This study demonstrated the contamination levels of polychlorinated biphenyls (PCBs), hydroxylated PCBs (OH-PCBs), polybrominated diphenyl ethers (PBDEs), methoxylated PBDEs (MeO-PBDEs), hydroxylated PBDEs (OH-PBDEs), and bromophenols (BPhs), and their relationships with thyroid hormones (THs), in the serum of human donors from an e-waste recycling site and a rural site in Hung Yen province, Vietnam. Occupationally related exposure was indicated by significantly higher residue levels of PCBs, OH-PCBs, PBDEs, and BPhs in the serum of donors from the e-waste recycling site (median: 420, 160, 290, and 300pgg(-1) wet wt, respectively) than those in the serum of donors from the rural site (median: 290, 82, 230, and 200pgg(-)(1) wet wt, respectively). On the other hand, levels of OH-/MeO-PBDEs were significantly higher in serum of donors from the reference site (median: 160 and 20pgg(-1) wet wt, respectively) than in those from the e-waste recycling site (median: 43 and 0.52pgg(-1) wet wt, respectively). In addition, we implemented stepwise generalized linear models to assess the association between the levels of TH and PCBs, PBDEs, and their related compounds. In females, we found positive associations of PCBs and OH-PCB concentrations with total thyroxine, free thyroxine, total triiodothyronine, and free triiodothyronine, and a negative association with thyroid-stimulating hormone concentrations.

BACKGROUND

Infants born preterm are at risk of both transiently reduced thyroid hormone levels and impaired neurocognitive development, including attention deficits. The objective of this study was to examine the effects of reduced thyroid hormone levels on general neurodevelopment and attention at 3 months corrected age.

METHODS

Sixty-four infants born 24 to 35 weeks gestation were stratified into four gestational age groups: Group A, 23-26 weeks (n = 10); Group B, 27-29 weeks (n = 23); Group C, 30-32 weeks (n = 20); Group D, 33-35 weeks (n = 11). Controls were 33 healthy infants born full-term (Group E). In preterm only, free thyroxine (FT(4)), triiodothyronine (T(3)), and thyrotropin (TSH) were measured at 2 and 4 weeks of life and at 40 weeks postconceptional age. At 3 months corrected age, all infants were assessed with the Bayley Scales of Infant Development-Second Edition (BSID-II), from which both mental development index (MDI) and psychomotor development index (PDI) scores and four indices of attention were derived: sustained attention, selective attention, attention shift, and total attention.

RESULTS

Gestational age-stratified preterm groups differed significantly in T(3) and FT(4) levels at 2 and 4 weeks of life in infants born less than 27 weeks gestation. Preterm infants overall scored significantly below full-term on BSID-II MDI and PDI, selective, sustained, and total attention scales. In the preterm group, FT(4) levels were positively associated with PDI and selective, sustained, and total attention.

CONCLUSIONS

Reduced levels of thyroid hormone in the neonatal period in preterm infants are associated with a reduced neurocognitive outcome in the attention domain at 3 months corrected age.

Resistance to thyroid hormone (RTH) is a rare autosomal dominant inherited syndrome of reduced end-organ responsiveness to thyroid hormone. Patients with RTH have elevated serum free thyroxine (FT4) and free triiodothyronine (FT3) concentrations and normal or slightly elevated serum thyroid stimulating hormone (TSH) level. Despite a variable clinical presentation, the common characteristic clinical features are goitre but an absence of the usual symptoms and metabolic consequences of thyroid hormone excess. Patients with RTH can be classified on clinical grounds alone into either generalized resistance (GRTH), pituitary resistance (PRTH) or combined. Mutations in the thyroid hormone receptor (TR) beta gene are responsible for RTH and 122 different mutations have now been identified belonging to 300 families. With the exception of one family found to have complete deletion of the TRbeta gene, all others have been demonstrated to have minor alterations at the DNA level. The differential diagnosis includes a TSH-secreting pituitary adenoma and the presence of endogenous antibodies directed against thyroxine (T4) and triiodothyronine (T3). Failure to differentiate RTH from primary thyrotoxicosis has resulted in the inappropriate treatment of nearly one-third of patients. Although occasionally desirable, no specific treatment is available for RTH; however, the diagnosis allows appropriate genetic counselling.

