DOCSLIB.ORG

Combination Hormonal Therapy Involving Aromatase Inhibitors in the Management of Women with Breast Cancer

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Combination Hormonal Therapy Involving Aromatase Inhibitors in the Management of Women with Breast Cancer Endocrine-Related Cancer (1999) 6 265-269 Combination hormonal therapy involving aromatase inhibitors in the management of women with breast cancer J N Ingle, V J Suman, V C Jordan1 and M Dowsett2 Mayo Clinic, Rochester, Minnesota 55905, USA 1Northwestern University, Chicago, Illinois 60611, USA 2Royal Marsden Hospital, London SW3 6JJ, UK (Requests for offprints should be addressed to J N Ingle, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA) Abstract Numerous comparative clinical trials have been conducted evaluating combination hormonal therapy involving the aromatase inhibitor aminoglutethimide, but there is no evidence for any superiority of this approach over single-agent therapy alone. The advent of new aromatase inhibitors with greater potency, selectivity, and better tolerability has prompted a reconsideration of the combined therapy approach, with attention being focused on pharmacologic and endocrinologic clinical research. The value of combining newer aromatase inhibitors with other hormonal agents remains to be established. Endocrine-Related Cancer (1999) 6 265-269 Introduction hormonal agents from other classes. In the case of combining aromatase inhibitors with tamoxifen (TAM), it Hormonal therapy remains an integral part of the is possible that the different mechanisms of action would management of most women with breast cancer both in the be complementary, with the aromatase inhibitor decreas- adjuvant and metastatic settings. A variety of hormonal ing estrogen levels and thus allowing TAM to act more agents are in clinical use today including antiestrogens, effectively as a competitive inhibitor with estradiol. progestins, androgens, estrogens, luteinizing hormone- releasing hormone analogs, and aromatase inhibitors. Numerous reports have been published evaluating Despite the availability of multiple agents and multiple aromatase inhibitors in combination with other hormonal classes of agents, a sizeable proportion of tumors will not agents but the most informative are those of a comparative respond to treatment and those tumors that do respond nature. This report will review the experience of will, in all likelihood, become resistant to treatment. The randomized trials evaluating combination hormonal desirability of finding more efficacious hormonal therapy therapy involving aromatase inhibitors and discuss pre- regimens is indisputable. The existence of multiple classes liminary studies utilizing letrozole plus TAM. of agents with different mechanisms of action and excellent tolerability which can be given at full therapeutic Randomized clinical trials evaluating doses in combination has formed the basis for the interest combination hormonal therapy in studying combination hormonal therapy. involving aromatase inhibitors The mechanism of action of the aromatase inhibitors is well defined in terms of reduction of circulating The randomized trials evaluating combination hormonal estrogens. The existence of aromatase activity in a therapy involving aromatase inhibitors are given in substantial proportion of breast carcinomas (Lipton et al. Table 1. The aromatase inhibitor utilized in all these 1987) is an additional incentive for their study. Recent studies was aminoglutethimide (AG) along with hydro- advances in aromatase inhibitor research has led to the cortisone. Five trials evaluated TAM alone or combined introduction of new more potent, more specific, and more with AG (Corkery et al. 1982, Milsted et al. 1985, Ingle et tolerable agents (Goss & Gwyn 1994). The aromatase al. 1986, Rose et al. 1986, Alonso-Muñoz et al. 1988). The inhibitors are particularly attractive for combining with trial with the largest sample size was that of Rose et al. Endocrine-Related Cancer (1999) 6 265-269 Online version via http://www.endocrinology.org 1351-0088/99/006-265 © 1999 Society for Endocrinology Printed in Great Britain Downloaded from Bioscientifica.com at 09/29/2021 02:33:53AM via free access Ingle et al.: Combination hormonal therapy with aromatase inhibitors Table 1 Randomized clinical trials of combination hormonal therapy involving aminoglutethimide No of Objective Median duration Time to treatment Median evaluable response of response failureA or survival Regimen patients rate (%) (months) progressionB (months) (months) Reference TAM 97 34 ~24 10A NA Rose et al. vs (1986) TAM + AG 82 28 ~24 8 NA TAM 49 43 15 7.2B 21.9 Ingle et al. vs (1986) TAM + AG 51 49 15 7.6 27.6 TAM 34 53 NA 15B NA Alonso-Munoz vs et al. (1988) AG 29 48 NA 13 NA vs TAM + AG 31 38 NA 14 NA TAM 26 19 86 NA NA Milsted et al. vs (1985) TAM + AG 26 23 56 NA NA TAM 9 33 NA 6A NA Corkery