High Thyroid Hormone Levels Research Articles

Charcoal Hemoperfusion in the Treatment of Levothyroxine Intoxication

Levothyroxine (l-thyroxine) intoxication may arise from intentional or accidental ingestion of excessive doses of the hormone and may cause symptoms equivalent to thyroid storm. We report a case of massive accidental l-thyroxine intoxication resulting from an error in the preparation of capsules to treat goiter. A 61-year-old woman was admitted showing high levels of thyroid hormones, with serum-free l-thyroxine level of 955.90 nmol/L (74.1 ng/mL) (normal values: 11.61-27.09 nmol/L or 0.9-2.1 ng/mL). It was discovered that she had ingested 50 mg instead of 50 microg/day of l-thyroxine during 9 days. Following charcoal hemoperfusion, the levels of total thyroxine, serum-free l-thyroxine, and triiodothyronine declined dramatically, with a reproducible pattern of reduction in hormone levels observed after each of the three sessions. The patient recovered from her stuporous mental state, atrial fibrillation, and acute respiratory failure. The use of hemoperfusion with a charcoal filter appears to be a very important therapeutic tool for the treatment of acute and severe forms of thyrotoxicosis due to l-thyroxine intoxication.

Resistance to Thyroid Hormone in a Patient with Coexisting Graves' Disease

Resistance to thyroid hormone (RTH) is a rare disorder in which an abnormality in the binding domain of the thyroid hormone receptor results in end-organ insensitivity to the actions of thyroid hormones. This disorder is sometimes misdiagnosed as Graves' disease due to the presence of a goiter with high Iodine-123 thyroid uptake and high levels of total and free thyroid hormones. Additionally, some patients with RTH may experience palpitations or tachycardia. There is a previous report of a patient with pituitary RTH and concurrent Graves' disease. We describe a patient who was found to have a goiter with signs and symptoms of hyperthyroidism by his primary care physician. Work-up revealed a low thyroid stimulating hormone (TSH), high thyroid-stimulating immunoglobulins, high Iodine-123 thyroid uptake, as well as increased homogenous activity in both thyroid glands on nuclear scan and a suppressed TSH. Diagnosis of Graves' disease was made, and the patient underwent radioactive ablation of the thyroid gland. The patient subsequently developed hypothyroidism and required a much higher dose of levothyroxine than his weight-based estimate of a full replacement dose to maintain euthyroidism. On 325 micog of daily levothyroxine the patient was clinically euthyroid and had a normal TSH although his levels of T3 and T4 were high. Work-up revealed a mutation in the thyroid hormone beta-receptor gene, consistent with diagnosis of RTH. RTH is often misdiagnosed as Graves' disease. However, these disorders can coexist, and the concurrent presence of both disorders in a patient can present diagnostic challenges. A previous report of a patient with Graves' disease associated with RTH was published before gene sequencing could be used to confirm diagnosis of RTH. We present a patient with Graves' disease and concurrent RTH that was confirmed by gene sequencing, showing a mutation in the thyroid hormone receptor beta gene.

Thyroid Hormone Beta Receptor Mutation Causes Renal Dysfunction and Impairment of ClC-2 Chloride Channel Expression in Mouse Kidney

Background/Aims: Mutations in the thyroid hormone receptor β (TR-β) gene result in resistance to thyroid hormone (RTH). Mutation Δ337T in the TR-β gene has been shown to have the characteristics of RTH syndrome in mice. The aim of this work was to study the possible involvement of TR-β receptor in thyroid modulation of ClC-2 in mouse kidney. Methods: Expression of mouse (Δ337T and normal C57BL/6) renal RNA and protein expression were studied by reverse transcriptase-polymerase chain reaction and Western blot, respectively, in mice with hyper- or hypothyroidism. Renal function was studied by analysis of urinary electrolyte excretion. Studies of the ClC-2 promoter region were performed in immortalized renal proximal tubule (IRPT) cells. Results: In RTH syndrome mice (Δ337T), renal dysfunction was found to be associated with changes in the fractional excretion of sodium (FE_Na) and chloride (FE_Cl). ClC-2 chloride channel mRNA and protein expression were found to be decreased by 40% in heterozygous and homozygous mutant mouse kidneys and high levels of plasma thyroid hormone were detected in both groups. Hypothyroidism induced by methimazole decreased the renal expression of ClC-2 in normal mice but not in Δ337T mutant mice. In in vitro studies performed on IRPT cells subjected to thyroid hormone treatment, the promoter region of the ClC-2 chloride channel was stimulated in a dose-dependent manner. Conclusions: This work emphasizes the importance of thyroid hormone in electrolyte handling along the nephron and suggests its participation in renal ClC-2 gene transcription via the TR-β receptor pathway.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 microg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

