Changes In Thyroid Hormones Research Articles

Noise Induces Hypothyroidism and Gonadal Dysfunction Via Stimulation of Pineal–Adrenal Axis in Chicks

Noise is a world-wide problem that causes nervous, endocrine and cardiovascular disorders, and eventually health hazards in humans and animals. Objective of the current work is to investigate endocrine interaction in noise stress, which subsequently affects other endocrine functions including gonads in a poultry bird like chicks. Gravimetric, ultrastructural and hormonal status of the endocrine organs were examined to ascertain the effects of noise stress. Acute noise at 60 dB had no effect, but at 80 and 100 dB each for 3 h, increased pineal and serum serotonin, and adrenal and serum corticosterone, epinephrine and norepinephrine concentrations, without any change in thyroid or gonadal hormones. Chronic noise exposure at 60, 80 and 100 dB each for 6 h, daily for 7 days, drastically disturbed normal behavior, and quantum of food consumption and water intake. Chronic exposure also significantly decreased body weight including thyroid, ovary and testis weight, and increased adrenal weight. Noise stress caused ultrastructural changes leading to stimulations of pinealocytes (with abundance of rough endoplasmic reticulum and mitochondria), adrenocortical cells (enlarged nuclei and abundance of smooth endoplasmic reticulum) and adrenomedullary cells (enlarged nuclei with presence of chromaffin granules) were observed in noise stress. Additionally, pineal and serum serotonin, N-acetyl serotonin and melatonin, and adrenal and serum corticosterone, epinephrine and norepinephrine levels were significantly elevated following chronic noise exposure. Contrarily, thyroid activity was suppressed with atrophied thyroid follicles followed by declined levels of serum T3 and T4 with elevation of TSH level. Simultaneously, serum 17β-estradiol (E2) and testosterone (T) concentrations were also significantly declined in all the doses of chronic noise. These changes were dose dependent of noise exposure. The findings suggest that (a) adrenal and pineal glands respond primarily to noise and secondarily act on other endocrine organs including gonads in chicks, (b) adrenal directly and/or indirectly causes thyroid and gonadal dysfunctions via pineal following noise exposure in chicks.

Thyroid function and neuropsychological status in older adults

Overt thyroid dysfunction is recognized as a risk factor for neuropsychological deficits in aging populations, yet evidence for how changes in levels of circulatory thyroid hormones impact specific neuropsychological domains is limited. Here we report cross-sectional associations between serum thyroid hormone concentrations and several neuropsychological function domains among men and women aged 55–74years. We administered neuropsychological tests to assess memory, learning, executive function, measures of attention, visuospatial function, affective state, and motor function. Multivariable linear regression analyses were performed adjusting for age, sex, education, and cigarette smoking. Effects were reported as differences in test scores per one interquartile range (IQR) increase in hormone concentration. Higher total thyroxine (T4) and free thyroxine (fT4) were associated with improved visuospatial function, as measured by Block Design Subtest total scores; associated increments per IQR differences in T4 and fT4 were 15% and 19%, respectively (false discovery rate q-values <0.05). We also detected statistical interactions between age and fT4 for effects in tasks of memory and learning. Concurrent increases in age and fT4 were associated with deficits in memory and learning as measured by California Verbal Learning Test subtests (10% and 16% deficits in t-score and short delay free recall score, respectively). Our findings suggest that changes in thyroid hormones may have important implications for neuropsychological function in aging populations. Further large-scale studies with comprehensive thyroid function and neuropsychological outcome assessments are warranted to confirm these results.

