ICD-9) Used in This Study

Total Page:16

File Type:pdf, Size:1020Kb

ICD-9) Used in This Study Supplementary Table 1 Diagnosis codes of International Classification of Diseases, Ninth Revision (ICD-9) used in this study Diagnoses † ICD-9 codes GIB UGIB 531.0, 531.2, 531.4, 531.6, 532.0, 532.2, 532.4, 532.6, 533.0, 533.2, 533.4, 533.6, 534.0, 534.2, 534.4, 534.6, 535.01, 535.11, 535.21, 535.31, 535.41, 535.51, 535.61, 535.71 LGIB 562.02, 562.03, 562.12, 562.13, 569.3, 569.85, 569.86 Unspecified GIB 578 (578.0, 578.1, 578.9) GIB or peptic ulcer 531, 532, 533, 534, and other codes of GIB Ischemic heart disease 410, 411, 412, 413, 414 Ischemic stroke, transient ischemic attack 433.x1, 434, 435, 436, 437.0, 437.1, 444, or systemic embolism 445 Hypertension 401, 402, 403, 404, 405 Diabetes 250 Renal disease 403, 404, 580, 581, 582, 583, 584, 585, 586, 590.0, 753.1 Intracranial hemorrhage 430, 431, 432 Cirrhosis 571.2, 571.5, 571.6 Gastrointestinal cancer 150, 151, 152, 153, 154 Inflammatory bowel disease 555, 556 Coagulant deficiency 286 Gastroenteritis or colitis due to radiation 558.1 Excision of gastrointestinal tract segment‡ V15.2, V45.89 † For GIB, the primary outcome, only inpatient records are included. For baseline medical condition, it is considered positive when the code is identified once in primary hospitalization diagnosis records or more than three times in outpatient records before the start date of the follow-up period; ‡ Also includes other diagnoses with description that mentioned gastrectomy, esophagectomy, enterotomy or colectomy. 1 Supplementary Table 2 Drug names used when extracting covariates of concurrent medications Medication Drug name Gastro-protective agents PPI Omeprazole, lansoprazole, dexlansoprazole, esomeprazole, pantoprazole, rabeprazole H2RA Famotidine, ranitidine, cimetidine, lafutidine, lavoltidine, loxtidine, niperotidine, nizatidine, roxatidine Other antiplatelet drugs Clopidogrel, dipyridamole, cilostazol, ticagrelor, ticlopidine, prasugrel, ticlopidine, aggrenox NSAIDs Naproxen, diclofenac, piroxicam, diclofenac, sulindac, ibuprofen, indomethacin, mefenamic, arcoxia, celecoxib, etoricoxib, apricoxib, lumiracoxib, rofecoxib, valdecoxib, parecoxib Anticoagulants Warfarin, dabigatran, rivaroxaban, apixaban, argatroban, efegatran, edoxaban, betrixaban, darexaban, darexaban, eribaxaban Corticosteroids Betamethasone, dexamethasone, fluocortolone, methylprednisolone, paramethasone, prednisolone, prednisone, triamcinolone, hydrocortisone, cortisone, prednylidene, rimexolone, intraarticular, deflazacort, cloprednol, meprednisone, cortivazol SSRI Zimeldine, fluoxetine, citalopram, paroxetine, sertraline, alaproclate, fluvoxamine, etoperidone, escitalopram Bisphosphonate Alendronate, alendronic acid, ibandronate, ibandronic acid, risedronate, risedronic acid, tidronate, etidronic acid, clodronate, clodronic acid, pamidronate, pamidronic acid, tiludronate, tiludronic acid, zoledronate, zoledronic acid PPI, proton pump inhibitors; H2RA, histamine type-2 receptor antagonists; NSAIDs, nonsteroidal anti-inflammatory drugs; SSRI, selective serotonin reuptake inhibitors. 2 Supplementary Table 3 Causes of gastrointestinal bleeding after H. pylori eradication in each group of aspirin users New users Chronic users Non-users Causes of GIB (ICD-9 codes) (%) (%) (%) UGIB Gastric ulcer (531.0, 531.2, 531.4, 531.6) 32 (12.3) 43 (14.2) 85 (6.6) Duodenal ulcer (532.0, 532.2, 532.4, 532.6) 23 (8.8) 22 (7.3) 127 (9.8) Peptic ulcer site unspecified (533.0, 533.2, 2 (0.8) 7 (2.3) 25 (19.3) 533.4, 533.6) Gastritis and duodenitis (535.01, 535.11, 535.21, 535.31, 535.41, 535.51, 535.61, 9 (3.4) 6 (1.9) 33 (2.5) 535.71) Other unspecified UGIB (578.0, 578.1, 30 (11.5) 36 (11.9) 166 (12.8) 578.9) † LGIB Diverticula of intestine (562.02, 562.03, 5 (1.9) 4 (1.4) 5 (0.4) 562.12, 562.13) Other disorders of intestine (569.3, 569.85, 27 (10.3) 10 (3.3) 115 (8.9) 569.86) Other unspecified intestinal bleeding 76 (29.1) 108 (35.6) 492 (38.0) (578.9) † Unspecified GIB Other unspecified (578.9) 57 (21.8) 67 (22.1) 247 (19.1) † Determined using diagnosis description and keywords recorded in the database. 