DDAVP Nasal Spray Is Provided As an Aqueous Solution for Intranasal Use
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Spray Desmopressin Acetate Nasal Spray 10 Μg/Spray
PRODUCT MONOGRAPH Pr DDAVP® Spray Desmopressin Acetate Nasal Spray 10 µg/spray Pr DDAVP® Rhinyle Desmopressin Acetate Nasal Solution 0.1 mg/mL Antidiuretic Ferring Inc. Date of Revision: 200 Yorkland Blvd, Suite 800 June 19, 2008 North York, Ontario M2J 5C1 Submission Control No: 119073 DDAVP® Spray and Rhinyle Page 1 of 23 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION.........................................................3 SUMMARY PRODUCT INFORMATION ........................................................................3 INDICATIONS AND CLINICAL USE..............................................................................3 WARNINGS AND PRECAUTIONS..................................................................................4 ADVERSE REACTIONS....................................................................................................6 DRUG INTERACTIONS ....................................................................................................7 DOSAGE AND ADMINISTRATION................................................................................7 OVERDOSAGE ..................................................................................................................9 ACTION AND CLINICAL PHARMACOLOGY ..............................................................9 STORAGE AND STABILITY..........................................................................................11 DOSAGE FORMS, COMPOSITION AND PACKAGING .............................................11 PART II: SCIENTIFIC INFORMATION -
Oxytocin Regulates the Expression of Aquaporin 5 in the Latepregnant Rat
RESEARCH ARTICLE Molecular Reproduction & Development 81:524–530 (2014) Oxytocin Regulates the Expression of Aquaporin 5 in the Late-Pregnant Rat Uterus ESZTER DUCZA,* ADRIENN B. SERES, JUDIT HAJAGOS-TOTH, GEORGE FALKAY, AND ROBERT GASPAR Department of Pharmacodynamics and Biopharmacy, Faculty of Pharmacy, University of Szeged, Szeged, Hungary SUMMARY Aquaporins (AQPs) are integral membrane channels responsible for the transport of water across a cell membrane. Based on reports that AQPs are present and accumulate in the female reproductive tract late in pregnancy, our aim was to study the expression of AQP isoforms (AQP1, 2, 3, 5, 8, and 9) at the end of pregnancy in rat in order to determine if they play a role in parturition. Reverse-transcriptase PCR revealed that specific Aqp mRNAs were detectable in the myometrium of non- pregnant and late-pregnancy (Days 18, 20, 21, and 22 of pregnancy) rat uteri. The expression of Aqp5 mRNA and protein were most pronounced on Days 18À21, and were dramatically decreased on Day 22 of pregnancy. In contrast, a significant increase was found in the level of Aqp5 transcript in whole-blood samples ÃCorresponding author: on the last day of pregnancy.The effect of oxytocin on myometrial Aqp5 expression in Department of Pharmacodynamics an organ bath was also investigated. The level of Aqp5 mRNA significantly decreased and Biopharmacy À8 University of Szeged, H-6720 5 min after oxytocin (10 M) administration, similarly to its profile on the day of Eotv€ os€ u. 6, Szeged 6270 delivery; this effect was sensitive to the oxytocin antagonist atosiban. The vasopres- Hungary. -
Corticotropin-Releasing Activity of Lysine Vasopressin Evelyn Joyce Weber Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1961 Corticotropin-releasing activity of lysine vasopressin Evelyn Joyce Weber Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Biochemistry Commons Recommended Citation Weber, Evelyn Joyce, "Corticotropin-releasing activity of lysine vasopressin " (1961). Retrospective Theses and Dissertations. 