The effect of thyroid hormones on the white adipose tissue gene expression of PAI-1 and its serum concentration

Metabolic syndrome is associated with an increased risk of developing cardiovascular diseases and Plasminogen activator inhibitor 1 (PAI-1) overexpression may play a significant role in this process. A positive correlation between adipose tissue gene expression of PAI-1 and its serum concentration has been reported. Furthermore, high serum levels of thyroid hormones (T3 and T4) and PAI-1 have been observed in obese children. The present study evaluates the impact of thyroid hormone treatment on white adipose tissue PAI-1 gene expression and its serum concentration. Male Wistar rats (60 days old) were treated for three weeks with T4 (50 µg/day, Hyper) or with saline (control). Additionally, 3T3-L1 adipocytes were treated for 24 h with T4 (100 nM) or T3 (100 nM). PAI-1 gene expression was determined by real-time PCR, while the serum concentration of PAI-1 was measured by ELISA using a commercial kit (Innovative Research, USA). Both the serum concentration of PAI-1 and mRNA levels were similar between groups in retroperitoneal and epididymal white adipose tissue. Using 3T3-L1 adipocytes, in vitro treatment with T4 and T3 increased the gene expression of PAI-1, suggesting non-genomic and genomic effects, respectively. These results demonstrate that thyroid hormones have different effects in vitro and in vivo on PAI-1 gene expression in adipocytes.

Paradigm Shift in the Pathophysiology of Postmenopausal and Thyrotoxic Osteoporosis

Bone loss is an inevitable result of getting older in both sexes. This loss is accelerated in women in the early years following menopause and in both sexes with drugs and diseases, prominently hyperthyroidism. Postmenopausal osteoporosis and hyperthyroid osteoporosis, both of which are widely recognized clinical entities, have been thought to arise from low estrogen levels and high thyroid hormone levels, respectively. However, when estrogen declines, follicle-stimulating hormone, an anterior pituitary hormone, rises. Likewise, when thyroid hormone levels rise in hyperthyroidism, thyroid-stimulating hormone levels fall. We have used a complement of mouse genetic, pharmacological, and cell biological approaches to unravel a direct action of follicle-stimulating hormone and thyroid-stimulating hormone on bone remodeling and bone mass. Apart from establishing a novel pituitary-bone axis of physiological significance, our studies challenge the existing 1-hormone, 1-disease paradigm in endocrinology and suggest that a plurality of hormonal disturbances involving pituitary hormones cause postmenopausal and hyperthyroid osteoporoses. New therapeutic targets thus emerge from these studies. Mt Sinai J Med 76:474-483, 2009. (c) 2009 Mount Sinai School of Medicine.

Thyreotropic effect of human Chorionic Gonadotropin (hCG) in mares at estrus

The β-subunits of thyroid stimulating hormone (TSH) and human chorionic gonadotropin (hCG) share a high homology, just like the ectodomains of their receptors, do. As a consequence, hCG was shown to exert a thyrotropic action in humans and hamsters. This study aimed to investigate whether hCG, used to induce ovulation, displays a thyrotropic effect in the equine species too. Forty mares at estrus were divided in two groups; 20 were intravenously treated with sterile saline solution (NaCl 0.9%) (group A); 20 were intravenously treated with 4000 I.U. of hCG (group B). All the mares were artificially inseminated 24 hours after the administration of the drugs and underwent blood collection at estrus detection (T1), 2, 6, 24 hours later (T2, T3, T4), and 3 and 6 days later (T5, T6), in order to detect serum fT3 and fT4 concentrations. fT3 concentrations gave rise to similar and constant trends in the two groups, without any statistically significant difference, whereas fT4 concentrations declined in both groups, remaining statistically higher in group B than in group A for 48 hours (p < 0.05), thus accounting for a thyrotropic effect of hCG. Pregnancy rate was 70% in group B and 40% in group A, respectively. The higher success in the outcome of pregnancy may result from the immunomodulating and steroidogenic effects of hCG and from the higher levels of thyroid hormones observed in the hCG treated group.

