Hypothalamic-Pituitary Axes
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The Endocrine System Brightside July, 2019 by Dr
The Endocrine System Brightside July, 2019 By Dr. Derek Conte How does the body regulate and balance itself from minute to minute, hour to hour and month to month? What is it that allows the food we eat to be utilized for growth, healing and energy? What causes the female egg to drop each month or a mother’s milk to flow? The answer is the endocrine system, which is comprised of the hypothalamus, pituitary gland, pineal gland, thyroid and parathyroid glands, thymus gland, the adrenals, pancreas, ovaries and testes. The brain signals these specialized glands to release hormones to initiate essential chemical actions that sustain life. The word “endocrine” literally means “to cry inside” and that is exactly what happens when the endocrine system works. An example is growth hormone (GH) or somatotropin, responsible for growth and tissue repair. During exercise or when we have low blood sugar or high blood amino acid levels, the hypothalamus leaks (“cries”) growth hormone releasing hormone (GHRH) through very small vessels into the anterior pituitary gland which then leaks growth hormone into the general circulation, acting on cells for growth or replacement of old or damaged tissues. Pro ballplayers looking for an edge have been using growth hormone. The hormone that shuts this process off is called growth hormone inhibiting hormone (GHIH) or somatostatin (“growth stop”), released when blood sugar levels are high. If there ever is an excess of growth hormone, it can result in gigantism or acromegaly depending on whether its onset occurred before or after the growth plates in the bones have closed around the age of 17. -
Growth Hormone Booklet
GROWTH HORMONE AND PRADER-WILLISECOND EDITION SYNDROME A REFerence For FaMILies and Care ProViders Donald G. Goranson, Jr., Editor Growth Hormone and Prader-Willi Syndrome — Second Edition Published By: Prader-Willi Syndrome Association (Usa) 8588 Potter Park Drive, Suite 500 Sarasota, Florida 34238 Toll Free: 800-926-4797 Local: 941-312-0400 Fax: 941-312-0142 www.pwsausa.org © Copyright 2011 A Reference for Families and Care Providers Growth HORMONE AND PraderSECOND-WILLI EDITION Syndrome A REFerence For FaMILies and Care ProViders Donald G. Goranson, Jr., Editor Growth Hormone and Prader-Willi Syndrome — Second Edition A Reference for Families and Care Providers CONTENTS Acknowledgments....................................................................... 5 Introduction and History .............................................................. 7 Prader-Willi Syndrome and Growth ...................................................... 9 Effects of Growth Hormone Treatment in Children with PWS ................................ 20 What Is Involved in Growth Hormone Treatment? .......................................... 26 Questions, Wisdom and Survey Data from our Families ..................................... 34 Appendix: A. Overview of Prader-Willi Syndrome................................................ 40 B. Information Resources on Prader-Willi Syndrome .................................... 42 C. Information Resources on Growth Hormone Use and Products ........................ 43 D. Glossary of Terms ............................................................ -
Growth and Growth Hormone I
Pediat. Res. 2: 43-63 (1968) Dwarfism, constitutional hypoglycemia dwarfism, psychosocial insulin gonadal dysgenesis maternal depriva- growth hormone tion syndrome growth retardation panhypopituitarism Growth and Growth Hormone I. Changes in Serum Level of Growth Hormone Following Hypoglycemia in 134 Children with Growth Retardation S.L.KAPLAN, C.A.L.ABRAMS, J.J.BELL, F.A.CONTE and M.M.GRUMBACH[41] Department of Pediatrics, University of California, San Francisco Medical Center, San Francisco, California, and College of Physicians and Surgeons, Columbia University, New York, New York, USA Extract The change in levels of growth hormone in serum (SGH) following insulin-induced hypoglycemia was evaluated in 134 prepubertal children with growth retardation and 10 control subjects with normal growth patterns by