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Hypothyroidism
Kinds of Hypothyroidism Selected AbstractsPREVALENCE OF SUBCLINICAL HYPOTHYROIDISM IN OLDER PATIENTS WITH DIABETES MELLITUS WITH POORLY CONTROLLED DYSLIPIDEMIA IN CHINAJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2009Shao-Hua Wang PhD No abstract is available for this article. [source] SEASONALITY IN THE INCIDENCE OF CONGENITAL HYPOTHYROIDISM IN JAPANJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7 2005Dr Makiko Nakamizo PhD No abstract is available for this article. [source] HIGH-DOSE TAURINE SUPPLEMENTATION INCREASES SERUM PARAOXONASE AND ARYLESTERASE ACTIVITIES IN EXPERIMENTAL HYPOTHYROIDISMCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2007Melahat Dirican SUMMARY 1Hypothyroidism is accompanied by hyperlipidaemia and oxidative stress and is associated with several complications, such as atherosclerosis. Paraoxonase activity has been reported to decrease in several situations associated with atherosclerosis and oxidative stress. In the present study, the effects of different doses of taurine on serum paraoxonase and arylesterase activities, as well as on the serum lipid profile, were investigated in hypothyroid rats. 2Forty male Sprague-Dawley rats were randomly divided into five groups as follows: Group 1, rats received normal rat chow and tap water; Group 2, rats received standard rat chow + 0.05% propylthiouracil (PTU) in the drinking water; and Groups 3,5, taurine-supplemented PTU groups (standard rat chow + 0.5, 2 or 3% taurine in the drinking water, respectively, in addition to PTU). Paraoxon or phenylacetate were used as substrates to measure paraoxonase and arylesterase activity, respectively. Plasma and tissue malondialdehyde (MDA) levels, indicators of lipid peroxidation, were determined using the thiobarbituric-acid reactive substances method. Serum triglyceride, total cholesterol and high-density lipoprotein,cholesterol (following precipitation with dextran sulphate,magnesium chloride) were determined using enzymatic methods. 3Serum paraoxonase and arylesterase activities were increased and plasma and tissue MDA levels and serum triglyceride levels were reduced in a dose-dependent manner in taurine-treated hypothyroid rats. Taurine concentrations were positively correlated with enzyme activities and negatively correlated with MDA and triglyceride levels. 4Further studies are needed to investigate the role of taurine supplementation in hypothyroidism in human subjects. [source] Hypothyroidism and acquired von Willebrand's syndrome: a systematic reviewHAEMOPHILIA, Issue 3 2008E. MANFREDI Summary., Acquired von Willebrand's syndrome type I is the supposed main underlying cause of bleeding tendency in hypothyroid patients. The purpose of this systematic review was to summarize the published evidence on the association between hypothyroidism and acquired von Willebrand's syndrome. All published clinical epidemiological and interventional studies, case reports and in vitro studies that investigated the association between hypothyroidism and acquired von Willebrand's syndrome were identified by a computer-assisted search of the MEDLINE and EMBASE electronic databases. A quality assessment was performed for clinical epidemiological studies. A total of 41 papers were included. A total of 22 epidemiological in vivo studies, two in vitro studies and 47 case reports were finally analyzed. No high quality in vivo study was identified. Almost all bleeding episodes described in the case reports were mucocutaneous. von Willebrand factor (VWF) antigen value was available for 23 patients: median value 28 U/dL (range: 4,45); VWF activity was available for 24 patients: median value 28.5 U/dL (range: <3,55); factor VIII activity was available for 16 patients: median value 47 U/dL (range: 9,74). Acquired von Willebrand's syndrome may be the main factor responsible for bleeding diathesis in overt hypothyroid patients. Even if bleeding episodes are mainly mild and mucocutaneous, blood transfusion, drug administration or surgical procedure may be required. [source] Effect of hypothyroidism on the nitrergic relaxant responses of corpus cavernosal smooth muscle in rabbitsINTERNATIONAL JOURNAL OF UROLOGY, Issue 1 2006BULENT SARAC Background:, The incidence of hormonal dysfunction as a cause of impotence remains controversial. However, several recent studies have reported evidence of hormonal abnormalities in 25,35% of impotent men. Hypothyroidism has been reported to occur in 6% of impotent men. Methods:, In the present study, we examined nitrergic responses in hypothyroidism in rabbit corpus cavernosum and compared them with controls. Results:, Carbachol-induced relaxation responses and electrical field stimulation (EFS)-induced frequency-dependent relaxations decreased significantly in hypothyroid rabbits. Papaverine and sodium nitroprusside (SNP)-induced relaxation responses did not change significantly in hypothyroid rabbits. The contraction responses of phenylephrine and EFS-induced frequency-dependent contractions were significantly decreased in the hypothyroid group. Conclusions:, We can speculate that the reduction of relaxant responses