et al. vs (1982) TAM + AG 11 36 NA 6 NA TAM 99 30.6 ~22.5 NA NA Powles et al. vs (P=0.05) (1984) TAM/AG/Danazol 99 43.2 ~17.5 NA NA AG 25 20 NA NA NA Hisamatsu et al. vs (1992) AG + TAM 21 19 NA NA NA MA 75 6* NA 5A 26 Russell et al. vs (1997) AG 80 24 NA 4 27 vs MA + AG 80 23 NA 7 26 AG 62 32 NA NA NA Wander et al. vs (1987) MPA + AG 69 32 NA NA NA MPA 29 31 9 NA NA Samonis et al. vs (1994) AG 28 36 9 NA NA vs MPA + AG 28 43 10 NA NA NA, not available; TAM, tamoxifen; AG, aminoglutethimide; MA, megestrol acetate; MPA, medroxyprogesterone acetate. *Response determined in total of 122 patients. (1986) which involved 179 patients evaluable for time AG was found to be associated with a significant analysis and 166 patients evaluable for response. There (P=0.032) decrease in the area under the curve (AUC) for was no indication of a therapeutic advantage, and the TAM, with the mean reduction being 73% (range: 56- toxicity was greater with the addition of AG. The other 80%), which corresponded to a mean increase in TAM four randomized trials (Corkery et al. 1982, Ingle et al. clearance of 222%. The impact of AG on five metabolites 1986, Milsted et al. 1985, Alonso-Muñoz et al. 1988) of TAM, including N-desmethyl-TAM and 4-hydroxy- contained smaller sample sizes but had similar results. TAM, was also examined, and the AUC for most After the completion of these studies of TAM plus AG, metabolites was also reduced, with a mean reduction of Lien et al. (1990) reported a study of pharmacokinetic about 50%. The authors concluded that their data were interactions between these two agents. They studied six most consistent with induction of TAM metabolism by postmenopausal women treated for more than 6 months AG. This reduction of TAM and its metabolites provided with TAM as a single agent. AG was then added, using a potential explanation for the failure of the studies noted 250 mg four times a day in five patients and three times a above to show superiority for TAM plus AG over TAM day in one patient, along with cortisone acetate (50 mg alone. twice a day for 2 weeks and 25 mg twice a day thereafter). 266 Downloaded from Bioscientifica.com at 09/29/2021 02:33:53AM via free access Endocrine-Related Cancer (1999) 6 265-269 In a variation on the TAM plus AG theme, Powles (1986), which demonstrated the antagonistic affect of AG et al. (1984) compared TAM plus AG plus danazol (a and danazol on estradiol levels. Before considering a synthetic progestin) with TAM alone. The combination phase III trial, it was considered necessary to evaluate regimen produced a higher response rate (43 vs 31%, patients for any pharmacokinetic interactions between P=0.05) but no advantage in terms of duration of TAM and letrozole. In order to examine the effects of response. The authors concluded that the trial did not show letrozole on TAM, we performed a pilot study in which a therapeutic advantage for the combination. Of note with patients received TAM (20 mg daily) for 6 weeks followed respect to the reported higher response rate for the three- by the addition of letrozole (2.5 mg daily) (JN Ingle, VJ agent combination is that it was subsequently Suman, PA Johnson, JE Krook, JA Mailliard, RH demonstrated that AG and danazol have opposing effects Wheeler, CL Loprinzi, EA Perez, VC Jordan & on the concentration of the free biologically active fraction M Dowsett, unpublished work). Dowsett et al. (1997a) of estradiol (Dowsett et al. 1986). Thus, the use of danazol concurrently performed the complementary study in combination with AG would be expected to be evaluating the effect of TAM on letrozole levels. counterproductive. In the former study which evaluated the impact of Three studies have evaluated the addition of AG to a letrozole on TAM pharmacokinetics, levels of TAM, progestin. The largest study compared megestrol acetate N-desmethyl-TAM, and 4-hydroxy-TAM were measured (MA) with AG or the combination of MA plus AG at 6 week intervals up to 18 weeks after the addition of (Russell et al. 1997). They studied a select group of letrozole. Seventeen patients were assessed with respect to women who were required to have estrogen receptor week 6 levels (before addition of letrozole) and week 24 positive tumors and prior treatment with TAM in the levels (18 weeks after addition of letrozole). There was no advanced disease setting with achievement of a partial indication of a systematic decrease in TAM, N-desmethyl response or stability for at least six months. The objective TAM or 4-hydroxy TAM following the addition of response rates were 6% (MA), 24% (AG), and 23% (MA letrozole. The variability in the percent change in TAM plus AG), with no significant difference being identified and that of the two metabolites was substantial but (χ2, 2 df, P=0.01). In addition, there was no difference in generally consistent and the median percent changes were time to treatment failure or survival.