Exposure to polychlorinated biphenyls and the thyroid gland – examining and discussing possible longitudinal health effects in humans

BackgroundMany previous studies have dealt with the effect of polychlorinated biphenyls (PCBs) on the thyroid gland, but their findings are inconsistent. One problem of these studies has been their use of cross-sectional designs. ObjectivesThe aim of the current study is to investigate longitudinal effects of PCBs on the thyroid gland, focusing on: morphological changes in thyroid tissue (i.e. thyroid volume), changes in thyroid hormones and in thyroid antibodies. MethodsA total of 122 individuals (Mage=44.7) were examined over a period of four years (t1 until t4). Medical history was collected via interviews, an ultrasound examination was performed and blood samples were taken to determine plasma PCB levels, thyroid stimulating hormone (TSH), free triiodthyronine (fT3), free thyroxine (fT4), thyroid peroxidase antibodies (TPOab), thyreoglobulin antibodies (TGab) and thyroid-stimulating hormone receptor antibodies (TSHRab). Rank correlation coefficients and mixed effect models were performed controlling for age and total lipids. ResultsThere were negative correlations between higher chlorinated biphenyls and fT3, cross-sectionally as well as longitudinally. We also found an interaction effect of higher-chlorinated PCBs over time for fT4 as well as TSHRab. In case of high exposure, a decrease in fT4 and an increase in TSHRab level were found over time. In regards to the other variables, our findings yielded no clear results in the examined time period. ConclusionThis is the first study to shows a PCB-related effect on fT3, fT4 and TSHRab over a four year period. The data also suggest that morphological and antibody findings remain inconsistent and do not allow for unambiguous interpretation.

Thyroid Hormone Indices in Computer Workers with Emphasis on the Role of Zinc Supplementation.

AIM:This study aimed to investigate the effects of computer monitor-emitted radiation on thyroid hormones and the possible protective role of zinc supplementation.MATERIAL AND METHODS:The study included three groups. The first group (group B) consisted of 42 computer workers. This group was given Zinc supplementation in the form of one tablet daily for eight weeks. The second group (group A) comprised the same 42 computer workers after zinc supplementation. A group of 63 subjects whose job does not entail computer use was recruited as a control Group (Group C). All participants filled a questionnaire including detailed medical and occupational histories. They were subjected to full clinical examination. Thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4) and zinc levels were measured in all participants.RESULTS:TSH, FT3, FT4 and zinc concentrations were decreased significantly in group B relative to group C. In group A, all tested parameters were improved when compared with group B. The obtained results revealed that radiation emitted from computers led to changes in TSH and thyroid hormones (FT3 and FT4) in the workers.CONCLUSION:Improvement after supplementation suggests that zinc can ameliorate hazards of such radiation on thyroid hormone indices.

Hyopmagnesium and treatment resistant depression

Our increasing knowledge about cellular and molecular level of brain functionality is changing the view on basis of psychological diseases, like depression, from brain functionality based diseases to organic based ones. It is known that changes in hormonal level, like thyroid, parathyroid, estrogen and progesterone hormones, could lead to mood deviations. Also the effect of some ions like lithium and calcium are represented over depression and mania. Here we introduce the case of a young patient who had a treatment resistant depression. However, his symptoms have been cured by adjusting the level of magnesium, which was idiopathically lower than normal lower limit.

Effect of L-carnitine and Hoodia gordonii Supplementation on Metabolic Markers and Physical Performance under Short Term Calorie Restriction in Rats

&lt;p&gt;Calorie restriction can occur as a consequence of food shortage due to natural calamities, war like situations or voluntarily for health benefits. This state of negative energy balance leads to decrease in performance and increase in feeling of hunger. A normal individual can sustain himself on stored energy in form of body fat for a period of time. It was hypothesised that use of an appetite suppressant like Hoodia gordonii along with L-carnintine, which helps in fat oxidation can be used as strategy for coping adverse situation without compromising physical performance. The aim of the study was to evaluate the combined effect of H. gordonii and L-carnitine supplementation on metabolic changes and appetite regulatory peptides during calorie restriction. Male albino rats were divided into two groups (n=12 in each) i.e. control (without treatment) and treated (H. gordonii organic solvent extract and L-carnitine, orally for 5 days at a dose of 100 mg/kg under 25 per cent calorie restriction). Biochemical variables including regulatory peptides were estimated along with physical efficiency tests. Significant changes in ghrelin, leptin, corticosterone and thyroid hormones were observed in comparison to control. While blood glucose, AMP kinase decreased significantly in the treated group, an increase in CPT-1 activity was observed compared with controls. It is concluded that approach could be practically suitable and effective in emergency situations of combat or food shortage.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Defence Science Journal, Vol. 66, No. 1, January 2016, pp. 11-18, DOI: http://dx.doi.org/10.14429/dsj.66.9178&lt;/strong&gt;&lt;/p&gt;