Seasonal levels of cortisol, growth hormone (GH), insulin like growth factor 1 (IGF-1), glucose, triiodothyronine (T3), free T3, thyroxine and free fatty acids (FFA) were measured every 3 weeks for 54 weeks in the plasma of five adult bulls, and four barren and five pregnant Alaskan reindeer (Rangifer tarandus) cows. Three consecutive samples were taken from each animal. Cortisol levels exhibited wide seasonal variation (9-45 ng/ml) [corrected] without any peak or difference in levels among groups. Rising levels were detected between the 3 consequent samples. Peak GH levels, detected during January and February, were higher in the non-pregnant group (54 ng/ml) than the pregnant (26 ng ml-1) and the male (27 ng ml-1) groups. Low GH levels (2-10 ng ml-1) were recorded between May and September. IGF-1 reached peak levels (715 ng ml-1) in males in August, in non-pregnant females in September (677 ng ml-1), and in the pregnant females in October (505 ng ml-1). Seasonal minima (404 in males, 172 and 93 in pregnant and non-pregnant groups) were detected in February. Glucose was fairly stable throughout the year (100-200 mg/100 ml). A rising levels were found between the three consecutive samples. Triiodothyronine (T3) (2.16-2.30 ng ml-1) peaked in all three groups during the spring and early summer, and minimal levels (0.61-0.97 ng ml-1) were detected from October to January. Conversely, thyroxine or free T3 did not exhibit seasonal variation. FFA fluctuated widely (97-1076 nmol l-1) throughout the year. Only in pregnant females were concentrations more stable (150-460 nmol l-1). Perhaps, because of ad libitum supply of food in captive reindeer, only T3 and GH exhibited pronounced seasonal fluctuations which could be related to the metabolic changes expected during the annual cycle.

Thyroid hormone plays an important role in cardiac function. Low levels of serum triiodothyronine (T3) due to nonthyroidal illness syndrome may have adverse effects in heart failure (HF). This study was designed to assess the ability of T3 to predict in-hospital outcomes in patients with acute HF. In total, 137 patients without thyroid disease or treatment with drugs which affect TH levels, who were hospitalized with acute HF were prospectively enrolled and studied. TH levels were tested upon hospital admission, and outcomes were compared between patients with low (<2.3 pg/ml) and normal (≥2.3 pg/ml) free T3 levels as well as between those with low (<0.6 ng/ml) and normal (≥0.6 ng/ml) total T3 levels. Low free T3 correlated with an increased length of stay in the hospital (median 11 vs 7 days, p <0.001) and higher rates of intensive care unit admission (31.8% vs 16.9%, p = 0.047), with a trend toward increased need for invasive mechanical ventilation (9.0% vs 1.4%, p = 0.056). Low total T3 correlated with an increased length of stay in the hospital (median 11 vs 7 days, p <0.001) and increased need for invasive mechanical ventilation (9.8% vs 1.3%, p = 0.045). In conclusion, low T3 predicts worse hospital outcomes in patients with acute HF and can be useful in the risk stratification of these patients.

OBJECTIVE

Altered thyroid hormone metabolism characterized by a low triiodothyronine (T3), so-called low-T3 syndrome, is a common finding in patients with severe systemic diseases. Additionally, subclinical thyroid dysfunction, defined as abnormal thyroid stimulating hormone (TSH) and normal thyroxine (T4), causes left ventricular dysfunction. Our objective was to identify the prevalence and prognostic impact of low-T3 syndrome and subclinical thyroid dysfunction in patients with acute decompensated heart failure (ADHF).

RESULTS

We examined 274 ADHF patients who were not receiving thyroid medication or amiodarone on admission (70 ± 15 years, 156 male), who underwent thyroid function tests. Euthyroidism was defined as TSH of 0.45 to 4.49 mIU/L; subclinical hypothyroidism as TSH of 4.5 to 19.9 mIU/L; and subclinical hyperthyroidism as TSH < 0.45 mIU/L, with normal free T4 level for the last two. Additionally, low-T3 syndrome was defined as free T3 < 4.0 pmol/L among euthyroidism subjects. On admission, 188 patients (69%) showed euthyroidism, 58 (21%) subclinical hypothyroidism, 5 (2%) subclinical hyperthyroidism, and 95 (35%) low-T3 syndrome. Cox proportional hazards models revealed that higher TSH, but not free T3 and free T4, was independently associated with composite cardiovascular events, including cardiac death and re-hospitalization for heart failure. Indeed, subclinical hypothyroidism was an independent predictor (hazard ratio: 2.31; 95% confidence interval: 1.44 to 3.67; P < 0.001), whereas low-T3 syndrome and subclinical hyperthyroidism were not.

