DOCSLIB.ORG

JPBMAL2832.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
JPBMAL2832.Pdf B. Kumar, JPBMAL, 2016, 4(2): 122-131 CODEN (USA): JPBAC9 | ISSN: 2347-4742 Journal of Pharmaceutical and Biomedical Analysis Letters Journal Home Page: www.pharmaresearchlibrary.com/jpbmal Review Article Open Access A Review on Thyroid Disease B. Kumar*, K. Durga Prasanna Roja, M. Gobinath Department of Pharmacy Practice, Ratnam Institute of Pharmacy, Pidthapolur, Nellore. A B S T R A C T The thyroid gland is one of the largest endocrine gland and consists of two connected lobes. The thyroid gland is found in the neck, below the thyroid cartilage. It participates in these processes by producing thyroid hormones, the principal ones being triiodothyronine (T3) and thyroxine (sometimes referred to as tetraiodothyronine (T4)). These hormones regulate the growth and rate of function of many other systems in the body. T3 and T4 are synthesized from iodine and tyrosine. The primary function of the thyroid is production of the hormones T3, T4 and calcitonin. Up to 80% of the T4 is converted to T3 by organs such as the liver, kidney and spleen. T3 is several times more powerful than T4, which is largely a prohormone, perhaps four or even ten times more active. Beta-blockers are used to decrease symptoms of hyperthyroidism such as increased heart rate, tremors, anxiety and heart palpitations, and anti-thyroid drugs are used to decrease the production of thyroid hormones, in particular, in the case of Graves' disease. The gland shrinks by 50-60% but can cause hypothyroidism and rarely pain syndrome, which arises due to radiation thyroiditis. It is short lived and treated by steroids. Keywords: Thyroid Gland, Thyroxine, Triiodothyronine, Graves ‘disease, Spleen and Kidney. A R T I C L E I N F O CONTENTS 1. Introduction . 123 2. Physiology. .123 3. Clinical Significance. .125 4. Pathophysiology. 126 5. Diagnosis. .127 6. Adverse Effects. .128 7. Drug Interactions. 128 8. Treatment. 129 9. Conclusion. 130 10. References . .130 Article History: Received 27 February 2016, Accepted 30 March 2016, Available Online 18 July 2016 *Corresponding Author B. Kumar Department of Pharmacy Practice, Ratnam Institute of Pharmacy, Nellore. Manuscript ID: JPBMAL2832 PAPER-QR CODE Citation: B. Kumar, et al. A Review on Thyroid Disease. J. Pharm. Biomed. A. Lett., 2016, 4(2): 122-131. Copyright© 2016 B. Kumar, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. Journal of Pharmaceutical and Biomedical Analysis Letters 122 B. Kumar, JPBMAL, 2016, 4(2): 122-131 CODEN (USA): JPBAC9 | ISSN: 2347-4742 1. Introduction The thyroid gland is one of the largest endocrine gland and the pyramidal lobe is present at the most anterior side of the consists of two connected lobes. The thyroid gland is found in lobe. In this region, the recurrent laryngeal nerve and the the neck, below the thyroid cartilage (which forms inferior thyroid artery pass next to or in the ligament and the laryngeal prominence, or "Adam's apple"). The thyroid tubercle. Between the two layers of the capsule and on the gland controls how quickly the body uses energy, posterior side of the lobes, there are on each side makes proteins, and controls how sensitive the body is to two parathyroid glands. The thyroid isthmus is variable in other hormones. It participates in these processes by producing presence and size, can change shape and size, and can thyroid hormones, the principal ones beingtriiodo- encompass the pyramidal lobe. The thyroid is one of the thyronine (T3) and thyroxine (sometimes referred to as larger endocrine glands, weighing 2-3 grams in neonates tetraiodothyronine (T4)). These hormones regulate the growth and 18-60 grams in adults, and increased in pregnancy. and rate of function of many other systems in the body. T3 and T4 are synthesized from iodine and tyrosine. The thyroid also producescalcitonin, which plays a role in calcium homeostasis.Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) produced by the anterior pituitary, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus. Figure 2: Isthmus showing pyramidal lobe In a healthy patient, the gland is not visible yet can be palpated as a soft mass. Examination of the thyroid gland is carried out by locating the thyroid cartilage and passing the fingers up and down, examining for abnormal masses and overall thyroid size. Then, place one hand on each of the trachea and gently displace the thyroid tissue to the contralateral side of the neck for both sides while the other Figure 1:The thyroid gland as present on the human hand manually palpates the displaced gland tissue; having trachea the patient flex the neck slightly to the side when being palpated may help in this examination. Next, the two lobes The thyroid gland is a butterfly-shaped organ and is of the gland should be compared