1990. https://lib.dr.iastate.edu/rtd/1990 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]. This dissertation has been 62-1374 microfilmed exactly as received WEBER, Evelyn Joyce, 1928- CORTICOTRO PIN-RE LEASING ACTIVITY OF LYSINE VASOPRESSIN. Iowa State University of Science and Technology Ph.D., 1961 Chemistry, biological University Microfilms, Inc., Ann Arbor, Michigan CORTICO TROPIN-RELEASING ACTIVITY OF LYSINE 7AS0PRESSII Evelyn Joyce Weber A Dissertation Submitted, to the Graduate Faculty in Partial Fulfillment of The Requirements for the Degree of DOCTOR OF PHILOSOPHY . kajor Subject: Biochemistry Approved: Signature was redacted for privacy. In Charge of l-.ejor V,rork Signature was redacted for privacy. Head, of kajor Department Signature was redacted for privacy. Deacf of Gradu/ue College Iowa State University Of Science and Technology Ames, loua 1961 il TABLE OF CONTENTS Page HISTORICAL . ; 1 Biological Activities of Vasopressin. ...... -3 Pressor activity 3 Antidiuretic activity 5 Oxytocic activity. £ Corticotropin releasing activity 10 Other activities of vasopressin. -
Management and Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus
REVIEW Management and treatment of lithium- induced nephrogenic diabetes insipidus Christopher K Finch†, Lithium carbonate is a well documented cause of nephrogenic diabetes insipidus, with as Tyson WA Brooks, many as 10 to 15% of patients taking lithium developing this condition. Clinicians have Peggy Yam & Kristi W Kelley been well aware of lithium toxicity for many years; however, the treatment of this drug- induced condition has generally been remedied by discontinuation of the medication or a †Author for correspondence Methodist University reduction in dose. For those patients unresponsive to traditional treatment measures, Hospital, Department several pharmacotherapeutic regimens have been documented as being effective for the of Pharmacy, University of management of lithium-induced diabetes insipidus including hydrochlorothiazide, Tennessee, College of Pharmacy, 1265 Union Ave., amiloride, indomethacin, desmopressin and correction of serum lithium levels. Memphis, TN 38104, USA Tel.: +1 901 516 2954 Fax: +1 901 516 8178 [email protected] Lithium carbonate is well known for its wide use associated with a mutation(s) of vasopressin in bipolar disorders due to its mood stabilizing receptors. Acquired causes are tubulointerstitial properties. It is also employed in aggression dis- disease (e.g., sickle cell disease, amyloidosis, orders, post-traumatic stress disorders, conduct obstructive uropathy), electrolyte disorders (e.g., disorders and even as adjunctive therapy in hypokalemia and hypercalcemia), pregnancy, or depression. Lithium has many well documented conditions induced by a drug (e.g., lithium, adverse effects as well as a relatively narrow ther- demeclocycline, amphotericin B and apeutic range of 0.4 to 0.8 mmol/l. Clinically vincristine) [3,4]. Lithium is the most common significant adverse effects include polyuria, mus- cause of drug-induced nephrogenic DI [5]. -
Vasopressin V2 Is a Promiscuous G Protein-Coupled Receptor That Is Biased by Its Peptide Ligands
bioRxiv preprint doi: https://doi.org/10.1101/2021.01.28.427950; this version posted January 28, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Vasopressin V2 is a promiscuous G protein-coupled receptor that is biased by its peptide ligands. Franziska M. Heydenreich1,2,3*, Bianca Plouffe2,4, Aurélien Rizk1, Dalibor Milić1,5, Joris Zhou2, Billy Breton2, Christian Le Gouill2, Asuka Inoue6, Michel Bouvier2,* and Dmitry B. Veprintsev1,7,8,* 1Laboratory of Biomolecular Research, Paul Scherrer Institute, 5232 Villigen PSI, Switzerland and Department of Biology, ETH Zürich, 8093 Zürich, Switzerland 2Department of Biochemistry and Molecular medicine, Institute for Research in Immunology and Cancer, Université de Montréal, Montréal, Québec, Canada 3Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA 4The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7BL, United Kingdom 5Department of Structural and Computational Biology, Max Perutz Labs, University of Vienna, Campus-Vienna-Biocenter 5, 1030 Vienna, Austria 6Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi 980-8578, Japan. 7Centre of Membrane Proteins and Receptors (COMPARE), University of Birmingham and University of Nottingham, Midlands, UK. 8Division of Physiology, Pharmacology & Neuroscience, School of Life Sciences, University of Nottingham, Nottingham, NG7 2UH, UK. *Correspondence should be addressed to: [email protected], [email protected], [email protected]. -