Evaluation of Thyroid Hormones Changes and CD4+ T-cell Count during Menstrual Cycle in Pulmonary TB Infected Women in Nnewi, Nigeria

Evaluation of Thyroid Hormones Changes and CD4+ T-cell Count during Menstrual Cycle in Pulmonary TB Infected Women in Nnewi, Nigeria

Relationship of Thyroid and Sex Hormones With Osteoarthritis in Postmenopausal Indian Women

Background: Osteoarthritis (OA) is the most frequent joint disease encountered in the clinical practice and is the most common cause of movement disability in the elderly. Females are found to have more severe OA, and prevalence and incidence increase after menopause. OA affects all articular tissues and finally leads to joint failure. Many experimental and clinical studies suggest that loss of hormone especially estrogen at the time of menopause increases a woman’s risk of getting OA and use of hormone replacement therapy (HRT) did seem to be associated with not only relieving of symptoms but also reduced rate of progression of OA. The aim of this case-control study was to investigate whether the thyroid and sex hormones are associated with OA in postmenopausal Indian women. Methods: One hundred twenty-five patients suffering from OA and 82 control subjects, all aged 45 - 65 years, were included in this study. Thyroid and sex hormones were measured in the serum by ELISA and chemiluminescent immunoassay technique. Results: Mean serum estrogen levels in the OA and control samples were 29.53 ± 3.27 and 49.21 ± 2.18 (P < 0.0001) which were significantly lower in OA patients compared with controls. Also these patients show significant change in thyroid hormones and progesterone hormone levels when compared with control subjects. Conclusion: The findings suggest that estrogen deficiency after menopause may contribute to developing OA in postmenopausal women. Estrogen can render help in such patients but with the current level of evidence, it cannot be recommended as a first-line treatment. J Clin Gynecol Obstet. 2016;5(4):117-120 doi: https://doi.org/10.14740/jcgo410e

Light-Regulated Thyroid Hormone Signaling Is Required for Rod Photoreceptor Development in the Mouse Retina.

Ambient light is both a stimulus for visual function and a regulator of photoreceptor physiology. However, it is not known if light can regulate any aspect of photoreceptor development. The purpose of this study was to investigate whether ambient light is required for the development of mouse rod photoreceptors. Newborn mouse pups (C57BL/6) were reared in either cyclic light (LD) or constant dark (DD). Pups were collected at postnatal day (P)5, P10, P17, or P24. We performed retinal morphometric and cell death analysis at P5, P10, and P17. Rhodopsin expression was assessed using immunofluorescence, Western blot, and quantitative RT-PCR analysis. Electroretinograms were performed at P17 and P24. Radioimmunoassay and ELISA were used to follow changes in thyroid hormone levels in the serum and vitreous. In the DD pups, the outer nuclear layer was significantly thinner at P10 and there were higher numbers of apoptotic cells at P5 compared to the LD pups. Rhodopsin expression was lower at P10 and P17 in DD pups. Electroretinogram a-waves were reduced in amplitude at P17 in the DD pups. The DD animals had lower levels of circulating thyroid hormones at P10. Light-mediated changes in thyroid hormones occur as early as P5, as we detected lower levels of total triiodothyronine in the vitreous from the DD animals. Drug-induced developmental hypothyroidism resulted in lower rhodopsin expression at P10. Our data demonstrate that light exposure during postnatal development is required for rod photoreceptor development and that this effect could be mediated by thyroid hormone signaling.