for size and texture using composed of two cone-like lobes or visual inspection, as well as manual or bimanual palpation. wings, lobusdexter (right lobe) and lobus sinister(left lobe), Finally, ask the patient to swallow to check for mobility of connected via the isthmus. Each lobe is about 5 cm long, the gland; many clinicians find that having the patient 3 cm wide and 2 cm thick. The organ is situated on the swallow water helps this part of the examination. In a anterior side of the neck, lying against and around the healthy state, the gland is mobile when swallowing occurs larynx and trachea, reaching posteriorly the oesophagus and due its fascial encasement. Thus when the patient swallows, carotid sheath. It starts cranially at the oblique line on the gland moves superiorly, as does the whole larynx. the thyroid cartilage (just below the laryngeal prominence, or 'Adam's Apple'), and extends inferiorly to approximately The thyroid is supplied with arterial blood from the superior the fifth or sixth tracheal ring. It is difficult to demarcate the thyroid artery, a branch of the external carotid artery, and gland's upper and lower border with vertebral levels the inferior thyroid artery, a branch of the thyrocervical because it moves position in relation to these during trunk, and sometimes by the thyroid ima artery, branching swallowing. There is occasionally a third lobe present directly from the subclavian artery. The venous blood is called the pyramidal lobe of the thyroid gland. It is of drained via superior thyroid veins, draining in the internal conical shape and extends from the upper part of the jugular vein, and via inferior thyroid veins, draining via isthmus, up across the thyroid cartilage to the hyoid bone. theplexus thyroideusimpar in the left brachiocephalic The pyramidal lobe is a remnant of the fetal thyroid stalk, vein.Lymphatic drainage passes frequently the lateral deep or thyroglossal duct. It is occasionally quite detached, or cervical lymph nodes and the pre- and paratracheal lymph may be divided into two or more parts. The pyramidal lobe nodes. The gland is supplied by parasympathetic nerve is also known as Lalouette's pyramid. On the posterior side, input from the superior laryngeal nerve and the recurrent the gland is fixed to the cricoids and tracheal cartilage laryngeal nerve. and cricopharyngeus muscle by a thickening of the fascia to form the posterior suspensory ligament of thyroid gland also known as Berry's ligament. The thyroid glands 2. Physiology: firm attachment to the underlying trachea is the reason The primary function of the thyroid is production of the behind its movement with swallowing. In variable extent, hormones T3, T4 and calcitonin. Up to 80% of the T4 is Journal of Pharmaceutical and Biomedical Analysis Letters 123 B. Kumar, JPBMAL, 2016, 4(2): 122-131 CODEN (USA): JPBAC9 | ISSN: 2347-4742 converted to T3 by organs such as the liver, kidney and "iodine trap" by the hydrogen peroxide generated by the spleen. T3 is several times more powerful than T4, which is enzyme thyroid peroxidase (TPO) and linked to the 3' and largely a prohormone, perhaps four or even ten times more 5' sites of the benzene ring of the tyrosine residues on Tg, active. and on free tyrosine. Upon stimulation by the thyroid- T3 and T4 production and action: stimulating hormone (TSH), the follicular cells reabsorb Tg and cleave the iodinated tyrosines from Tg in lysosomes, forming T4 and T3 (in T3, one iodine atom is absent compared to T4), and releasing them into the blood. Deiodinase enzymes convert T4 to T3. Thyroid hormone secreted from the gland is about 80-90% T4 and about 10-20% T3. Cells of the developing brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play a particularly crucial role in brain maturation during fetal development, A transport protein that seems to be important for T4 transport across the blood–brain barrier (OATP1C1) has been identified. A second transport protein (MCT8) is important for Figure 3:The system of the thyroid hormones T3 and T4 T3transport across brain cell membranes. Non-genomic actions of T4 are those that are not initiated by liganding of the hormone to intranuclear thyroid receptor. These may begin at the plasma membrane or within cytoplasm. Plasma membrane-initiated actions begin at a receptor on the integrin alphaV beta3 that activates ERK1/2. This binding culminates in local membrane actions on ion transport systems such as the Na(+)/H(+) exchanger or complex cellular events including cell proliferation. These integrins are concentrated on cells of the vasculature and on some types of tumor cells, which in part explains the proangiogenic effects of iodothyronines Figure 4: Synthesis of the thyroid hormones, as seen on an and proliferative actions of thyroid hormone on some individual thyroid follicular cell.