to EFS and carbachol in hypothyroid rabbits can depend on a decreased release of nitric oxide (NO) from nitrergic nerves and endothelium or a reduction of muscarinic receptor density. Also, decreases in contraction responses may depend on diminished adrenoceptor density. [source] Induced hypothyroidism accelerates the regression of liver fibrosis in ratsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2007Rafael Bruck Abstract Background and Aim:, It has been shown in previous studies that hypothyroidism prevents the development of liver fibrosis in bile duct ligated rats and in rats chronically treated with thioacetamide (TAA). In recent years, regression of liver fibrosis (occurring spontaneously or during treatment) has been demonstrated in rodent models such as bile duct ligation and CCl4 administration. Therefore, in the present study, the potential therapeutic effect of hypothyroidism on liver fibrosis was investigated. Methods:, Liver fibrosis was induced in rats by administration of TAA (200 mg/kg, i.p., twice weekly) for 12 weeks. Hypothyroidism was then induced by either methimazole (0.04%) or propylthiouracil (0.05%) administered in drinking water for 8 weeks. Control euthyroid rats received normal drinking water. Hypothyroidism was confirmed by a significant elevation of serum thyroid-stimulating hormone levels. Results:, Eight weeks after the cessation of TAA administration, spleen weight, histological score of liver fibrosis, and hepatic hydroxyproline content were significantly lower in both groups of hypothyroid rats as compared to euthyroid controls (P < 0.001). In vitro studies using the rat hepatic stellate cell line HSC-T6 using northern blot analysis and zymography, respectively, showed that high concentrations of triiodotyronine (T3) enhanced transforming growth factor (TGF)-,-induced collagen I gene expression, and reduced metalloproteinase (MMP)-2 secretion, implying that reducing the levels of T3 may contribute to resolution of fibrosis. Additionally, low T3 concentration inhibited HSC-T6 proliferation. Conclusion:, Pharmacologically induced hypothyroidism accelerates the resolution of liver fibrosis in rats. This beneficial effect may in part be due to prevention of T3 -induced stimulation of collagen synthesis and reduction of MMP-2 secretion. [source] Gastric emptying function changes in patients with thyroid cancer after withdrawal of thyroid hormone therapyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2004PAN-FU KAO Abstract Background:, Hypothyroidism is commonly thought to cause decreased gastric emptying but is mostly associated with autoimmune disease. In the present study the gastric emptying function of thyroid cancer patients with severe hypothyroidism of short duration was evaluated with a radionuclide solid meal gastric emptying study. Methods:, Twenty-two patients who had undergone surgical operation and 131I ablation for thyroid cancer participated in solid meal gastric emptying studies before the withdrawal of thyroxine and then again 4 weeks after the withdrawal of thyroxine. Eleven patients had an additional gastric emptying study at 6 weeks after withdrawal of thyroxine. Gastric emptying curves and emptying parameters were calculated. Student's paired t -test was used for statistical analysis of data for all cases between the baseline and at 4 weeks after withdrawal. An additional repeated measure anova with multiple comparisons was performed on data between baseline, 4 weeks and 6 weeks after withdrawal for the other 11 patients. All P values presented are two-tailed and the significance level is 0.05. Results:, Hypothyroidism status was confirmed by the marked change of the serum thyroxine and thyroid-stimulating hormone 4 weeks and 6 weeks after withdrawal of the thyroxine replacement (P < 0.001). The gastric half-emptying time and emptying rate changed significantly after short-term severe thyroid hormone deficiency (P < 0.005). However, the length of the lag phase did not have a statistically significant change at 4 weeks or 6 weeks after withdrawal of the thyroxin replacement (P = 0.219 and 0.142). Conclusions:, Hypothyroidism following the withdrawal of the thyroxine replacement in thyroid cancer patients preparing for 131I cancer work-up can significantly prolong gastric half-emptying time and emptying rate. [source] Altered Thyroid Hormones and Behavioural Change in a Sub-Population of Rats Following Chronic Constriction InjuryJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2010E. Kilburn-Watt Hypothyroidism is associated with a disturbance of behaviour and mood. There are also individuals, not classified as hypothyroid, with low to ,low normal' thyroid hormone levels and normal thyroid-stimulating hormone (TSH) levels who have mood and behavioural changes. As the peripheral thyroid hormones decrease, TSH is expected to increase. However, there are a number of physiological mechanisms known to suppress TSH. In the present study, we report on thyroid hormone regulation in a rat model of neuropathic pain and altered social behaviour that is usually transient, but is persistent in a sub-group of the population. Following ligation of the sciatic nerve, male