No abstract available.
Thyrotropin* ; Thyrotropin-Releasing Hormone*

GTP-Binding Proteins ; Receptors, Thyrotropin-Releasing Hormone ; Thyrotropin-Releasing Hormone*

A 45-year-old woman who complained of weight gain and irregular menstruation was diagnosed as having Cushing's syndrome due to a 3 cm sized left adrenal adenoma. She underwent left adrenalectomy, and she also underwent combined anterior pituitary tests before and 9 months after the surgery. The growth hormone and adrenocorticotropic hormone levels failed to respond to hypoglycemia before the surgery, but their responses recovered after the surgery. Cortisol and thyroid stimulating hormone failed to respond to hypoglycemia and thyrotropin releasing hormone (TRH) before the surgery, respectively, but these were improved after the surgery. Luteinizing hormone, follicle stimulating hormone, and prolactin adequately responded to gonadotropin-releasing hormone and TRH, respectively, before and after the surgery. However, the basal levels of these hormones were higher after adrenalectomy, suggesting that hypercortisolemia had a significant influence on all the pituitary hormones.
Adenoma* ; Adrenalectomy ; Adrenocorticotropic Hormone ; Cushing Syndrome* ; Female ; Follicle Stimulating Hormone ; Gonadotropin-Releasing Hormone ; Growth Hormone ; Humans ; Hydrocortisone ; Hypoglycemia ; Hypopituitarism ; Luteinizing Hormone ; Menstruation ; Middle Aged ; Pituitary Hormones ; Prolactin ; Thyrotropin ; Thyrotropin-Releasing Hormone ; Weight Gain

OBJECTIVE: To investigate the prevalence of subclinical hypothyroidism (SH) diagnosed by thyrotropin-releasing hormone (TRH) stimulating test in infertile women with basal thyroid-stimulating hormone (TSH) levels of 2.5 to 5.0 mIU/L. METHODS: This study was performed in 39 infertile women with ovulatory disorders (group 1) and 27 infertile women with male infertility only (group 2, controls) who had basal serum TSH levels of 2.5 to 5.0 mIU/L and a TRH stimulating test. Serum TSH levels were measured before TRH injection (TSH0) and also measured at 20 minutes (TSH1) and 40 minutes (TSH2) following intravenous injection of 400 microg TRH. Exaggerated TSH response above 30 mIU/L following TRH injection was diagnosed as SH. Group 1 was composed of poor responders (subgroup A), patients with polycystic ovary syndrome (subgroup B) and patients with WHO group II anovulation except poor responder or polycystic ovary syndrome (subgroup C). RESULTS: The prevalence of SH was significantly higher in group 1 of 46.2% (18/39) compared with 7.4% (2/27) in group 2 (P=0.001). TSH0, TSH1, and TSH2 levels were significantly higher in group 1 than the corresponding values in group 2 (P<0.001, P<0.001, P<0.001). In group 1, TSH1 and TSH2 levels were significantly lower in subgroup C compared with those in subgroup A and B (P=0.008, P=0.006, respectively). CONCLUSION: TRH stimulation test had better be performed in infertile women with ovulatory disorders who have TSH levels between 2.5 and 5.0 mIU/L for early detection and appropriate treatment of SH.
Anovulation ; Female ; Humans ; Hypothyroidism* ; Infertility ; Infertility, Male ; Injections, Intravenous ; Male ; Polycystic Ovary Syndrome ; Prevalence ; Thyrotropin* ; Thyrotropin-Releasing Hormone*

