Dry Eye: an Evidence-Based Approach to Diagnosis and Management

Total Page:16

File Type:pdf, Size:1020Kb

Dry Eye: an Evidence-Based Approach to Diagnosis and Management Dry Eye: An Evidence-based Approach to Diagnosis and Management Jennifer Gould OD, MS, FAAO Disclosures • Aerie • Allergan • Zeiss Dry Eye Definition “Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and DEWS II hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles” Definition – DEWS II Definition of dry eye Classification Evaluation Treatment Tear Film Neurosensory Ocular Surface Hyperosmolarity Instability Abnormalities Inflammation Dry eye disease is an interplay of aqueous deficiency and evaporative etiologies Dry Eye Evaluation American Society of cataract and “DED can cause a reduced visual function refractive surgery and might compromise the overall result of (ASCRS) corneal, cataract, and refractive surgery.” Preoperative “The impact of DED and OSD on topography, biometry, keratometry, and higher order diagnosis and aberrations is one of the major causes of treatment of ocular disappointing postoperative outcomes.” surface disorders Published 12/2018 Dry eye Screening • Symptoms - • Questionnaire – OSDI vs speed vs speed II • Signs - • Osmolality • Inflammatory Marker Further evaluation should be performed is one of these areas is abnormal Speed Score Interpretation Sum of scores / 28 Asymptomatic: ≤ 2 Mild: 3-4 Moderate: 5-7 Speed Survey Severe: ≥ 8 Speed II Survey OSDI Survey OSDI Score Interpretation Sum of scores x 25 / # Questions answered Normal: 0-12 Mild: 13-22 Moderate: 23-32 Severe: ≥ 33 Point of Care testing: Identify non-symptomatic patients MMP-9: Non-specific inflammatory marker > 307 mOsm/L = abnormal > 8 difference between eyes is significant Non-invasive - Objective testing • Meibomian gland imaging • Lipid Layer thickness • >=60 thickness highly indicative of Meibomian gland dysfunction • Non-invasive TBUT • Corneal topography • Surface irregularity indicative of dry eye disease • Sjogren’s antibody testing Clinical Examination • Performed on all patients – (+) or (-) screening • Goal to determine type, severity and visual significance of dry eye Clinical Examination • Look: • Lagophthalmos, proptosis • Lid abnormalities (i.e., entropion, trichiasis) • Anterior/posterior blepharitis (i.e., scurf, collarettes, foamy tears, demodex, capped mg, lid telangiectasia) • Palpebral conjunctiva (i.e., injection, follicles, conjunctivochalasis, pterygium) • Cornea (i.e., filaments, ebmd, prominent punctate keratitis) LOOK Don’t forget to watch the patient blink! Clinical Examination • LIFT AND PULL: • Examine superior cornea (superior limbic keratitis) • Lid laxity (Floppy eyelid syndrome) https://www.reviewofopto metry.co m/article/get-taut-on-floppy-eyelid-syndrome PUSH STAIN Evaluate for Lid Wiper Epitheliopathy Dry Eye Management Step 1: Modification Systemic and Lid Patient Dietary Topical of local topical hygiene/warm Education modification lubricants environment medications? compresses EDUCATION • Systemic associations • Chronicity • Iatrogenic causes • Surgery • Set expectations • Contact Lens Wear • Cosmetic Makeup • Humidifiers • Preservatives in other topical medications Risk factors (Modified from DEWS II) CONSISTENT ASSOCIATION SUGGESTIVE ASSOCIATION POSSIBLE ASSOCIATION Aging Diabetes Hispanic ethnicity Female sex Rosacea Menopause Asian race Viral infection Acne Non-modifiable Meibomian gland dysfunction Thyroid disease Sarcoidosis Connective tissue diseases Psychiatric conditions Sjögren Syndrome Pterygium Androgen deficiency Low fatty acids