IGF-I led to an elevation of FT3 in the face of unchanged T4 levels. Growth hormone alone and GH plus IGF-I resulted in a more pronounced elevation in T3 level. The results suggest that IGF-I partially mediates the well-known effects of GH on peripheral conversion of T4 to T3. However, GH has more pronounced effects on thyroid hormones that apparently are not mediated by IGF-I.

The present study was designed to investigate the effect of chronic heat exposure (32 degrees constant) on plasma metabolites and hormone concentrations in broiler chickens. At 2 and 4 weeks of age, fifty-four male Shaver broiler chickens were allocated to one of three treatments: 22 degrees, ad lib. feeding (22AL), 32 degrees, ad lib. feeding (32AL) and 22 degrees, pair-feeding with the 32AL group (22PF). Ambient temperature was kept constant at either 22 or 32 degrees for 2 weeks. Plasma glucose, triacylglycerols, phospholipids, non-esterified fatty acids (NEFA), individual amino acids, uric acid, insulin, triiodothyronine (T3), thyroxine, corticosterone were determined. Sensitivity to exogenous insulin was also measured at 7 weeks of age. At 4 and 6 weeks of age, i.e. after 2 weeks at high ambient temperature, fasted 32AL chickens displayed similar concentrations of glucose and triacylglycerols to those of 22AL birds. When fed, 32AL chickens exhibited higher plasma levels of glucose and decreased concentrations of NEFA and amino acids. Feed restriction resulted in intermediate values. Concentrations of all plasma free amino acids were decreased under heat exposure except for aspartic acid, glutamic acid and phenylalanine. At 6 weeks of age, plasma T3 was reduced irrespective of the nutritional state, while plasma corticosterone concentrations were increased in 32AL birds compared with 22AL birds. Heat exposure did not change plasma insulin concentration in either fasted or fed chickens. The 32AL chickens displayed significantly reduced sensitivity to exogenous insulin when fasted, but an enhanced response to insulin when fed, compared with both 22 degrees groups. Such endocrinological changes could stimulate lipid accumulation through increased de novo lipogenesis, reduced lipolysis and enhanced amino acid catabolism under chronic heat exposure.