3 Supplementary Table 4 The effects of gastroprotective agents on risk of GIB and UGIB in different subgroups Subgroups HR (95% CI) for all GIB HR (95% CI) for UGIB All aspirin users 0.34 (0.25-0.46) 0.27 (0.19-0.37) New users 0.31 (0.23-0.42) 0.22 (0.14-0.34) Chronic users 0.53 (0.40-0.70) 0.32 (0.21-0.48) Age 60 0.39 (0.31-0.48) 0.28 (0.20-0.38) Age < 60 0.84 (0.43-1.66) 0.25 (0.09-0.72) Male 0.42 (0.32-0.55) 0.36 (0.24-0.53) Female 0.41 (0.30-0.57) 0.17 (0.10-0.28) NSAIDs users 0.28 (0.17-0.47) 0.14 (0.06-0.35) Other antiplatelet drugs 0.51 (0.30-0.87) 0.27 (0.14-0.55) users Anticoagulants users 0.50 (0.09-2.83) 0.27 (0.03-2.58) Corticosteroids 0.50 (0.19-1.30) 0.28 (0.05-1.61) All patients 0.74 (0.65-0.85) 0.51 (0.40-0.65) Non-users 0.93 (0.80-1.07) 0.71 (0.54-0.92) 4 Supplementary Figure 1 The schematic diagram of the study design. 5 Supplementary Figure 2 Flow chart of patient’s selection. (HP, Helicobacter pylori; GI, gastrointestinal; IBD, inflammatory bowel disease) 6 Supplementary Figure 3 Absolute standardized differences for baseline covariates comparing new aspirin users and chronic aspirin users in the original, the matched and weighted sample. IPTW, inverse probability of treatment weighting. 7 Supplementary Figure 4 The individual Schoenfeld test of new aspirin users with chronic aspirin users as the control in multivariate Cox regression mode for GIB. According to the proportional hazards assumption tests, the coefficients of the aspirin status (new users vs. chronic users) were time-dependent in all models of GIB, and in weighting and multivariate models of UGIB. Therefore, the interaction of aspirin usage status and time was introduced into the time-dependent regression models. 8 .
Recommended publications
  • Nizatidine) Oral Solution
    Axid® (nizatidine) Oral Solution Description: Nizatidine (USP) is a histamine H2-receptor antagonist. Chemically, it is N-[2-[[[2-[(dimethylamino)methyl]-4-thiazolyl]methyl]thio]ethyl]-N'-methyl-2-nitro-1,1- ethenediamine. The structural formula is as follows: Nizatidine has the empirical formula C12H21N5O2S2 representing a molecular weight of 331.47. It is an off-white to buff crystalline solid that is soluble in water. Nizatidine has a bitter taste and mild sulfur-like odor. Axid® Oral Solution is formulated as a clear, yellow, oral solution with bubble gum flavor and each 1 mL contains 15 mg of nizatidine. Axid® Oral Solution also contains the inactive ingredients methylparaben, propylparaben, glycerin, sodium alginate, purified water, sodium chloride, saccharin sodium, sodium citrate dihydrate, citric acid anhydrous, sucrose, bubble gum flavor, artificial sweetness enhancer, and sodium hydroxide. Clinical Pharmacology in Adults: Nizatidine is a competitive, reversible inhibitor of histamine at the histamine H2-receptors, particularly those in the gastric parietal cells. Antisecretory Activity—1. Effects on Acid Secretion: Nizatidine significantly inhibited nocturnal gastric acid secretion for up to 12 hours. Nizatidine also significantly inhibited gastric acid secretion stimulated by food, caffeine, betazole, and pentagastrin (Table 1). Table 1. Effect of Oral Nizatidine on Gastric Acid Secretion % Inhibition of Gastric Acid Output by Dose (mg) Time After Dose (h) 20-50 75 100 150 300 Nocturnal Up to 10 57 - 73 - 90 Betazole Up to 3 - 93 - 100 99 Pentagon Up to 6 - 25 - 64 67 Meal Up to 4 41 64 - 98 97 Caffeine Up to 3 - 73 - 85 96 2. Effects on Other Gastrointestinal Secretions—Pepsin: Oral administration of 75 to 300 mg of nizatidine did not affect pepsin activity in gastric secretions.