Thyroid hormone and vitamin D regulate VGF expression and promoter activity.

The Siberian hamster (Phodopus sungorus) survives winter by decreasing food intake and catabolizing abdominal fat reserves, resulting in a sustained, profound loss of body weight. Hypothalamic tanycytes are pivotal for this process. In these cells, short-winter photoperiods upregulate deiodinase 3, an enzyme that regulates thyroid hormone availability, and downregulate genes encoding components of retinoic acid (RA) uptake and signaling. The aim of the current studies was to identify mechanisms by which seasonal changes in thyroid hormone and RA signaling from tanycytes might ultimately regulate appetite and energy expenditure. proVGF is one of the most abundant peptides in the mammalian brain, and studies have suggested a role for VGF-derived peptides in the photoperiodic regulation of body weight in the Siberian hamster. In silico studies identified possible thyroid and vitamin D response elements in the VGF promoter. Using the human neuroblastoma SH-SY5Y cell line, we demonstrate that RA increases endogenous VGF expression (P<0.05) and VGF promoter activity (P<0.0001). Similarly, treatment with 1,25-dihydroxyvitamin D3 increased endogenous VGF mRNA expression (P<0.05) and VGF promoter activity (P<0.0001), whereas triiodothyronine (T3) decreased both (P<0.01 and P<0.0001). Finally, intra-hypothalamic administration of T3 blocked the short day-induced increase in VGF expression in the dorsomedial posterior arcuate nucleus of Siberian hamsters. Thus, we conclude that VGF expression is a likely target of photoperiod-induced changes in tanycyte-derived signals and is potentially a regulator of seasonal changes in appetite and energy expenditure.

The Effect of Laparoscopic Gastric Plication Surgery on Body Composition, Resting Energy Expenditure, Thyroid Hormones, and Physical Activity in Morbidly Obese Patients

Introduction: Laparoscopic gastric placation (LGP) is one of the innovative bariatric surgeries for weight loss. Several studies have shown that after LGP, resting energy expenditure (REE) has decreased may be as a result of changes in free-fat mass (FFM) and thyroid stimulating hormone (TSH) level. The aim of this study was to assess the changes in body composition, REE, and thyroid hormones in patients undergoing LGP between baseline and 3 months after LGP compared to controls. Methods: This study was performed on 42 patients (21 patients undergoing LGP and 21 age- and weight-matched subjects as controls). Weight, body mass index, body composition, resting metabolic rate, and thyroid hormones are measured at baseline in case and 3 months after the surgery in case and control groups. Results: The patients lost an average of 22.38 ± 4.00 kg weight and fat mass (FM), FFM, and REE decreased after surgery. An increase in T4 and a reduction of T3 and TSH at 3 months after LGP observed that was significant onl...

Apoptotic Marker Alternations in the Spleen of Experimentally Hyperthyroid and Hypothyroid Rat.

Apoptosis plays a critical role in the development and homeostasis of multicellular organisms, especially those with high cell turnover such as the lymphoid system. The current study aimed to examined the effects of changes in thyroid hormones on apoptosis of spleen in male rats. 30 rats were equally divided into three groups (10 animals each). G1, control group in which animals did not received any treatment; G2, Hypothyroid group in which rats received 0.05% 6-n-propyl-2-thiouracil (PTU) in drinking water for 6 weeks; G3, Hyperthyroid group in which rats received 100 μg/Kg L-Thyroxin sodium administration in drinking water for 6 weeks. In the present study; serum T3 and T4 concentrations were depressed and serum TSH concentration was significantly elevated in rats receiving PTU-induced hypothyroidism. On the other hand; serum T3 and T4 concentrations were significantly elevated and serum TSH concentration was depressed in rats receiving L-Thyroxin sodium-induced hyperthyroidism. In the current study; spleen in both hypothyroid and hyperthyroid rats revealed many of abnormalities as marked disruption of spleen structure, loss in distinction between the white and red pulps, degeneration and vacuolation with an increased in the lymphocyte population. Also, a significant increase in p53 and Caspase3 apoptotic cells and a significant decrease in Bcl-2 antiapoptotic cells in the spleen tissues revealed the possibility of the apoptosis occurrence after PTU or Thyroxin administration in the case of hypothyroidism and hyperthyroidism.