Load more

Recommended publications
  • PRODUCT INFORMATION Propylthiouracil-D5 Item No
    PRODUCT INFORMATION Propylthiouracil-d5 Item No. 30743 CAS Registry No.: 1189423-94-6 Formal Name: 2,3-dihydro-6-(propyl-2,2,3,3,3-d5)-2- thioxo-4(1H)-pyrimidinone S Synonyms: 6-n-Propylthiouracil-d5, PTU-d5 MF: C H D N OS H H 7 5 5 2 N N FW: 175.3 D D Chemical Purity: ≥98% (Propylthiouracil) D O Deuterium D Incorporation: ≥99% deuterated forms (d1-d5); ≤1% d0 D Supplied as: A solid Storage: -20°C Stability: ≥2 years Information represents the product specifications. Batch specific analytical results are provided on each certificate of analysis. Laboratory Procedures Propylthiouracil-d5 is intended for use as an internal standard for the quantification of propylthiouracil (Item No. 14069) by GC- or LC-MS. The accuracy of the sample weight in this vial is between 5% over and 2% under the amount shown on the vial. If better precision is required, the deuterated standard should be quantitated against a more precisely weighed unlabeled standard by constructing a standard curve of peak intensity ratios (deuterated versus unlabeled). Propylthiouracil-d5 is supplied as a solid. A stock solution may be made by dissolving the propylthiouracil-d5 in the solvent of choice, which should be purged with an inert gas. Propylthiouracil-d5 is slightly soluble in DMSO and methanol. Description Propylthiouracil (PTU) is a thioamide antithyroid agent.1 It inhibits thyroid peroxidase activity in rat and monkey thyroid microsomes (IC50s = 0.081 and 4.1 μM, respectively). PTU (30 mg/kg) increases thyroid weight and serum thyroid stimulating hormone levels and decreases serum 3,5,3’-triiodothyronine and thyroxine levels in rats.