Load more

Recommended publications
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]
  • Corticosteroids in Terminal Cancer-A Prospective Analysis of Current Practice
    Postgraduate Medical Journal (November 1983) 59, 702-706 Postgrad Med J: first published as 10.1136/pgmj.59.697.702 on 1 November 1983. Downloaded from Corticosteroids in terminal cancer-a prospective analysis of current practice G. W. HANKS* T. TRUEMAN B.Sc., M.B., B.S., M.R.C.P.(U.K.) S.R.N. R. G. TWYCROSS M.A., D.M., F.R.C.P. Sir Michael Sobell House, The Churchill Hospital, Headington, Oxford OX3 7LJ Summary Introduction Over half of a group of 373 inpatients with advanced Corticosteroids have a major role to play in the malignant disease were treated with corticosteroids control of symptoms in patients with advanced for a variety of reasons. They received either pred- malignant disease. They may be employed in a non- nisolone or dexamethasone, or replacement therapy specific way to improve mood and appetite; or they with cortisone acetate. Forty percent of those receiv- may be indicated as specific adjunctive therapy in the ing corticosteroids benefited from them. A higher relief of symptoms related to a large tumour mass or response rate was seen when corticosteroids were to nerve compression. The management of a numberProtected by copyright. prescribed for nerve compression pain, for raised of other symptoms and syndromes may also be intracranial pressure, and when used in conjunction facilitated by treatment with corticosteroids (Table with chemotherapy. No significant difference in 1). efficacy was noted between the 2 drugs. The results, The use of corticosteroids in patients with ad- however, suggest that with a larger sample, dexame- vanced cancer is empirical, as it is in other non- thasone would have been shown to be significantly endocrine indications.
    [Show full text]
  • 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
    [Show full text]
  • Replacement Therapy for Adrenal Insufficiency
    Group 4: Replacement therapy for adrenal insufficiency Frederic Castinetti, Laurence Guignat, Claire Bouvattier, Dinane Samara-Boustani, Yves Reznik To cite this version: Frederic Castinetti, Laurence Guignat, Claire Bouvattier, Dinane Samara-Boustani, Yves Reznik. Group 4: Replacement therapy for adrenal insufficiency . Annales d’Endocrinologie, Elsevier Masson, 2017, 78 (6), pp.525-534. 10.1016/j.ando.2017.10.007. hal-01724179 HAL Id: hal-01724179 https://hal-amu.archives-ouvertes.fr/hal-01724179 Submitted on 10 Apr 2018 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. Consensus Group 4: Replacement therapy for adrenal insufficiencyଝ Groupe 4 : traitement substitutif de l’insuffisance surrénale Frédéric Castinettia,∗, Laurence Guignatb, Claire Bouvattierc, Dinane Samara-Boustanid, Yves Reznike,f a UMR7286, CNRS, CRN2M, service d’endocrinologie, hôpital La Conception, Aix Marseille université, AP–HM, 13005 Marseille, France b Service d’endocrinologie et maladies métaboliques, hôpital Cochin, CHU Paris Centre, 75014 Paris, France c Service d’endocrinologie
    [Show full text]
  • 21 CFR Ch. I (4–1–01 Edition)
    § 524.86 21 CFR Ch. I (4–1–01 Edition) 524.1044b Gentamicin sulfate, 524.1600 Nystatin ophthalmic and topical betamethasone valerate otic solution. dosage forms. 524.1044c Gentamicin ophthalmic ointment. 524.1600a Nystatin, neomycin, thiostrepton, 524.1044d Gentamicin sulfate, and triamcinolone acetonide ointment. betamethasone valerate ointment. 524.1600b Nystatin, neomycin, thiostrepton, 524.1044e Gentamicin sulfate spray. and triamcinolone acetonide ophthalmic 524.1044f Gentamicin sulfate, ointment. betamethasone valerate topical spray. 524.1662 Oxytetracycline hydrochloride oph- 524.1044g Gentamicin sulfate, thalmic and topical dosage forms. betamethasone valerate, clotrimazole 524.1662a Oxytetracycline hydrochloride and ointment. hydrocortisone spray. 524.1044h Gentamicin sulfate, mometasone 524.1662b Oxytetracycline hydrochloride, furoate, clotrimazole otic suspension. polymyxin B sulfate ophthalmic oint- 524.1193 Ivermectin pour-on. ment. 524.1195 Ivermectin otic suspension. 524.1742 N-(Mercaptomethyl) phthalimide S- 524.1200 Kanamycin ophthalmic and topical (O,O-dimethyl phosphorodithioate) emul- dosage forms. sifiable liquid. 524.1200a Kanamycin ophthalmic ointment. 524.1880 Prednisolone-neomycin sulfate oph- 524.1200b Kanamycin ophthalmic aqueous thalmic ointment. solution. 524.1881 Prednisolone acetate ophthalmic 524.1204 Kanamycin sulfate, calcium and topical dosage forms. amphomycin, and hydrocortisone ace- 524.1881a [Reserved] tate. 524.1240 Levamisole. 524.1881b Prednisolone acetate-neomycin 524.1376 2-Mercaptobenzothiazole solution. sulfate sterile suspension. 524.1443 Miconazole nitrate cream; 524.1883 Prednisolone sodium phosphate-ne- miconazole nitrate lotion; miconazole ni- omycin sulfate ophthalmic ointment. trate spray. 524.1982 Proparacaine hydrochloride oph- 524.1446 Milbemycin oxime solution. thalmic solution. 524.1451 Moxidectin. 524.2098 Selamectin. 524.1465 Mupirocin ointment. 524.2101 Selenium disulfide suspension. 524.1484 Neomycin sulfate ophthalmic and 524.2140 Squalane, pyrethrins and piperonyl topical dosage forms.