    [Show full text]
  • Product List March 2019 - Page 1 of 53
    Wessex has been sourcing and supplying active substances to medicine manufacturers since its incorporation in 1994. We supply from known, trusted partners working to full cGMP and with full regulatory support. Please contact us for details of the following products. Product CAS No. ( R)-2-Methyl-CBS-oxazaborolidine 112022-83-0 (-) (1R) Menthyl Chloroformate 14602-86-9 (+)-Sotalol Hydrochloride 959-24-0 (2R)-2-[(4-Ethyl-2, 3-dioxopiperazinyl) carbonylamino]-2-phenylacetic 63422-71-9 acid (2R)-2-[(4-Ethyl-2-3-dioxopiperazinyl) carbonylamino]-2-(4- 62893-24-7 hydroxyphenyl) acetic acid (r)-(+)-α-Lipoic Acid 1200-22-2 (S)-1-(2-Chloroacetyl) pyrrolidine-2-carbonitrile 207557-35-5 1,1'-Carbonyl diimidazole 530-62-1 1,3-Cyclohexanedione 504-02-9 1-[2-amino-1-(4-methoxyphenyl) ethyl] cyclohexanol acetate 839705-03-2 1-[2-Amino-1-(4-methoxyphenyl) ethyl] cyclohexanol Hydrochloride 130198-05-9 1-[Cyano-(4-methoxyphenyl) methyl] cyclohexanol 93413-76-4 1-Chloroethyl-4-nitrophenyl carbonate 101623-69-2 2-(2-Aminothiazol-4-yl) acetic acid Hydrochloride 66659-20-9 2-(4-Nitrophenyl)ethanamine Hydrochloride 29968-78-3 2,4 Dichlorobenzyl Alcohol (2,4 DCBA) 1777-82-8 2,6-Dichlorophenol 87-65-0 2.6 Diamino Pyridine 136-40-3 2-Aminoheptane Sulfate 6411-75-2 2-Ethylhexanoyl Chloride 760-67-8 2-Ethylhexyl Chloroformate 24468-13-1 2-Isopropyl-4-(N-methylaminomethyl) thiazole Hydrochloride 908591-25-3 4,4,4-Trifluoro-1-(4-methylphenyl)-1,3-butane dione 720-94-5 4,5,6,7-Tetrahydrothieno[3,2,c] pyridine Hydrochloride 28783-41-7 4-Chloro-N-methyl-piperidine 5570-77-4
    [Show full text]
  • Do Intra-Articular Steroid Injections Affect Glycemic Control in Patients
    Evidence-based answers from the Family Physicians Inquiries Network Erin Kallock, MD; Do intra-articular steroid Jon O. Neher, MD Valley Family Medicine Residency, Renton, Wash. injections aff ect glycemic control Leilani St. Anna, MLIS, AHIP University of Washington in patients with diabetes? Health Services Library, Seattle EVIDENCE-BASED ANSWER yes, but the clinical importance mendation [SOR]: B, small cohort studies). A is minimal. A single intra-articular Intra-articular steroid injections into the steroid injection into the knee produces shoulder may briefl y raise postprandial (but acute hyperglycemia for 2 or 3 days in pa- not mean) glucose levels with larger and re- tients with diabetes who otherwise have peated doses (SOR: C, extrapolated from het- good glucose control (strength of recom- erogenous and mixed cohort studies). A single steroid injection into the knee joint Evidence summary 1 week; investigators measured fructosamine causes acute Two prospective cohort studies evaluated the levels (a measure of intermediate-term hyperglycemia eff ect on glycemic control of a single gluco- glucose control) at baseline and again for 2 or 3 days corticoid injection into the knee of patients 2 weeks after injection. in patients with with controlled type 2 diabetes (glycosylated Th e injection produced hyperglycemia in diabetes who hemoglobin A1c Ͻ7.0%). Th e fi rst enrolled all participants, with peak blood glucose lev- otherwise have 9 patients with symptomatic osteoarthritis of els ranging from 251 to 430 mg/dL and time to good glucose the knee unresponsive to 3 months of nonste- peak glucose usually less than 6 hours. Fruc- control.