Exposure to difenoconazole causes changes of thyroid hormone and gene expression levels in zebrafish larvae.

Difenoconazole was believed to induce a large suite of symptoms during zebrafish development, but little is known about the negative invisible effect known as endocrine disruption. In this study, zebrafish (Danio rerio) embryos were exposed to various concentrations of difenoconazole from fertilization to 120 h post-fertilization (hpf), and the whole body content of thyroid hormone and gene transcription in the hypothalamic-pituitary-thyroid (HPT) axis were investigated. Results showed thyroxine (T4) levels were significantly decreased, while triiodothyronine (T3) concentrations were not changed. Moreover, the mRNA transcription of corticotrophin-releasing hormone (crh), thyroid-stimulating hormone (tshβ), transthyretin (ttr), thyronine deiodinase (dio1 and dio2), uridine diphosphate glucuronosyltransferase (ugt1ab) in the HPT axis were significantly up-regulated, but the transcriptions of thyroglobulin (tg), sodium/iodide symporter (nis) and thyroid hormone receptors trβ were not changed. The overall results showed that exposure to difenoconazole could alter thyroid hormone levels and gene transcription in zebrafish larvae, indicating thyroid endocrine disruption.

Thyroid Hormones and Moderate Exposure to Perchlorate during Pregnancy in Women in Southern California.

Background:Findings from national surveys suggest that everyone in the United States is exposed to perchlorate. At high doses, perchlorate, thiocyanate, and nitrate inhibit iodide uptake into the thyroid and decrease thyroid hormone production. Small changes in thyroid hormones during pregnancy, including changes within normal reference ranges, have been linked to cognitive function declines in the offspring.Objectives:We evaluated the potential effects of low environmental exposures to perchlorate on thyroid function.Methods:Serum thyroid hormones and anti-thyroid antibodies and urinary perchlorate, thiocyanate, nitrate, and iodide concentrations were measured in 1,880 pregnant women from San Diego County, California, during 2000–2003, a period when much of the area’s water supply was contaminated from an industrial plant with perchlorate at levels near the 2007 California regulatory standard of 6 μg/L. Linear regression was used to evaluate associations between urinary perchlorate and serum thyroid hormone concentrations in models adjusted for urinary creatinine and thiocyanate, maternal age and education, ethnicity, and gestational age at serum collection.Results:The median urinary perchlorate concentration was 6.5 μg/L, about two times higher than in the general U.S. population. Adjusted associations were identified between increasing log10 perchlorate and decreasing total thyroxine (T4) [regression coefficient (β) = –0.70; 95% CI: –1.06, –0.34], decreasing free thyroxine (fT4) (β = –0.053; 95% CI: –0.092, –0.013), and increasing log10 thyroid-stimulating hormone (β = 0.071; 95% CI: 0.008, 0.133).Conclusions:These results suggest that environmental perchlorate exposures may affect thyroid hormone production during pregnancy. This could have implications for public health given widespread perchlorate exposure and the importance of thyroid hormone in fetal neurodevelopment.Citation:Steinmaus C, Pearl M, Kharrazi M, Blount BC, Miller MD, Pearce EN, Valentin-Blasini L, DeLorenze G, Hoofnagle AN, Liaw J. 2016. Thyroid hormones and moderate exposure to perchlorate during pregnancy in women in Southern California. Environ Health Perspect 124:861–867; http://dx.doi.org/10.1289/ehp.1409614

Effects of Alcoholic Extract of Myrtus communis L. on the Hypothalamic-Pituitary-Thyroid Axis in Rats

