Showing posts with label TSH. Show all posts
Showing posts with label TSH. Show all posts

Tuesday, May 14, 2013

Hyperthyroidism due to thyroid stimulating hormone secretion after surgery for Cushing's syndrome: A novel cause of the syndrome of inappropriate secretion of thyroid stimulating hormone


  1. Iichiro Shimomura, MD, PhD1
Author Affiliations
  1. 1Department of Metabolic Medicine, Osaka University Graduate School of Medicine, Osaka, Japan
  2. 2Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
  1. Address all correspondence and requests for reprints to: Michio Otsuki, MD, PhD, Department of Metabolic Medicine, Osaka University Graduate School of Medicine, 2–2 Yamada-oka, Suita, Osaka 565-0871, Japan, Telephone: +81-6-6879-3732. Fax: +81-6-6879-3739, E-mail: otsuki@endmet.med.osaka-u.ac.jp.

Abstract

Context: Hyperthyroidism with the syndrome of inappropriate secretion of thyroid stimulating hormone (TSH) (SITSH) occurred by a decrease in hydrocortisone dose after surgery for Cushing's syndrome. This is a novel cause of SITSH.

Objective: The aim of this study was to describe and discuss the two cases of SITSH patients who were found after surgery for Cushing's syndrome. We also checked whether SITSH occurred in the consecutive 7 patients with Cushing's syndrome after surgery.

Patients and Methods: A 45-year-old Japanese woman with adrenocorticotropin (ACTH)-independent Cushing's syndrome and a 37-year-old Japanese man with ACTH-dependent Cushing's syndrome presented SITSH caused by insufficient replacement of hydrocortisone for postoperative adrenal insufficiency. When the dose of hydrocortisone was reduced to less than 20 mg/day within 18 days after operation, SITSH occurred in both cases. We examined whether the change of the hydrocortisone dose induced the secretion of TSH. Free T3 and TSH were normalized by the hydrocortisone dose increase of 30 mg/day and these were elevated by the dose decrease of 10 mg/day. We also checked TSH and thyroid hormone the consecutive 7 patients with Cushing's syndrome after surgery. Six (66.6 %) of nine patients showed SITSH.

Conclusions: This is the first report that insufficient replacement of hydrocortisone after the surgery of Cushing's syndrome caused SITSH. Hyperthyroidism by SITSH as well as adrenal insufficiency can contribute to withdrawal symptoms of hydrocortisone replacement. So we need to consider the possibility of SITSH for the pathological evaluation of withdrawal syndrome of hydrocortisone replacement.
  • Received May 4, 2013.
  • Accepted May 8, 2013.

Saturday, May 7, 2011

Pituitary Hormones

Pituitary
The pituitary gland is a small gland, located below the brain and connected to the hypothalamus. The pituitary gland regulates the secretions of hormones in the body, and hormones impact metabolism, growth and development, reproduction and urine production. It is important to note that the hypothalamus and pituitary gland are connected by blood vessels and nerves.

When the body experiences changes, perhaps in temperature, the hypothalamus responds to restore our body’s balance (homeostasis). The hypothalamus stimulates the pituitary gland to release hormones that in term stimulate various organs in the body to respond. The pituitary gland has cells that respond independently to the stimulus. Some cells make one type of hormone, other cells produce other hormones. The pituitary gland is often referred to as the master gland.

The hormones produced and the body’s response follows:

Growth Hormone (GH) signals certain liver cells to produce somatomedin-C, which is needed for growth in childhood

Prolactin stimulates breast milk production and controls menstrual periods.

Adrenocorticotropic hormone (ACTH) stimulates the adrenal glands to release cortisol and aldosterone that helps the body to regulate stress.

Thyroid-stimulating hormone (TSH) stimulates the release of thyroid hormones, which play a major role in basal metabolic rate, the way the body’s cells convert food into energy.

Follicle Stimulating Hormone (FSH) stimulates the production of testosterone and estrogen and progesterone.

Luteinizing Hormone (LH) also stimulates the hormones that regulate reproduction.

Melanocyte stimulating hormone controls skin pigmentation.

Antidiuretic hormone (ADH), also referred to as vasopressin, increases the absorption of water by the kidneys into the blood.

Oxytocin is produced by the hypothalamus and stored in the pituitary gland until released. Ocytocin causes the uterus to contract during childbirth and stimulates milk production.