    [Show full text]
  • Carboxylic Acid Derivates
    Europaisches Patentamt 0 367 484 J> European Patent Office CO Publication number: A1 Office europeen des brevets © EUROPEAN PATENT APPLICATION A61K 31/29 © Application number: 89310994.2 © int. ci.5: C07D 233/64 , C07D 277/42 C07D 277/28 @ Date of filing: 25.10.89 C07D 295/08 C07D 249/14 C07D 211/20 C07D 417/04 © Priority: 26.10.88 GB 8825058 © Applicant: GLAXO GROUP LIMITED 26.06.89 GB 8914631 Clarges House 6-12 Clarges Street London W1Y8DH(GB) © Date of publication of application: 09.05.90 Bulletin 90/19 © Inventor: Clitherow, John Watson 54, Gilders © Designated Contracting States: Sawbridgeworth Hertfordshire(GB) AT BE CH DE ES FR GB GR IT LI LU NL SE © Representative: Marchant, James Ian et al Elkington and Fife Beacon House 113 Kingsway London WC2B 6PP(GB) © Carboxylic acid derivates. © The invention relates to salts formed between basic H2-receptor antagonists and a complex of bismuth with a carboxylic acid, and solvate of such salts, excluding salts in which the basic H2-receptor antagonist is ranitidine. Examples of suitable carboxylic acids are citric acid and tartaric acid. Examples of basic rVreceptor antagonists are cimetidine, sufotidine famotidine and nizatidine. The salts ares useful in the treatment of gastrointestinal disorders, particularly gastroduodenal conditions. The salts show the antisecretory activity associated with the basic H2-receptor antagonist together with antibacterial activity against Campylobacter pylori and they also possess cytoprotective properties. 00 (0 a. LU Xerox Copy Centre EP 0 367 484 A1 CARBOXYLIC ACID DERIVATIVES This invention relates to salts of compounds having antagonist activity at histamine H2- receptors, to a process for the preparation thereof, to pharmaceutical compositions containing them and to their use in therapeutics.
    [Show full text]
  • The In¯Uence of Medication on Erectile Function
    International Journal of Impotence Research (1997) 9, 17±26 ß 1997 Stockton Press All rights reserved 0955-9930/97 $12.00 The in¯uence of medication on erectile function W Meinhardt1, RF Kropman2, P Vermeij3, AAB Lycklama aÁ Nijeholt4 and J Zwartendijk4 1Department of Urology, Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; 2Department of Urology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands; 3Pharmacy; and 4Department of Urology, Leiden University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands Keywords: impotence; side-effect; antipsychotic; antihypertensive; physiology; erectile function Introduction stopped their antihypertensive treatment over a ®ve year period, because of side-effects on sexual function.5 In the drug registration procedures sexual Several physiological mechanisms are involved in function is not a major issue. This means that erectile function. A negative in¯uence of prescrip- knowledge of the problem is mainly dependent on tion-drugs on these mechanisms will not always case reports and the lists from side effect registries.6±8 come to the attention of the clinician, whereas a Another way of looking at the problem is drug causing priapism will rarely escape the atten- combining available data on mechanisms of action tion. of drugs with the knowledge of the physiological When erectile function is in¯uenced in a negative mechanisms involved in erectile function. The way compensation may occur. For example, age- advantage of this approach is that remedies may related penile sensory disorders may be compen- evolve from it. sated for by extra stimulation.1 Diminished in¯ux of In this paper we will discuss the subject in the blood will lead to a slower onset of the erection, but following order: may be accepted.