radioimmunoassay, utilizing 131I-HGH and rabbit antiserum to human growth hormone. Mean maximum growth hormone concentration (m^g/ml) at any time during the test was: 10 Control subjects 12.4 53 Hypopituitarism 2.5 m^g or less in 52/53 20 Constitutional shortness of stature 12.5 22 Primordial dwarfism 12.1 9 XO gonadal dysgenesis 13.4 5 Delayed adolescence 11.8 5 Maternal deprivation 16.7 9 Psychosocial dwarfism 10.9 11 Miscellaneous disorders 7.0 Among factors found to affect the SGH response to insulin-induced hypoglycemia were: a) elevated fasting concentration of SGH which appeared to alter the responsiveness to stimulation; and b) age. The mean maximum SGH concentration of the control subjects following insulin-induced hypo- glycemia was 12.4 m^Mg/ml. In 52/53 patients with hypopituitarism, the SGH concentration was 1 m/*g or less at rest, with no increase or an increase to a maximum of 2.5 m^Mg/ml following hypoglycemia. -
HORMONES and SPORT Insulin, Growth Hormone and Sport
13 HORMONES AND SPORT Insulin, growth hormone and sport P H Sonksen Guy’s, King’s and St Thomas’ School of Medicine, St Thomas’ Hospital, London SE1 7EH, UK; Email: [email protected] Abstract This review examines some interesting ‘new’ histories of blood rather than urine samples. The first method has a insulin and reviews our current understanding of its window of opportunity lasting about 24 h after an injec- physiological actions and synergy with GH in the regu- tion and is most suitable for ‘out of competition’ testing. lation of metabolism and body composition. It reviews the The second method has reasonable sensitivity for as long as history of GH abuse that antedates by many years the 2 weeks after the last injection of GH and is uninfluenced awareness of endocrinologists to its potent anabolic actions. by extreme exercise and suitable for post-competition Promising methods for detection of GH abuse have been samples. This method has a greater sensitivity in men than developed but have yet to be sufficiently well validated to in women. The specificity of both methods seems accept- be ready for introduction into competitive sport. So far, ably high but lawyers need to decide what level of there are two promising avenues for detecting GH abuse. scientific probability is needed to obtain a conviction. Both The first uses immunoassays that can distinguish the methods need further validation before implementation. isomers of pituitary-derived GH from the monomer of Research work carried out as part of the fight against recombinant human GH. The second works through doping in sport has opened up a new and exciting area of demonstrating circulating concentrations of one or more endocrinology. -
Drug Code List
HCPCS/Drug Code List Version 13.2 Revised 6/1/21 List will be updated routinely Disclaimer: For drug codes that require an NDC, coverage depends on the drug NDC status (rebate eligible, Non-DESI, non-termed, etc) on the date of service. Note: Physician/Facility-administered medications are reimbursed using the Centers for Medicare and Medicaid Services (CMS) Part B Drug pricing file found on the CMS website--www.cms.gov. In the absence of a fee, pricing may reflect the methodolgy used for retail pharmacies. Go to data.medicaid.gov for a complete list of drug NDCs participating in the Medicaid drug rebate program. Consult with each Managed Care Organization (MCO) about their coverage guidelines and prior authroization requirements, if applicable. Highlights represent updated material for each specific revision of the Drug Code List. Code Description Brand Name NDC NDC unit Category Service AC CAH P NP MW MH HS PO OPH HI ID DC Special Instructions req. of Limits OP OP TF for measure drug rebate ? 90281 human ig, im Gamastan Yes ML Antisera NONE X X X X Closed 3/31/13. 90283 human ig, iv Gamimune, Yes ML Antisera NONE X X X X Closed 3/31/13. Cost invoice required with claim. Restricted to ICD-9 diagnoses codes 204.10 - 204.12, Flebogamma, 279.02, 279.04, 279.06, 279.12, 287.31, and 446.1, and must be included on claim form, effective 10/1/09. Gammagard 90287 botulinum antitoxin N/A Antisera Not Covered 90288 botulism ig, iv No ML NONE X X X X Requires documentation and medical review 90291 cmv ig, iv Cytogam Yes ML Antisera NONE X X X X Closed 3/31/13. -