Functional defects of the pituitary gland are a rare cause of pubertal delay. The pituitary stalk is an important structure that connects the hypothalamus and pituitary gland. A defect in fusion of the pituitary stalk and anterior pituitary gland will block the function of the anterior pituitary gland. A 28-year-old man was referred to our clinic with poorly developed secondary sexual characteristics. He had undeveloped facial, axillary, and pubic hair and was Tanner stage I. Laboratory tests gave random serum testosterone < 0.025 ng/mL, luteinizing hormone (LH) < 0.1 mIU/mL, follicle-stimulating hormone (FSH) 0.626 mIU/mL, thyroid-stimulating hormone (TSH) 6.85 microIU/mL, and fT4 6.96 pmol/L. Sella magnetic resonance imaging (MRI) showed no pituitary stalk enhancement. The response in the combined pituitary function test revealed multiple hormonal defects, while the TSH response to thyrotropin-releasing hormone (TRH) was exaggerated and delayed. Therefore, we concluded that pituitary stalk dysgenesis had led to hypothalamic-type panhypopituitarism.
Adult ; Follicle Stimulating Hormone ; Hair ; Humans ; Hypopituitarism ; Hypothalamus ; Luteinizing Hormone ; Magnetic Resonance Imaging ; Pituitary Function Tests ; Pituitary Gland ; Pituitary Gland, Anterior ; Puberty, Delayed ; Testosterone ; Thyrotropin ; Thyrotropin-Releasing Hormone

Authors report the clinical study on the usefulness of thyrotropin-releasing hormone tartrate(TRH-T) in the treatment of mild disturbance of consciousness. 20 patients suffering head trauma, subarachnoid hemorrhage, and intracerebral hemorrhage were given TRH-T intravenously for ten days. TRH-T was effective for the patients in whom the consciousness disturbance was mild, the duration in fixed consciousness level was short, and the brain was not distorted on CT scan. These features were most prominent in patients with subarachnoid hemorrhage. Three was no significant side effect, and TRH-T turned out to be safe.
Brain ; Cerebral Hemorrhage ; Consciousness* ; Craniocerebral Trauma ; Humans ; Subarachnoid Hemorrhage ; Thyrotropin-Releasing Hormone ; Tomography, X-Ray Computed

Phthalates widely used in the manufacture of plastics have deeply penetrated into our everyday lives. Recently, a concern over the toxicity of phthalates on thyroid, has been raised but in most of cases, the doses employed were unrealistically high. To investigate the effects of phthalates on thyroid, we investigated the effects of the repeated oral exposure to low to high doses (0.3, 3, 30 and 150 mg/kg) di-2-ethylhexylphthalate (DEHP) from weaning to maturity for 90 days in juvenile rats on the thyroid. The histological examination revealed that DEHP significantly induced hyperplasia in the thyroid from the doses of 30 mg/kg, which was confirmed with Ki67 staining. In line with this finding, increased mRNA expression of thyrotropin releasing hormone (Trh) was observed in the thyroid of female at 0.3 mg/kg and 150 mg/kg as determined by RNAseq analysis. Moreover, significantly increased expression of parathyroid hormone (Pth) in the female at 0.3 mg/kg, and thyroglobulin (Tg) and thyroid hormone responsive (Thrsp) in the male at 0.3 mg/kg were noted in the blood, of which changes were substantially attenuated at 150 m/kg, alluding the meaningful effects of low dose DEHP on the thyroid hormone regulation. Urinary excretion of mono-2-ethylhexyl-phthalate (MEHP), a major metabolite of DEHP was determined to be 4.10 and 12.26 ppb in male, 6.65 and 324 ppb in female at 0.3 and 30 mg/kg DEHP, respectively, which fell within reported human urine levels. Collectively, these results suggest a potential adverse effects of low dose phthalates on the thyroid.
Animals ; Diethylhexyl Phthalate* ; Female ; Humans ; Hyperplasia ; Male ; Parathyroid Hormone ; Plastics ; Rats* ; RNA, Messenger ; Thyroglobulin ; Thyroid Gland* ; Thyrotropin-Releasing Hormone ; Weaning

The syndrome of resistance to thyroid hormone (RTH) is characterized by reduced tissue sensitivity to thyroid hormone (TH). In the majority of subjects, RTH is caused by mutations in the thyroid hormone receptor beta (TRbeta) gene, located on the chromosome locus 3p24.3. RTH is inherited in an autosomal dominant manner. The clinical presentation of RTH is variable, but common features include elevated serum levels of thyroid hormone (TH), a normal or slightly increased thyrotropin (thyroid stimulating hormone, TSH) level that responds to thyrotropin releasing hormone (TRH), and goiter. We report a 4 year-old girl, who was clinically euthyroid in spite of high total and free T4, and T3 concentrations, while TSH was slightly increased. Sequence analysis of the thyroid hormone receptor beta gene (THRB) confirmed a heterozygous C to T change at nucleotide number 1303, resulting in a substitution of histidine by tyrosine at codon 435 (H435Y). Further analysis of her parents revealed that the H435Y variation was a de novo mutation since neither parents had the variation. Her parents' TH and TSH levels were within normal range.
Child, Preschool ; Codon ; Female ; Genes, erbA* ; Goiter ; Histidine ; Humans ; Parents ; Reference Values ; Sequence Analysis ; Thyroid Gland* ; Thyroid Hormone Receptors beta ; Thyrotropin ; Thyrotropin-Releasing Hormone ; Tyrosine