    [Show full text]
  • Comparative Effects of Cimetidine and Famotidine on the Vagally Stimulated Acid Secretion in the Isolated Mouse Whole Stomach
    Comparative Effects of Cimetidine and Famotidine on the Vagally Stimulated Acid Secretion in the Isolated Mouse Whole Stomach Kazuo Watanabe1, Shingo Yano1, Masayuki Yamamoto1 and Shoko Kanaoka2 1Laboratory of Chemical Pharmacology, Department of Drug Evaluation and Toxicological Sciences, Faculty of Pharmaceutical Sciences, Chiba University, 1-33, Yayoi-cho, Inage-ku, Chiba 263, Japan 2Research Institute for Wakan-Yaku, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan Received July 15, 1992 Accepted December 10, 1992 ABSTRACT-We investigated the effects of cimetidine and famotidine on the acid secretory response to elec trical vagal stimulation, bethanechol and histamine in the isolated mouse whole stomach preparation. The acid secretion elicited by electrical vagal stimulation at the position of the esophagus (10 Hz, 0.3 msec, 10 V for 5 min) was reproducible by repeated stimulation in each preparation, and it was abolished by tetrodo toxin, atropine and hexamethonium. This vagally stimulated acid secretion was abolished by cimetidine (3 mM), while it was only partly inhibited by famotidine (10-100 ƒÊM). Histamine (100 ƒÊM)-induced acid secre tion was inhibited by cimetidine and famotidine, and the doses of these drugs required for complete inhibi tion were 3 mM and 10 ƒÊM, respectively. In contrast, bethanechol (10 ƒÊM)-induced acid secretion was slight ly reduced by famotidine (1-100 ƒÊM), but markedly reduced by cimetidine (3 mM). In the guinea pig ileum, millimolar concentrations of cimetidine and famotidine shifted the dose-response curve of the contractile response to acetylcholine rightward. These findings suggest that the inhibitory effect of cimetidine on the vagally stimulated or bethanechol-induced acid secretion is elicited at least partly through mechanisms different from H2-antagonism.
    [Show full text]
  • A Comparative Evaluation of Lafutidine and 2 Rabeprazole in The
    1 *Original research paper 2 A comparative evaluation of Lafutidine and 3 Rabeprazole in the treatment of gastritis and 4 peptic ulcer: A double-blind, randomized study 5 in Indian patients. 6 Dr. Sanjay Kumar 1, Dr. Bhupesh Dewan 2*, Deepashri Shah 2 7 8 1Global Liver and Gastroenterology Centre, Bhopal, India 2 9 Medical Department, Zuventus Healthcare Ltd., Mumbai, India 10 11 . 12 ABSTRACT 13 Aims: To assess the efficacy of lafutidine therapy versus rabeprazole in Indian patients with endoscopically and histologically proven gastritis and peptic ulcer. Study design: A double blind, double dummy, randomized, comparative study. Place and Duration of Study: Global Liver and Gastroenterology Centre, Bhopal, India, between March 2010 and October 2010. Methodology: A total of 100 patients were enrolled, including 50 with endoscopically and histologically proven gastritis and other 50 with peptic ulcer (over 5 mm in diameter). Each group was randomized to receive either lafutidine or rabeprazole tablet and their corresponding competitor placebo dummy tablet, for a period of 4 weeks. Gastritis/ulcer cure rates confirmed by endoscopic histology, symptom response and Helicobacter pylori (H. Pylori) eradication were compared among the two drugs Results: Complete cure of gastritis was observed in all the patients (100%) treated with lafutidine and 95.24% [20/21; 95% CI: 76.18 to 99.88%] patients treated with rabeprazole. Complete cure of ulcer was observed in 72.0% (18/25, 95% CI = 50.61 to 87.93%) and 79.16% (19/24, 95% CI = 57.85 to 92.87%) patients treated with lafutidine and rabeprazole respectively. There was no significant difference in gastritis/ulcer cure rate and symptom response rate between the two treatment groups at the end of the study.