Successful Treatment of Plasma Exchange for Severe Cerebral Venous Thrombosis with Thyrotoxicosis

Although cerebral venous thrombosis (CVT) is generally treated with anticoagulants, some patients have a poor prognosis. We report a 34-year-old woman who developed severe CVT with mental symptoms and intracerebral hemorrhage with central herniation. She had a hypercoagulable state accompanied by thyrotoxicosis. Aggressive medical therapies including unfractionated heparin, a mixture of concentrated glycerin and fructose, and intravenous administration of thiamazole, iohexol, and propranolol were ineffective. The patient was treated with plasma exchange (PE) two times, in addition to aggressive medical therapies. The neurologic symptoms and laboratory data including high levels of thyroid hormones began to improve soon after the first PE. Activated partial thromboplastin time was prolonged after PE although the heparin dose was not changed. After 6 months, her modified Rankin Scale score was 2. PE should be considered for severe CVT as a result of a hypercoagulable state accompanied by thyrotoxicosis, because it not only reduces thyroid hormones, but also might remove multiple prothrombotic factors.

Thyroid responsiveness of the large African barb Labeobarbus intermedius (Teleostei; Cyprinidae): Individual variability and morphological consequences

Thyroid hormones (THs), produced by the thyroidgland, play an important role in the regulation of ontog-eny in bony fishes. They influence the rate of individualdevelopment of the body as a whole, as well as the ratesof growth and differentiation of its particular structures[1]. Definitive morphology of fishes is a result of inter-action between the developing body and a hormone,and depending on the TH level and an ability of thebody to respond to TH, i.e., TH-responsiveness.The TH level depends on the functional activity ofthe thyroid gland. A low activity and, as a result, lowTH levels lead to slowing down the ontogeny. On thecontrary, high TH levels accelerate the ontogeny [1, 2].Differences in the activity of the thyroid gland canresult in variability of the expression of morphologicalfeatures [2]. Recently, indirect data on individual vari-ability of TH-responsiveness in the large African barbLabeobarbus intermedius were reported. They demon-strated that juveniles of this fish differently respondedto similar doses of exogenous THs under experimentalconditions [3, 4]. Taking into account an important roleof TH-responsiveness in the ontogeny control, we stud-ied individual variability of TH-responsiveness and itsinvolvement in intraspecific morphological diversifica-tion in fishes.We compared morphological changes inL. intermedius siblings grown at a high level of exoge-nous TH. We focused our attention on the serial struc-tures that usually decrease in number when theL. intermedius siblings are growing under a high THlevel [3, 4].The eggs were obtained from the crossing ofL. intermedius spawners taken from a Lake Tana tribu-tary, the Gumara River (Ethiopia) and divided into twogroups. The first experimental group was put into amedium with a high TH content, namely, 2 × 10

Interference of a Mutant Thyroid Hormone Receptor α1 with Hepatic Glucose Metabolism

Mice expressing the mutant thyroid hormone receptor TRalpha1R384C, which has a 10-fold reduced affinity to the ligand T(3), exhibit hypermetabolism due to an overactivation of the sympathetic nervous system. To define the consequences in the liver, we analyzed hepatic metabolism and the regulation of liver genes in the mutant mice. Our results showed that hepatic phosphoenolpyruvate-carboxykinase was up-regulated and pyruvate kinase mRNA down-regulated, contrary to what observed after T(3) treatment. In contrast, mice expressing a mutant TRalpha1L400R specifically in the liver did not show a dysregulation of these genes; however, when the TRalpha1L400R was expressed ubiquitously, the hepatic phenotype differed from TRalpha1R384C animals, suggesting that the localization of the mutation plays an important role for its consequences on glucose metabolism. Furthermore, we observed that glycogen stores were completely depleted in TRalpha1R384C animals, despite increased gluconeogenesis and decreased glycolysis. Exposure of the mutant mice to high maternal levels of thyroid hormone during fetal development leads to a normal liver phenotype in the adult. Our results show how genetic and maternal factors interact to determine the metabolic setpoint of the offspring and indicate an important role for maternal thyroid hormone in the susceptibility to metabolic disorders in adulthood.