Sprague-Dawley rats were assessed for social dominance towards an intruder: 20% showed persistently decreased social dominance. Plasma levels of thyroid hormones, TSH and corticosterone were measured before and on days 2, 3, 4, 5 and 6 after injury in 21 rats. The mean plasma thyroxine (T4), free thyroxine (fT4) and triiodothyronine (T3) levels decreased significantly post-injury in rats with persistently changed behaviour compared to rats with unchanged behaviour (P , 0.002). There was no significant difference between groups for mean change in free triiodothyronine (fT3) or TSH. There was a correlation between decreased dominance behaviour and decrease in both T4 (r = 0.62, P = 0.009) and fT4 (r = 0.71, P = 0.001), but no correlation with TSH. In a sub-population of rats, decreased thyroid hormones did not result in the expected increased levels of TSH to restore pre-injury levels, nor did they show increased hypothalamic thyrotrophin-releasing hormone mRNA expression, indicating altered hypothalamic-pituitary-thyroid axis regulation. Because T3 availability to the brain is dependent on both circulating T3 and T4, decreased peripheral thyroid hormones may result in changed neural function, as expressed in altered complex behaviours in this sub-population of rats. [source] A Genomic Analysis of Subclinical Hypothyroidism in Hippocampus and Neocortex of the Developing rat BrainJOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2009J. E. Royland No abstract is available for this article. [source] Nicotine reverses adult-onset hypothyroidism-induced impairment of learning and memory: Behavioral and electrophysiological studiesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2006K.H. Alzoubi Abstract Nicotine alleviates cognitive impairment associated with a variety of health conditions. We examined the effect of chronic nicotine treatment on adult-onset hypothyroidism-induced impairment of learning and memory in rats. Hypothyroidism was induced by surgical removal of thyroid glands (thyroidectomy). One month later, chronic nicotine treatment (1 mg/kg sc, twice/day) was instituted for 4,6 weeks. Test of hippocampus-dependent spatial learning and memory in the radial arm water maze showed that hypothyroidism impaired learning as well as short-term and long-term memory retention. Chronic nicotine treatment reversed the hypothyroidism-induced learning and memory impairment. In normal rats, chronic nicotine treatment had no effect on learning and memory. Extracellular recordings from the CA1 region of anesthetized hypothyroid rats showed severe reduction of both early-phase and late-phase long-term potentiation (LTP) magnitude, which was reversed in nicotine-treated hypothyroid rats. These results show that chronic nicotine treatment prevents hypothyroidism-induced impairment of spatial cognition and LTP. © 2006 Wiley-Liss, Inc. [source] Thyroid hormone stimulates ,-glutamyl transpeptidase in the developing rat cerebra and in astroglial culturesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2005Asmita Dasgupta Abstract Hypothyroidism in the developing rat brain is associated with enhanced oxidative stress, one of the earliest manifestations of which is a decline in the level of glutathione (GSH). To investigate the role of thyroid hormone (TH) on GSH homeostasis, the effect of TH on ,-glutamyl transpeptidase (,GT), the key enzyme involved in the catalysis of GSH, was studied. Hypothyroidism declined the specific activity of cerebral ,GT at all postnatal ages examined (postnatal day 1,20) with a maximum inhibition of 42% at postnatal day 10. Intraperitoneal injection of TH to 15-day-old rat pups increased the specific activity of ,GT by 25-30% within 4,6 hr. Treatment of primary cultures of astrocytes by TH also enhanced the specific activity of ,GT by 30,40% within 4,6 hr. The induction of ,GT by TH was blocked by actinomycin D or cycloheximide. ,GT is an ectoenzyme that is normally involved in the catabolism of GSH released by astrocytes. In the presence of the ,GT-inhibitor, acivicin, GSH released in the culture medium of astrocytes increased linearly for at least 6 hr and TH had no effect on this accumulation pattern. In the absence of acivicin, GSH content of the medium from TH-treated cells was significantly lower than that of untreated controls due to activation of ,GT by TH and a faster processing of GSH. Because the products of ,GT reaction are putative precursors for neuronal GSH, the activation of ,GT by TH may be conducive to GSH synthesis in neurons and their protection from oxidative stress. © 2005 Wiley-Liss, Inc. [source] Evaluation and Treatment of Hyperthyroidism and HypothyroidismJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 10 2004ANP-C, FAANP, Mary Jo Goolsby EdD ABSTRACT This month's clinical practice guideline (CPG) review is on the diagnosis and treatment of hyperthyroidism and hypothyroidism as provided by the American Association of Clinical Endocrinologists. An estimated 27 million Americans have thyroid disease, and about 13 million of them are undiagnosed. The risk of thyroid disease increases with age, and women are seven times more likely than men to develop thyroid