Pharmacological Management of Acromegaly: a Current Perspective
Neurosurg Focus 29 (4):E14, 2010 Pharmacological management of acromegaly: a current perspective SUNIL MANJILA , M.D.,1 Osmo N D C. WU, B.A.,1 FAH D R. KHAN , M.D., M.S.E.,1 ME H ree N M. KHAN , M.D.,2 BAHA M. AR A F AH , M.D.,2 AN D WA rre N R. SE L M AN , M.D.1 1Department of Neurological Surgery, The Neurological Institute, and 2Division of Clinical and Molecular Endocrinology, University Hospitals Case Medical Center, Cleveland, Ohio Acromegaly is a chronic disorder of enhanced growth hormone (GH) secretion and elevated insulin-like growth factor–I (IGF-I) levels, the most frequent cause of which is a pituitary adenoma. Persistently elevated GH and IGF-I levels lead to substantial morbidity and mortality. Treatment goals include complete removal of the tumor causing the disease, symptomatic relief, reduction of multisystem complications, and control of local mass effect. While trans- sphenoidal tumor resection is considered first-line treatment of patients in whom a surgical cure can be expected, pharmacological therapy is playing an increased role in the armamentarium against acromegaly in patients unsuitable for or refusing surgery, after failure of surgical treatment (inadequate resection, cavernous sinus invasion, or transcap- sular intraarachnoid invasion), or in select cases as primary treatment. Three broad drug classes are available for the treatment of acromegaly: somatostatin analogs, dopamine agonists, and GH receptor antagonists. Somatostatin analogs are considered as the first-line pharmacological treatment of acromegaly, although effica- cy varies among the different formulations. Octreotide long-acting release (LAR) appears to be more efficacious than lanreotide sustained release (SR). -
Cross Discipline Team Leader Review
CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 203255Orig1s000 CROSS DISCIPLINE TEAM LEADER REVIEW Cross Discipline Team Leader Review pituitary adenoma (pituitary acromegaly) and only very rarely to an ectopic source of GH. Therefore for practical purposes, acromegaly is a pituitary disease. Although the treatment of choice of pituitary acromegaly is surgical removal of the pituitary mass via transsfenoidal route, the success rate is variable (90% in patients with microadenoma and below 50% in patients with macroadenomas). Patients who fail surgery (or cannot undergo surgery for a variety of reasons) benefit from radiation or pharmacological therapy. Because the effects of radiation may take years to reach effectiveness, medical therapy is almost invariably used in patients who respond poorly or incompletely to surgical management. Tight GH control and a normalization of serum IGF-1 are the goals of medical treatment. GH reductions to ≤1 μg/L using a modern sensitive immunoassay (approximately equivalent to 2.5 μg/L measured by RAI)2 following an oral glucose load are desirable. There are three drug products that have been approved by the FDA for the medical treatment of acromegaly. From a mechanism of action perspective they belong to two distinct classes: somatostatin analogs (octreotide and lanreotide) and GH receptor antagonists (pegvisomant). Pegvisomant (SOMAVERT) is a pegylated GH analog and acts as a GH receptor antagonist. It competes with endogenous GH for GH receptor binding. Once bound to the GH receptor it prevents receptor dimerization and subsequent intracellular signaling, thus blocking generation of IGF-1. The major safety signal identified with pegvisomant is transient liver enzyme elevation; however, no drug-induced liver failure has been documented to date. -
Pyrexia of Unknown Origin. Presenting Sign of Hypothalamic Hypopituitarism R