Somatotropin adenoma and resistance to thyroid hormone

Resistance to thyroid hormone (RTH) is a rare disease characterized by non-suppressed TSH in spite of high free thyroid hormone levels. Up to date, in the literature, there are more than 600 RTH cases, but co-incidental hypophyseal adenoma was reported in only 1 case. In the literature, despite reported cases with thyrotropinoma accompanying RTH, we could not find a case with somatotropinoma accompanying RTH. Here, we report a 34-yr-old male patient, who was admitted to the hospital with complaints of dyspnea, chest pain, and palpitation in 2003. His alpha- subunit value was normal and the alpha-subunit/TSH molar ratio was <1. His response to TRH stimulation test was normal. His TSH level was suppressed in the T3 suppression test. Hypophyseal magnetic resonance imaging showed a 6-mm hypophyseal microadenoma. Levels of all anterior hypophyseal hormones, including GH and IGF-I, were normal. Oral glucose tolerance test (OGTT)-GH suppression test was normal. The patient was followed with the diagnosis of RTH and incidental hypophyseal adenoma. After 3 yr, because of high levels of IGF-I: 901 ng/ml (68-324), the OGTT-GH suppression test was reported and no suppression was detected. Thus, the patient was referred to surgery with the pre-diagnosis of RTH and acromegaly. Immunohistochemistry was showed as strong GH staining with low Ki 67 index while TSH and other anterior hypophyseal hormones stainings were negative. Post-operative thyroid hormones were still high.

Avaliação das metaloproteinases de matriz -2 e -9 em gatos com desmineralização óssea secundária à tirotoxicose induzida

Observou-se significativo aumento de atividade das formas ativas das metaloproteinases -2 e -9 em gatos com tirotoxicose induzida e desmineralização óssea. As formas pró e intermediária da metaloproteinase -2 elevaram-se com 14 dias de administração hormonal, porém, posteriormente, houve uma tendência de queda. Observou-se correlação negativa entre a forma ativa das metaloproteinases de matriz -2 e -9 e a densidade mineral óssea da extremidade distal do rádio. Os resultados sugerem aumento da degradação da matriz colágena secundária com a elevação dos hormônios tiroidianos.

A Child with Resistance to Thyroid Hormone without Thyroid Hormone Receptor Gene Mutation: A 20-Year Follow-Up

We report here the 20-year follow-up study of a male subject diagnosed at 15 months of age as a sporadic case of pituitary resistance to thyroid hormone on the combination of clinical hyperthyroidism, elevated serum thyroid hormone (TH) levels and inappropriate thyrotropin (TSH). On D-thyroxine (D-T(4)) therapy from 30 months of age to 12.5 years, hyperactivity and hyperthyroid signs and symptoms as well as growth abnormalities improved, serum L-thyroxine (L-T(4)) enantiomer normalized, and basal and stimulated TSH decreased significantly without complete suppression. After 8 years off D-T(4), at 20 years of age, clinical status was normal despite persisting high TH levels and inappropriate TSH. Evolution of serum markers of TH action and echocardiography measurements followed up from 15 months to 20 years of age either in basal condition or on triiodothyronine (T(3)), as well as the sequential determination of bone mineral density suggest differences in the tissue responses to T(3): normal in bone with a high remodelling rate, heterogeneity for various hepatic markers, and decreased at heart level. No mutations were found in the coding sequence of TRbeta1, TRbeta2, TRalpha1, RXRgamma, SMRT, NCoR1, and NCoA1. In this patient the putative long-term effects of the persisting high bone resorption are unknown.

Low TSH levels are not associated with osteoporosis in childhood

A recent study on TSH receptor (TSHR) null mice suggested that skeletal loss occurring in hyperthyroidism is caused by the low TSH rather than high thyroid hormone levels. The aim of this study was to examine whether low TSH results in osteoporosis in the human. We determined bone mineral density (BMD) and markers of bone metabolism in two male siblings aged 9.8 and 6.8 years with isolated TSH deficiency, due to a mutation of the TSH beta-subunit gene. BMD was measured in the lumbar spine (L1-L4) by dual-energy X-ray absorptiometry. Laboratory investigation included the determination of serum calcium, phosphate, 25-hydroxy-vitamin D, parathyroid hormone concentrations, and urine calcium (Ca)/creatinine (Cr) ratio. Osteoblast activity was measured by serum bone alkaline phosphatase and osteocalcin levels, and osteoclast activity by urine cross-linked amino-terminal, carboxy-terminal telopeptides of type I collagen and deoxypyridinoline concentrations. BMD of both patients was within the normal range for age and sex; z-scores were -0.55 and -0.23 for patients 1 and 2 respectively. Serum calcium, phosphate, urine Ca/Cr ratio, and specific markers of bone metabolism were also within normal range. In childhood, chronic extremely low TSH levels, in the face of normal thyroid hormone levels, are not related to bone loss.