A 58-year-old male with a pituitary adenoma was investigated and demonstrated to have hypersecretion of both gonadotropins in the basal state. Presenting symptoms included visual disturbance, headache, loss of libido, impotence, cold intolerance and urinary frequency. The patient denied alteration of hair distribution and did not disclosed the aral features, galactorrheaor gynecomastia. Dynamic assay with synthetic thyrotropin-releasing hormone and synthetic gonadotropin-releasing hormone result in increase of serum luteinizing hormone(LH) and follicle stimulating hormone(FSH). Immunochemically, tumor cell revealed positive reaction for chromogranin and FSH, but negative for LH. Electron microscopic examination using paraffin embedded block was failed to demonstrate classic neurosecretory granule, but some electron dense granules were found in the cytoplasm. Gonadotropin-producing pituitary adenomas are rare, but have been diagnosed more frequently as radiographic techniques and biochemical assays have improved. A review of the literatures documents pituitary tumor secreting both FSH and LH in the basal state and we report a case of gonadotropin-producing pituitary adenoma.
Cytoplasm ; Erectile Dysfunction ; Gonadotropin-Releasing Hormone ; Gonadotropins ; Gynecomastia ; Hair ; Headache ; Humans ; Libido ; Lutein ; Male ; Middle Aged ; Paraffin ; Pituitary Neoplasms* ; Thyrotropin-Releasing Hormone

We investigated the effect of alpha-subunit of the stimulatory GTP-binding protein (Galphas) gene mutation on the expression of the thyrotropin-releasing hormone (TRH) receptor (TRH-R) gene in GH3 cells and in growth hormone (GH)-secreting adenomas of acromegalic patients. In the presence of cycloheximide, forskolin and isobutylmethylxanthine, cholera toxin, and GH-releasing hormone (GBRH) decreased rat TRH-R (rTRH-R) gene expression by about 39%, 43.7%, and 46.7%, respectively. Transient expression of a vector expressing mutant-type Galphas decreased the rTRH-R gene expression by about 50% at 24 h of transfection, whereas a wild-type Galphas expression vector did not. The transcript of human TRH-R (hTRH-R) gene was detected in 6 of 8 (75%) tumors. Three of them (50%) showed the paradoxical GH response to TRH and the other three patients did not show the response. The relative expression of hTRH-R mRNA in the tumors from patients with the paradoxical response of GH to TRH did not differ from that in the tumors from patients without the paradoxical response. Direct PCR sequencing of GALPHAs gene disclosed a mutant allele and a normal allele only at codon 201 in 4 of 8 tumors. The paradoxical response to TRH was observed in 2 of 4 patients without the mutation, and 2 of 4 patients with the mutation. The hTRH-R gene expression of pituitary adenomas did not differ between the tumors without the mutation and those with mutation. The present study suggests that the expression of TRH-R gene is not likely to be a main determinant for the paradoxical response of GH to TRH, and that Galphas mutation may suppress the gene expression of TRH-R in GH-secreting adenoma. However, a certain predisposing factor(s) may play an important role in determining the expression of TRH-R.
Acromegaly ; Adenoma ; Alleles ; Animals ; Cholera Toxin ; Codon ; Colforsin ; Cycloheximide ; Gene Expression ; Growth Hormone ; GTP-Binding Proteins ; Humans ; Pituitary Neoplasms ; Polymerase Chain Reaction ; Rats ; Receptors, Thyrotropin-Releasing Hormone* ; RNA, Messenger* ; Thyrotropin-Releasing Hormone ; Transfection