    [Show full text]
  • Chapter 38 Thyroid & Antithyroid Drugs
    Chapter 38 Thyroid & antithyroid drugs Right Lobe Left Lobe Thyroglobulin Thyroid gland Structure: • The thyroid gland consists of two lobes & is situated in the lower neck • The functional unit of the thyroid gland is the follicle • Each follicle consists of a single layer of epithelial cells (follicular cells) around a cavity, >>> • the follicle lumen, which is filled with a thick colloid containing thyroglobulin – Thyroglobulin is a large glycoprotein, – each molecule of which contains about 115 tyrosine residues Thyroid homones • The thyroid gland secretes: triiodothyronine (T3) thyroxine (T4)…iodothyronines • The thyroid gland also secretes calcitonin • T3 and T4 are critically important for: – normal growth and development, – normalize body temp. – normalize energy levels • Calcitonin is involved in the control of plasma Ca2+ (Ch. 42) Synthesis, storage, release, and interconversion of thyroid hormones Iodine intake Iodide is ingested by food, water, medication… rapidly absorbed (best absorbed in the duodenum and ileum) The daily intake is: 150mcg (200mcg during pregnancy) The thyroid gland removes 75mcg daily Synthesis, storage, release, and interconversion of thyroid hormones 1) Iodide ion (I-) is uptaken by the follicular cell (Na/I- symporter)…that incorporate it into active thyroid hormone. 2) Iodide is oxidized by thyroidal peroxidase into iodine 3) Iodine iodinates tyrosine residues of thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)….iodine organification 4) Two molecules of diiodotyrosine combine
    [Show full text]
  • Carbimazole-Induced Hepatotoxicity - Avoid Rechallenging
    Central JSM Thyroid Disorders and Management Bringing Excellence in Open Access Case Report *Corresponding author Marianne Elston, Department of Endocrinology, Waikato Hospital, Private Bag 3200, Hamilton 3240, New Carbimazole-Induced Zealand, Tel: +647 839 8899; Email: Submitted: 01 August 2016 Hepatotoxicity - Avoid Accepted: 10 August 2016 Published: 11 August 2016 Rechallenging Copyright © 2016 Elston et al. Karalus M, Jade Tamatea AU, Conaglen JV, and Elston MS* Waikato Clinical Campus, University of Auckland, New Zealand OPEN ACCESS Keywords Abstract • Antithyroid agents All thioamide anti - thyroid medications are known to be associated with liver • Drug-induced liver injury dysfunction. Cholestasis is most commonly reported in association with carbimazole/ • Thyrotoxicosis methimazole. We report a patient with Graves’ disease, who developed acute • Graves’s disease Hepatocellular dysfunction associated with carbimazole. There is limited data available on re -exposure in this situation. The patient rechallenged herself twice and subsequent exposures resulted in an increasingly shorter time to symptom onset until finally even a single 5mg tablet rapidly provoked severe symptoms and abnormal liver function tests. This case supports the need to avoid anti - thyroid medication rechallenge in patients who develop significant liver dysfunction following their use and identifies that carbimazole may be associated with acute Hepatocellular dysfunction and not just Cholestasis. ABBREVIATIONS thyrotoxicosis with normal liver function tests (LFTs) (Figure 1 and Table 1). Initial therapy with 20mg CBZ once daily was ATD: Anti - Thyroid Drugs; PTU: Propylthiouracil; CBZ: reduced after 2 weeks to 10mg per day. One month after starting Carbimazole; MMZ: Methimazole; ALT: Alanine Transaminase CBZ, routine liver function testing revealed abnormal LFTs INTRODUCTION particularly alanine transaminase (ALT) (Figure 1 and Table 1).
    [Show full text]
  • Thyrotoxic Hypokalaemic Periodic Paralysis
    Thyrotoxic Hypokalaemic Periodic Paralysis: A Case Series from Trinidad, West Indies M Ramdath1, J Teelucksingh1, A Ramnath1, K Ramcharan2, L Conyette2, A Ramesar2, RP King3, S Teelucksingh4 ABSTRACT We report our experience with seven cases of thyrotoxicosis associated with hypokalaemic periodic paralysis seen over a 25-year period in Trinidad, West Indies, an ethnically diverse island. All the cases were males, one was a Chinese, two were of East Indian and four of African descent, with a mean age 31.4 years (range 22–54 years). Early diagnosis and appropriate treatment led to the prompt resolution of the symptoms. Although rare in the Caribbean region, clinicians should be aware of the features of this potentially fatal but readily remediable com- plication of thyrotoxicosis. Keywords: Hypokalaemia, hypokalaemic periodic paralysis, periodic paralysis, thyrotoxic periodic paralysis, Trinidad and Tobago, West Indies Parálisis Periódica Hipocalémica Tirotóxica: Un Estudio de Serie de Casos de Trinidad, West Indies M Ramdath1, J Teelucksingh1, A Ramnath1, K Ramcharan2, L Conyette2, A Ramesar2, RP King3, S Teelucksingh4 RESUMEN Reportamos nuestra experiencia con siete casos de tirotoxicosis asociada con parálisis perió- dica hipocalémica observada por un período de 25 años en Trinidad, West Indies – una isla ca- racterizada por su diversidad étnica. En todos los casos se trató de hombres: uno era un chino, dos eran de la India, y cuatro de ascendencia africana, con una edad promedio de 31.4 años (rango 22 a 54 años). El diagnóstico precoz y un tratamiento adecuado llevaron a la pronta re- solución de los síntomas. Aunque sea raro en la región del Caribe, los clínicos deben tener en cuenta que las características de esta complicación de la tirotoxicosis, potencialmente fatal pero fácilmente remediable.