Environmental influences on hypothalamic–pituitary–thyroid function and behavior in Antarctica

We examined the physiological and psychological status of men and women who spent the summer ( n = 100) and/or winter ( n = 85) seasons in Antarctica at McMurdo (latitude 78.48 S, elevation 12 m) and South Pole (latitude 90 S, elevation 3880 m) stations to determine whether there were any significant differences by severity of the stations' physical environment. Physiological measures (body mass index, blood pressure, heart rate, tympanic temperature), serum measures of thyroid hormones, cortisol, and lipids and plasma catecholamines were obtained at predeployment (Sep–Oct) and the beginning of the summer (November) and winter (Mar–Apr) seasons. Cognitive performance and mood were assessed using the Automatic Neuropsychological Assessment Metric — Isolated and Confined Environments (ANAM-ICE), a computerized test battery. South Pole residents had a lower body mass index ( p < 0.05) and body temperature ( p < 0.01) and higher levels of plasma norepinephrine ( p < 0.05) in summer and winter than McMurdo residents. Upon deployment from the United States and during the summer, South Pole residents experienced significantly higher thyroid hormone values (free and total T 3 and T 4) ( p < 0.01) than McMurdo residents; in summer they also experienced lower levels of triglycerides ( p < 0.01) cortisol ( p < 0.05) and LDL ( p < 0.05). In winter, South Pole residents also experienced a 39% decrease in serum TSH compared with a 31.9% increase in McMurdo ( p < 0.05). South Pole residents also were significantly more accurate ( p < 0.05) and efficient ( p < 0.01) in performance of complex cognitive tasks in summer and winter. Higher thyroid hormone levels, combined with lower BMI and body temperature, may reflect increased metabolic and physiological responses to colder temperatures and/or higher altitude at South Pole with no apparent adverse effect on mood and cognition.

Functional Thyroid Gland Adenoma in a Dog Treated with Surgical Excision Alone

An 11-year-old male Golden Retriever presented with progressive weight loss, tachycardia, hyperthermia, polyuria and polydipsia. A freely movable mass, 4.5 x 4 cm in size, was palpated at the cranioventral cervical region. Hormonal study revealed high levels of serum thyroid hormones, and a tentative diagnosis of hyperthyroidism due to a thyroid tumor was made. The tumor was removed surgically and diagnosed histopathologically as thyroid gland adenoma. Serum thyroid hormone levels decreased after surgery with improved clinical signs. At 12 months after surgery, the dog maintained a good physical condition with no evidence of recurrence.

Thyroid Hormones Selectively Regulate the Posttranslational Processing of Prothyrotropin-Releasing Hormone in the Paraventricular Nucleus of the Hypothalamus

Over the last few years, our laboratory has demonstrated that different physiological conditions or stressors affect the posttranslational processing of hypophysiotropic and nonhypophysiotropic proTRH and, consequently, the output of TRH and other proTRH-derived peptides. These alterations in proTRH processing are generally associated with parallel changes in the levels of two members of the family of prohormone convertases 1/3 and 2 (PC1/3 and PC2). An important regulator of proTRH is thyroid hormone, which is the peripheral end product of the hypothalamic (TRH)-pituitary (TSH)-thyroid (T3/4) (HPT) axis. In this study we investigated the effect of thyroid status on the processing of proTRH inside and outside the HPT axis. Our data showed that high levels of thyroid hormone down-regulated PC1/3 and PC2 and TRH synthesis, which led to an accumulation of intermediate forms of proTRH processing. Conversely, low levels of thyroid hormone up-regulated proTRH synthesis and PC1/3 and PC2 levels. Control of the activity of PCs and proTRH processing occurred specifically in the paraventricular nucleus, whereas no change due to thyroid status was found in the lateral hypothalamus or preoptic area. The posttranslational regulation of proTRH processing in the paraventricular nucleus by thyroid status is a novel aspect of the regulation of the HPT axis, which may have important implications for the pathophysiology of hypo- and hyperthyroidism.