    [Show full text]
  • Tanibirumab (CUI C3490677) Add to Cart
    5/17/2018 NCI Metathesaurus Contains Exact Match Begins With Name Code Property Relationship Source ALL Advanced Search NCIm Version: 201706 Version 2.8 (using LexEVS 6.5) Home | NCIt Hierarchy | Sources | Help Suggest changes to this concept Tanibirumab (CUI C3490677) Add to Cart Table of Contents Terms & Properties Synonym Details Relationships By Source Terms & Properties Concept Unique Identifier (CUI): C3490677 NCI Thesaurus Code: C102877 (see NCI Thesaurus info) Semantic Type: Immunologic Factor Semantic Type: Amino Acid, Peptide, or Protein Semantic Type: Pharmacologic Substance NCIt Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression. PDQ Definition: A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor
    [Show full text]
  • A New Robust Technique for Testing of Glucocorticosteroids in Dogs and Horses Terry E
    Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 2007 A new robust technique for testing of glucocorticosteroids in dogs and horses Terry E. Webster Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Veterinary Toxicology and Pharmacology Commons Recommended Citation Webster, Terry E., "A new robust technique for testing of glucocorticosteroids in dogs and horses" (2007). Retrospective Theses and Dissertations. 15029. https://lib.dr.iastate.edu/rtd/15029 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]. A new robust technique for testing of glucocorticosteroids in dogs and horses by Terry E. Webster A thesis submitted to the graduate faculty in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Major: Toxicology Program o f Study Committee: Walter G. Hyde, Major Professor Steve Ensley Thomas Isenhart Iowa State University Ames, Iowa 2007 Copyright © Terry Edward Webster, 2007. All rights reserved UMI Number: 1446027 Copyright 2007 by Webster, Terry E. All rights reserved. UMI Microform 1446027 Copyright 2007 by ProQuest Information and Learning Company. All rights reserved. This microform edition is protected against unauthorized copying under Title 17, United States Code. ProQuest Information and Learning Company 300 North Zeeb Road P.O. Box 1346 Ann Arbor, MI 48106-1346 ii DEDICATION I want to dedicate this project to my wife, Jackie, and my children, Shauna, Luke and Jake for their patience and understanding without which this project would not have been possible.
    [Show full text]
  • PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
    Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names INN which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service CAS registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known.
    [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]
  • Histamine H2-Receptor Antagonists Improve Non-Steroidal Anti-Inflammatory Drug-Induced Intestinal Dysbiosis
    International Journal of Molecular Sciences Article Histamine H2-Receptor Antagonists Improve Non-Steroidal Anti-Inflammatory Drug-Induced Intestinal Dysbiosis Rei Kawashima, Shun Tamaki, Fumitaka Kawakami, Tatsunori Maekawa and Takafumi Ichikawa * Department of Regulation Biochemistry, Kitasato University Graduate School of Medical Sciences, Kanagawa 252-0374, Japan; [email protected] (R.K.); [email protected] (S.T.); [email protected] (F.K.); [email protected] (T.M.) * Correspondence: [email protected]; Tel.: +81-42-778-8863 Received: 8 October 2020; Accepted: 30 October 2020; Published: 31 October 2020 Abstract: Dysbiosis, an imbalance of intestinal flora, can cause serious conditions such as obesity, cancer, and psychoneurological disorders. One cause of dysbiosis is inflammation. Ulcerative enteritis is a side effect of non-steroidal anti-inflammatory drugs (NSAIDs). To counteract this side effect, we proposed the concurrent use of histamine H2 receptor antagonists (H2RA), and we examined the effect on the intestinal flora. We generated a murine model of NSAID-induced intestinal mucosal injury, and we administered oral H2RA to the mice. We collected stool samples, compared the composition of intestinal flora using terminal restriction fragment length polymorphism, and performed organic acid analysis using high-performance liquid chromatography. The intestinal flora analysis revealed that NSAID [indomethacin (IDM)] administration increased Erysipelotrichaceae and decreased Clostridiales but that both had improved with the concurrent administration of H2RA. Fecal levels of acetic, propionic, and n-butyric acids increased with IDM administration and decreased with the concurrent administration of H2RA. Although in NSAID-induced gastroenteritis the proportion of intestinal microorganisms changes, leading to the deterioration of the intestinal environment, concurrent administration of H2RA can normalize the intestinal flora.
    [Show full text]