problems. Unfortunately, thyroid symptoms are usually very nonspecific and should be kept in the differential diagnosis of many clinical complaints. The format of this month's column is a little different because we received two independent manuscripts, each of which had merit. We made a decision to present both points of view and deleted repetitive material. This is an example of variable approaches one can take with reviewing and critiquing CPGs. [source] Neurologic Dysfunction in Hypothyroid, Hyperlipidemic Labrador RetrieversJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2007Christina L. Vitale Background: Hypothyroidism has been associated with a variety of neurologic signs, but the mechanism for this association is not completely understood. Hypothyroidism also is associated with hyperlipidemia that predisposes to atherosclerosis, increased blood viscosity, and thromboembolic events. Objective: The objective is to characterize neurologic signs potentially associated with hyperlipidemia and atherosclerosis in canine hypothyroidism. Animals: This study used dogs referred to North Carolina State University Veterinary Teaching Hospital for evaluation of neurologic signs. Materials and Methods: A retrospective study was conducted in which medical records of dogs with neurologic signs and a diagnosis of hypothyroidism and hyperlipidemia were reviewed. Details of the history, presenting signs, results of routine blood tests, thyroid tests, cerebrospinal fluid (CSF) analysis and diagnostic imaging, and response to therapy were compiled. Results: Three Labrador Retrievers and one Labrador Retriever cross fit the inclusion criteria. All dogs were hypothyroid and severely hyperlipidemic. Neurologic signs included tetraparesis, central and peripheral vestibular signs, facial paralysis, and paraparesis. Two dogs had an acute history and rapid resolution of signs consistent with an infarct, the presence of which was confirmed in 1 of the dogs by magnetic resonance imaging. Two dogs had chronic histories of cranial neuropathies and paraparesis. One of these dogs had evidence of iliac thrombosis and atherosclerosis on ultrasound examination. All dogs improved with thyroid hormone supplementation. Clinical Relevance: Labrador Retrievers may be predisposed to the development of severe hyperlipidemia in association with hypothyroidism. One possible consequence of severe hyperlipidemia is the development of neurologic signs due to atherosclerosis and thromboembolic events. [source] Atrial Lead Dysfunction: An Unusual Feature of HypothyroidismPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2008KRISTEN K. PATTON M.D. Hypothyroidism is known to have a multitude of cardiac electrophysiologic effects, including bradycardia, atrioventricular block, prolonged QT interval, and elevated ventricular pacing thresholds. We report the case of a 36-year-old woman who presented with isolated dysfunction of her atrial pacemaker lead, which reversed with thyroid hormone replacement. [source] Hypothyroidism in Netherton SyndromePEDIATRIC DERMATOLOGY, Issue 1 2008BEN ZION GARTY M.D. Letters to the Editor are welcomed for publication (subject to editing). Letters must be signed by all authors, and must not exceed two pages of text including references. Letters should not duplicate material submitted or published in other journals. Prepublication proofs will not be provided. [source] Psoriasiform Lesions and Abscesses as Initial Manifestations of Severe Hypothyroidism in a Previously Healthy 15-Year-Old GirlPEDIATRIC DERMATOLOGY, Issue 3 2007JENNIFER KWINTER B.A. We describe a previously healthy 15-year-old girl with psoriasiform lesions, abscesses, and extremely severe hypothyroidism, all presenting simultaneously. The pathophysiology of the connection is unclear, but several hypotheses are discussed. The temporal relationship of these conditions and the significant improvement of the skin lesions upon normalization of T4 levels following initiation of thyroid supplementation illustrate a direct association. It is probable that the extreme severity of hypothyroidism in our patient is implicated in the etiology of these skin lesions. This unique case illustrates that novel cutaneous manifestations may sometimes act as an early presenting sign of hypothyroidism and may be associated with more severe forms of the disorder. [source] Harlequin Ichthyosis in Association with Hypothyroidism and Juvenile Rheumatoid ArthritisPEDIATRIC DERMATOLOGY, Issue 5 2003Yuin-Chew Chan M.D. Two Chinese children, a 2-year-old boy and an 11-year-old girl, presented with these classic features as well as alopecia and loss of eyebrows and eyelashes. The boy was small for his age and was found to have hypothyroidism at the age of 18 months; he is currently on thyroxine replacement therapy. At 6 years of age, the girl developed symmetrical polyarthritis associated with positive rheumatoid factor and radiologic evidence of erosive arthritis, suggestive of juvenile rheumatoid arthritis. She received prednisolone, nonsteroidal anti-inflammatory drugs (NSAIDs), and subsequently methotrexate for her arthritis, with clinical and radiologic improvement. Early therapy with oral