intake Smoking Computer use Refractive surgery Alcohol Contact lens wear Allergic conjunctivitis Pregnancy Hormone replacement therapy Demodex infestation Modifiable Hematopoietic stem cell transplantation Botulinum toxin injection Environment: pollution, low humidity, sick building syndrome Medications: antihistamines, antidepressants, anxiolytics, Medications: anticholinergic, diuretics, beta- Medications: multivitamins, oral isotretinoin blockers contraceptives Category Subcategory Drugs Antirheumatic Aspirin, Ibuprofen Analgesic Cannabinoid Dronabinol, Tetrahydrocannabinol Opioid Buprenorphine, Fentanyl, Methadone, Morphine, Opium, Oxymorphone, Tapentadol Anesthesia Ether, Nitrous Oxide Antiarrythmic/Bronchodilating Atropine, Diphenhydramine, Disopyramide, Homatropine, Ipratropium, Methscopolamine, Scopolamine, Tiotropium, Tolterodine Azelastine, Brompheniramine, Carbinoxamine, Cetirizine, Chlorpheniramine, Clemastine, Cyproheptadine, Desloratidine, Dexchlorphenamine, Diphenhydramine, Doxylamine, Epinastine, Fexofenadine, Hydroxyzine, Ketotifen, Loratidine, Olopatadine, Antihistamine Promethazine, Pseudoephedrine, Tripelennamine, Triprolidine Agomelatine, Amitriptyline, Bupropion, Chlomipramine, Cialopram, Desipramine, Doxepin, Duloxetine, Fluoxetine, Fluvoxamine, Anticholinergic (antimuscarinic) Antidepressant Imipramine, Mianserine, Mirtazapine, Nortripty, Paroxetine, Reboxetine, Sertraline, Tianeptine, Trazodone, Venlafexine Anti-Parkinson's Benapryzine, Benzhexol, Benztropine, Bornaprine, Levodopa, Methixine, Orphenadrine, Pamipexole, Procyclidine Aiprasidone, Aripiprazole, Brompheniramine, Carbinoxamine, Chlorpheniramine, Chlorpromazine, Clemastine, Clozapine, Cyproheptadine, Dexchlorphiniramine, Fluphenazine, Haloperidol, Lithium carbonate, Olanzepine, Perphenazine, Promethazine, Antipsychotic Quetiapine, Risperidone, Sulpiride, Thiethylperazine, Thioridazine Thiothixene, Trifluoperazine Antispasmodic Fesoterodine, Homatropine, Oxybutynin, Propantheline, Propiverine, Solifenacin, Tolterodine, Trospium Decongestant Oxymetazoline, Phenylephrine, Phenylpropanolamine, Pseudoephedrine, Xylometazoline Drugs associated with dry eye (adapted from DEWS II) Drugs associated with dry eye (continued) Category Subcategory Drugs Antihypertensive Adrenergic blocking Acebutolol, Atenolol, Carvedilol, Labetalol, Metoprolol, Nadolol, Pindolol, Clonidine, Prazosin, Oxprenolol, Propranolol Na+Cl- Co-transporter (diuretic) Bendroflumethiazide, Chlorothiazide, Chlortalidone, Hydrochlorothiazide, Hydroflumethiazide, Indapamide, Methyclothiazide, Metolazone, Polythiazide, Trichlormethiazide Antileprosy Clofazimine Antimalarial Chloroquine, Hydrochloroquine Antineoplastic Busulfan, Cetuximab, Cyclophosphamide, Docetaxel, Erlotinib, Gefitinib, Interferon, Methotrexate, Mitomicin C, Panitumumab, Vinblastine, Vertiporphin Anxiolytic/hypnotic Alprazolam, Diazepam, Eszopiclone, Lorazepam, Zolpidem, Zopiclone Chelator/Calcium Regulator Methoxsalen, Alendronate, Pamidronate, Risedronate Depressant Ethanol Herbal and Vitamins Isotretinoin*, Niacin, Echinacea, Kava Hormonal Antiandrogen/Estrogen replacement Alfuzosin, Doxazosin, Finasteride, Leuprorelin, Tamsulosin, Terazosin, Estrogen/progesterone, Medroxyprogesterone Neurotoxin Botulinum A or B Sedative Primidone, Phenylbarbitol Lubricants LID HYGIENE Step 2: Prescription Tear drugs conservation Intense pulsed Restasis Preservative Tea tree oil Overnight Gland Xiidra • Punctal occlusion light therapy for free lubricants treatment treatment Expression Cequa • Moisture chamber MGD spectacles/goggles Topical Antibiotics Topical