VASOPRESSIN and OXYTOCIN Molecular, Cellular, and Clinical Advances ADVANCES in EXPERIMENTAL MEDICINE and BIOLOGY
VASOPRESSIN AND OXYTOCIN Molecular, Cellular, and Clinical Advances ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo IRUN R. COHEN, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, N. S. Kline Institutefor Psychiatric Research RODOLFO PAOLETTI, University of Milan Recent Volumes in this Series Volume 443 ADV ANCES IN LACTOFERRIN RESEARCH Edited by Genevieve Spik, Dominique Legrand, Joel Mazurier, Annick Pierce, and Jean-Paul Perraudin Volume 444 REPRODUCTIVE TOXICOLOGY: In Vitro Germ Cell Developmental Toxicology, from Science to Social and Industrial Demand Edited by Jesus del Mazo Volume 445 MA THEMA TICAL MODELING IN EXPERIMENTAL NUTRITION Edited by Andrew J. Clifford and Hans-Georg MUlier Volume 446 MOLECULAR AND CELLULAR MECHANISMS OF NEURONAL PLASTICITY: Basic and Clinical Implications Edited by Yigal H. Ehrlich Volume 447 LIPOXYGENASES AND THEIR METABOLITES: Biological Functions Edited by Santosh Nigam and Cecil R. Pace-Asciak Volume 448 COPPER TRANSPORT AND ITS DISORDERS: Molecular aIfd Cellular Aspects Edited by Arturo Leone and Julian F. B. Mercer Volume 449 VASOPRESSIN AND OXYTOCIN: Molecular, Cellular, and Clinical Advances Edited by Harts H.Zingg, Charles W. Bourque, and Daniel G. Bichet Volume 450 ADV ANCES IN MODELING AND CONTROL OF VENTILATION Edited by Richard L. Hughson, David A. Cunningham, and James Duffin Volume 451 GENE THERAPY OF CANCER Edited by Peter Walden, Uwe Trefzer, Wolfram Sterry, and Farzin Farzaneh Volume 452 MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION VII: Molecular Determinants of Microbial Immunity Edited by Sudhir Gupta, Alan Sher, and Rafi Ahmed A Continuation Order Plan is available for this series. -
Oral Desmopressin in Central Diabetes Insipidus
Arch Dis Child: first published as 10.1136/adc.61.3.247 on 1 March 1986. Downloaded from Archives of Disease in Childhood, 1986, 61, 247-250 Oral desmopressin in central diabetes insipidus U WESTGREN, C WITTSTROM, AND A S HARRIS Department of Pediatrics, University Hospital, Lund, and Faculty of Pharmacy, Biomedicum, Uppsala, Sweden SUMMARY Seven paediatric patients with central diabetes insipidus were studied in an open dose ranging study in hospital followed by a six month study on an outpatient basis to assess the efficacy and safety of peroral administration of DDAVP (desmopressin) tablets. In the dose ranging study a dose dependent antidiuretic response was observed. The response to 12-5-50 mcg was, however, less effective in correcting baseline polyuria than were doses of 100 mcg and above. Patients were discharged from hospital on a preliminary dosage regimen ranging from 100 to 400 mcg three times daily. After an initial adjustment in dosage in three patients at one week follow up, all patients were stabilised on treatment with tablets and reported an adequate water turnover at six months. As with the intranasal route of administration dosage requirements varied from patient to patient, and a dose range rather than standard doses were required. A significant correlation, however, was found for the relation between previous intranasal and present oral daily dosage. No adver-se reactions were reported. No clinically significant changes were noted in blood chemistry and urinalysis. All patients expressed a preference for the oral over existing intranasal copyright. treatment. Treatment with tablets offers a beneficial alternative to the intranasal route, particularly in patients with chronic rhinitis or impaired vision. -
Demeclocycline in the Treatment of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone
Thorax: first published as 10.1136/thx.34.3.324 on 1 June 1979. Downloaded from Thorax, 1979, 34, 324-327 Demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone W H PERKS, E H WALTERS,' I P TAMS, AND K PROWSE From the Department of Respiratory Physiology, City General Hospital, Stoke-on-Trent, Staffordshire, UK ABSTRACT Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (> 135 mmol/l) in all patients after a mean of 8-6 days (SD+5-3 days). Blood urea rose significantly from the pretreatment level of 4-2±2-3 mmol/l to 10-1±5-1 mmol/l at ten days (p<0 001). The average maximum blood urea was 13-4-6-8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of this rise. The azotaemia could be attributed to a combination of increased urea production and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent. The syndrome of inappropriate secretion of anti- Methods http://thorax.bmj.com/ diuretic hormone (SIADH) has become increas- ingly recognised as a treatable cause of stupor and Fourteen patients with a diagnosis of SIADH confusion in patients with a wide variety of based on the criteria of De Troyer and Demanet diseases (De Troyer and Demanet, 1976). -
Hypernatremia: 2 Months Back When He Had Progressive Decrease in Vision (Right > Left)
Correspondence to increased intrathoracic pressure and central radiologist regarding vascular injury when there is venous pressure, decreased venous return from the refractory hypotension so that necessary steps can be brain and increased ICP[4] taken to identify and treat iatrogenic complications that • Patients with aneurysmal SAH have disturbed might compound the pre‑existing morbidity. autoregulation of cerebral blood flow. Hence, intraoperative hypotension of any cause has an REFERENCES adverse effect on the outcome of SAH[5,6] • Patients with poor grade SAH (Fischer III/IV) and 1. Young WL, Pile-Spellman J. Anesthetic considerations for interventional Neuroradiolgy (Review). Anesthesiology angiographic evidence of vasospasm which our 1994;80:427-56. patient had, are at risk for cerebral hypoperfusion 2. Varma MK, Price K, Jayakrishnan V, Manickam B, Kessell G. because of impaired cerebral autoregulation and Anaesthetic considerations for interventional neuroradiology. thus intraoperative hypotension and cerebral Br J Anaesth 2007;99:75-85. [6,7] 3. Kent KC, Moscucci M, Mansour KA, Dimattia S, Gallagher S, hypoperfusion compounds the poor outcome Kuntz R, et al. Retroperitoneal hematoma after cardiac • Blood loss leading to severe anaemia (Hb 3.8 g%) catheterization: Prevalence, risk factors, and optimal during the procedure might have lead to decreased management. J Vasc Surg 1994;20:905-10. oxygen‑carrying capacity of blood and further 4. De Laet I, Citerio G, Malbrain ML. The influence of exacerbate the hypoxic injury to brain. intraabdominal hypertension on the central nervous system: Current insights and clinical recommendations, is it all in the Thus a combination of age, poor grade SAH, diffuse head? Acta Clin Belg Suppl 2007;1:89-97. -
Structural and Functional Evolution of the Vasopressin/Oxytocin Superfamily
The Journal of Neuroscience, September 1995, 15(g): 5989-5998 Structural and Functional Evolution of the Vasopressin/Oxytocin Superfamily: Vasopressin-Related Conopressin Is the Only Member Present in Lymnaea, and Is Involved in the Control of Sexual Behavior R. E. Van Kesteren,’ A. B. Smit,’ R. P. J. De Lange,’ K. S. Kits,’ F. A. Van Golen,’ R. C. Van Der Schors,’ N. D. De With,’ J. F. Burke,* and W. P. M. Geraertsl ‘Graduate School Neurosciences Amsterdam, Institute of Neurosciences, Faculty of Biology, Department of Experimental Zoology, Vrije Universiteit, Amsterdam, The Netherlands and *Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Brighton, United Kingdom It has been suggested that the gene duplication that led to Vasopressin and oxytocin are nonapeptides that are present in the formation of the vasopressin/oxytocin two-gene family all placental mammals. Although similar in structure, they serve occurred early during vertebrate evolution. However, the different functions (Ramsay, 1983). Vasopressin has anti-diuretic existence of both vasopressin- and oxytocin-related pep- activities and is involved in hydromineral regulation, whereas tides in invertebrates suggests that this duplication may oxytocin has uterotonic and milk-ejection activities and regulates have occurred much earlier, although there is no evidence aspects of reproductive behavior. Peptides related to both vaso- for the co-occurrence of vasopressin- and oxytocin-related pressin and oxytocin are present in all vertebrate classes, except peptides in the same invertebrate species. We report here the cyclostomes, which have only the vasopressin-related pep- that in Lymnaea only the vasopressin-related peptide Lys- tide vasotocin (reviewed by Acher, 1993). -