    [Show full text]
  • Thyroidectomy for the Treatment of Graves' Thyrotoxicosis in Thioamide- Induced Agranulocytosis and Sepsis
    Thyroidectomy for the treatment of Graves' thyrotoxicosis in thioamide- induced agranulocytosis and sepsis Citation: Knight, Colin L., Cooray, Shamil D., Kulkarni, Jaideep, Borschmann, Michael and Kotowicz, Mark 2017, Thyroidectomy for the treatment of Graves' thyrotoxicosis in thioamide- induced agranulocytosis and sepsis, Endocrinology, diabetes & metabolism, Article ID: 17- 0071, pp. 1-6. DOI: http://www.dx.doi.org/10.1530/EDM-17-0071 © 2017, The Authors Reproduced by Deakin University under the terms of the Creative Commons Attribution Non- Commercial No-Derivatives Licence Downloaded from DRO: http://hdl.handle.net/10536/DRO/DU:30109157 DRO Deakin Research Online, Deakin University’s Research Repository Deakin University CRICOS Provider Code: 00113B ID: 17-0071 10.1530/EDM-17-0071 C L Knight and others Thyroidectomy when thyrotoxic ID: 17-0071; September 2017 with agranulocytosis DOI: 10.1530/EDM-17-0071 Thyroidectomy for the treatment of Graves’ thyrotoxicosis in thioamide-induced agranulocytosis and sepsis Colin L Knight1, Shamil D Cooray1, Jaideep Kulkarni1, Michael Borschmann2,3 and Mark Kotowicz1,4,5 1Department of Endocrinology and Diabetes, University Hospital Geelong, Geelong, Victoria, Australia, Correspondence 2Ear, Nose and Throat, Head and Neck Surgery, St. John of God Hospital, Geelong, Victoria, Australia, should be addressed 3Director of Otolaryngology, University Hospital Geelong, Geelong, Victoria, Australia, 4Deakin University to C Knight School of Medicine, Geelong, Victoria, Australia, and 5Melbourne Clinical School-Western Campus, Email Department of Medicine, The University of Melbourne, St. Albans, Victoria, Australia [email protected] Summary A 51 year old man presented with sepsis in the setting of thioamide-induced agranulocytosis. Empiric broad-spectrum antibiotics was followed by directed narrow-spectrum antibiotics, and his neutrophil count recovered with support from granulocyte-colony stimulating factor (G-CSF) analogue transfusions.
