Corticosteroids in Terminal Cancer-A Prospective Analysis of Current Practice
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Adrenal Disorders
Adrenal Disorders Dual-release Hydrocortisone in Addison’s Disease— A Review of the Literature Roberta Giordano, MD,1 Federica Guaraldi, MD,2 Rita Berardelli, MD,2 Ioannis Karamouzis, MD,2 Valentina D’Angelo, MD,2 Clizia Zichi, MD,2 Silvia Grottoli, MD,2 Ezio Ghigo, PhD2 and Emanuela Arvat, PhD3 1. Department of Clinical and Biological Sciences; 2. Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences; 3. Division of Oncological Endocrinology, Department of Medical Sciences, University of Turin, Turin, Italy Abstract In patients with adrenal insufficiency, glucocorticoids (GCs) are insufficiently secreted and GC replacement is essential for health and, indeed, life. Despite GC-replacement therapy, patients with adrenal insufficiency have a greater cardiovascular risk than the general population, and suffer from impaired health-related quality of life. Although the aim of the replacement GC therapy is to reproduce as much as possible the physiologic pattern of cortisol secretion by the normal adrenal gland, the pharmacokinetics of available oral immediate-release hydrocortisone or cortisone make it impossible to fully mimic the cortisol rhythm. Therefore, there is an unmet clinical need for the development of novel pharmaceutical preparations of hydrocortisone, in order to guarantee a more physiologic serum cortisol concentration time-profile, and to improve the long-term outcome in patients under GC substitution therapy. Keywords Addison’s disease, glucocorticoids, hydrocortisone, Plenadren®, limits, advantages Disclosure: The authors have no conflicts of interest to declare. Received: June 28, 2013 Accepted: August 9, 2013 Citation: US Endocrinology 2013;9(2):177–80 DOI: 10.17925/USE.2013.09.02.177 Correspondence: Roberta Giordano, MD, Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences, Azienda Ospedaliera Città della Salute e della Scienza di Torino, C so Dogliotti 14, 10126 Turin, Italy. -
Frequently Asked Questions for Addison Patients
FREQUENTLY ASKED QUESTIONS FOR ADDISON PATIENTS TABLE OF CONTENT (Place your cursor over the subject line, hold down the Control Button and Click your mouse. To get back to the Table of Content, hold down the Control Button and press the Home key) ADDISONIAN CRISIS / EMERGENCY ADDISONS AND OTHER DISORDERS ADDISONS AND OTHER MEDICATIONS ADRENALINE BLOOD PRESSURE COMMON COLD/FLU/OTHER ILLNESS CORTISOL DAY CURVE CORTISOL MEDICATION CRAMPS DIABETES DIAGNOSING ADDISONS EXERCISE / SPORTS FATIGUE FLORINEF / SALT / SODIUM HERBAL / VITAMIN SUPPLEMENTS HYPERPIGMENTATION IMMUNIZATION MENOPAUSE, PREGNANCY, HORMONE REPLACEMENT, BIRTH CONTROL, HYSTERECTOMY MISCELLANEOUS OSTEOPOROSIS SECONDARY ADDISON’S SHIFT WORK SLEEP 1 STRESS DOSING SURGICAL, MEDICAL, DENTAL PROCEDURES THYROID TRAVEL WEIGHT GAIN 2 ADDISONIAN CRISIS / EMERGENCY How do you know when to call an ambulance? If you are careful, you should not have to call an ambulance. If someone with adrenal insufficiency has gastrointestinal problems and is unable to keep down their cortisol or other glucocorticoid for more than 24 hrs, they should be taken to an emergency department so they can be given intravenous solucortef and saline. It is not appropriate to wait until they are so ill that they cannot be taken to the hospital by a family member. If the individual is unable to retain anything by mouth and is very ill, or if they have had a sudden stress such as a fall or an infection, then it would be necessary for them to go by ambulance as soon as possible. It is important that you should have an emergency kit at home and that someone in the household knows how to use it. -
Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids
Canine vascular tissues are targets for androgens, estrogens, progestins, and glucocorticoids. K B Horwitz, L D Horwitz J Clin Invest. 1982;69(4):750-758. https://doi.org/10.1172/JCI110513. Research Article Sex differences and steroid hormones are known to influence the vascular system as shown by the different incidence of atherosclerosis in men and premenopausal women, or by the increased risk of cardiovascular diseases in women taking birth control pills or men taking estrogens. However, the mechanisms for these effects in vascular tissues are not known. Since steroid actions in target tissues are mediated by receptors, we have looked for cytoplasmic steroid receptor proteins in vascular tissues of dogs. We find specific saturable receptors, sedimenting at 8S on sucrose density gradients for estrogens (measured with [3H]estradiol +/- unlabeled diethylstilbestrol), androgens (measured with [3H]R1881 +/- unlabeled R1881 and triamcinolone acetonide), and glucocorticoids (measured with [3H]dexamethasone +/- unlabeled dexamethasone); they are absent for progesterone (measured with [3H]R5020 +/- unlabeled R5020 and dihydrotestosterone). Progesterone receptors can, however, be induced by 1-wk treatment of dogs with physiological estradiol concentrations (100 pg/ml serum estrogen), indicating a functional estrogen receptor. Receptor levels range from 20 to 2,000 fmol/mg DNA. They are specific for each hormone; unrelated steroids fail to complete for binding. Low dissociation constants, measured by Scatchard analyses, show that binding is of high affinity. Steroid binding sites are in the media and/or adventitia since they persist when the intima is removed. Compared with the arteries, receptor levels are reduced 80% in inferior venae cavae of […] Find the latest version: https://jci.me/110513/pdf Canine Vascular Tissues Are Targets for Androgens, Estrogens, Progestins, and Glucocorticoids KATHRYN B. -
Dexamethasone Inhibits the Induction of NAD+-Dependent 15
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Biochimica et Biophysica Acta 1497 (2000) 61^68 www.elsevier.com/locate/bba Dexamethasone inhibits the induction of NAD-dependent 15-hydroxyprostaglandin dehydrogenase by phorbol ester in human promonocytic U937 cells Min Tong 1, Hsin-Hsiung Tai * Division of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536-0082, USA Received 29 December 1999; received in revised form 2 March 2000; accepted 9 March 2000 Abstract Pro-inflammatory prostaglandins are known to be first catabolized by NAD-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) to inactive metabolites. This enzyme is under regulatory control by various inflammation-related agents. Regulation of this enzyme was investigated in human promonocytic U937 cells. 15-PGDH activity was found to be optimally induced by phorbol 12-myristate 13-acetate (PMA) at 10 nM after 24 h of treatment. The induction was blocked by staurosporine or GF 109203X indicating that the induction was mediated by protein kinase C. The induction by PMA was inhibited by the concurrent addition of dexamethasone. Nearly complete inhibition was observed at 50 nM. Other glucocorticoids, such as hydrocortisone and corticosterone, but not sex hormones, were also inhibitory. Inhibition by dexamethasone could be reversed by the concurrent addition of antagonist mifepristone (RU-486) indicating that the inhibition was a receptor-mediated event. Either induction by PMA or inhibition by dexamethasone the 15-PGDH activity correlated well with the enzyme protein expression as shown by the Western blot analysis. These results provide the first evidence that prostaglandin catabolism is regulated by glucocorticoids at the therapeutic level. -
Dexamethasone in Patients with Acute Lung Injury from Acute Monocytic Leukaemia
Eur Respir J 2012; 39: 648–653 DOI: 10.1183/09031936.00057711 CopyrightßERS 2012 Dexamethasone in patients with acute lung injury from acute monocytic leukaemia E´. Azoulay*, E. Canet*, E. Raffoux#, E. Lengline´#, V. Lemiale*, F. Vincent*, A. de Labarthe#, A. Seguin*, N. Boissel#, H. Dombret# and B. Schlemmer* ABSTRACT: The use of steroids is not required in myeloid malignancies and remains AFFILIATIONS controversial in patients with acute lung injury (ALI) or acute respiratory distress syndrome *Medical ICU and #Hematology Dept, Saint-Louis (ARDS). We sought to evaluate dexamethasone in patients with ALI/ARDS caused by acute Hospital, Paris, France. monocytic leukaemia (AML FAB-M5) via either leukostasis or leukaemic infiltration. Dexamethasone (10 mg every 6 h until neutropenia) was added to chemotherapy and intensive CORRESPONDENCE ´ care unit (ICU) management in 20 consecutive patients between 2005 and 2008, whose data were E. Azoulay AP-HP compared with those from 20 historical controls (1994–2002). ICU mortality was the primary Hoˆpital Saint-Louis criterion. We also compared respiratory deterioration rates, need for ventilation and nosocomial Medical ICU infections. 