CONCLUSIONS

Subclinical hypothyroidism on admission was an independent predictor of adverse cardiovascular outcomes in ADHF patients, suggesting a possible interaction between thyroid dysfunction and the pathophysiology of ADHF.

A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its alpha-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas beta-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. L-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH. Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, alpha-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its alpha-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour. It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.

In a prospective study to determine which factors would predict remission or relapse, 65 patients with hyperthyroid Graves' disease were treated for six months with a blocking replacement regimen of carbimazole, 40 mg daily, and triiodothyronine (T3). They were followed for one year after stopping treatment, by which time 32 (49 per cent) had relapsed. Although the treatment protocol, relapse rate and frequency of the HLA-DR3 antigen in this population were similar to those of a regionally separate Graves' population investigated previously, the predictive value of HLA-DR3 status together with thyroid stimulating antibody (TSAB) levels was strikingly different. In the present study there was no significantly abnormal distribution of any HLA antigen in the relapse group compared with those patients who achieved remission. Thyroid stimulating antibodies were detected in 62 patients (95 per cent) and fell significantly (p less than 0.05) after carbimazole treatment, irrespective of DR3 status or outcome; TSAB levels only became undetectable in nine patients (28 per cent) who subsequently relapsed and in nine patients (30 per cent) who maintained remission. T3-suppressed 20 min 123I uptake fell equally after treatment in the relapse and remission groups but continued to fall thereafter in the group which maintained remission. In these patients, 123I uptake was significantly lower at the end of the study period than at the end of treatment (p less than 0.05). Serum free T4 levels were higher before treatment in the patients who later relapsed than in those whose disease remitted (p less than 0.02). This proved the only significant marker associated with outcome but was of little predictive value in any patient. This study highlights the problem in predicting the outcome of antithyroid drug treatment, since even within the same country under similar conditions, divergent results have been obtained. It appears that the loci controlling the immune response in Graves' disease are likely to include genes lying outside the HLA-DR region. The results also suggest that the immunological effects of antithyroid drugs are maintained after stopping treatment in those patients whose disease remits.

BACKGROUND

We previously reported a unique hypothalamic-pituitary-thyroid (HPT) axis profile in women with a menstrually related mood disorder (MRMD) who also had a history of sexual abuse (SA). In the present study, we sought to extend that work by examining the association of an SA history with HPT-axis disturbance in both women with MRMD and women without MRMD.

METHODS

Fifty-seven women met the prospective criteria for MRMD (23 with an SA history), and 52 women were non-MRMD (18 with an SA history). Thyroid-stimulating hormone, thyroxin (T4; total and free), and triiodothyronine (T3; total and free) were evaluated in serum, together with thyroid hormone ratios reflecting T4 to T3 conversion.

RESULTS

Women with MRMD, compared with women without MRMD, had elevated T3/T4 ratios (p values ≤ .01; reflecting increased conversion of T4 to T3) and lower free and total T4 concentrations (p values = .01). Higher T3/T4 ratios and lower T4 concentrations predicted more severe premenstrual symptoms in all women. An SA history, irrespective of MRMD status, was associated with elevated thyroid-stimulating hormone concentrations (p = .03). However, in women with MRMD, an SA history was associated with elevated T3 concentrations (p = .049), whereas in women without MRMD, an SA history was associated with decreased T3 concentrations (p = .02).

CONCLUSIONS

An MRMD and an SA history are associated with independent and interactive effects on the HPT axis. The evidence that an MRMD moderates the influence of SA on T3 concentrations contributes to a growing body of work suggesting that an SA history may identify a distinct subgroup of women with MRMD.

Recent studies have shown a possible relationship between cigarette smoking and endocrine function. Since changes in thyroid hormone concentrations can have a profound effect on overall metabolism as well as influencing both androgenic and estrogenic steroid activity, we investigated the relationship between cigarette smoking and thyroid function. Volunteers were divided into four groups according to self-reported and biochemical data, including blood carboxyhemoglobin, plasma cotinine, and thiocyanate, and were described as nonsmokers, light, moderate, and heavy smokers. Substantial decreases were found in serum thyroxine (T4) and triiodothyronine (T3) concentrations in heavy smokers compared with nonsmokers. Reduced serum thyroid hormone levels were not accompanied by a substantial change in serum thyrotropin concentrations. The free T4 index, free T3 index, and T4-T3 ratio were not substantially different for either group.