Postgrad Med J: first published as 10.1136/pgmj.57.667.310 on 1 May 1981. Downloaded from Postgraduate Medical Journal (May 1981) 57, 310-313 Pyrexia of unknown origin. Presenting sign of hypothalamic hypopituitarism R. MARILUS* A. BARKAN* M.D. M.D. S. LEIBAt R. ARIE* M.D. M.D. I. BLUM* M.D. *Department of Internal Medicine 'B' and tDepartment ofEndocrinology, Beilinson Medical Center, Petah Tiqva, The Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Israel Summary least 10 such admissions because offever of unknown A 62-year-old man was admitted to hospital 10 times origin had been recorded. During this period, he over 12 years because of pyrexia of unknown origin. was extensively investigated for possible infectious, Hypothalamic hypopituitarism was diagnosed by neoplastic, inflammatory and collagen diseases, but dynamic tests including clomiphene, LRH, TRH and the various tests failed to reveal the cause of theby copyright. chlorpromazine stimulation. Lack of ACTH was fever. demonstrated by long and short tetracosactrin tests. A detailed past history of the patient was non- The aetiology of the disorder was believed to be contributory. However, further questioning at a previous encephalitis. later period of his admission revealed interesting Following substitution therapy with adrenal and pertinent facts. Twelve years before the present gonadal steroids there were no further episodes of admission his body hair and sex activity had been fever. normal. At that time he had an acute febrile illness with severe headache which lasted for about one Introduction week. He was not admitted to hospital and did not http://pmj.bmj.com/ Pyrexia of unknown origin (PUO) may present receive any specific therapy. -
To Download a List of Prescription Drugs Requiring Prior Authorization
Essential Health Benefits Standard Specialty PA and QL List July 2016 The following products require prior authorization. In addition, there may be quantity limits for these drugs, which is notated below. Therapeutic Category Drug Name Quantity Limit Anti-infectives Antiretrovirals, HIV SELZENTRY (maraviroc) None Cardiology Antilipemic JUXTAPID (lomitapide) 1 tab/day PRALUENT (alirocumab) 2 syringes/28 days REPATHA (evolocumab) 3 syringes/28 days Pulmonary Arterial Hypertension ADCIRCA (tadalafil) 2 tabs/day ADEMPAS (riociguat) 3 tabs/day FLOLAN (epoprostenol) None LETAIRIS (ambrisentan) 1 tab/day OPSUMIT (macitentan) 1 tab/day ORENITRAM (treprostinil diolamine) None REMODULIN (treprostinil) None REVATIO (sildenafil) Soln None REVATIO (sildenafil) Tabs 3 tabs/day TRACLEER (bosentan) 2 tabs/day TYVASO (treprostinil) 1 ampule/day UPTRAVI (selexipag) 2 tabs/day UPTRAVI (selexipag) Pack 2 packs/year VELETRI (epoprostenol) None VENTAVIS (iloprost) 9 ampules/day Central Nervous System Anticonvulsants SABRIL (vigabatrin) pack None Depressant XYREM (sodium oxybate) 3 bottles (540 mL)/30 days Neurotoxins BOTOX (onabotulinumtoxinA) None DYSPORT (abobotulinumtoxinA) None MYOBLOC (rimabotulinumtoxinB) None XEOMIN (incobotulinumtoxinA) None Parkinson's APOKYN (apomorphine) 20 cartridges/30 days Sleep Disorder HETLIOZ (tasimelteon) 1 cap/day Dermatology Alkylating Agents VALCHLOR (mechlorethamine) Gel None Electrolyte & Renal Agents Diuretics KEVEYIS (dichlorphenamide) 4 tabs/day Endocrinology & Metabolism Gonadotropins ELIGARD (leuprolide) 22.5 mg -
Somatostatin Analogues in the Treatment of Neuroendocrine Tumors: Past, Present and Future
International Journal of Molecular Sciences Review Somatostatin Analogues in the Treatment of Neuroendocrine Tumors: Past, Present and Future Anna Kathrin Stueven 1, Antonin Kayser 1, Christoph Wetz 2, Holger Amthauer 2, Alexander Wree 1, Frank Tacke 1, Bertram Wiedenmann 1, Christoph Roderburg 1,* and Henning Jann 1 1 Charité, Campus Virchow Klinikum and Charité, Campus Mitte, Department of Hepatology and Gastroenterology, Universitätsmedizin Berlin, 10117 Berlin, Germany; [email protected] (A.K.S.); [email protected] (A.K.); [email protected] (A.W.); [email protected] (F.T.); [email protected] (B.W.); [email protected] (H.J.) 2 Charité, Campus Virchow Klinikum and Charité, Campus Mitte, Department of Nuclear Medicine, Universitätsmedizin Berlin, 10117 Berlin, Germany; [email protected] (C.W.); [email protected] (H.A.) * Correspondence: [email protected]; Tel.: +49-30-450-553022 Received: 3 May 2019; Accepted: 19 June 2019; Published: 22 June 2019 Abstract: In recent decades, the incidence of neuroendocrine tumors (NETs) has steadily increased. Due to the slow-growing nature of these tumors and the lack of early symptoms, most cases are diagnosed at advanced stages, when curative treatment options are no longer available. Prognosis and survival of patients with NETs are determined by the location of the primary lesion, biochemical functional status, differentiation, initial staging, and response to treatment. Somatostatin analogue (SSA) therapy has been a mainstay of antisecretory therapy in functioning neuroendocrine tumors, which cause various clinical symptoms depending on hormonal hypersecretion. Beyond symptomatic management, recent research demonstrates that SSAs exert antiproliferative effects and inhibit tumor growth via the somatostatin receptor 2 (SSTR2). -