retinoids in both children accelerated shedding of the hyperkeratotic plates as well as improved ectropion and eclabium. There was no major adverse reaction to oral retinoids. The development of juvenile rheumatoid arthritis in survivors with harlequin ichthyosis has not been previously described. The use of prednisolone and NSAIDs in the girl did not affect the skin condition, but the addition of methotrexate led to a decrease in erythema. The association with autoimmune disease is probably coincidental. The psychosocial impact of this severe lifelong disease on the two families was enormous. Early retinoid therapy may improve the disorder and help increase survival rates. A multidisciplinary approach, including psychosocial support of the affected families, is vital in the management of this lifelong disease. [source] Hypothyroidism in neonates post-iodinated contrast media: a systematic reviewACTA PAEDIATRICA, Issue 10 2009Alexandra Ahmet Abstract Aim:, To determine if neonates exposed to iodinated contrast media are at risk of hypothyroidism. Methods:, A systematic review was conducted by searching electronic databases (e.g. MEDLINE), contacting experts and scanning reference lists. Studies examining the effects of contrast media on neonatal thyroid function were included. Two reviewers independently screened the literature and assessed the risk of bias, while one reviewer abstracted data. Results:, Eleven studies were included; nine studies directly examined the risk of hypothyroidism (n = 182 neonates exposed to contrast media). All were highly affected by bias. In the three studies including term infants, one showed a trend towards increased thyroid-stimulating hormone (TSH) and decreased free thyroxine (FT4) among exposed groups. Six of 72 (8.3%) term infants exposed were treated for hypothyroidism. In studies of premature infants, there was a trend towards increased TSH (n = 3/7 studies), lower total thyroxine (n = 1), decreased triidothyronine and FT4 (n = 3) and hypothyroidism (n = 5). Twenty of 110 (18.2%) premature infants exposed were treated for hypothyroidism. Conclusion:, Hospitalized neonates exposed to iodinated contrast media are at risk for abnormal thyroid function and development of hypothyroidism. Premature infants might be at increased risk. Well-controlled studies are required to replicate our findings because the included studies were highly affected by bias. [source] Review of animal models for autism: implication of thyroid hormoneCONGENITAL ANOMALIES, Issue 1 2006Miyuki Sadamatsu ABSTRACT,, Autism is a behaviorally defined disorder associated with characteristic impairments in social interactions and communication, as well as restricted and repetitive behaviors and interest. Its prevalence was once thought to be 2/10 000, but recently several large autism prevalence reviews revealed that the rate of occurrence was roughly 30/10 000. While it has been considered a developmental disorder, little is certain about its etiology. Neuroanatomical studies at the histological level in the brains of autistic patients provide many arguments in the etiology of autism. Results from postmortem and imaging studies have implicated many major structures of the brain including the limbic system, cerebellum, corpus callosum, basal ganglia and brainstem. There is no single biological or clinical marker for autism. While several promising candidate genes have been presented, the critical loci are yet unknown. Environmental influences such as rubella virus, valproic acid, and thalidomide exposure during pregnancy are also considered important, as concordance in monozygotic twins is less than 100% and the phenotypic expression of the disorder varies widely. It is thus hypothesized that non-genetic mechanisms contribute to the onset of autistic syndrome. In light of these ambiguities, hope is held that an animal model of autism may help elucidate matters. In this article, we overview most of the currently available animal models for autism, and propose the rat with mild and transient neonatal hypothyroidism as a novel model for autism. [source] Developmental delay and unstable state of the testes in the rdw rat with congenital hypothyroidismDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 4 2004Yasuhiro Sakai From the present study of the rdw rat, it is clear that the thyroid hormone is essential for the development and maintenance of the testes. In previous studies, the thyroid hormone has few serious effects on the testes except during the neonatal stage when the thyroid hormone receptor is mainly present. However, there is little knowledge concerning the prolonged effect of thyroid hormone deficiency throughout the rat's life span. In the present study, a morphological analysis was performed on the testes of rdw rats with congenital hypothyroidism. The rdw testes required a longer time to develop into the normal adult structure. Moreover, the developed, normal structure began to degenerate after full maturation. Specific characteristics of the rdw testes include: (i) a prolonged proliferation of Sertoli cells during postnatal development; (ii) a developmental delay in the appearance of spermatocytes and