Forty-seven chloralkali workers exposed to mercury vapour for an average of 13.3 years were compared with 47 referents matched for age in a cross-sectional study of thyroid function. The mean urinary mercury concentration in the exposed workers was low compared with other studies of chloralkali workers: 5.9 nmol mmol-1 creatinine (range 1.1-16.8) vs 1.3 nmol mmol-1 creatinine (range 0.2-5.0) in the reference group. The median serum concentration of reverse triiodothyronine (rT3) was statistically significantly higher in the exposed subjects compared with the referents (268 pmol l (-1) and range 161-422 vs 240 pmol l(-1) and range 129-352; P = 0.009). The difference between the exposed subjects and the referents was most pronounced in the highest exposed sub-groups. The free thyroxine (T4)/free T3 ratio was also higher in the highest exposed subgroups compared with the referents. The median serum concentration of tumour necrosis factor alpha (TNF-alpha) was lower in the exposed subjects (7.3 pg ml(-1) and range 4.4-69.7 vs 8.0 pg ml(-1) and range 6.0-34.6; P = 0.004). Exposed subjects with the lowest urinary iodine (<67.8 nmol mmol(-1) Cr) had higher serum concentrations of reverse T 3 and a higher free T4/free T3 ratio than the other subjects, suggesting that a low concentration of iodine in urine may be a risk factor for increased serum concentrations of reverse T3 and the free T4/free T3 ratio in subjects exposed occupationally to mercury vapour. The study could indicate a slight effect of low mercury vapour exposure on the function of the enzyme type I iodothyronine deiodinase, possibly modified by comparatively low urinary iodine concentrations.

Serum concentrations of iodothyronines, cortisol, prolactin, testosterone and the respective tropic hormones were measured in 32 noncirrhotic male alcoholics, aged 28-51 years, at the end of a long drinking period and subsequently during ethanol withdrawal over 1-2 weeks. Seven men had testicular atrophy. On admission one patient had high values for serum thyroxine (T4) and free thyroxine index (FT4I). A blunted response of serum thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) was found in 9 men. Apart from a blunted TSH-response in one man the abnormalities disappeared during the first week of alcohol abstinence. Simultaneously the mean levels of serum T4, FT4I, triiodothyronine, free triiodothyronine index and reverse triiodothyronine were reduced by 12, 14, 5, 8 and 21%, respectively, and the mean of the maximum TSH-response to TRH was increased by 55%. At the time of stopping drinking two men had high morning values and six an abnormal diurnal rhythm of serum cortisol. High serum ACTH-levels associated with normal serum cortisol concentrations were found in 12 men. During the first week of alcohol abstinence the mean morning values for serum cortisol and ACTH were reduced by 18 and 42%, respectively. The serum ACTH-levels remained high in 6 men but the abnormalities in cortisol secretion disappeared. On admission four men had low serum concentrations of testosterone which were normalized during ethanol withdrawal over one week. At the same time the mean level of serum testosterone was increased by 19%. Mild hyperprolactinaemia found in 7 patients on admission disappeared in 4 men during the first week of ethanol withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)

OBJECTIVE

We studied the impact of radiofrequency ablation (RFA) on health-related quality of life (HRQL) in patients with benign thyroid nodules (TN) in a 2-year follow-up.

METHODS

Forty patients (35 women and 5 men; age, 54.9 ± 14.3 years) with cold thyroid solitary nodules or a dominant nodule within a normofunctioning multi-nodular goiter (volume range, 6.5 to 90.0 mL) underwent RFA of thyroid nodular tissue under ultrasound real-time assistance.

RESULTS

Data are mean and standard deviation. Energy delivered was 37,154 ± 18,092 joules, with an output power of 37.4 ± 8.8 watts. Two years after RFA, nodule volume decreased from 30.0 ± 18.2 mL to 7.9 ± 9.8 mL (-80.1 ± 16.1% of initial volume; P<.0001). Thyroid-stimulating hormone, free triiodothyronine, and free thyroxine levels remained stable. Symptom score measured on a 0- to 10-cm visual analogue scale (VAS) declined from 5.6 ± 3.1 cm to 1.9 ± 1.3 cm (P<.0001). Cosmetic score (VAS 0-10 cm) declined from 5.7 ± 3.2 cm to 1.9 ± 1.5 cm (P<.0001). Two patients became anti-thyroglobulin antibody-positive. Physical Component Summary (PCS)-12 improved from 50.4 ± 8.9 to 54.5 ± 5.3, and the Mental Component Summary (MCS)-12 improved from 36.0 ± 13.3 to 50.3 ± 6.3 (P<.0001 for both score changes).