Steroids? Oral Antibiotics PRESERVATIVE FREE TEARS IN OFFICE - LID HYGIENE LID HYGIENE - DEMODEX Overnight treatment PUNCTAL OCCLUSION Oasis PLUS – 2-5 days Oasis PLUS Extended – 3 months DuraPlug – 6 months IN OFFICE MANUAL LID HYGIENE TREATMENT PRESCRIPTION TREATMENT Cequa (cyclosporin Restasis (cyclosporin Xiidra (lifitegrast 0.09% with NCELL 0.05%) 5%) technology) Keratoconjunctivitis Keratoconjunctivitis Indication Dry eye syndrome sicca sicca Blocks LFA-1/ICAM-1 Immunosuppressive; Immunosuppressive; interaction. reduce ocular reduce ocular Mechanism of Minimizing Tcell inflammation to inflammation to activation; Inhibits Action increase tear increase tear inflammatory production production cytokines Burning, dysgeusia, Burning blurry vision Burning Hyperemia, FB Headache, Hyperemia, FB Side Effects sensation, blurry increased sensation, blurry vision lacrimation, vision hyperemia Onset of Symptom 3 months 3-4 weeks 3-4 weeks Reduction Step 3: Therapeutic contact lens options Autologous/allogeneic • Soft bandage lenses Oral secretagogues serum eye drops • Rigid scleral lenses Oral secretagogues • Pilocarpine (salagen) 5mg four times daily AUTOLOGOUS TEARS Keratoconjunctivitis sicca, dry eye Donated blood is centrifuged to extract serum and diluted (20-100%) most common 20% ~$100 per month Step 4: Topical Other surgical Amniotic Surgical corticosteroid approaches membrane punctal for longer (tarsorrhaphy, grafts occlusion salivary gland duration transplantation) Step 4 Summary • Combining Using the ASCRS Protocol for Dry Eye Evaluation with the DEWSII staged treatment approach can provide a systematic approach to patient diagnosis and management • Comprehensive Dry Eye Management can improve refractive outcomes (glasses and contact), and surgical outcomes. Putting it all Together Tear Lab: 289/305 Inflammadry: negative OU Thank you! [email protected].
Recommended publications
  • 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]
  • Deficits in Cholinergic Neurotransmission and Their Clinical
    www.nature.com/npjparkd All rights reserved 2373-8057/16 REVIEW ARTICLE OPEN Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease Santiago Perez-Lloret1 and Francisco J Barrantes2 In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic, cholinergic and other monoaminergic neuronal populations. In this work, the characteristics of cholinergic deficits in PD and their clinical correlates are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions remit to cholinergic neurotransmission at the synaptic, pathway, and circuital levels. The bulk of evidence highlights the link between cholinergic alterations and PD motor symptoms, gait dysfunction, levodopa-induced dyskinesias, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction, and altered olfactory function. The pathophysiology of these symptoms is related to alteration of the cholinergic tone in the striatum and/or to degeneration of cholinergic nuclei, most importantly the nucleus basalis magnocellularis and the pedunculopontine nucleus. Several results suggest the clinical usefulness of antimuscarinic drugs for treating PD motor symptoms and of inhibitors of the enzyme acetylcholinesterase for the treatment of dementia. Data also suggest that these inhibitors and pedunculopontine nucleus deep-brain stimulation might also be effective in preventing falls. Finally, several drugs acting on nicotinic receptors have proved efficacious for treating levodopa-induced dyskinesias and cognitive impairment and as neuroprotective agents in PD animal models. Results in human patients are still lacking.