Fetal Loss Associated With Excess Thyroid Hormone Exposure

Both maternal hypothyroidism and hyperthyroidism have adverse effects on pregnancy outcomes. The effects of thyroid hormone (TH) deprivation on the fetus can be studied in infants having congenital hypothyroidism, but this is not the case for those with fetal thyrotoxicosis. This retrospective family study examined the effects of excessive TH in fetuses whose mothers were resistant to TH (THR) secondary to mutations of the TH receptor β gene. These women maintain an euthyroid state despite high TH levels. The study focused on 167 members of an Azorean family with RTH. Those affected had high serum levels of free thyroxine and triiodothyronine but no suppression of thyrotropin. They had the Arg2 (→) gln mutation of the TH receptor β gene. Among 36 couples with complete information, 9 had an affected mother, 9 an affected father, and 18 were unaffected. Miscarriage rates averaged 22.9%, 2.0%, and 4.4%, respectively. Affected mothers had 20 affected and 11 unaffected children, whereas affected fathers had 15 affected and 12 unaffected children. Unaffected infants born to affected mothers were significantly smaller than affected infants. Only in unaffected infants born to affected mothers were blood levels of thyrotropin undetectable. These findings indicate that high levels of TH may have direct toxic effects on fetal development. They include an increased risk of miscarriage and lower birth weights of unaffected infants born to euthyroid mothers with high TH levels. There is no question that even mildly hypothyroid pregnant women should have TH replacement, but it also must be recognized that overreplacement may have adverse effects on the developing fetus.

Fetal Loss Associated With Excess Thyroid Hormone Exposure

ContextMaternal hypothyroidism and hyperthyroidism have deleterious effects on the outcome of pregnancy. While the effects of thyroid hormone (TH) deprivation on the fetus, independently from that on the mother, can be studied in infants with congenital hypothyroidism, this is not the case in those with fetal thyrotoxicosis.ObjectiveTo study the effects of TH excess on fetuses carried by mothers with resistance to TH (RTH) who are euthyroid despite high TH levels but who may carry normal fetuses that are exposed to high maternal hormone levels.Design, Setting, and ParticipantsRetrospective study of 167 members of an Azorean family with RTH. Affected individuals had the RTH phenotype (high serum concentration of free thyroxine and triiodothyronine without suppressed thyrotropin) confirmed by genotyping to identify the Arg243→Gln mutation in the TH receptor β gene.Main Outcome MeasuresPregnancy outcome of affected mothers vs that of unaffected mothers carrying fetuses conceived by affected fathers, as well as that of unaffected first-degree relatives and outcomes from the general island population. Comparison of birth weights and blood concentrations of thyrotropin (TSH) obtained during routine neonatal screening of infants born to these 3 groups.ResultsThirty-six couples with complete information belonged to 1 of 3 groups: affected mothers (n = 9), affected fathers (n = 9), and unaffected relatives (n = 18). Mean miscarriage rates were 22.9%, 2.0%, and 4.4%, respectively (χ2 = 8.66, P = .01). Affected mothers had an increased rate of miscarriage (z = 3.10, P = .002, by Wilcoxon rank-sum test). They had marginally higher than expected numbers of affected offspring, ie, 20 affected and 11 unaffected children (P = .07), while affected fathers had 15 affected and 12 unaffected children (P = .35). Unaffected infants born to affected mothers were significantly smaller than affected infants, having a mean SD score for gestational age of –1.79 (SD, 0.86) vs −0.06 (SD, 1.11) to –0.22 (SD, 0.70) for all other groups (P<.001). Only unaffected infants born to affected mothers had undetectable blood levels of TSH.ConclusionThere was a higher rate of miscarriage in mothers affected by RTH that may have involved predominantly unaffected fetuses. The lower birth weight and suppressed levels of TSH in unaffected infants born to affected mothers indicates that the high maternal TH levels produce fetal thyrotoxicosis. These data indicate a direct toxic effect of TH excess on the fetus.

Effects of iodized feed on stress modulation in steelhead trout, Oncorhynchus mykiss (Walbaum)

In the aquaculture industry, the physiological systems of fish can be chronically stressed by various biological, chemical and physical factors. Chronic stress leads to a decrease in the overall health and growth of the fish, making them more prone to diseases. Dietary iodine has been shown to reduce this stress response in chickens and increase disease resistance in dairy cattle, but the mechanisms by which iodine affects stress resistance and immunocompetency is not completely understood and has not been extensively studied in fish. This study investigated the effects of iodized feed as a nutritional supplement in relation to stress modulation in steelhead trout (Oncorhynchus mykiss). We investigated effects on primary, secondary and tertiary stress responses by measuring plasma levels of cortisol, glucose and thyroid hormones as well as haematocrit percentage and average growth rate in steelhead trout. Iodine-supplemented fish, on average, had lower levels of plasma cortisol and glucose and lower packed cell volumes than fish fed with regular commercial feed (P<0.05). Iodine-supplemented fish also showed higher levels of thyroid hormones and exhibited better growth over the period of the experiment (P<0.05). It was concluded that, used with other husbandry practices, use of iodine-supplemented feed could lead to better host defence, growth and survival in fish raised in the aquaculture industry.