CONCLUSIONS

Our 2-year follow-up study confirms that RFA of benign TNs is effective in reducing nodular volume and compressive and cosmetic symptoms, without causing thyroid dysfunction or life-threatening complications. Our data indicate that the achievement of these secondary endpoints is associated with HRQL improvement, measured both as PCS and MCS.

OBJECTIVE

To investigate the association between low free triiodothyronine (fT3) levels and the severity and prognosis of patients with acute myocardial infarction.

METHODS

A total of 501 patients with acute myocardial infarctions were enrolled in our study. The circulating levels of thyroid hormones and clinical parameters were assayed. The patients were categorized into either the low fT3 group or the normal fT3 group according to the fT3 level on admission. All patients underwent a follow-up for 10±2 months for mortality from any cause and the occurrence of any adverse major cardiac events (MACE).

RESULTS

There were 171 patients in the low fT3 group (fT3<3.5 pmol/L) and 330 patients in the normal fT3 group (≥3.5 pmol/L). During the follow-up period, 33 patients died (6.6%) and the overall survival rates were 86.0% and 97.3% in patients with a low fT3 level and a normal fT3 level, respectively. The rates of MACE were 66.7% and 45.5% in the patients with and those without low fT3 levels, respectively. Using a multivariable Cox proportional hazards model, the fT3 level was found to be the most important predictor of cumulative death and MACE (hazard ratio [HR] for death: 0.142, p<0.001 and HR for major adverse cardiac events: 0.748, p=0.007). A Kaplan-Meier analysis revealed that those patients with low fT3 levels had higher rates of MACE and death.

CONCLUSIONS

A low fT3 level, a common phenomenon in patients with acute myocardial infarctions, is a strong predictor of short-term and long-term poor prognoses in patients with acute myocardial infarctions.

BACKGROUND

Both low free triiodothyronine (fT3) and high brain natriuretic peptide (BNP) have been separately described as prognostic predictors for mortality in heart failure (HF). We investigated whether their prognostic value is independent.

RESULTS

From January of 2001 to December of 2006, we prospectively evaluated 442 consecutive patients with systolic HF and no thyroid disease or treatment with drugs affecting thyroid function (age 65+/-12 years, mean +/- standard deviation, 75% were male, left ventricular ejection fraction 33% +/- 10%, New York Heart Association (NYHA) class I and II: 63%, NYHA class III and IV: 37%). All patients underwent full clinical and echocardiographic evaluation and assessment of BNP and thyroid function. Both cardiac and all-cause mortality (cumulative) were considered as end points. During a median 36-month follow-up (range 1-86 months), 110 patients (24.8%) died, 64 (14.4%) of cardiac causes. Univariate Cox model predictors of all-cause mortality and cardiac death were age, body mass index, creatinine, hemoglobin, ejection fraction, NYHA class, BNP, fT3, and thyroxine level. Multivariate analysis selected age, NYHA class, hemoglobin, BNP, and fT3 as independent predictors for all-cause mortality and NYHA class, BNP, and fT3 as independent predictors for cardiac mortality. Patients with low fT3 and higher BNP showed the highest risk of all-cause and cardiac death (odds ratio 11.6, confidence interval, 5.8-22.9; odds ratio 13.8, confidence interval, 5.4-35.2, respectively, compared with patients with normal fT3 and low BNP).

CONCLUSIONS

fT3 and BNP hold an independent and additive prognostic value in HF.

BACKGROUND

The current approach for calculating the starting dose of levothyroxine (LT4) after total thyroidectomy is based on the patient's body weight (BW). The aim of the study was to identify the major predictive factors of LT4 requirement and to elaborate a new method to improve the accuracy of the LT4 starting dose after total thyroidectomy.

METHODS

The study consists of two parts. The first part consisted of the retrospective identification of 92 adult patients (retrospective cohort) who had undergone a total thyroidectomy for benign disease and who had begun LT4 treatment at a dose of 1.6 μg/kg/day. Adjustments to optimize the LT4 dose were then performed at the post-surgery follow-up on the basis of serum thyrotropin (TSH) levels. The results of this retrospective analysis were used to formulate a nomogram for a proper calculation of the LT4 starting dose that was then used prospectively in the second part of the study on 31 consecutive patients (prospective cohort).