Background: Myrtus communis leaves have the potential to affect thyroid hormone functions. Objectives: In this study, the effects of hydroalcoholic extract of M. communis on the hypothalamus-pituitary-thyroid axis and histological changes were studied. Materials and Methods: In this experimental study, 40 male rats were divided in 5 groups (n = 8): control, sham, and three experimental groups which received the extract of M. communis leaves in a minimal (0.75 mg/kg), Medium (1.5 mg/kg) and maximal amounts (3 mg/ kg), respectively. At the end of the 15th day blood samples were collected to measure triiodothyronine (T 3 ), thyroxine (T 4 ) and thyroidstimulating hormone (TSH) and to study thyroid gland tissue Results: Serum levels of T 4 and TSH in groups receiving maximum dose of the extract showed a significant decrease compared to sham group (P < 0.05). Conclusions: It is probable that some compounds in the alcoholic extract of M. communis leaves may be cause changes in serum TSH concentration and thyroid hormones.

Sequential Amniotic Fluid Thyroid Hormone Changes Correlate with Goiter Shrinkage following in utero Thyroxine Therapy

Several isolated reports of fetal goiter treatment have shown limited generalizability of approaches and provide no real guidance for optimal timing, dosages, and treatment strategies. Graves' disease accounts for >60% of these cases. Maternal treatments of hyperthyroidism include antithyroid medications such as methimazole and more commonly propylthiouracil (PTU). Here, our management of a patient with a fetal thyroid goiter from maternal exposure to PTU diagnosed at 23.6 weeks' gestation and the management of other cases allow us propose a general strategy for treatment. Intrauterine therapy with 200 and then 400 μg of levothyroxine (3 weeks apart) showed an 85% reduction in fetal thyroid goiter volume. We collected amniotic fluid samples at the time of treatments and assayed thyroid hormones and associated antibodies which closely reflected the changes in thyroid goiter mass volume. Our observations suggest a weekly or biweekly therapeutic intervention schedule. Utilizing both goiter size as well as a novel approach in using amniotic fluid hormone levels to monitor therapy efficacy might improve the quality of treatments. Only with a standardized approach and collection of amniotic fluid thyroid panels do we have the opportunity to develop the database required to determine the number and timing of treatments needed.

Neurotoxicological and thyroid evaluations of rats developmentally exposed to tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) and tris(2-chloro-2-ethyl)phosphate (TCEP)

Tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) and tris(2-chloro-2-ethyl)phosphate (TCEP) are organophosphorous flame retardants with widespread usage and human exposures through food, inhalation, and dust ingestion. They have been detected in human tissues including urine and breast milk. Reports of disrupted neural growth in vitro, abnormal development in larval zebrafish, and altered thyroid hormones in several species have raised concern for neurodevelopmental toxicity. This is especially the case for TDCIPP, which is more potent and has more activity in those assays than does TCEP. We evaluated the potential for developmental neurotoxicity of TDCIPP and TCEP in a mammalian model. Pregnant Long–Evans rats were administered TDCIPP (15, 50, or 150mg/kg/day) or TCEP (12, 40, 90mg/kg/day) via oral gavage from gestational day 10 to weaning. Corn oil was the vehicle control in both studies. Body weight and righting reflex development were monitored in all pups. A subset of offspring at culling and weaning, and dams at weaning, were sacrificed for serum and organ collection for measurement of brain, liver, and thyroid weights, serum thyroid levels, and serum and brain acetylcholinesterase activities. Brain weights were also measured in a group of adult TDCIPP-treated offspring. One male and one female from each litter were allocated for behavioral testing at several ages: standard locomotor activity (preweaning, postweaning, adults), locomotor activity including a lighting change mid-way (postweaning, adults), elevated zero maze (postweaning, adults), functional observational battery (FOB; postweaning, adults), and Morris water maze (place learning, reference and working memory; adults). Neither chemical produced changes in maternal body weight or serum thyroid hormones, but relative liver weight was increased at the high doses of both TDCIPP and TCEP. In offspring, there were no effects on viability, litter size, or birth weight. With TDCIPP, absolute liver weights were lower at weaning and weight gain was lower in the high-dose offspring until about two months of age. Thyroid hormones and brain weights were not altered and acetylcholinesterase (both brain and serum) was not inhibited by either chemical. TDCIPP-treated offspring showed slight differences in floating in the water maze, hindlimb grip strength, and altered activity habituation, whereas TCEP-treated rats showed differences in quadrant time (probe) and middle-zone preference in the water maze. Regarding these few changes, the effects were minimal, mostly not related to dose, and did not appear treatment-related or biologically significant. Overall, these data do not support the potential for thyrotoxicity or developmental neurotoxicity produced by TDCIPP or TCEP.