    [Show full text]
  • Fisiopatologia Dei Tremori
    FISIOPATOLOGIA DEI TREMORI Enrico Alfonsi Neurofisiopatologia IRCCS-Istituto Neurologico Nazionale «Casimiro Mondino» Pavia TREMOR A rhythmic involuntary movement of one or several regions of the body. It represents the most common neurological sign, as everyone has a ‘’physiological’’ tremor, which can only be measured with instrumental tools. 1 BACKGROUND Relation to Voluntary Movement Relation to Body Part Rest tremor Head tremor Parkinson’s disease Cerebellar disease Other parkinsonian syndromes Dystonia Tardive (drug-induced) parkinsonism Essential tremor (rarely when isolated) Vascular parkinsonism Chin tremor Hydrocephalus Parkinson’s disease Common Psychogenic (functional) tremor Hereditary geniospasm tremor Action tremor Jaw tremor disorders Postural tremor Parkinson’s disease classified Physiologic tremor and enhanced physiologic tremor Dystonia according Essential tremor Palatal tremor to two main Dystonic tremor Idiopathic (essential) criteria Parkinsonism Owing to brainstem lesions (secondary) Fragile X premutation (fragile X tremor–ataxia syndrome) Owing to degenerative disease (adult-onset Alexander’s disease) Neuropathies Arm tremor Tardive tremor Cerebellar disease Toxins (e.g., mercury) Dystonia Metabolic disorder (e.g., hyperthyroidism, hypoglycemia) Essential tremor Psychogenic (functional) tremor Parkinson’s disease Kinetic tremor Leg tremor Cerebellar disease Parkinson’s disease Holmes’ tremor Orthostatic tremor Wilson’s disease Psychogenic (functional) tremor 2 Essential tremor Features considered typical of the essential tremor syndrome Feature Description Tremor 4–12 Hz action tremor that occurs when patients voluntarily attempt • A resting tremor can appear only in advanced to maintain a steady posture stages. Other neurological signs (with the against gravity (postural tremor) or move (kinetic tremor) exception of cog-wheel phenomenon and Tremor may be suppressed by difficulties with tandem gait) are typically performing skilled manual tasks absent.
    [Show full text]
  • Partial Agreement in the Social and Public Health Field
    COUNCIL OF EUROPE COMMITTEE OF MINISTERS (PARTIAL AGREEMENT IN THE SOCIAL AND PUBLIC HEALTH FIELD) RESOLUTION AP (88) 2 ON THE CLASSIFICATION OF MEDICINES WHICH ARE OBTAINABLE ONLY ON MEDICAL PRESCRIPTION (Adopted by the Committee of Ministers on 22 September 1988 at the 419th meeting of the Ministers' Deputies, and superseding Resolution AP (82) 2) AND APPENDIX I Alphabetical list of medicines adopted by the Public Health Committee (Partial Agreement) updated to 1 July 1988 APPENDIX II Pharmaco-therapeutic classification of medicines appearing in the alphabetical list in Appendix I updated to 1 July 1988 RESOLUTION AP (88) 2 ON THE CLASSIFICATION OF MEDICINES WHICH ARE OBTAINABLE ONLY ON MEDICAL PRESCRIPTION (superseding Resolution AP (82) 2) (Adopted by the Committee of Ministers on 22 September 1988 at the 419th meeting of the Ministers' Deputies) The Representatives on the Committee