75010 Paris 17 (85%) patients had hyperleukocytosis, 19 (95%) had leukaemic masses, and all 20 had France E-mail: [email protected] severe pancytopenia. All patients presented with respiratory symptoms and pulmonary infiltrates paris.fr prior to AML FAB-M5 diagnosis. Compared with historical controls, dexamethasone-treated patients had a significantly lower ICU mortality rate (20% versus 50%; p50.04) and a trend for less Received: respiratory deterioration (50% versus 80%; p50.07). There were no significant increases in the May 24 2011 Accepted after revision: rates of infections with dexamethasone. -
Steroid Use in Prednisone Allergy Abby Shuck, Pharmd Candidate
Steroid Use in Prednisone Allergy Abby Shuck, PharmD candidate 2015 University of Findlay If a patient has an allergy to prednisone and methylprednisolone, what (if any) other corticosteroid can the patient use to avoid an allergic reaction? Corticosteroids very rarely cause allergic reactions in patients that receive them. Since corticosteroids are typically used to treat severe allergic reactions and anaphylaxis, it seems unlikely that these drugs could actually induce an allergic reaction of their own. However, between 0.5-5% of people have reported any sort of reaction to a corticosteroid that they have received.1 Corticosteroids can cause anything from minor skin irritations to full blown anaphylactic shock. Worsening of allergic symptoms during corticosteroid treatment may not always mean that the patient has failed treatment, although it may appear to be so.2,3 There are essentially four classes of corticosteroids: Class A, hydrocortisone-type, Class B, triamcinolone acetonide type, Class C, betamethasone type, and Class D, hydrocortisone-17-butyrate and clobetasone-17-butyrate type. Major* corticosteroids in Class A include cortisone, hydrocortisone, methylprednisolone, prednisolone, and prednisone. Major* corticosteroids in Class B include budesonide, fluocinolone, and triamcinolone. Major* corticosteroids in Class C include beclomethasone and dexamethasone. Finally, major* corticosteroids in Class D include betamethasone, fluticasone, and mometasone.4,5 Class D was later subdivided into Class D1 and D2 depending on the presence or 5,6 absence of a C16 methyl substitution and/or halogenation on C9 of the steroid B-ring. It is often hard to determine what exactly a patient is allergic to if they experience a reaction to a corticosteroid. -
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Cr
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Crizotinib (PF-02341066) 1 4 55 Docetaxel 1 5 98 Anastrozole 1 6 25 Cladribine 1 7 23 Methotrexate 1 8 -187 Letrozole 1 9 65 Entecavir Hydrate 1 10 48 Roxadustat (FG-4592) 1 11 19 Imatinib Mesylate (STI571) 1 12 0 Sunitinib Malate 1 13 34 Vismodegib (GDC-0449) 1 14 64 Paclitaxel 1 15 89 Aprepitant 1 16 94 Decitabine 1 17 -79 Bendamustine HCl 1 18 19 Temozolomide 1 19 -111 Nepafenac 1 20 24 Nintedanib (BIBF 1120) 1 21 -43 Lapatinib (GW-572016) Ditosylate 1 22 88 Temsirolimus (CCI-779, NSC 683864) 1 23 96 Belinostat (PXD101) 1 24 46 Capecitabine 1 25 19 Bicalutamide 1 26 83 Dutasteride 1 27 68 Epirubicin HCl 1 28 -59 Tamoxifen 1 29 30 Rufinamide 1 30 96 Afatinib (BIBW2992) 1 31 -54 Lenalidomide (CC-5013) 1 32 19 Vorinostat (SAHA, MK0683) 1 33 38 Rucaparib (AG-014699,PF-01367338) phosphate1 34 14 Lenvatinib (E7080) 1 35 80 Fulvestrant 1 36 76 Melatonin 1 37 15 Etoposide 1 38 -69 Vincristine sulfate 1 39 61 Posaconazole 1 40 97 Bortezomib (PS-341) 1 41 71 Panobinostat (LBH589) 1 42 41 Entinostat (MS-275) 1 43 26 Cabozantinib (XL184, BMS-907351) 1 44 79 Valproic acid sodium salt (Sodium valproate) 1 45 7 Raltitrexed 1 46 39 Bisoprolol fumarate 1 47 -23 Raloxifene HCl 1 48 97 Agomelatine 1 49 35 Prasugrel 1 50 -24 Bosutinib (SKI-606) 1 51 85 Nilotinib (AMN-107) 1 52 99 Enzastaurin (LY317615) 1 53 -12 Everolimus (RAD001) 1 54 94 Regorafenib (BAY 73-4506) 1 55 24 Thalidomide 1 56 40 Tivozanib (AV-951) 1 57 86 Fludarabine -