Estonian Statistics on Medicines 2013 1/44
Estonian Statistics on Medicines 2013 DDD/1000/ ATC code ATC group / INN (rout of admin.) Quantity sold Unit DDD Unit day A ALIMENTARY TRACT AND METABOLISM 146,8152 A01 STOMATOLOGICAL PREPARATIONS 0,0760 A01A STOMATOLOGICAL PREPARATIONS 0,0760 A01AB Antiinfectives and antiseptics for local oral treatment 0,0760 A01AB09 Miconazole(O) 7139,2 g 0,2 g 0,0760 A01AB12 Hexetidine(O) 1541120 ml A01AB81 Neomycin+Benzocaine(C) 23900 pieces A01AC Corticosteroids for local oral treatment A01AC81 Dexamethasone+Thymol(dental) 2639 ml A01AD Other agents for local oral treatment A01AD80 Lidocaine+Cetylpyridinium chloride(gingival) 179340 g A01AD81 Lidocaine+Cetrimide(O) 23565 g A01AD82 Choline salicylate(O) 824240 pieces A01AD83 Lidocaine+Chamomille extract(O) 317140 g A01AD86 Lidocaine+Eugenol(gingival) 1128 g A02 DRUGS FOR ACID RELATED DISORDERS 35,6598 A02A ANTACIDS 0,9596 Combinations and complexes of aluminium, calcium and A02AD 0,9596 magnesium compounds A02AD81 Aluminium hydroxide+Magnesium hydroxide(O) 591680 pieces 10 pieces 0,1261 A02AD81 Aluminium hydroxide+Magnesium hydroxide(O) 1998558 ml 50 ml 0,0852 A02AD82 Aluminium aminoacetate+Magnesium oxide(O) 463540 pieces 10 pieces 0,0988 A02AD83 Calcium carbonate+Magnesium carbonate(O) 3049560 pieces 10 pieces 0,6497 A02AF Antacids with antiflatulents Aluminium hydroxide+Magnesium A02AF80 1000790 ml hydroxide+Simeticone(O) DRUGS FOR PEPTIC ULCER AND GASTRO- A02B 34,7001 OESOPHAGEAL REFLUX DISEASE (GORD) A02BA H2-receptor antagonists 3,5364 A02BA02 Ranitidine(O) 494352,3 g 0,3 g 3,5106 A02BA02 Ranitidine(P) -
Diabetes Insipidus: Diagnosis and Treatment of a Complex Disease
REVIEW AMGAD N. MAKARYUS, MD SAMY I. McFARLANE, MD, MPH CME North Shore University Hospital, New York University State University of New York-Downstate and Kings CREDIT School of Medicine, Manhasset, NY County Hospital Center, Brooklyn, NY Diabetes insipidus: Diagnosis and treatment of a complex disease ■ ABSTRACT ATIENTS WHO PRESENT with diabetes P insipidus need immediate care because Diabetes insipidus, characterized by excretion of copious the body’s delicate water and electrolyte bal- volumes of dilute urine, can be life-threatening if not ance is threatened. It is essential to perform a properly diagnosed and managed. It can be caused by knowledgeable assessment based on character- two fundamentally different defects: inadequate or izing features, intervene rapidly with the prop- impaired secretion of antidiuretic hormone (ADH) from er treatment, and continue to reevaluate the the posterior pituitary gland (neurogenic or central patient’s condition. diabetes insipidus) or impaired or insufficient renal Complicating matters, the proper treat- response to ADH (nephrogenic diabetes insipidus). The ment depends on the cause in the individual distinction is essential for effective treatment. patient. Therefore, the physician must deter- mine whether the defect is in the brain or in ■ KEY POINTS the kidney. ■ Urine osmolality is easy to measure and helps in INABILITY TO CONSERVE WATER determining whether polyuria is due to diabetes insipidus or another condition. Diabetes insipidus is caused by the inability to conserve water and maintain an optimum free water level. The kidneys pass large The water deprivation test can help in distinguishing amounts of dilute urine regardless of the central diabetes insipidus from nephrogenic diabetes body’s hydration state, leading to symptoms of insipidus.