DOCSLIB.ORG

Cushing's Syndromedue to Unilateral Adrenocortical Hyperplasia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cushing's Syndromedue to Unilateral Adrenocortical Hyperplasia CASE REPORT Cushing's Syndrome due to Unilateral Adrenocortical Hyperplasia Fumio Otsuka, Toshio Ogura*, Kazushi Nakao, Nobuhiko Hayakawa, Yukari Mimura, Takayoshi Yamauchi and Hirofumi Makino A 49-year-old womanwith Cushing's syndrome due to unilateral adrenal hyperplasia is presented. She had developed obesity and menopausefor 2 years, but no hypertension or hypertrichosis was observed. Althoughplasma adrenocorticotropin and serum cortisol levels were within normal ranges, the circadian rhythm has completely disappeared. Free thyroxine and triiodothyronine levels were decreased. Adrenocorticotropin did not respond to corticotropin- releasing hormone, and urinary excretion of 17-hydroxycorticosteroids was not suppressed by dexamethasone. Abdominal computed tomography and 131I-Adosterol scintigraphy demonstrated a unilateral functioning mass in the left adrenal gland. The resected left adrenal mass was pathologically diagnosed as the rare condition of adrenocortical nodular hyperplasia. (Internal Medicine 37: 385-390, 1998) Key words: glucocorticoid, adrenalectomy, dexamethasone suppression test, thyroid Introduction The examination findings of lung, heart and nervous system revealed nothing in particular. The laboratory examination Cushing's syndromeis caused by adrenocortical hyperse- revealed the following: white blood cell count, 9,300/|il with cretion of cortisol, most of which results from adrenocortical 15%lymphocytes and 1%eosinophils; red blood cell count, adenoma or pituitary adenoma, i.e. Cushing's disease. The 419x104/jli1; hemoglobin, 13.5 g/dl; hematocrit, 40.6%; plate- present case of Cushing's syndrome is attributable to a unilat- let, 3 10x103/|ll1; total protein, 6. 1 1 g/dl; serum albumin, 3.58 g/ eral adrenocortical hyperplasia. This rare pathology has been dl; serum sodium, 144 mmol//; serum potassium, 3.9 mmol//; documented in only 5 cases ofCushing's syndrome (1-5). This serum chloride, 105 mmol//, serum calcium, 8.6 mg/dl; serum case report not only introduces a clinical variety of Cushing's inorganic phosphate, 3. 1 mg/dl; alkaline phosphatase, 107 IU/ syndrome, but also illustrates the clinical influence of adrenal /; creatinine phosphokinase, 73 IU//; total cholesterol, 227 mg/ function on the thyroid. dl; and triglyceride, 108 mg/dl; liver, renal functions and urinalysis were normal. Fasting blood glucose was 86 mg/dl, Case Report and hemoglobin Alc was 6.4% (normal: 4-6). Oral glucose (75 g) tolerance test revealed an impaired glucose tolerance. The A 49-year-old womaninitially presented a complaint of bone density in her lumbar spine (QDR- 1000) was decreased to pretibial edema in 1989. She has been free of both hypertension 0.609 g/cm2 (mean ± SD in a normal 49-year-old female: 0.993 and diabetes, but she has suffered general fatigue and has gained + 0. 139). The endocrinological data on admission are shown in 5 kg over 2 years. Menopause occurred at the age of47 years Table 1. Free triiodothyronine (FT3) and thyroxine (FT4) con- old. She was admitted to our hospital for evaluation of endo- centrations were decreased, while thyrotropin (TSH) level was crine function in 1996. The physical examination on admission normal. Reverse triiodothyronine (rT3) and thyroxine binding revealed the following: height, 147.9 cm; weight, 55.7 kg, globulin (TBG) were normal. The serum cortisol (F) concentra- featuring mild obesity with a round face; blood pressure, 136/ tion in the morningwasnormal, and the plasma adrenocortico- 80 mmHg;pulse, 75 bpm and regular. No goiter or lymphade- tropin (ACTH)obtained at the sametime was at the lower limit nopathy wasobserved. Nostriae cutis wasfound on abdomen of the normal range. Urinary excretion of both 17-hydroxy- or extremities. Pretibial and pedal pitting edema were noted. corticosteroids (17-OHCS) and 17-ketosteroids (17-KS) were From the Department of Medicine III, Okayama University Medical School and *Health and Medical Center, Okayama University, Okayama Received for publication July 25, 