The location of the pituitary gland should be noted as well. The pituitary gland sits below the crossing fibers of the optic nerves. On either side of the pituitary gland are the carotid arteries and nerves that control eye movements.

Diseases and symptoms involving the pituitary gland are varied. Some diseases are related to an overproduction of a specific hormone, or too little to no production. A growth in the pituitary gland could put pressure on the optic nerve or the carotid artery. Surgery involving the pituitary gland is done using minimally invasive, microscopic surgery. The surgeon can go through the sphenoid sinus and there are no visible scars.

Adapted from http://www.independentmail.com/news/2011/may/07/pituitary-gland-produces-several-hormones/

Friday, March 11, 2011

Pituitary Terms

ACTH

ACTH is important in controlling the adrenal gland’s secretion of cortisol and androgens (male hormones). Too much ACTH causes a disease called Cushing’s disease and too little ACTH causes adrenal insufficiency. Symptoms of adrenal insufficiency include weight loss, decrease in appetite, abdominal pain, and muscle aches. Please see the additional patient education material on this Web site for further information. 

ADH

ADH is a critical hormone that regulates water balance in the body by controlling how much water the kidneys release into the urine. Too much ADH secretion by the pituitary causes the syndrome of inappropriate antidiuretic hormone (SIADH), in which the salt levels in the body can drop dangerously low due to holding on to too much water. Treatments may include fluid restriction and salt supplementation. Too little ADH results in diabetes insipidus (DI), in which the body constantly produces a clear high volume of urine accompanied by extreme thirst. The treatment is fluids and a medicine called DDAVP. Additional information regarding diabetes insipidus may be found in patient education material on this Web site.

Acromegaly

A rare disorder called acromegaly occurs when a person’s pituitary gland secretes too much growth hormone, usually from a pituitary tumor. Symptoms of this disorder may include broadening of the lips and nose, irregular menstrual periods, excessive sweating and increasing ring and shoe size. Surgery is generally indicated for the treatment of acromegaly. There are several medications that are frequently used in addition to surgery to control acromegaly, and, occasionally, radiation therapy is required as well.

Cushing's Disease

Too much ACTH secretion is rare and may be from a pituitary tumor; this is called Cushing’s disease. Symptoms of too much ACTH include weight gain, a round and red face, increased acne, purple stretch marks, hair growth and muscle weakness. Special testing is necessary to make the diagnosis. Surgery is generally indicated for the treatment of Cushing’s disease. Medications are also available to lower cortisol production, and radiation therapy is sometimes required as well.

Gonadotropins

The gonadotropins are responsible for the initiation and maintenance of sexual characteristics and fertility (ability to have children). LH and FSH act on the gonads (ovaries and testes) to cause production of estrogen and testosterone and ultimately make eggs and sperm. Too little secretion of LH and FSH can cause infertility and hypogonadism, manifesting primarily as erectile dysfunction in men and irregular or absent menstrual periods in women as well as low sex drive in both. Treatment includes various forms of testosterone or estrogen replacement.  Fertility can be possible with the assistance of injectable forms of gonadotropins.

Growth Hormone

As its name implies, growth hormone is important for childhood growth. In adults, it is also important in order to maintain bone mass and normal body composition. Symptoms of growth hormone deficiency include fatigue, an increase in fat around the abdomen, decreased ability to exercise and poor sense of well-being. Treatment includes subcutaneous injections of growth hormone.

Oxytocin

Oxytocin is a hormone that is important for uterine contractions during childbirth and for release of milk during breastfeeding. It is, therefore, frequently used in the induction of labor.

Pituitary

The pituitary is a pea-sized gland located at the base of the brain in the middle of the head and right below the optic nerves. It serves as the “master gland” that regulates the secretion of the majority of hormones in the body from all of the other glands, such as the thyroid and adrenal glands, as well as the ovary and testicles. The pituitary gland is divided into the anterior and posterior lobes, both of which secrete different hormones that have unique functions in the body. The anterior pituitary secretes prolactin, growth hormone and the gonadotropins, which include luteinizing hormone (LH) and follicle stimulating hormone (FSH), adrenocorticotrophic hormone (ACTH) and thyroid stimulating hormone (TSH). The posterior pituitary makes antidiuretic hormone (ADH) and oxytocin. The secretion of the hormones from the pituitary gland itself is also controlled by hormones coming from part of the brain directly above the pituitary called the hypothalamus. The hypothalamus and the pituitary gland are connected by the pituitary stalk.