    [Show full text]
  • Thyroid Disease Testing AHS – G2045
    Corporate Medical Policy Thyroid Disease Testing AHS – G2045 File Name: thyroid_disease_testing Origination: 4/2019 Last CAP Review: 6/2021 Next CAP Review: 6/2022 Last Review: 6/2021 Description of Procedure or Service Definition Thyroid hormones are necessary for prenatal and postnatal development, as well as metabolic activity in adults (Brent, 2020). Thyroid disease includes conditions which cause hypothyroidism, hyperthyroidism, goiter, thyroiditis (which can present as either hypo- or hyper-thyroidism) a nd thyroid tumors (Rugge, Bougatsos, & Chou, 2015). Thyroid function tests are used in a variety of clinical settings to assess thyroid function, monitor treatment, and screen asymptomatic populations for subclinical or otherwise undiagnosed thyroid dysfunction (Ross, 2019c). Related Policies: Genetic Cancer Susceptibility Using Next Generation Sequencing Genetic Testing for Germline Mutations of the RET Proto-Oncogene Molecular Markers in Fine Needle Aspirates of the Thyroid Molecular Panel Testing of Cancers to Identify Targeted Therapy Prenatal Screening ***Note: This Medical Policy is complex and technical. For questions concerning the technical language and/or specific clinical indications for its use, please consult your physician. Policy BCBSNC will provide coverage for thyroid disease testing when it is determined the medical criteria or reimbursement guidelines below are met Benefits Application This medical policy relates only to the services or supplies described herein. Please refer to the Member's Benefit Booklet for availability of benefits. Member's benefits may vary according to benefit design; therefore member benefit language should be reviewed before applying the terms of this medical policy. When thyroid disease testing is covered 1) Reimbursement for thyroid function testing is a llowed in the following situations: A.
    [Show full text]
  • PTU™ 50 Mg Tablets
    PRODUCT INFORMATION PTU™ 50 mg Tablets PTU™ 50 mg Tablets NAME OF THE MEDICINE Propylthiouracil Chemical Name: 1,2-dihydro-6-propyl-2-thioxopyrimidine-4-one The molecular weight of the compound is 170.2, the molecular formula is C 7H10 N2OS and the CAS registry number is 51-52-5. Structural Formula : DESCRIPTION Propythiouracil is a thioamide derivative which occurs as a white crystalline powder, odourless with a bitter taste, very slightly soluble in water, sparingly soluble in ethanol and soluble in solutions of alkali hydroxides or ammonia. PTU™ 50 mg Tablets are white, round, biconvex and uncoated. One side is debossed ‘PRESTAB’ and other side is plain. PHARMACOLOGY Category: Antithyroid Propylthiouracil blocks the peripheral conversion of thyroxine (T 4) to triiodothyronine (T 3) by inhibiting incorporation of iodide into tyrosine. Propylthiouracil is rapidly absorbed. The half-life in plasma approximates 2 hours (in anuric patients T½ 8.5 hours). Protein binding of propylthiouracil is approximately 75%. The drug is metabolized in the liver and is excreted in the bile (primary route) with approximately 30% being excreted in the urine as metabolites or whole drug. Propylthiouracil does not interfere with the action and the release of exogenous thyroid hormone. Clinical response, therefore, does not occur until circulating and colloid-stored thyroid hormone is utilised, and as such depends in part on the amount of colloid in the gland. The rapid fall in serum triiodothyronine T 3 concentration, before serum thyroxine (T 4) levels fall, parallels a clinical improvement in the thyrotoxic patient, and is generally seen after the first week.