RESULTS

At the first follow-up, 37 (40%) patients from the retrospective cohort were euthyroid. Univariate analysis indicated significant correlations between the optimal dose of LT4 and BW, body mass index (BMI), age, preoperative mean corpuscular volume, and free triiodothyronine (fT3). The optimal dose of LT4, analyzed for BMI and age, showed an inverse relationship with these two parameters, and ranged from 1.4 to 1.8 μg/kg/day. In the prospective cohort, the use of an age- and BMI-related nomogram improved the prediction of the optimal LT4 starting dose, with 68% of patients being euthyroid at the first follow-up compared to 41% of patients reported to have reached euthyroid state using the best strategy proposed in the literature.

CONCLUSIONS

This study confirms that BW is not the only variable for predicting LT4 requirement, as it decreases with the increase in age and BMI, probably due to the relative decrease of lean body mass. A new correlation between optimal dose and presurgical levels of fT3 and mean corpuscular volume was observed. We propose an easy and more efficient method of calculating LT4 starting dose after total thyroidectomy for benign disease.

BACKGROUND

Although hyperthyroidism predisposes to atrial fibrillation, previous trials have suggested decreased triiodothyronine (T3) concentrations to be associated with postoperative atrial fibrillation (POAF). Therapy with thyroid hormones (TH), however, did not reduce the risk of POAF. This study reevaluates the relation between thyroid hormone status, atrial electromechanical function and POAF.

METHODS

Thirty-nine patients with sinus rhythm and no history of atrial fibrillation or thyroid disease undergoing cardiac surgery were prospectively enrolled. Serum concentrations of thyrotropin, free (F) and total (T) thyroxine (T4) and T3, reverse (r)T3, 3-iodothyronamine (3-T1AM) and 3,5-diiodothyronine (3,5-T2) were measured preoperatively, complemented by evaluation of echocardiographic and electrophysiological parameters of cardiac function. Holter-ECG and telemetry were used to screen for POAF for 10 days following cardiac surgery.

RESULTS

Seven of 17 patients who developed POAF demonstrated nonthyroidal illness syndrome (NTIS; defined as low T3 and/or low T4 syndrome), compared to 2 of 22 (p < 0.05) patients who maintained sinus rhythm. In patients with POAF, serum FT3 concentrations were significantly decreased, but still within their reference ranges. 3,5-T2 concentrations directly correlated with rT3 concentrations and inversely correlated with FT3 concentrations. Furthermore, 3,5-T2 concentrations were significantly elevated in patients with NTIS and in subjects who eventually developed POAF. In multivariable logistic regression FT3, 3,5-T2, total atrial conduction time, left atrial volume index and Fas ligand were independent predictors of POAF.

CONCLUSIONS

This study confirms reduced FT3 concentrations in patients with POAF and is the first to report on elevated 3,5-T2 concentrations in cardiac NTIS. The pathogenesis of NTIS therefore seems to involve more differentiated allostatic mechanisms.

BACKGROUND

The coexistence of hyperthyroidism and primary hyperparathyroidism (pHPT) has been reported. We have questioned whether hypercalcemia or surgical trauma contribute to transient hyperthyroidism following parathyroid surgery.

METHODS

Twenty-six pHPT and eleven breast cancer patients were compared regarding pre-, peri- and postoperative thyrotropin (TSH), free thyroxine (T4) and free triiodothyronine (T3) concentrations. Thyroglobulin concentration, occurrence of autonomous thyroid nodules, and variables reflecting surgical trauma were compared in pHPT patients with and without postoperative hyperthyroidism.

RESULTS

Postoperatively, eleven pHPT patients demonstrated T4 and T3 concentrations above normal, and nine developed symptoms of mild thyrotoxicosis. A parallel rise in TSH and T4 concentrations was seen during both parathyroid and breast cancer surgery. Compared with patients with no postoperative hyperthyroidism, patients with postoperative hyperthyroidism showed a parallel rise in mean thyroglobulin and T4/T3 concentrations as well as higher thyroglobulin concentrations. However, there was no difference in variables assessing surgical trauma nor in occurrence of autonomous thyroid nodules. The peri-operative rise in TSH was preceded by a decrease in calcium.

CONCLUSIONS

Transient hyperthyroidism after parathyroid surgery is not infrequent. The condition seems to be self-limiting, since symptoms invariably subsided without treatment. Manipulation of the thyroid gland is most likely the major contributing factor to postoperative hyperthyroidism. However, it may not be the sole explanation, since our data suggest a more multifactorial scenario.