of Ministers of Belgium, France, the Federal Republic of Germany, Italy, Luxembourg, the Netherlands and the United Kingdom of Great Britain and Northern Ireland, these states being parties to the Partial Agreement in the social and public health field, and the Representatives of Austria, Denmark, Ireland, Spain and Switzerland, states which have participated in the public health activities carried out within the above-mentioned Partial Agreement since 1 October 1974, 2 April 1968, 23 September 1969, 21 April 1988 and 5 May 1964, respectively, Considering that the aim of the Council of Europe is to achieve greater unity between its members and that this
    [Show full text]
  • National Ribat University Institute of Forensic Evidence Sciences
    National Ribat University Institute of Forensic Evidence Sciences Assessment of Trihexyphenidyl (kharsha) Knowledge and Abuse Among Students of one of Khartoum state Universities Bsc. Pharmacy,University of Science andTechnology (2005) A Thesis Submitted to National Ribat University for Partial Fulfillment of the Requirements for the Master Degree in Forensic Science Submitted By Hawari Salih AbdElrahman Supervised By Associate Prof. Ahmed AwadElgamel 2016 I Dedication I dedicate this work to my father who generously dedicated his life for us. To my dear mother that the secret of my success is her du'aa. To my wife and my beautiful children who are the joy of my life for their patience and support. To my friend Musaab for his support and endless help. HawariSalih I Acknowledgment I wish to record my thanks to all those who assisted me in the completion of this work either by support or consultation. I owe a great deal to my academic supervisor Dr.Ahmed AwadElgamel for the patience careful direction and never-ending support. II الملخ صِ بنزهكسول ِهيدروكلوريد ِ)تريهكسفينيديل(، ِيعتبراحد ِمضادات ِالكولين ِالقوية ِ ِوقد ِاكتسب ِاستخدام ِعلىِ نطاقِواسعِفيِعﻻجِمرضِالشللِالرعاشِوفيِالسيطرةِعلىِاﻵثارِالجانبيةِﻻدويةِالشللِالرعاش.ِعلىِ الرغمِمنِالتقاريرالتيِتحدثتِفيِوقتِمبكرِﻻفتةِاﻻنتباهِإلىِتاثيراتهِالنفسيةِوإمكانيةِادمانهِمنِالناحيةِ النظريةِعليِاﻻقل،ِحيثِانهِلمِيتمِاثباتهِسريرياِحتىِوقتِقريب،ِقدِلوحظِسوءِاستخدامِبنزهكسولِبوتيرةِ متزايدةِفيِالسنواتِاﻷخيرةِبينِالشبانِالساخطينِوالمحرومينِالمترددينِعلىِعياداتِالطبِالنفسي،ِوقدِ أفادوا ِأن ِاستخدامهم
    [Show full text]
  • Toxic, and Comatose-Fatal Blood-Plasma Concentrations (Mg/L) in Man
    Therapeutic (“normal”), toxic, and comatose-fatal blood-plasma concentrations (mg/L) in man Substance Blood-plasma concentration (mg/L) t½ (h) Ref. therapeutic (“normal”) toxic (from) comatose-fatal (from) Abacavir (ABC) 0.9-3.9308 appr. 1.5 [1,2] Acamprosate appr. 0.25-0.7231 1311 13-20232 [3], [4], [5] Acebutolol1 0.2-2 (0.5-1.26)1 15-20 3-11 [6], [7], [8] Acecainide see (N-Acetyl-) Procainamide Acecarbromal(um) 10-20 (sum) 25-30 Acemetacin see Indomet(h)acin Acenocoumarol 0.03-0.1197 0.1-0.15 3-11 [9], [3], [10], [11] Acetaldehyde 0-30 100-125 [10], [11] Acetaminophen see Paracetamol Acetazolamide (4-) 10-20267 25-30 2-6 (-13) [3], [12], [13], [14], [11] Acetohexamide 20-70 500 1.3 [15] Acetone (2-) 5-20 100-400; 20008 550 (6-)8-31 [11], [16], [17] Acetonitrile 0.77 32 [11] Acetyldigoxin 0.0005-0.00083 0.0025-0.003 0.005 40-70 [18], [19], [20], [21], [22], [23], [24], [25], [26], [27] 1 Substance Blood-plasma concentration (mg/L) t½ (h) Ref. therapeutic (“normal”) toxic (from) comatose-fatal (from) Acetylsalicylic acid (ASS, ASA) 20-2002 300-3502 (400-) 5002 3-202; 37 [28], [29], [30], [31], [32], [33], [34] Acitretin appr. 0.01-0.05112 2-46 [35], [36] Acrivastine -0.07 1-2 [8] Acyclovir 0.4-1.5203 2-583 [37], [3], [38], [39], [10] Adalimumab (TNF-antibody) appr. 5-9 146 [40] Adipiodone(-meglumine) 850-1200 0.5 [41] Äthanol see Ethanol -139 Agomelatine 0.007-0.3310 0.6311 1-2 [4] Ajmaline (0.1-) 0.53-2.21 (?) 5.58 1.3-1.6, 5-6 [3], [42] Albendazole 0.5-1.592 8-992 [43], [44], [45], [46] Albuterol see Salbutamol Alcuronium 0.3-3353 3.3±1.3 [47] Aldrin -0.0015 0.0035 50-1676 (as dieldrin) [11], [48] Alendronate (Alendronic acid) < 0.005322 -6 [49], [50], [51] Alfentanil 0.03-0.64 0.6-2.396 [52], [53], [54], [55] Alfuzosine 0.003-0.06 3-9 [8] 2 Substance Blood-plasma concentration (mg/L) t½ (h) Ref.
    [Show full text]
  • Successful Treatment of Tardive Oculogyric Crisis with Bornaprine
    Isr J Psychiatry - Vol. 56 - No 3 (2019) Şengül KOCamer ŞAHIN ET AL. Successful Treatment of Tardive Oculogyric Crisis with Bornaprine Şengül Kocamer Şahin, MD,1 Ayşegül Şahin Ekici, MD,1 Gulcin Elboga, MD,1 Abdurrahman Altindag, MD,1 and Atil Bisgin, MD2 1 Department of Psychiatry, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey 2 Adana Genetics Diseases Diagnosis and Treatment Center and Medical Genetics Department of the Medical Faculty, Cukurova University, Adana, Turkey The presentation is a specific dystonic reaction. Recurrent ABSTRACT oculogyric crisis is different from the acute adverse drug event (4). It has been variously considered to be a form Tardive oculogyric crisis is one of the tardive syndromes of tardive dyskinesia (4). characterized by a spasmodic deviation of eyes typically Antipsychotic discontinuation is still the primary turning upwards after long-term use of high-potency suggestion regarding the management of tardive syn- typical or rarely atypical antipsychotics. Antipsychotic dromes, although no definitive evidence is supported. discontinuation is suggested as a treatment option with If this is not possible, changing to an antipsychotic with changing to an antipsychotic with a lower tardive dystonia a lower tardive dystonia (TDt) risk is the next option risk. Anticholinergic drugs such as trihexyphenidyl may (5). Antidyskinetic agents may be added to treatment also improve the symptoms of tardive dystonia, but these in patients whose symptoms persist despite drug regula- drugs may trigger or aggravate tardive dyskinesia. We tion. Antioxidants that reduce free oxygen radicals such report on a case with tardive syndromes and treatment as Ginkgo biloba, vitamin E, vitamin B6, clonazepam, challenge.