1997; Accepted for publication December 24, 1997 Reprint requests should be addressed to Dr. Fumio Otsuka, the Department of Medicine III, OkayamaUniversity Medical School, 2-5- 1 Shikata-cho, Okayama 700-8558 Internal Medicine Vol. 37, No. 4 (April 1998) 385 Otsuka et al also within normal limits. No thyroid autoantibodies including adrenal mass was discovered on abdominal computed tomo- anti-thyroid peroxidase (TPO) antibody, anti-thyroglobulin graphy (CT; Fig. 1A), while no nodular formation was de- (TG) antibody, or thyrotropin binding inhibitory immunoglobu- tected in right adrenal gland (Fig. IB). The 131I-Adosterol lin (TBII) were detected. The responses of ACTHand F to scintigraphy exhibited a fine accumulation in the left adrenal corticotropin-releasing hormone (CRH)were completely sup- mass, in contrast to no accumulation in the right adrenal gland pressed, and the response of TSHto thyrotropin-releasing (Fig. 2). Because the diagnosis of Cushing's syndrome was hormone (TRH) was also markedly suppressed (Table 2a). confirmed, left adrenalectomy was performed on July 23, 1996. Cranial magnetic resonance imaging (MRI) demonstrated a Histological examination of the resected mass was consistent normal pituitary. The circadian rhythm of ACTHand F was with adrenal macronodular hyperplasia, predominantly con- completely eliminated (Table 3a), and the adrenal response to sisting of compact cells (Fig. 3). Following adrenalectomy, ACTHinjection (0.25 mg) was impaired. Administration of 1 intravenous administration of hydrocortisone (100 to 50 mg/ mg dexamethasone did not suppress serum F level, and the day) was initiated for 3 days, and oral administration with 25 suppression test using 2 or 8 mg dexamethasone revealed a mg/day ofhydrocortisone has been maintained. One weekafter paradoxic increase of urinary 17-OHCS (Table 4). A left the surgery, serum F change in a day has taken the form of a Table 1. Preoperative Endocrinological Data Blood sample: ACTH 4.4 -pg/ml (4.4-48) PRL 26.5 ng/ml (<30) F 16.3 (ig/dl (5-21) GH 1.13 ng/ml (0.28-8.7) FT3 2.30 pg/ml (4-5.8) PAC 53.0 pg/ml (57-150) TSH 2.2 |LiU/ml (0.55-4.8) FT4 0.70 ng/dl (1.03-2.21) DHEAS 26 |ig/dl (33-262) LH 26.57 mlU/ml (>15) rT3 141 pg/ml (140-410) HANP 25.7 pg/ml (<43) FSH 80.43 mIU/ml (>15) TBG 15.4 jig/ml (12-30) AVP 4.4 pg/ml (0.8-6.3) Urine sample: U-AD 6 |Lig/day (3-23) U-NA 80 |ig/day (25-131) U-DA 1,000 jig/day (150-1,000) U-17OHCS 6.0 mg/day (2.6-7.8) U-17KS 3.5 mg/day (1-8) U-CPR 65 Jig/day (20-130) ACTH:adrenocorticotropin, GH: growth hormone, TSH: thyroid stimulating hormone, LH: luteinizing hormone, FSH: follicle stimulating hormone, PRL: prolactin, FT3: free triiodothyronine, FT4: free thyroxine, rT3: reverse triiodothyronine, TBG: thyroxine binding globulin, F: cortisol, PAC: plasma aldosterone concentration, DHEAS: dehydroepiandrosterone sulfate, AVP: arginine vasopressin, HANP: human antinatriuretic hormone, U-AD: urinary adrenaline, NA: noradrenaline, DA: dopamine, 17OHCS: 17-hydroxycorticosteroids, 17KS: 17- ketosteroids, CPR: c-peptide immunoreactivity. Parentheses include the normal ranges. Table 2. Provocative Tests by CRH (100 |jg) and TRH (500 jig) Table 3. Daily Profile ofACTH and F a) Preoperative data a) Preoperative data Time after the injection (min) 0 1 5 30 60 90 1 20 Time 8:00 ll:00 14:00 16:00 20:00 23:00 ACTH (pg/ml) 4.0 4.0 4.0 4.3 4.0 5.1 ACTH (pg/ml) 4.0 4.0 4.0 4.1 4.0 4.0 F (jLig/dl) 17.4 17.2 16.1 17.0 16.6 16.9 F (|ig/dl) 19.5 20.8 18.8 19.1 17.1 18.5 TSH ((lU/ml) 0.06 2.39 3.10 2.46 1.66 1.17 PRL (ng/ml) 28.9 277.3 244.8 156.9 110.8 76.2 Abbreviations and normal values are shownin Table 1. Abbreviations and normal values are shownin Table 1. b) Postoperative data (1 week after the surgery) b) Postoperative data (3 months after the surgery) Time 8:00 ll:00 14:00 16:00 20:00 23:00 Time after the injection (min) 0 15 30 60 90 1 20 ACTH (pg/ml) 18.0 33.3 47.5 47.4 31.5 31.1 I hydrocortisone 25 mg ip.o.) F (]Lig/dl) 0.10 0.10 0.20 0.10 0.10 0.20 ACTH (pg/ml) 4.0 4.1 4.0 4.0 4.0 4.0 TSH QxU/ml) 2.29 14.41 18.48 14.81 10.35 8.08 F (Jig/dl) 0.30 15.3 17.8 6.1 2.0 0.50 PRL (ng/ml) 29.4 368.4 405.9 276.6 175.4 158.6 Abbreviations and normal values are shown in Table 1. Abbreviations and normal values are shown in Table 1. 