spermatid; (iii) direct contact with each other for both spermatocytes and spermatids, without Sertoli cell cytoplasm completely intervening between adjacent germ cells; (iv) subsequent apoptosis of germ cells after maturation; (v) reduction in the height of the seminiferous epithelium; and (vi) lower testosterone levels in the rdw rats, especially during old age. Thus, we conclude that the thyroid hormone plays an important role in developing and maintaining normal function of testes. [source] Universal newborn screening and adverse medical outcomes: A historical noteDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 4 2006Jeffrey P. Brosco Abstract Universal newborn screening programs for metabolic disorders are typically described as a triumph of medicine and public policy in the US over the last 50 years. Advances in science and technology, including the Human Genome Project, offer the opportunity to expand universal newborn screening programs to include many additional metabolic and genetic conditions. Although the benefits of such screening programs appear to outweigh their costs, some critics have claimed that historical examples of inadvertent harm ensuing from false-positive screening results and subsequent inappropriate medical treatment should make us wary of expanding universal newborn screening. In this essay, we report the results of a review of the published literature to assess whether the extension of screening from at risk populations to all newborns led to substantial morbidity and mortality from misguided medical treatment. We provide a historical overview of universal newborn screening programs in the United States, and then focus on six early NBS programs: congenital hypothyroidism, phenylketonuria, congenital adrenal hyperplasia, galactosemia, sickle cell disease, and maple syrup urine disease. Our comprehensive search of published sources did not reveal a widespread problem of harm ensuing from medical treatment of children with false positive screening test results. © 2006 Wiley-Liss, Inc. MRDD Research Reviews 2006;12:262,269. [source] Changes in mid-to-late latency auditory evoked reponses in the chicken during neural maturationDEVELOPMENTAL PSYCHOBIOLOGY, Issue 1 2010Rebbekah Atkinson Abstract Utilizing the special advantages offered by the protracted maturation of neural circuits in chicken forebrain this study investigates the functional consequence of maturation using auditory evoked response potentials (AERPs) in behaving animals. Repeated measures AERP recordings were undertaken between weeks 1 and 8 posthatch. Quantitative analysis revealed a significant decrease in amplitude of the positive AERP component and a decrease in latency of the negative AERP component with maturation. AERPs were also utilized to investigate perturbed maturation via the induction of chemically induced hypothyroidism. Results from this study showed that the induction of late onset hypothyroidism produces measurable effects on the chicken AERP consistent with perturbation in maturation of neuronal circuits and synapses. This suggests that AERPs may be useful noninvasive functional measures of brain maturation that can be used to study the effects of endogenous or exogenous factors on brain maturation in the chicken. Since human brain also exhibits a protracted maturation period the availability of a well-characterized animal model for protracted brain maturation provides an opportunity to identify molecules, genes and environmental factors that are important in the regulation of maturation. The protracted maturation of neuronal circuits observed in chicken forebrain offers such a model. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 52: 24,34, 2010 [source] Treatment emergent mania responding to valproate in a Chinese female adolescent population with eating disorders: A case seriesEUROPEAN EATING DISORDERS REVIEW, Issue 6 2008Phern Chern Tor Abstract Eating disorders are commonly associated with depressive symptoms. In an adolescent and binge eating population fluoxetine is commonly used to treat co-morbid depression associated with eating disorders. In some patients this may precipitate treatment emergent mania (TEM). Risk factors in the adolescent population include being older, female, having a longer duration of illness, more previous mood episodes, a higher prevalence of subclinical hypothyroidism, early-onset anxiety and recent exposure to a mood-elevating agent. Diagnosis and management of these co-morbid conditions is challenging due to the overlapping symptomatology and the adverse effects of both conditions complicating pharmacological management. This is illustrated with three cases in a Chinese female adolescent population that experienced TEM while on fluoxetine and responded to valproate. Copyright © 2008 John Wiley & Sons, Ltd and Eating Disorders Association. [source] Interference in thyroid-stimulating hormone determinationEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2010Mauro Imperiali Eur J Clin Invest 2010; 40 (8): 756,758 Abstract Background, Thyroid-stimulating hormone (TSH) measurement plays a major role in the diagnosis of thyroid disorders. Despite the good quality of