Glial cultures were obtained from the brains of 1-week-old rats and were grown in a chemically defined, serum-free medium. We investigated the development of oligodendrocytes in these cultures and the synthesis of sulfolipids in the presence and absence of triiodothyronine (T3) in the medium: (1) In the presence of T3, the incorporation of [35S]sulfate into sulfolipids exhibited a developmental profile which is comparable to that found in the developing brain in vivo. A sharp peak of sulfolipid synthesis was observed at day 5 in vitro, which is equivalent to day 12 after birth. As observed in vivo, the percentage of label incorporated into sulfogalactosyldiradylglycerols decreased with time in culture. (2) Addition of T3 to the medium stimulated sulfolipid synthesis by oligodendrocytes in a dose-related manner (optimal T3 concentration, 30 nM). The hormone also enhanced the rates of cholesterogenesis and lipogenesis but to a lesser extent than sulfolipid synthesis. (3) The temporary omission of T3 from the medium resulted in lower rates of sulfolipid synthesis that could not be restored by readdition of T3. This inhibitory effect was most pronounced if the hormone was omitted from the medium on days 2 and 3 in culture. (4) Omission of T3 also resulted in the development of fewer oligodendrocytes in the cultures. Our results show that T3 is essential for the development of oligodendrocytes in our neurone-free culture system. They also indicate that the stimulation of myelination by thyroid hormones can, at least partially, be explained as a direct effect of T3 on oligodendrocytes, independent of an effect of T3 on neuronal growth.

OBJECTIVE

We investigated dialysis duration, dose of erythropoietin (EPO), and clinical manifestations in peritoneal dialysis (PD) patients with subclinical hypothyroidism.

METHODS

This cross-sectional study, performed in 3 centers, assessed 122 adult patients on PD for more than 6 months with regard to demographic data, dialysis duration, thyroid function, biochemical data, EPO dose, and clinical manifestations. Thyroid dysfunction was determined by serum thyroid-stimulating hormone, free thyroxine, total thyroxine, total triiodothyronine, antithyroid peroxidase antibodies, and auto-antibodies against thyroglobulin.

RESULTS

Of the 122 study patients, 98 (80.3%) were assessed as having euthyroidism; 19 (15.6%), subclinical hypothyroidism; and 5 (4.1%), subclinical hyperthyroidism. The proportion of women (74.2% vs. 57.1%, p = 0.038), the mean duration of PD (58.1 months vs. 37.9 months, p = 0.032), and the weighted mean monthly EPO dose (1.22 μg/kg vs. 1.64 μg/kg, p = 0.009) were significantly higher in the subclinical hypothyroidism group than in the euthyroidism group, but the prevalences of coronary artery disease and cerebrovascular disease were not. From the multivariate model, PD duration was more significant than sex as a risk factor for subclinical hypothyroidism (p = 0.0132).

CONCLUSIONS

Subclinical hypothyroidism is frequent in PD patients, especially female patients and patients with a longer PD duration. Compared with euthyroid patients, patients with subclinical hyperthyroidism need a higher dose of EPO to maintain a stable hemoglobin level.

Objective. To investigate the association of thyroid function and diabetic nephropathy (DN) in euthyroid patients with type 2 diabetes. Methods. A total of 421 patients were included in this cross-sectional study. The following parameters were assessed: anthropometric measurements, fast plasma glucose, serum creatinine, lipid profile, HbA1c, free triiodothyronine (FT3), free thyroxine, thyroid-stimulating hormone levels, and urinary albumin-to-creatinine ratio (UACR). Patients with UACR of ≥30 mg/g were defined as those suffering from DN. Results. Of the 421 patients, 203 (48.2%) suffered from DN, and no difference was found between males and females. The patients with DN yielded significantly lower FT3 levels than those without DN (P < 0.01). The prevalence of DN showed a significantly decreasing trend across the three tertiles based on FT3 levels (59.6%, 46.4%, and 38.6%, P < 0.01). After adjustment for gender and age, FT3 levels were found to correlate positively with estimated glomerular filtration rate (P = 0.03) and negatively with UACR (P < 0.01). Multiple linear regression analysis showed that FT3 level was independently associated with UACR (β = -0.18, t = -3.70, and P < 0.01). Conclusion. Serum FT3 levels are inversely associated with DN in euthyroid patients with type 2 diabetes, independent of traditional risk factors.

BACKGROUND

Although thyroid dysfunction is a known prognostic factor for cardiovascular disease, the relationship between thyroid function and prognosis in patients with acute decompensated heart failure (ADHF) is poorly understood. Herein, we investigated the association between thyroid hormone levels and outcome in patients hospitalized for ADHF.

METHODS

We evaluated 270 hospitalized ADHF patients with thyroid hormone levels measured at admission between April 2007 and May 2012.