386 Internal Medicine Vol. 37, No. 4 (April '. Cushing' s Syndrome and Hyperplasia Table 4. DexamethasoneSuppression Test Day 0 1 2 3 4 5 6 7 Dexamethasoneip.o.) - - 2mg 2mg 8mg 8mg Urinary17-OHCS (mg/day) 4.1 7.8 10.8 13.3 12.0 12.8 12.7 16.0 Urinary17-KS (mg/day) 2.9 4.0 3.7 3.7 2.7 2.6 3.2 4.7 Abbreviations and normal values are shown in Table 1. Figure 1. Abdominal computed tomography (CT). Plain abdominal CT revealed a left adrenal mass with 19 HUof CT number (arrow, A), while the right adrenal was presented as a normal shape (arrow, B). circadian rhythm under the replacement therapy (Table 3b), and both FT3 and FT4 concentrations were also normalized. Serum TSH level has gradually increased, and reached the peak on day 8 after surgery, and consequently decreased to within the normal limit (Fig.
Load more

Recommended publications
  • Te2, Part Iii
    TERMINOLOGIA EMBRYOLOGICA Second Edition International Embryological Terminology FIPAT The Federative International Programme for Anatomical Terminology A programme of the International Federation of Associations of Anatomists (IFAA) TE2, PART III Contents Caput V: Organogenesis Chapter 5: Organogenesis (continued) Systema respiratorium Respiratory system Systema urinarium Urinary system Systemata genitalia Genital systems Coeloma Coelom Glandulae endocrinae Endocrine glands Systema cardiovasculare Cardiovascular system Systema lymphoideum Lymphoid system Bibliographic Reference Citation: FIPAT. Terminologia Embryologica. 2nd ed. FIPAT.library.dal.ca. Federative International Programme for Anatomical Terminology, February 2017 Published pending approval by the General Assembly at the next Congress of IFAA (2019) Creative Commons License: The publication of Terminologia Embryologica is under a Creative Commons Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0) license The individual terms in this terminology are within the public domain. Statements about terms being part of this international standard terminology should use the above bibliographic reference to cite this terminology. The unaltered PDF files of this terminology may be freely copied and distributed by users. IFAA member societies are authorized to publish translations of this terminology. Authors of other works that might be considered derivative should write to the Chair of FIPAT for permission to publish a derivative work. Caput V: ORGANOGENESIS Chapter 5: ORGANOGENESIS
    [Show full text]
  • Quantitation of Corticotrophs in the Pars Distalis of Stress-Prone Swine Beverly Ann Bedford Iowa State University
    Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1-1-1976 Quantitation of corticotrophs in the pars distalis of stress-prone swine Beverly Ann Bedford Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Veterinary Anatomy Commons Recommended Citation Bedford, Beverly Ann, "Quantitation of corticotrophs in the pars distalis of stress-prone swine" (1976). Retrospective Theses and Dissertations. 17953. https://lib.dr.iastate.edu/rtd/17953 This Thesis is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Quantitation of corticotrophs in the pars distalis of stress-prone swine by Beverly Ann Bedford A Thesis Submitted to the Graduate Faculty in Partial Fulfillment of The Requirements for the Degr~e of MASTER OF SCIENCE Department: Veterinary Anatomy, Pharmacology and Physiology Major: Veterinary Anatomy ., Signatures have been redacted for privacy ' I Iowa State University Ames, Iowa 1976 ii :E5 ll I q7(p ,g3r TABLE OF CONTENTS c,J. Page INTRODUCTION 1 LITERATURE REVIEW 4 Pituitary Gland 4 General morphology 4 Development 5 Blood supply 7 Staining techniques 7 Pars distalis 13 . Pars tuberalis 25 ·pars intermedia 28 Process of secretion 36 Neurohypophysis 41 Porcine Stress Syndrome 45 MATERIALS AND MET!iODS' 52 RESULTS 56 DISCUSSION 64 SUMMARY AND CONCLUSIONS 72 BIBLIOGRAPHY 73 ACKNOWLEDGMENTS 85 APPENDIX 86 1111408 1 INTRODUCTION As early as 1953, there came reports (Ludvigsen, 1953; Briskey et al., 1959) of pale soft exudative (PSE) post-mortem porcine muscu- lature which later stimulated research into the mechanisms responsible for this condition.