    [Show full text]
  • BASED NASAL FORMULATIONS of LEVOTHYROXINE by Esomchukwu
    DEVELOPMENT AND IN VITRO CHARACTERIZATION OF POLYMER- BASED NASAL FORMULATIONS OF LEVOTHYROXINE by Esomchukwu Vin-Boris Obinna Submitted in partial fulfilment of the requirements for the degree of Masters of Science at Dalhousie University Halifax, Nova Scotia August 2020 © Copyright by Esomchukwu Vin-Boris Obinna, 2020 TABLE OF CONTENT LIST OF TABLES……………………………………………………………………… v LIST OF FIGURES……………………………………………………………………. vi ABSTRACT………………………………………………………………………………x LIST OF ABBREVIATIONS AND SYMBOLS USED………………………………xi ACKNOWLEDGEMENTS…….………………………………………………….… xii CHAPTER 1 INTRODUCTION ............................................................................. 1 1.1 ANATOMY AND PHYSIOLOGY OF THE THYROID GLAND .............................. 1 1.2 DISEASES OF THE THYROID GLAND ............................................................. 2 1.2.1 Hyperthyroidism ................................................................................. 2 1.2.2 Hypothyroidism .................................................................................. 3 1.3 LEVOTHYROXINE REPLACEMENT THERAPY ................................................. 4 1.3.1 Chemical and Physical Properties of Levothyroxine .......................... 5 1.3.2 Current Levothyroxine Delivery Methods .......................................... 6 1.4 ANATOMY AND PHYSIOLOGY OF THE NOSE ................................................. 8 1.5 NASAL DRUG DELIVERY .............................................................................. 9 1.5.1 Mechanisms of Nasal Drug Absorption
    [Show full text]
  • Acting Via a Cell Surface Receptor, Thyroid Hormone Is a Growth Factor for Glioma Cells
    Research Article Acting via a Cell Surface Receptor, Thyroid Hormone Is a Growth Factor for Glioma Cells Faith B. Davis,1 Heng-Yuan Tang,2 Ai Shih,1 Travis Keating,2 Lawrence Lansing,1 Aleck Hercbergs,5 Robert A. Fenstermaker,6 Ahmed Mousa,3 Shaker A. Mousa,3 Paul J. Davis,1,2,4 and Hung-Yun Lin1,2 1Ordway Research Institute, Inc.; 2Research Service, Stratton Veterans Affairs Medical Center; 3Albany College of Pharmacy; 4Wadsworth Center, New York State Department of Health, Albany, New York; 5Department of Radiation Oncology, The Cleveland Clinic, Cleveland, Ohio; and 6Department of Neurosurgery, Roswell Park Cancer Institute, Buffalo, New York Abstract RGD (arginine-glycine-aspartate) recognition site that is essential to the interactions of the integrin with its extracellular matrix Recent evidence suggests that the thyroid hormone L-thyroxine (ECM) protein ligands (2, 3). We have presented evidence that the (T4) stimulates growth of cancer cells via a plasma membrane thyroid hormone–binding site on integrin aVh3 is at or near the receptor on integrin AVB3.The contribution of this recently described receptor for thyroid hormone and receptor-based RGD recognition site and that an RGD peptide will displace stimulation of cellular mitogen-activated protein kinase thyroid hormone from integrin and will block the cellular actions [MAPK; extracellular signal-regulated kinase 1/2 (ERK1/2)] of the hormone (1). An interesting feature of this hormone activity, to enhancement of cell proliferation by thyroid receptor is that tetraiodothyroacetic acid, a hormone analogue hormone was quantitated functionally and by immunologic with reduced thyromimetic activity (4), competes with T4 at the means in three glioma cell lines exposed to T .At concen- receptor site (1).
    [Show full text]
  • Pharm Endocrine Review
    Pharm Endocrine Review Oral Hypoglycemic Medications α‐Glucosidase Insulin Secretagouges Insulin Sensitizer Inihibitors Sulfonylureas Meglitinides Phenylalanine Biguanides Thiazolidinediones Acarbose Miglitol Tolbutamide (1) Repaglinide Nateglinide Metformin Rosiglitazone Chloropramide (1) Pioglitazone Glyburide (2) Glipizide (2) Glimepiride (2) INSULIN SECRETAGOUGES The goal of these medications is simply to increase secretion of insulin from the pancreas. Each has its own nuances and proper usage, but essentially, they all regulate potassium efflux in the pancreatic β‐ islets causing an increased release of insulin in a still‐functioning pancreas Sulfonylureas. There are two generations of Sulfonylureas. The first generation (Tolbutamide and Chloropramide) are generally not used anymore because they have a risk of sulfur allergies. The second generation (Glyburide, Glipizide, Glimepiride) have no risk of sulfur allergies and are used much more frequently. Regardless of the generation, these function by blocking potassium efflux leading to depolarization of the pancreatic cells, calcium influx, and the release of insulin. Sulfonylureas can be taken just one time a day and are generally well tolerated. However, they run the risk of hypoglycemia, especially in those with hepatic failure. Meglitanides (Repaglinide). This functions just like a sulfonylurea: blocking potassium channels Æ increased insulin release. This differs from the sulfonylureas in that it has a rapid onset and short duration so is used as a supplement when eating. These are taken just prior to meals. When taken appropriately (i.e. you eat right after you take this) there is a lower risk of hypoglycemia. Of course, these drugs are new, which means expensive, and you must have a diligent diabetic who remembers to take his pill every time he eats.