Pituitary tumors result from a single cell losing the ability to control its growth. These tumors are almost always benign or non-cancerous. Very rarely can a pituitary tumor become malignant or cancerous. A tumor that is less than 1 cm in size is called a microadenoma, and a tumor that is larger than 1 cm is a macroadenoma.

Microadenomas usually do not cause symptoms related to their size, but macroadenomas can cause headaches as well as visual loss secondary to compression of the optic nerves. In addition, the normal pituitary tissue can be compressed by a macroadenoma, so deficiencies of anterior pituitary hormones can be identified on blood tests and based on symptoms. Pituitary tumors are also categorized according to their ability to make hormones and cause symptoms. 

The functional tumors include those that secrete prolactin (prolactinomas), ACTH (Cushing’s disease), growth hormone (acromegaly) and TSH. Tumors that do not secrete functional hormones are called non-functioning pituitary tumors. The most common tumors in adults are prolactinomas followed by non-functioning tumors, ACTH-secreting tumors, GH-secreting tumors and TSH-secreting tumors. In children, the most common tumor is also a prolactin-secreting tumor followed by ACTH-secreting tumors, GH-secreting tumors, non-functioning tumors and TSH-secreting tumors. 

Prolactin

Prolactin is a hormone that is important for the production of breast milk. 

Prolactinoma

A pituitary tumor that secretes prolactin is called a prolactinoma. In women, too much prolactin is associated with milk production outside of pregnancy and irregular menstrual periods or a lack of periods altogether. In men, excess prolactin levels cause low testosterone levels, which will typically manifest as low sex drive. Medical treatment with a pill is available for a prolactinoma. Women with too little prolactin production will be unable to make breast milk but otherwise there are no obvious symptoms of prolactin deficiency.

TSH

Thyroid stimulating hormone (TSH) directs the thyroid gland to produce thyroid hormones, which are important in regulating the body’s metabolism. Rarely, a pituitary tumor can secrete too much TSH. This would cause hyperthyroidism, as manifested by increased sweating, intolerance to heat, tremors, fast heart rate, heart palpitations, anxiety and/or weight loss. Treatment includes medications and surgery. Too little TSH results in hypothyroidism, a condition in which a person would have intolerance to cold, fatigue, dry skin, constipation, a slow heart rate and/or weight gain due to water retention. Treatment includes taking daily thyroid hormone.

From http://www.mdanderson.org/patient-and-cancer-information/care-centers-and-cli...

Friday, March 19, 2010

Magnetic Resonance Imaging and Pituitary Function in Children with Panhypopituitarism

Free Abstract Article (Fulltext) Article (PDF 148 KB)


Original Paper

Magnetic Resonance Imaging and Pituitary Function in Children with Panhypopituitarism
Guimei Li, Peng Shao, Xiaojun Sun, Qian Wang, Lijuan Zhang
Provincial Hospital Affiliated to Shandong University, Shandong, PR China

Address of Corresponding Author

Horm Res Paediatr 2010;73:205-209 (DOI: 10.1159/000284363)


 Key Words

  • Magnetic resonance imaging
  • Insulin-like growth factor-1
  • Multiple pituitary hormone
  • Panhypopituitarism

 Abstract

Background: To explore the relationship between magnetic resonance imaging (MRI) findings and multiple pituitary-target hormones in patients with panhypopituitarism or multiple pituitary hormone deficiency (MPHD).

Methods: 125 patients with MPHD (102 boys, MPHD group) and 90 age-, sex- and Tanner stage-matched normal children (control group) were enrolled. 96 of the patients with MPHD underwent MRI scans of the hypothalamic-pituitary area. The patients were subdivided into five stages according to their MRI findings. The serum concentrations of GH, IGF-1, FT4, TSH, ACTH, cortisol, FSH, LH, prolactin, testosterone and estradiol were measured in patients and in controls.

Results: MRI stage was significantly positively correlated with the number of pituitary hormone deficiencies (r = 0.9, p < 0.001). MRI stage was negatively correlated with peak GH, IGF-1, FT4, cortisol and anterior pituitary height (r = –0.43, –0.47, –0.67, –0.54, and –0.49, respectively, p < 0.01). Diabetes insipidus patients could be stratified according to their MRI stage; diabetes insipidus was found mainly in patients with absence of the posterior pituitary bright spot or small ectopic posterior pituitary bright spot on MRI.