    [Show full text]
  • Nomina Histologica Veterinaria, First Edition
    NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria.
    [Show full text]
  • BGD B Lecture Notes Docx
    BGD B Lecture notes Lecture 1: GIT Development Mark Hill Trilaminar contributions • Overview: o A simple tube is converted into a complex muscular, glandular and duct network that is associated with many organs • Contributions: o Endoderm – epithelium of the tract, glands, organs such as the liver/pancreas/lungs o Mesoderm (splanchnic) – muscular wall, connective tissue o Ectoderm (neural crest – muscular wall neural plexus Gastrulation • Process of cell migration from the epiblast through the primitive streak o Primitive streak forms on the bilaminar disk o Primitive streak contains the primitive groove, the primitive pit and the primitive node o Primitive streak defines the body axis, the rostral caudal ends, and left and right sides Thus forms the trilaminar embryo – ectoderm, mesoderm, endoderm • Germ cell layers: o ectoderm – forms the nervous system and the epidermis epithelia 2 main parts • midline neural plate – columnar epithelium • lateral surface ectoderm – cuboidal, containing sensory placodes and skin/hair/glands/enamel/anterior pituitary epidermis o mesoderm – forms the muscle, skeleton, and connective tissue cells migrate second migrate laterally, caudally, rostrally until week 4 o endoderm – forms the gastrointestinal tract epithelia, the respiratory tract and the endocrine system cells migrate first and overtake the hypoblast layer line the primary yolk sac to form the secondary yolk sac • Membranes: o Rostrocaudal axis Ectoderm and endoderm form ends of the gut tube, no mesoderm At each end, form the buccopharyngeal
    [Show full text]
  • The Physiology of Corticotropin-Releasing Factor (CRF)
    The physiology of corticotropin-releasing factor (CRF) Marie-Charles RAUX-DEMAY F. GIRARD Hôpital Trousseau, 26, avenue du Dr A. Netter, 75012 Paris, France. Summary. Corticotropin-releasing factor (CRF) was characterized, purified and synthesized in 1981 by Vale. The composition of this 41 amino-acid peptide varies slightly from one species to another. Its principal origin is the paraventricular nucleus of the hypothalamus and, by the portal vessels, it reaches the adenohypophysis where it stimulates the corticotrophs. The effects of CRF have been analysed by in vitro and in vivo experiments. Some actions on the autonomic nervous system have been described. The action of CRF on adrenocorticotrophic hormone (ACTH) secretion is predominant, but it acts in relation with arginine-vasopressin and accessorily with angiotensin and catecholamines. Adrenal steroids act on feedback control of CRF secretion in the hypothalamus and also on pituitary corticotrophs. The CRF function starts between the 16th and 19th day in the fetal rat. The placenta is ’ able to produce CRF. Hypothalamic regulation of adrenocorticotrophic hormone (ACTH) secretion in the anterior pituitary has been recognized since 1948 (Harris, 1948). Thereafter, hypothalamic extracts were seen to have CRF activity (Guillemin and Rosemberg, 1955) which since then has been shown to be polymorphic, i.e. shared by arginine vasopressin (AVP1, angiotensin II (A II) and adrenaline. The purification of a molecule comprising 41 amino acids from half a million ovine hypothamami (oCRF) has opened up a vast potential field of research (Vale et al., 19811.). Characterization of 1-41 CRF The purification of ovine CRF (OCRF) was rapidly followed by the determination of its primary structure and the synthesis of the molecule (Vale et a/., 19811.).