    [Show full text]
  • Pharmacologic Characteristics of Corticosteroids 대한신경집중치료학회
    REVIEW J Neurocrit Care 2017;10(2):53-59 https://doi.org/10.18700/jnc.170035 eISSN 2508-1349 Pharmacologic Characteristics of Corticosteroids 대한신경집중치료학회 Sophie Samuel, PharmD1, Thuy Nguyen, PharmD1, H. Alex Choi, MD2 1Department of Pharmacy, Memorial Hermann Texas Medical Center, Houston, TX; 2Department of Neurosurgery and Neurology, The University of Texas Medical School at Houston, Houston, TX, USA Corticosteroids (CSs) are used frequently in the neurocritical care unit mainly for their anti- Received December 7, 2017 inflammatory and immunosuppressive effects. Despite their broad use, limited evidence Revised December 7, 2017 exists for their efficacy in diseases confronted in the neurocritical care setting. There are Accepted December 17, 2017 considerable safety concerns associated with administering these drugs and should be limited Corresponding Author: to specific conditions in which their benefits outweigh the risks. The application of CSs in H. Alex Choi, MD neurologic diseases, range from traumatic head and spinal cord injuries to central nervous Department of Pharmacy, Memorial system infections. Based on animal studies, it is speculated that the benefit of CSs therapy Hermann Texas Medical Center, 6411 in brain and spinal cord, include neuroprotection from free radicals, specifically when given Fannin Street, Houston, TX 77030, at a higher supraphysiologic doses. Regardless of these advantages and promising results in USA animal studies, clinical trials have failed to show a significant benefit of CSs administration Tel: +1-713-500-6128 on neurologic outcomes or mortality in patients with head and acute spinal injuries. This Fax: +1-713-500-0665 article reviews various chemical structures between natural and synthetic steroids, discuss its E-mail: [email protected] pharmacokinetic and pharmacodynamic profiles, and describe their use in clinical practice.
    [Show full text]
  • Conversion of Cortisone to Cortisol and Prednisone to Prednisolone
    22 April 1967 Histocompatibility Tests-Johnson and Russell MEBRITJSH 205 Bach, F., and Hirschhorn, K. (1964). Science, 143, 813. Harris, R., Clarke, C. A., Jones, A. L., Sheppard, P. M., Lehane, D., Bain, B., and Lowenstein, L. (1964). Ibid., 145, 1315. McCarthy, M., Lawler, S. D., and Shatwell, H. S. (1966). Brit. Vas, M. R., and Lowenstein, L. (1964). Blood, 23, 108. med. 7., 1, 509. Brent, L., and Medawar, P. B. (1963). Brit. med. 7., 2, 269. Hirschhorn, K. (1965). In Histocompatibility Testing, edited by P. S. - (1964). Nature (Lond.), 204, 90. Russell and H. J. Winn, Publication No. 1229, Nat. Acad. Sci., Bridges, J. M., Nelson, S. D., and McGeown, M. G. (1964). Lancet, 1, Washington, p. 177. 581. Huggins, C. E. (1964). Ann. Surg., 160, 643. Chen, P. S. (1958). Proc. Soc. exp. Biol. (N.Y.), 98, 546. Johnson, G. J., and Russell, P. S. (1965). Nature (Lond.), 208, 343. Gray, J. G., and Russell, P. S. (1963). Lancet, 2, 863. Moorhead, J. F., and Patel, A. R. (1964). Brit. med. 7., 2, 1111. - (1965). In Histocompatibility Testing, edited by P. S. Russell Russell, P. S. (1966). In Histocompatibility Testing 1965, edited by HE and H. J. Winn. Publication No. 1229, Nat. Acad. Sci., Washington, Balner, F. J. Cleton, and J. G. Eernissc, p. 233. Copenhagen. p. 105. Streilein, J. W. (1966). Ibid., p. 241. Conversion of Cortisone to Cortisol and Prednisone to Prednisolone J. S. JENKINS,* M.D., M.R.C.P.; P. A. SAMPSON,t M.B., CH.B. Brit. med. J., 1967, 2, 205-207 Though cortisone has been widely used since Hench et al.