Dexamethasone and Fludrocortisone Inhibit Hedgehog Signaling In
This is an open access article published under an ACS AuthorChoice License, which permits copying and redistribution of the article or any adaptations for non-commercial purposes. Article Cite This: ACS Omega 2018, 3, 12019−12025 http://pubs.acs.org/journal/acsodf Dexamethasone and Fludrocortisone Inhibit Hedgehog Signaling in Embryonic Cells † ‡ † ‡ Kirti Kandhwal Chahal,*, , Milind Parle, and Ruben Abagyan*, † Department of Pharmaceutical Sciences, G. J. University of Science and Technology, Hisar 125001, India ‡ Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92037, United States ABSTRACT: The hedgehog (Hh) pathway plays a central role in the development and repair of our bodies. Therefore, dysregulation of the Hh pathway is responsible for many developmental diseases and cancers. Basal cell carcinoma and medulloblastoma have well- established links to the Hh pathway, as well as many other cancers with Hh-dysregulated subtypes. A smoothened (SMO) receptor plays a central role in regulating the Hh signaling in the cells. However, the complexities of the receptor structural mechanism of action and other pathway members make it difficult to find Hh pathway inhibitors efficient in a wide range. Recent crystal structure of SMO with cholesterol indicates that it may be a natural ligand for SMO activation. Structural similarity of fluorinated corticosterone derivatives to cholesterol motivated us to study the effect of dexamethasone, fludrocortisone, and corticosterone on the Hh pathway activity. We identified an inhibitory effect of these three drugs on the Hh pathway using a functional assay in NIH3T3 glioma response element cells. Studies using BODIPY-cyclopamine and 20(S)-hydroxy cholesterol [20(S)-OHC] as competitors for the transmembrane (TM) and extracellular cysteine-rich domain (CRD) binding sites showed a non-competitive effect and suggested an alternative or allosteric binding site for the three drugs. -
Ketoconazole Revisited: a Preoperative Or Postoperative Treatment in Cushing's Disease
European Journal of Endocrinology (2008) 158 91–99 ISSN 0804-4643 CLINICAL STUDY Ketoconazole revisited: a preoperative or postoperative treatment in Cushing’s disease F Castinetti, I Morange, P Jaquet, B Conte-Devolx and T Brue Department of Endocrinology, Diabetes, Metabolic Diseases and Nutrition, Hoˆpital de la Timone, Centre Hospitalier Universitaire de Marseille and Faculte´ de Me´decine, Universite´ de la Me´diterrane´e, 264 rue St Pierre, Cedex 5, 13385 Marseille, France (Correspondence should be addressed to T Brue; Email: [email protected]) Abstract Context: Although transsphenoidal surgery remains the first-line treatment in Cushing’s disease (CD), recurrence is observed in about 20% of cases. Adjunctive treatments each have specific drawbacks. Despite its inhibitory effects on steroidogenesis, the antifungal drug ketoconazole was only evaluated in series with few patients and/or short-term follow-up. Objective: Analysis of long-term hormonal effects and tolerance of ketoconazole in CD. Design: A total of 38 patients were retrospectively studied with a mean follow-up of 23 months (6–72). Setting: All patients were treated at the same Department of Endocrinology in Marseille, France. Patients: The 38 patients with CD, of whom 17 had previous transsphenoidal surgery. Intervention: Ketoconazole was begun at 200–400 mg/day and titrated up to 1200 mg/day until biochemical remission. Main outcome measures: Patients were considered controlled if 24-h urinary free cortisol was normalized. Results: Five patients stopped ketoconazole during the first week because of clinical or biological intolerance. On an intention to treat basis, 45% of the patients were controlled as were 51% of those treated long term. -