    [Show full text]
  • |||GET||| Pancreatic Islet Biology 1St Edition
    PANCREATIC ISLET BIOLOGY 1ST EDITION DOWNLOAD FREE Anandwardhan A Hardikar | 9783319453057 | | | | | The Evolution of Pancreatic Islets Advanced search. The field of regenerative medicine is rapidly evolving and offers great hope for the nearest future. Easily read eBooks on Pancreatic Islet Biology 1st edition phones, computers, or any eBook readers, including Kindle. Help Learn to edit Community portal Recent changes Upload file. Pancreatic Islet Biologypart of the Stem Cell Biology and Regenerative Medicine series, is essential reading for researchers and clinicians in stem cells or endocrinology, especially those focusing on diabetes. Because the beta cells in the pancreatic islets Pancreatic Islet Biology 1st edition selectively destroyed by an autoimmune process in type 1 diabetesclinicians and researchers are actively pursuing islet transplantation as a means of restoring physiological beta cell function, which would offer an alternative to a complete pancreas transplant or artificial pancreas. Strategies to improve islet yield from chronic pancreatitis pancreases intended for islet auto-transplantation 6. About this book This comprehensive volume discusses in vitro laboratory development of insulin-producing cells. Junghyo Jo, Deborah A. Show all. Comparative Analysis of Islet Development. Leibson A. However, type 1 diabetes is the result of the autoimmune destruction of beta cells in the pancreas. Islets can influence each other through paracrine and autocrine communication, and beta cells are coupled electrically to six to seven other beta cells but not to other cell types. Pancreatic Islet Biologypart of the Stem Cell Biology and Regenerative Medicine Pancreatic Islet Biology 1st edition, is essential reading for researchers and clinicians in stem cells or endocrinology, especially those focusing on diabetes.
    [Show full text]
  • Neonatal Thymulin Gene Therapy in Nude Mice: Effects on the Morphology of the Pituitary Corticotrope Population
    Histol Histopathol (2011) 26: 471-479 Histology and http://www.hh.um.es Histopathology Cellular and Molecular Biology Neonatal thymulin gene therapy in nude mice: Effects on the morphology of the pituitary corticotrope population Eliana Martines1,2*, Paula C. Reggiani1,3*, José I. Schwerdt1,3, Rodolfo G. Goya1,3 and Gloria Cónsole1,4 1Department of Cytology, Histology and Embryology, Faculty of Medicine, National University of La Plata, 2Adventist University of La Plata (UAP), Entre Ríos, 3INIBIOLP-UNLP and 4CICPBA, Argentina *These two authors contributed equally to this study Summary. The integrity of the thymus during early life and athymic mice. Athymic mice showed only a is necessary for a proper maturation of the marginal reduction in corticotrope CD, VD and CS. In neuroendocrine system, including the adrenal axis. The these mutants hypothalamic CRH content was slightly thymic metallopeptide thymulin seems to be a increased, whereas adrenal corticosterone tended to be central physiologic mediator of thymus-pituitary lower. Thymulin administration to adult mice tended to communication. Furthermore, neonatal thymulin gene reverse these changes. Our results suggest a possible therapy has been shown to prevent the typical alterations modulating effect of thymulin on the corticotrope of gonadotrophic cell number and morphology and population and the adrenal gland, confirming the serum gonadotropin levels in nude female mice. In the existence of a bidirectional thymus-pituitary-adrenal present study we assessed the impact of athymia and the axis. effect of neonatal thymulin gene therapy on the corticotropic cell population in nude mice. The effect of Key words: Thymus-pituitary axis, Thymulin gene thymulin administration to adult nudes on their therapy, Nude mice, Hypophysiotropic activity, RAd- hypothalamic content of corticotropin-releasing hormone FTS (CRH) and the adrenal content of corticosterone was also determined.