Conclusion: An abnormal MRI finding is evidence of MPHD and, correspondingly, there is a noteworthy correlation between MRI and pituitary function.

Copyright © 2010 S. Karger AG, Basel

From http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ArtikelNr=284363&Ausgabe=253980&ProduktNr=224036

Thursday, December 3, 2009

Abnormalities of thyroid function in Japanese patients with metastatic renal cell carcinoma treated with sorafenib: A prospective evaluation

Hideaki Miyake, M.D., Ph.D.aCorresponding Author Informationemail address, Toshifumi Kurahashi, M.D., Ph.D.a, Kazuki Yamanaka, M.D., Ph.D.b, Yutaka Kondo, M.D., Ph.D.b, Mototsugu Muramaki, M.D., Ph.D.a, Atsushi Takenaka, M.D., Ph.D.a, Taka-aki Inoue, M.D., Ph.D.b, Masato Fujisawa, M.D., Ph.D.a

Received 29 June 2009; received in revised form 17 August 2009; accepted 17 August 2009. published online 16 November 2009.
Corrected Proof

Abstract

The objective of this study was to characterize features of thyroid dysfunction in Japanese patients with metastatic renal cell carcinoma (RCC) who were treated with sorafenib. We performed a prospective observational study including 69 Japanese patients who were diagnosed as having metastatic RCC refractory to cytokine therapy and subsequently treated with sorafenib for at least 12 weeks. Thyroid function was assessed before and every 4 weeks after the initiation of sorafenib treatment. Of the 69 patients, 23 (33.3%) did not show any biochemical thyroid abnormality, while the remaining 46 (67.7%) developed hypothyroidism. However, 11 (23.9%) of these 46 hypothyroid patients initially had a suppressed thyroid-stimulating hormone (TSH) value accompanying the increase in free triiodothyronine (T3) and/or free thyroxine (T4) before developing hypothyroidism, suggesting sorafenib-induced thyroiditis. During the observation period of this study, 4 patients (5.8%) demonstrated severe clinical symptoms caused by hypothyroidism and received thyroid hormone replacement. Among several factors examined, only age was significantly associated with the risk for hypothyroidism. These findings suggest that although the incidence of clinically significant hypothyroidism requiring thyroid hormone replacement therapy was not very high, biochemical thyroid abnormality was frequently observed in Japanese RCC patients treated with sorafenib. Accordingly, regular surveillance of thyroid function by the measurement of TSH, free T3, and T4 is warranted during sorafenib treatment in Japanese RCC patients.

Keywords: Renal cell carcinoma, Thyroid function, Sorafenib, Hypothyroidism

a Division of Urology, Kobe University Graduate School of Medicine, Kobe, Japan

b Department of Urology, Hyogo Cancer Center, Akashi, Japan

Corresponding Author InformationCorresponding author. Tel.: +81-78-382-6155; fax: +81-78-382-6169.

PII: S1078-1439(09)00263-4

doi:10.1016/j.urolonc.2009.08.011

© 2009 Elsevier Inc. All rights reserved.

 

From http://www.urologiconcology.org/article/PIIS1078143909002634/abstract?rss=yes

Tuesday, August 18, 2009

Diminished and irregular thyrotropin secretion with delayed acrophase in patients with Cushing’s syndrome

F Roelfsema, A Pereira, N Biermasz, Marijke Frölich, Daniel Keenan, Johannes Veldhuis and J Romijn

F Roelfsema, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, 2333ZA, Netherlands
A Pereira, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Netherlands
N Biermasz, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Netherlands
M Frölich, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Netherlands
D Keenan, Statistics, University of Virginia, Charlottesville, United States
J Veldhuis, Endocrine Research Unit, Mayo Clinic, Rochester, United States
J Romijn, Department of Endocrinology, C4-R, Leiden University Medical Center, Leiden, 2300 RC, Netherlands

Correspondence: F Roelfsema, Email: f.roelfsema@lumc.nl

Abstract

Context. The hypothalamo-pituitary-thyroid axis in Cushing’ syndrome may be altered.

Objective. We analyzed serum TSH profiles in relation to cortisol profiles in patients with hypercortisolism of pituitary (n=16) or primary-adrenal origin (n=11) and after remission by pituitary surgery (n=7) in order to delineate aberrations in the hypothalamo-pituitary-thyroid system.