Age-Related Hearing Loss and Degeneration of Cochlear Hair Cells in Mice Lacking Thyroid Hormone Receptor β1.

A key function of the thyroid hormone receptor β (Thrb) gene is in the development of auditory function. However, the roles of the 2 receptor isoforms, TRβ1 and TRβ2, expressed by the Thrb gene are unclear, and it is unknown whether these isoforms promote the maintenance as well as development of hearing. We investigated the function of TRβ1 in mice with a Thrb(b1) reporter allele that expresses β-galactosidase instead of TRβ1. In the immature cochlea, β-galactosidase was detected in the greater epithelial ridge, sensory hair cells, spiral ligament, and spiral ganglion and in adulthood, at low levels in the hair cells, support cells and root cells of the outer sulcus. Although deletion of all TRβ isoforms causes severe, early-onset deafness, deletion of TRβ1 or TRβ2 individually caused no obvious hearing loss in juvenile mice. However, over subsequent months, TRβ1 deficiency resulted in progressive loss of hearing and loss of hair cells. TRβ1-deficient mice had minimal changes in serum thyroid hormone and thyrotropin levels, indicating that hormonal imbalances were unlikely to cause hearing loss. The results suggest mutually shared roles for TRβ1 and TRβ2 in cochlear development and an unexpected requirement for TRβ1 in the maintenance of hearing in adulthood.

Changes in thyroid hormones in patients undergoing liver transplantation

Changes in thyroid hormones in patients undergoing liver transplantation

The influence of end-stage liver disease and liver transplantation on thyroid hormones.

Thyroid dysfunction has been reported in most chronic illnesses including severe liver disease. These defects in thyroid hormone metabolism result in the sick euthyroid syndrome, also known as low T3 syndrome. Our objective was to evaluate the thyroid function in patients with end stage liver disease prior and after deceased donor liver transplantation and to correlate thyroid hormonal changes with the MELD score (Model for End stage Liver Disease). In a prospective study, serum levels of thyrotropin (thyroid stimulating hormone TSH), total thyroxine (tT4), free thyroxine (fT4) and triiodothyronine (T3) from 30 male adult patients with end stage liver disease were measured two to four hours before and 6 months after liver transplantation (LT). MELD was determined on the day of transplant. For this analysis, extra points were not added for patients with hepatocellular carcinoma. The patients had normal TSH and fT4 levels before LT and there was no change after the procedure. Total thyroxine and triiodothyronine were within the normal range before LT, except for four patients (13.3%) whose values were lower. Both hormones increased to normal values in all four patients after LT (P=0.02 and P<0.001, respectively). When the patients were divided into two groups (MELD <18 and MELD >18), it was observed that there was no change in the TSH, freeT4, and total T4 levels in both groups after LT. Although there was no significant variation in the level of T3 in MELD <18 group (P=0.055), there was an increase in the MELD >18 group after LT (P=0.003). Patients with end stage liver disease subjected to liver transplantation had normal TSH and fT4 levels before and after LT. In a few patients with lower tT4 and T3 levels before LT, the level of these hormones increased to normal after LT.