immunochemical tests measuring TSH levels, the presence of interfering substances can sometimes alter the TSH results. Design, We reported the case of a 79-year-old man affected by primary autoimmune hypothyroidism hospitalized for pneumonia. A TSH value > 100 mIU L -1 (reference: 0.44 mIU L -1) was found at admission. No signs and symptoms of hypothyroidism were found upon clinical examination and serum concentration of the free thyroxine (FT4) was normal. Results, Serum treatment in heterophile antibody blocking tubes did not change the TSH result in our assay, while normal levels were found in a different immunoassay method. An abnormal pattern was found in protein electrophoresis at admission, with IgG / j and IgM / k monoclonal bands proved in immunofixation. Interestingly, the disappearance of monoclonal bands was paralleled with a normalization of the TSH value. Conclusions, We suggest in this study that the TSH determination might be influenced by the presence of transient paraproteins. [source] Hypothyroidism and acquired von Willebrand's syndrome: a systematic reviewHAEMOPHILIA, Issue 3 2008E. MANFREDI Summary., Acquired von Willebrand's syndrome type I is the supposed main underlying cause of bleeding tendency in hypothyroid patients. The purpose of this systematic review was to summarize the published evidence on the association between hypothyroidism and acquired von Willebrand's syndrome. All published clinical epidemiological and interventional studies, case reports and in vitro studies that investigated the association between hypothyroidism and acquired von Willebrand's syndrome were identified by a computer-assisted search of the MEDLINE and EMBASE electronic databases. A quality assessment was performed for clinical epidemiological studies. A total of 41 papers were included. A total of 22 epidemiological in vivo studies, two in vitro studies and 47 case reports were finally analyzed. No high quality in vivo study was identified. Almost all bleeding episodes described in the case reports were mucocutaneous. von Willebrand factor (VWF) antigen value was available for 23 patients: median value 28 U/dL (range: 4,45); VWF activity was available for 24 patients: median value 28.5 U/dL (range: <3,55); factor VIII activity was available for 16 patients: median value 47 U/dL (range: 9,74). Acquired von Willebrand's syndrome may be the main factor responsible for bleeding diathesis in overt hypothyroid patients. Even if bleeding episodes are mainly mild and mucocutaneous, blood transfusion, drug administration or surgical procedure may be required. [source] Acquired von Willebrand's syndrome resulting from untreated hypothyroidism in two prepubertal girlsHAEMOPHILIA, Issue 6 2006A. GALLI-TSINOPOULOU Summary., Acquired von Willebrand syndrome (AvWS) is a rare bleeding disorder associated with a number of different diseases, including hypothyroidism. We describe two prepubertal girls with AvWS and undiagnosed hypothyroidism due to thyroiditis Hashimoto. The patients had neither family history nor symptoms of bleeding disorders. Substitution therapy with levothyroxine led to normalization of the coagulation parameters. We report these cases in order to raise awareness among paediatricians so that the AvWS should be suspected and searched for with the appropriate laboratary tests in all cases of hypothyroidism. Moreover, patients with bleeding diathesis of unknown origin should also be investigated for hypothyroidism. [source] Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis: Selected practical issues in their evaluation and management,HEPATOLOGY, Issue 1 2009Raj Vuppalanchi Nonalcoholic fatty liver disease (NAFLD) is among the most common causes of chronic liver disease in the western world. It is now recognized that these patients have myriad of important co-morbidities (e.g., diabetes, hypothyroidism and metabolic syndrome). The workup of patients with suspected NAFLD should consist of excluding competing etiologies and systemic evaluation of metabolic comorbidities. NAFLD is histologically categorized into steatosis and steatohepatitis, two states with fairly dichotomous natural history. While significant progress has been made in terms of noninvasively predicting advanced fibrosis, insufficient progress has been made in predicting steatohepatitis. Currently, liver biopsy remains the gold standard for the histological stratification of NAFLD. While sustained weight loss can be effective to treat NASH, it is often difficult to achieve. Foregut bariatric surgery can be quite effective in improving hepatic histology in selected patients without liver failure or significant portal hypertension. Thiazolidinediones have shown promise and the results from the ongoing, large multicenter study should become available soon. Large multicenter studies of CB, receptor anatagonists are also underway but their results will not be available for several years. Several recent studies have highlighted that cardiovascular disease is the single most important cause of morbidity and mortality in this patient population. Conclusion: Health care providers should not only focus on liver disease but also concentrate on aggressively