    [Show full text]
  • Recent Advances in the Analysis of Steroid Hormones and Related Drugs
    ANALYTICAL SCIENCES MAY 2004, VOL. 20 767 2004 © The Japan Society for Analytical Chemistry Reviews Recent Advances in the Analysis of Steroid Hormones and Related Drugs Sándor GÖRÖG Gedeon Richter Ltd., P.O.B. 27, H-1475 Budapest, Hungary The development during the last 15 years and the state-of-the-art in the analysis of bulk steroid hormone drugs and hormone-like structures and pharmaceutical formulations made thereof are summarized. Other steroids (sterols, bile acids, cardiac glycosides, vitamins D) as well as biological-clinical aspects and pharmacokinetic and metabolic studies are excluded from this review. The state-of-the-art is summarized based on comparisons of monographs in the latest editions of the European Pharmacopoeia, United States Pharmacopoeia and the Japanese Pharmacopoeia. This is followed by sections dealing with new developments in the methodology for the fields of spectroscopic and spectrophotometric, chromatographic, electrophoretic and hyphenated techniques as well electroanalytical methods. The review is terminated by two problem-oriented sections: examples on impurity and degradation profiling as well as enantiomeric analysis. (Received January 14, 2004; Accepted February 2, 2004) 1 Introduction 767 4·3 Supercritical fluid chromatography (SFC) 2 Steroid Hormone Drugs in Pharmacopoeias 768 4·4 High-performance liquid chromatography 2·1 Assay of bulk drug materials (HPLC) and HPLC-MS 2·2 Related impurities test of bulk drug materials 5 Electrophoretic and Related Methods 776 2·3 Assay of steroid hormone formulations
    [Show full text]
  • Prednisone in Rheumatoid Arthritis: Metabolic and Clinical Effects
    Ann Rheum Dis: first published as 10.1136/ard.17.2.145 on 1 June 1958. Downloaded from Ann. rheum. Dis. (1958), 17, 145. PREDNISONE IN RHEUMATOID ARTHRITIS: METABOLIC AND CLINICAL EFFECTS BY L. EMMERSON WARD, HOWARD F. POLLEY, MARSCHELLE H. POWER, HAROLD L. MASON, CHARLES H. SLOCUMB, AND PHILIP S. HENCH Mayo Clinic and Mayo Foundation,* Rochester, Minn. The initial reports (Hench, Kendall, Slocumb, and strated that chemists could alter the steroid molecule Polley, 1949; Sprague, Power, Mason, Albert, so as to prepare synthetic compounds with even Mathieson, Hench, Kendall, Slocumb, and Polley, more selective effects. This paved the way for the 1950; Hench and others, 1950) of the antirheumatic dissociation of one effect from another, so that one potency of cortisone emphasized the fact that or more of these effects could be enhanced rela- excessive doses produced not only desirable but also tively. certain undesirable effects. At that time (1949), we The chemical structure of prednisone (delta expressed our hope and belief that analogues 1-cortisone) and prednisolone (delta I-hydro- superior to cortisone would be discovered. Since cortisone) differs from that of cortisone and hydro- then, at least seven more cortisone-like steroids have cortisone, respectively, only in the possession of a copyright. been found useful clinically; these include hydro- double bond (hence the designation "delta") between cortisone, 9-alpha-fluorohydrocortisone (Fludro- the first and second carbon atoms in ring A of the cortisone), prednisone, prednisolone, a compound molecule (Fig. 1, overleaf). It is this slight change whose structure is 9-alpha-fluoro, delta 1-hydro- that invests these synthetic cortisone-like steroids cortisone, and the two most recent additions, with an increased antirheumatic potency and a de- namely triamcinolone and 6-methyl, delta I-hydro- creased effect on the metabolism ofelectrolytes when cortisone.
    [Show full text]