    [Show full text]
  • On Rana Pipiens Metamorphosis and Development
    UNLV Theses, Dissertations, Professional Papers, and Capstones 2004 The Effects of environmentally relevant doses of Perchlorate (ClO4-) on Rana Pipiens metamorphosis and development Andrea N. Golli University of Nevada Las Vegas Follow this and additional works at: https://digitalscholarship.unlv.edu/thesesdissertations Part of the Desert Ecology Commons, Environmental Indicators and Impact Assessment Commons, and the Zoology Commons Repository Citation Golli, Andrea N., "The Effects of environmentally relevant doses of Perchlorate (ClO4-) on Rana Pipiens metamorphosis and development" (2004). UNLV Theses, Dissertations, Professional Papers, and Capstones. 183. http://dx.doi.org/10.34917/1436436 This Thesis is protected by copyright and/or related rights. It has been brought to you by Digital Scholarship@UNLV with permission from the rights-holder(s). You are free to use this Thesis in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Thesis has been accepted for inclusion in UNLV Theses, Dissertations, Professional Papers, and Capstones by an authorized administrator of Digital Scholarship@UNLV. For more information, please contact [email protected]. THE EFFECTS OF ENVIRONMENTALLY RELEVANT DOSES - OF PERCHLORATE (ClO4 ) ON RANA PIPIENS METAMORPHOSIS AND DEVELOPMENT by Andrea N. Golli Bachelor of Science University of Findlay 2001 Master of Science University of Nevada, Las Vegas 2004 A thesis submitted in partial fulfillment of the requirements for the Master of Science Degree in Environmental Science Department of Environmental Studies Greenspun College of Urban Affairs Graduate College University of Nevada, Las Vegas May 2004 ABSTRACT The Effects of Environmentally Relevant Doses - of Perchlorate (ClO4 ) on Rana pipiens Metamorphosis and Development by Andrea N.
    [Show full text]
  • Thiamazole "Uni-Pharma"
    EU-RISK MANAGEMENT PLAN THIAMAZOLE UNI-PHARMA 5 MG TABLETS VI.2 Elements for a public summary VI.2.1 Overview of disease epidemiology The most common forms of hyperthyroidism include Graves’ disease, Plummer disease, and toxic adenoma; but approximately 1-2% of patients with hyperthyroidism progress to thyroid storm, a rare disorder. (3) (4) (5) The overall incidence of hyperthyroidism (condition in which the thyroid gland is overactive and makes excessive amounts of thyroid hormone) is estimated between 0.05% and 1.3%, with the majority consisting of subclinical disease. A population-based study in the United Kingdom and Ireland found an incidence of 0.9 cases per 100,000 children younger than 15 years, showing that the disease incidence increases with age. The incidences of Graves’ disease and Plummer disease change with iodine intake. The prevalence of hyperthyroidism is approximately 5-10 times less than hypothyroidism (condition in which the body lacks sufficient thyroid hormone). (4) (5) Autoimmune thyroid disease (when the immune system creates antibodies that cause the thyroid to grow and make more thyroid hormone than the body needs) occurs with the same frequency in Caucasians, Hispanics, and Asians but at lower rates in African Americans; but all thyroid diseases occur more frequently in women than in men. (4) (5) VI.2.2 Summary of treatment benefits Thiamazole was introduced into use in 1954 and is still widely used for the temporary relief of hyperthyroidism in Graves’ disease, particularly in patients with mild or self-limited hyperthyroidism or who wish to avoid removal of the thyroid gland (thyroidectomy) or radiation therapy.
    [Show full text]