modifying and treating their cardiovascular risk factors. (HEPATOLOGY 2009;49:306-317.) [source] NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in "Brain-Lung-Thyroid Syndrome",HUMAN MUTATION, Issue 2 2010Loïc Guillot Abstract NKX2-1 (NK2 homeobox 1) is a critical regulator of transcription for the surfactant protein (SP)-B and -C genes (SFTPB and SFTPC, respectively). We identified and functionally characterized two new de novo NKX2-1 mutations c.493C>T (p.R165W) and c.786_787del2 (p.L263fs) in infants with closely similar severe interstitial lung disease (ILD), hypotonia, and congenital hypothyroidism. Functional analyses using A549 and HeLa cells revealed that NKX2-1-p.L263fs induced neither SFTPB nor SFTPC promoter activation and had a dominant negative effect on wild-type (WT) NKX2-1. In contrast,NKX2-1-p.R165W activated SFTPC, to a significantly greater extent than did WTNKX2-1,whileSFTPB activation was only significantly reduced in HeLa cells. In accordance with our in vitro data, we found decreased amounts of SP-B and SP-C by western blot in bronchoalveolar lavage fluid (patient with p.L263fs) and features of altered surfactant protein metabolism on lung histology (patient with NKX2-1-p.R165W). In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in "Brain-Lung-Thyroid syndrome". © 2009 Wiley-Liss, Inc. [source] Chronic hypothyroidism only marginally affects adult-type Leydig cell regeneration after EDS administrationINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2010Eddy Rijntjes Summary Chronic prenatally induced dietary hypothyroidism delays adult-type Leydig cell development, but does not block this process. Using a chemical model to induce hypothyroidism, it was suggested that development of a new population of Leydig cells was completely inhibited following the addition of the cytotoxic compound ethane-1,2-dimethyl sulphonate (EDS). In this study, we used a dietary approach to induce hypothyroidism and reinvestigated the regeneration of the Leydig cell population following EDS administration. Eighty-four day old euthyroid and chronically hypothyroid rats received an injection of EDS and were killed directly before or at regular intervals up to 77 days after EDS. In some control and hypothyroid animals, the first progenitor-type Leydig cells were observed at day 12 after EDS. At day 16, Leydig cell progenitors were present in all rats. The percentage of proliferating Leydig cells peaked in the euthyroid animals at day 21 after EDS. In the hypothyroid testis such a peak was not observed, although the percentage of proliferating regenerating Leydig cells was significantly higher from days 35 to 56 compared with the controls. This suggested that the wave of Leydig cell proliferation was delayed in the hypothyroid animals as compared with the euthyroid controls. On the day of EDS injection, the Leydig/Sertoli cell ratio was 37% lower in the hypothyroid rats compared with the controls. The Leydig/Sertoli cell ratio remained lower in the EDS-treated hypothyroid animals compared with the controls at all time points investigated. At day 77 after EDS, the Leydig cell population had returned to its pre-treatment size in both groups. Plasma testosterone production was reduced to below detectable levels immediately after EDS injection, and started to increase again on day 16, reaching pre-treatment values on day 21 in both groups. Taken together, severely reduced thyroid hormone levels did not block the regeneration of the adult-type Leydig cell population following EDS, as has been suggested previously. [source] Are germ cell factors essential in the testicular enlargement after neonatal hypothyroidism recovery?INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2002A study using W/Wv mutant mice model We examined the issue of whether germ cell factors are required for testicular enlargement that occurs after recovery from neonatal hypothyroidism. Experiments were performed using W/Wv mutant mice (lacking germ cells) and normal mice (ICR). The pups in experimental group (neonatal hypothyroid) received 6 propyl 2-thio-uracil (PTU) treatment, administered by adding 0.1% (w/v) to the water provided to the mother from day 1 of birth through day 25 postpartum, while the pups of control group received drinking water only. Mice were sacrificed at the age of day 25, 50 and 90, in the case of ICR mice, or at day 25 and 90 in the case of W/Wv mutant mice. In both groups, early hypothyroidism caused a partial recoverable decrease in body growth and testicular development. Both ICR and W/Wv mutant mice, those recovered from neonatal hypothyroidism showed an increase in testis weights, the number of Sertoli cells, and the diameter of the semniferous tubules. This study demonstrates that neonatal hypothyroidism led recovery caused testicular enlargement not only in ICR mice but also in germ cell depleted W/Wv mutant mice. Hence these findings deny direct involvement of the germ cell factors in the process of testicular enlargement in recovered mice even in vivo, and reaffirm the notion that thyroid hormone directly regulates the dynamics of Sertoli cell maturation. [source] | ||||||||||||||||||||||||||||||||||||||||