    [Show full text]
  • The Physiology of Corticotropin-Releasing Factor (CRF) Marie-Charles Raux-Demay, F
    The physiology of corticotropin-releasing factor (CRF) Marie-Charles Raux-Demay, F. Girard To cite this version: Marie-Charles Raux-Demay, F. Girard. The physiology of corticotropin-releasing factor (CRF). Re- production Nutrition Développement, 1985, 25 (5), pp.931-943. hal-00898355 HAL Id: hal-00898355 https://hal.archives-ouvertes.fr/hal-00898355 Submitted on 1 Jan 1985 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. The physiology of corticotropin-releasing factor (CRF) Marie-Charles RAUX-DEMAY F. GIRARD Hôpital Trousseau, 26, avenue du Dr A. Netter, 75012 Paris, France. Summary. Corticotropin-releasing factor (CRF) was characterized, purified and synthesized in 1981 by Vale. The composition of this 41 amino-acid peptide varies slightly from one species to another. Its principal origin is the paraventricular nucleus of the hypothalamus and, by the portal vessels, it reaches the adenohypophysis where it stimulates the corticotrophs. The effects of CRF have been analysed by in vitro and in vivo experiments. Some actions on the autonomic nervous system have been described. The action of CRF on adrenocorticotrophic hormone (ACTH) secretion is predominant, but it acts in relation with arginine-vasopressin and accessorily with angiotensin and catecholamines.
    [Show full text]
  • 26 April 2010 TE Prepublication Page 1 Nomina Generalia General Terms
    26 April 2010 TE PrePublication Page 1 Nomina generalia General terms E1.0.0.0.0.0.1 Modus reproductionis Reproductive mode E1.0.0.0.0.0.2 Reproductio sexualis Sexual reproduction E1.0.0.0.0.0.3 Viviparitas Viviparity E1.0.0.0.0.0.4 Heterogamia Heterogamy E1.0.0.0.0.0.5 Endogamia Endogamy E1.0.0.0.0.0.6 Sequentia reproductionis Reproductive sequence E1.0.0.0.0.0.7 Ovulatio Ovulation E1.0.0.0.0.0.8 Erectio Erection E1.0.0.0.0.0.9 Coitus Coitus; Sexual intercourse E1.0.0.0.0.0.10 Ejaculatio1 Ejaculation E1.0.0.0.0.0.11 Emissio Emission E1.0.0.0.0.0.12 Ejaculatio vera Ejaculation proper E1.0.0.0.0.0.13 Semen Semen; Ejaculate E1.0.0.0.0.0.14 Inseminatio Insemination E1.0.0.0.0.0.15 Fertilisatio Fertilization E1.0.0.0.0.0.16 Fecundatio Fecundation; Impregnation E1.0.0.0.0.0.17 Superfecundatio Superfecundation E1.0.0.0.0.0.18 Superimpregnatio Superimpregnation E1.0.0.0.0.0.19 Superfetatio Superfetation E1.0.0.0.0.0.20 Ontogenesis Ontogeny E1.0.0.0.0.0.21 Ontogenesis praenatalis Prenatal ontogeny E1.0.0.0.0.0.22 Tempus praenatale; Tempus gestationis Prenatal period; Gestation period E1.0.0.0.0.0.23 Vita praenatalis Prenatal life E1.0.0.0.0.0.24 Vita intrauterina Intra-uterine life E1.0.0.0.0.0.25 Embryogenesis2 Embryogenesis; Embryogeny E1.0.0.0.0.0.26 Fetogenesis3 Fetogenesis E1.0.0.0.0.0.27 Tempus natale Birth period E1.0.0.0.0.0.28 Ontogenesis postnatalis Postnatal ontogeny E1.0.0.0.0.0.29 Vita postnatalis Postnatal life E1.0.1.0.0.0.1 Mensurae embryonicae et fetales4 Embryonic and fetal measurements E1.0.1.0.0.0.2 Aetas a fecundatione5 Fertilization
    [Show full text]
  • Quantitative and Histomorphological Studies on Age-Correlated Changes in Canine and Porcine Hypophysis Lakshminarayana Das Iowa State University
    Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1971 Quantitative and histomorphological studies on age-correlated changes in canine and porcine hypophysis Lakshminarayana Das Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Structures Commons, and the Veterinary Anatomy Commons Recommended Citation Das, Lakshminarayana, "Quantitative and histomorphological studies on age-correlated changes in canine and porcine hypophysis" (1971). Retrospective Theses and Dissertations. 4873. https://lib.dr.iastate.edu/rtd/4873 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. 71-26,847 DAS, Lakshminarayana, 1936- QUANTITATIVE AND HISTOMORPHOLOGICAL STUDIES ON AGE-CORRELATED CHANGES IN CANINE AND PORCINE HYPOPHYSIS (VOLUMES I AND II). Iowa State University, Ph.D., 1971 Anatomy• University Microfilms, A XEROX Company, Ann Arbor. Michigan Quantitative and histomorphological studies on age-correlated changes in canine and porcine hypophysis py Lakshminarayana Das Volume 1 of 2 A Dissertation Submitted to the Graduate Faculty in Partial Fulfillment of The Requirements for the Degree of DOCTOR OP PHILOSOPHY Major Subject:
    [Show full text]
  • Expression Cloning of a Human Corticotropin-Releasing
    Proc. Natl. Acad. Sci. USA Vol. 90, pp. 8967-8971, October 1993 Biochemistry Expression cloning of a human corticotropin-releasing- factor receptor (G protein-coupled receptor/yDthalamic-oitulitarv-aldrenocortlcal Iax/cyclic AMP/peptide hormone receptor) RUOPING CHEN, KATHY A. LEWIS, MARILYN H. PERRIN*, AND WYLIE W. VALE The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, La Jolla, CA 92037 Contributed by Wylie W. Vale, July 19, 1993 ABSTRACT Corticotropin-releasing factor (CRF) is the Here we present the expression cloning and functional principal neuroregulator of the hypothalamic-pituitary- expression of a cDNA encoding a CRF receptor from a adrenocortical axis and plays an important role In coordinating human Cushing corticotropic cell tumor. We also report a the endocrine, autonomic, and behavioral responses to stress variant of the receptor produced by alternative splicing.t and immune chaLenge. We report here the cloning of a cDNA coding for a CRF receptor from a human corticotropic tumor MATERIALS AND library. The cloned cDNA encodes a 415-amino acid protein METHODS comprisng seven putative membrane-saning domains and Is Library Construction. A human corticotropic adenoma structurally related to the calcitonin/vasoactive intestnal pep- removed from a patient with Cushing disease was generously tide/growth hormone-releasing hormone subfamlly of G pro- provided by Mary Lee Vance and the neurosurgery unit tein-coupled receptors. The receptor expressed in COS cells headed by Edward Laws (University of Virginia School of binds rat/human CRF with high affnity (Kd = 3.3 t 0.45 nM) Medicine). Total RNA was prepared by guanidine extraction and specficity and is functionally coupled to adenylate cyclase.
    [Show full text]
  • The Cellular Origins of Corticotropin and Melanotropin As Revealed by Immunochemical Staining ’
    The Cellular Origins of Corticotropin and Melanotropin as Revealed by Immunochemical Staining ’ BURTON L. BAKER AND SISTER THaRBSE DRUMMOND2 Department of Anatomy, The University of Michigan Medical School, Ann Arbor, Michigan 481 04 ABSTRACT The cellular origins of corticotropin and melanotropin were studied by observing the response of the rat hypophysis to adrenalectomy and cortisol administration when stained immunochemically with peroxidase-labeled antibody following application of antiserums to P1-24-corticotropin,pp17-39-cortico- tropin, human p-melanotropin, and a-melanotropin. The presence of corticotropin in the pars intermedia is indicated since this lobe, in addition to corticotropic cells of the pars distalis, stained with antiserum to pp17-39-~orti~otropin.However, the concentration of corticotropin is less in the pars intermedia than in cortico- tropic cells since at higher dilutions of antiserum the latter cells stained intensely while the pars intermedia was unstained. Also, corticotropic cells exhibited strik- ing hypertrophy after adrenalectomy and regression after cortisol administration, while morphological and tinctorial properties of the pars intermedia were min- imally altered. These observations suggest that the pars distalis is primarily responsible for supplying the corticotropin required to meet the changing re- quirements of the body. With antiserum to human P-melanotropin, the pars intermedia stained in- tensely. Since the antiserum was ineffective after absorption the staining re- action appears to be specific for p-melanotropin. Except for a rare cell, the pars distalis did not stain. Thus p-melanotropin is restricted primarily to the pars intermedia. Sever a1 observations implicate the pars tropin content. Also in microscopic sections intermedia of the rat hypophysis in the prepared with histological staining pro- secretion of corticotropin.
    [Show full text]