18-Dehydrogenase Deficiency W
Arch Dis Child: first published as 10.1136/adc.51.8.576 on 1 August 1976. Downloaded from Archives of Disease in Childhood, 1976, 51, 576. Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency W. HAMILTON, A. E. McCANDLESS, J. T. IRELAND, and C. E. GRAY From the University Departments of Child Health, Liverpool and Glasgow Hamilton, W., McCandless, A. E., Ireland, J. T., and Gray, C. E. (1976). Archives of Disease in Childhood, 51, 576. Hypoaldosteronism in three sibs due to 18-dehydrogenase deficiency. Three sibs all presented in the early neonatal period with a salt-losing syndrome. The salt-losing form of congenital adrenal hyperplasia was diagnosed and appropriate treatment with glucocorticosteroids, mineralocorticosteroids, and additional dietary salt started. Although early life was maintained with difficulty, with age all3 children required decreasingamounts ofreplace- ment steroids to maintain normal plasma electrolyte balance. They were reinvestigated at the ages of 15 years and 8 years (twins), when cortisol synthesis and metabolism proved normal, but aldosterone synthesis was blocked by deficiency of 18-dehydro- genase. Rational treatment of these cases of a salt-losing syndrome in which aldo- sterone synthesis alone is blocked due to lack of the enzyme 18-dehydrogenase requires the administration of a mineralocorticosteroid drug only. Since deoxycor- ticosterone (acetate or pivalate) requires intramuscular administration, as life-long therapy oral fludrocortisone is preferable. Although fludrocortisone has glucocorti- coid activity, the 'hydrocortisone equivalent' effect of the small dosage used was un- likely to inhibit either pituitary corticotrophin or growth hormone production. Salt-loss of adrenal origin is recognized as a female external genitalia or macrogenitosomia http://adc.bmj.com/ feature of 3/1-hydroxysteroid dehydrogenase de- praecox in the male. -
And Function by Progesterone TLR4-Mediated Dendritic Cell
Differential Modulation of TLR3- and TLR4-Mediated Dendritic Cell Maturation and Function by Progesterone This information is current as Leigh A. Jones, Shrook Kreem, Muhannad Shweash, of September 23, 2021. Andrew Paul, James Alexander and Craig W. Roberts J Immunol 2010; 185:4525-4534; Prepublished online 15 September 2010; doi: 10.4049/jimmunol.0901155 http://www.jimmunol.org/content/185/8/4525 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2010/09/13/jimmunol.090115 Material 5.DC1 http://www.jimmunol.org/ References This article cites 56 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/185/8/4525.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 23, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Differential Modulation of TLR3- and TLR4-Mediated Dendritic Cell Maturation and Function by Progesterone Leigh A. -
Cortisone Acetate Tablets, Usp
CORTISONE ACETATE- cortisone acetate tablet Hikma Pharmaceuticals USA Inc. ---------- CORTISONE ACETATE TABLETS, USP Rev. 07/09 Rx Only DESCRIPTION: Glucocorticoids are adrenocortical steroids, both naturally occurring and synthetic, which are readily absorbed from the gastrointestinal tract. Cortisone acetate is a white or practically white, odorless, crystalline powder. It is stable in air. It is insoluble in water. The molecular weight is 402.49. It is designated chemically as 21-(acetyloxy)-17- hydroxypregn-4-ene-3,11,20-trione. The molecular formula is C23H30O6 and the structural formula is: Cortisone Acetate tablets contain 25 mg of cortisone acetate in each tablet. Inactive ingredients are Anhydrous Lactose, Colloidal Silicon Dioxide, Magnesium Stearate, Microcrystalline Cellulose, Sodium Lauryl Sulfate, and Sodium Starch Glycolate. CLINICAL PHARMACOLOGY: Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. They are also used for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli. INDICATIONS AND USAGE: 1. Endocrine Disorders Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the first choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy mineralocorticoid supplementation