Intervention. Patients and controls (n=27) underwent a 24-h blood sampling study. Serum TSH and cortisol were measured with precise methods and data were analyzed with a deconvolution program, approximate entropy (ApEn) and cosinor regression.

Results. Pulsatile TSH secretion, and mean TSH pulse mass, were diminished during hypercortisolism, independently of etiology (P<0.001). TSH secretion was increased in patients in remission only during day-time due to increased basal secretion (P<0.01). Pulse frequency and half life of TSH were similar in patients and controls. TSH ApEn (irregularity) was increased in patients with hypercortisolism (P<0.01), but was normal in cured patients. Cross-ApEn between TSH and cortisol, a measure of pattern-synchrony loss, was increased in active disease, indicating (partial) loss of secretory synchrony. The TSH rhythm was phase-delayed in hypercortisolemic patients, but normal in cured patients (P<0.01). Free thyroxine levels were decreased only in pituitary-dependent hypercortisolism compared with controls (P=0.003). Total 24-h TSH correlated negatively and linearly with log-transformed cortisol secretion (R=0.43, P=0.001).

Conclusion: Cortisol excess decreases TSH secretion by diminishing pulsatile release, whereas surgically cured patients have elevated non-pulsatile TSH release. Diminished TSH secretory regularity in active disease suggests glucocorticoid-induced dysregulation of TRH or somatostatinergic / annexin-1 control.

From http://www.eje.org/cgi/content/abstract/EJE-09-0580v1

Sunday, May 24, 2009

Pituitary-thyroid feedback in a patient with a sporadic activating TSH-R mutation

From http://www.unboundmedicine.com/medline/ebm/record/19454581/full_citation/Pituitary_thyroid_feedback_in_a_patient_with_a_sporadic_activating_TSH_R_mutation:_implication_that_thyroid_secreted_factors_other_than_thyroid_hormones_contribute_to_serum_TSH_levels

Title:    Pituitary-thyroid feedback in a patient with a sporadic activating TSH-R mutation: implication that thyroid-secreted factors other than thyroid hormones contribute to serum TSH levels.


Author(s)    Gelwane G, de Roux N, Chevenne D, Carel JC, Léger J
Institution    Pediatric Endocrinology Department, Centre de Référence Maladies Endocriniennes de la Croissance and Institut National de la Santé et de la Recherche Médicale (INSERM) Unit 690, Pediatric Biochemistry and Hormonology Unit, Assistance Publique-Hôpitaux de Paris, Robert Debré Hospital, Université Paris-Diderot Paris 7, Paris, France.


Source:    J Clin Endocrinol Metab 2009 May 19.


Abstract:    Context: Constitutive mutations of the TSH receptor gene are a rare cause of severe congenital hyperthyroidism. Persistent TSH suppression has been described in euthyroid Graves' disease patients treated with antithyroid drugs. An ultra-short negative feedback loop affecting TSH secretion by activating the pituitary TSH receptor with TSH receptor autoantibodies has been suggested as a possible mechanism of TSH suppression in these patients.

Objective and Design:  To determine whether TSH suppression also occurs in euthyroid treated patients with non-autoimmune hyperthyroidism. We investigated the outcome of pituitary-thyroid feedback in a patient carrying an activating mutation of the TSH-R gene, in an observational prospective study. Repeated clinical investigations from birth until the age of 14 years are presented for the patient on drug treatment and following radical treatment.


Results: TSH was consistently undetectable or present at very low concentrations in the serum for several years, although FT4 and FT3 concentrations remained mostly in the normal range. Moreover, serum TSH concentrations increased only slightly when serum FT4 concentrations fell below normal levels. During drug treatment, serum TSH concentrations expressed as a function of serum FT4 and FT3 concentrations were significantly lower than those for control or congenital hypothyroid populations. By contrast, after radical treatment, serum TSH levels increased, reaching the normal range, and low serum FT4 and FT3 concentrations were associated with appropriate increases in serum TSH concentrations.


Conclusion: These data provide insight into the regulation of serum TSH concentrations and suggest an alternative mechanism, in addition to serum thyroid hormone levels, for adjusting TSH secretion.


Language    ENG
Pub Type(s)    JOURNAL ARTICLE
PubMed ID    19454581