RESULTS

The median (interquartile range) thyroid stimulating hormone, free triiodothyronine (fT3), and free thyroxine were 2.79 (1.49-4.96)μU/ml, 2.32 (1.93-2.75)pg/ml, and 14.0 (12.1-15.7)pg/dl, respectively. Receiver operating characteristic (ROC) curve analysis was applied to assess their prognostic value for in-hospital outcome. The fT3 had the most favorable performance, with an area under the ROC curve of 0.791 (optimal cutoff point ≤2.05; sensitivity 85.0%; specificity 72.0%). Although patients in the low fT3 group (≤2.05) had higher age and lower body mass index, there were no significant differences with respect to systolic blood pressure and heart rate between the groups. In multivariate analysis adjusted for various markers of disease severity and amiodarone use, low fT3 level was independently associated with higher in-hospital mortality (odds ratio 14.4; p<0.001). In addition, the probability of 1-year total death among patients with low fT3 was significantly higher than that among patients with normal fT3 (log-rank p<0.001).

CONCLUSIONS

Low fT3 level was associated with adverse outcomes in patients hospitalized for ADHF. Thyroid hormone measurements might be useful in the risk stratification of ADHF patients.

OBJECTIVE

To describe the clinical picture and laboratory features of Chinese children with newly diagnosed type 1 diabetes mellitus.

METHODS

The clinical and laboratory data of a total of 203 children who presented with newly diagnosed type 1 diabetes mellitus during a 5-year period (2004-2008) were retrospectively analysed based on hospital records.

RESULTS

There were 88 boys (43.3%) and 115 girls (56.7%) with a median age of 8.3 years. The age distribution was categorised as 0-4 years: 52 (25.6%), 5-9 years: 57 (28.1%) and 10-14 years: 94 (46.3%). We found a peak incidence rate in the older age group. No significant seasonality was observed. The most common symptoms were polydipsia, polyuria and weight loss. Eighty-five (41.9%) of all patients presented with diabetic ketoacidosis (DKA). The average duration of presenting symptoms before the hospital encounter was 24.5 days. Young age group children had shorter duration (17.1 days, P = 0.03) and significantly lower levels of C-peptide (P = 0.003) and haemoglobin A1c (P = 0.049) than the other groups. Children with DKA had a higher incidence of preceding infections (P = 0.032), lower free triiodothyronine and free thyroxine levels (P= 0.035, 0.046), and higher white blood cell counts (P = 0.000) than the non-DKA group.

CONCLUSIONS

The duration between the onset of the symptoms and diagnosis was long, and the proportion of DKA in children with newly diagnosed diabetes mellitus was high. These findings call for a collaborative effort for the early recognition of symptoms by patients and physicians in order to avoid more severe types of presentation.

OBJECTIVE

Hyperthyroidism is frequently associated with pronounced neuropsychiatric symptoms such as impulsiveness, irritability, poor concentration, and memory impairments. Functional neuroimaging has revealed changes in cerebral metabolism in hyperthyroidism, but regional changes in cortical morphology associated with specific neurological deficits have not been studied so far. To investigate the pathophysiology underlying hyperthyroid-associated neural dysfunction, we compared grey matter volume (GMV) between adult hyperthyroid patients and matched healthy controls using voxel-based morphometry (VBM).

METHODS

High resolution 3D T1-weighted images were acquired by 3T MRI from 51 hyperthyroid patients and 51 controls. VBM analysis was performed using SPM8. Correlations between regional GMV and both serum free thyroid hormone (TH) concentrations and disease duration were assessed by multiple regression analysis.

RESULTS

Compared to controls, GM volumes in the bilateral hippocampus, parahippocampal gyrus, calcarine, lingual gyrus, and left temporal pole were lower and bilateral supplementary motor area GMV higher in hyperthyroid patients. Serum free triiodothyronine (FT3) concentration was negatively correlated with the normalized regional volume (NRV) of the left parahippocampal gyrus and serum free thyroxine (FT4) concentration negatively correlated with the NRV of the left hippocampus and right parahippocampal gyrus. Disease duration was negatively correlated with the NRV of the left hippocampus, bilateral parahippocampal gyrus, and left temporal pole.

CONCLUSIONS

Hyperthyroid patients exhibited reduced GMV in regions associated with memory, attention, emotion, vision, and motor planning. Negative correlations between GMV and both free TH and disease duration suggest that chronic TH elevation induces abnormalities in the adult cortex.