Regulatory Mechanisms of Somatostatin Expression
International Journal of Molecular Sciences Review Regulatory Mechanisms of Somatostatin Expression Emmanuel Ampofo * , Lisa Nalbach, Michael D. Menger and Matthias W. Laschke Institute for Clinical & Experimental Surgery, Saarland University, 66421 Homburg/Saar, Germany; [email protected] (L.N.); [email protected] (M.D.M.); [email protected] (M.W.L.) * Correspondence: [email protected]; Tel.: +49-6841-162-6561; Fax: +49-6841-162-6553 Received: 25 May 2020; Accepted: 9 June 2020; Published: 11 June 2020 Abstract: Somatostatin is a peptide hormone, which most commonly is produced by endocrine cells and the central nervous system. In mammals, somatostatin originates from pre-prosomatostatin and is processed to a shorter form, i.e., somatostatin-14, and a longer form, i.e., somatostatin-28. The two peptides repress growth hormone secretion and are involved in the regulation of glucagon and insulin synthesis in the pancreas. In recent years, the processing and secretion of somatostatin have been studied intensively. However, little attention has been paid to the regulatory mechanisms that control its expression. This review provides an up-to-date overview of these mechanisms. In particular, it focuses on the role of enhancers and silencers within the promoter region as well as on the binding of modulatory transcription factors to these elements. Moreover, it addresses extracellular factors, which trigger key signaling pathways, leading to an enhanced somatostatin expression in health and disease. Keywords: somatostatin; pre-prosomatostatin; δ-cells; central nervous system (CNS); gut; hypothalamus; cAMP resonse element (CRE); pancreas/duodenum homeobox protein (PDX)1; paired box protein (PAX)6; growth hormone (GH); brain-derived neurotrophic factor (BDNF); glutamateric system; pancreas 1. -
Influence of the Endocrine System on Growth and Development R
331. INFLUENCE OF THE ENDOCRINE SYSTEM ON GROWTH AND DEVELOPMENT R. J. GERRITS A. R. S., U. S. D. A. Introduction The field of endocrinology cannot be defined in a manner entirely acceptable to all biologists or animal scientists. This is understandable as there are many points of view and many voids in our knowledge in this area. It is very hard to give a precise definition for an endocrine gland because all cells possess some secretory capacity and therefore contribute to the internal environment of the organism. For the most part the term "hormone" is probably applied too loosely and to a great variety of unrelated substances. Hormones can be identified as chemical agents which are synthesized by circumscribed parts of the body, generally specialized ductless glands, and are carried by the circulatory system to another part of the body where they evoke systemic adjustments by acting on rather specific target tissues or organs (Turner, 1966). In general, hormones regulate many processes such as growth, regeneration, reproduction, blood chemistry, metabolic rate, etc. Hormones act on the organs and tissues of the body by regulating the rate of specific metabolic reactions without contributing much at all to the constituent cell. It can be said that ad- justments to hormone levels require duration rather than speed, as opposed to the rapid coordinations of the body that are controlled by the nervous system. These biochemical adjustments are accomplished at the cellular level by virtue of their power to augwnt or restrain special enzyme sys- tems. It is important that hormones be released at the right time and in the proper amounts of the normal organism if they are to accomplish their specific mission.