    [Show full text]
  • Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DIX to the HTSUS—Continued
    20558 Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DEPARMENT OF THE TREASURY Services, U.S. Customs Service, 1301 TABLE 1.ÐPHARMACEUTICAL APPEN- Constitution Avenue NW, Washington, DIX TO THE HTSUSÐContinued Customs Service D.C. 20229 at (202) 927±1060. CAS No. Pharmaceutical [T.D. 95±33] Dated: April 14, 1995. 52±78±8 ..................... NORETHANDROLONE. A. W. Tennant, 52±86±8 ..................... HALOPERIDOL. Pharmaceutical Tables 1 and 3 of the Director, Office of Laboratories and Scientific 52±88±0 ..................... ATROPINE METHONITRATE. HTSUS 52±90±4 ..................... CYSTEINE. Services. 53±03±2 ..................... PREDNISONE. 53±06±5 ..................... CORTISONE. AGENCY: Customs Service, Department TABLE 1.ÐPHARMACEUTICAL 53±10±1 ..................... HYDROXYDIONE SODIUM SUCCI- of the Treasury. NATE. APPENDIX TO THE HTSUS 53±16±7 ..................... ESTRONE. ACTION: Listing of the products found in 53±18±9 ..................... BIETASERPINE. Table 1 and Table 3 of the CAS No. Pharmaceutical 53±19±0 ..................... MITOTANE. 53±31±6 ..................... MEDIBAZINE. Pharmaceutical Appendix to the N/A ............................. ACTAGARDIN. 53±33±8 ..................... PARAMETHASONE. Harmonized Tariff Schedule of the N/A ............................. ARDACIN. 53±34±9 ..................... FLUPREDNISOLONE. N/A ............................. BICIROMAB. 53±39±4 ..................... OXANDROLONE. United States of America in Chemical N/A ............................. CELUCLORAL. 53±43±0
    [Show full text]
  • PHARMACEUTICAL APPENDIX to the HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2008) (Rev
    Harmonized Tariff Schedule of the United States (2008) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2008) (Rev. 2) 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. ABACAVIR 136470-78-5 ACIDUM GADOCOLETICUM 280776-87-6 ABAFUNGIN 129639-79-8 ACIDUM LIDADRONICUM 63132-38-7 ABAMECTIN 65195-55-3 ACIDUM SALCAPROZICUM 183990-46-7 ABANOQUIL 90402-40-7 ACIDUM SALCLOBUZICUM 387825-03-8 ABAPERIDONUM 183849-43-6 ACIFRAN 72420-38-3 ABARELIX 183552-38-7 ACIPIMOX 51037-30-0 ABATACEPTUM 332348-12-6 ACITAZANOLAST 114607-46-4 ABCIXIMAB 143653-53-6 ACITEMATE 101197-99-3 ABECARNIL 111841-85-1 ACITRETIN 55079-83-9 ABETIMUSUM 167362-48-3 ACIVICIN 42228-92-2 ABIRATERONE 154229-19-3 ACLANTATE 39633-62-0 ABITESARTAN 137882-98-5 ACLARUBICIN 57576-44-0 ABLUKAST 96566-25-5 ACLATONIUM NAPADISILATE 55077-30-0 ABRINEURINUM 178535-93-8 ACODAZOLE 79152-85-5 ABUNIDAZOLE 91017-58-2 ACOLBIFENUM 182167-02-8 ACADESINE 2627-69-2 ACONIAZIDE 13410-86-1 ACAMPROSATE
    [Show full text]
  • Emulated Clinical Trials from Longitudinal Real-World
    Supplemental Material for “Emulated Clinical Trials from Longitudinal Real-World Data Efficiently Identify Candidates for Neurological Disease Modification: Examples from Parkinson's Disease” Table S1. ICD codes for PD cohort definition Type System Code Name icd9 3320 Paralysis agitans Inclusion icd10 G20 Parkinson's disease icd9 3316 Corticobasal degeneration icd9 3321 Secondary parkinsonism icd9 3330 Other degenerative diseases of the basal ganglia Exclusion icd10 G21 Secondary parkinsonism Progressive supranuclear ophthalmoplegia [Steele- icd10 G231 Richardson-Olszewski] icd10 G3185 Corticobasal degeneration Table S2. PD-indicated drugs and their corresponding ATC class names. The list below has been compiled by a domain expert based on the following sources: National Drug File – Reference Terminology (NDF-RT), Anatomical Therapeutic Chemical Classification System (ATC), and DrugBank (45). Drug ATC class code(s) ATC class name(s) Amantadine N04BB Adamantane derivatives Drugs used in erectile dysfunction; dopamine Apomorphine G04BE; N04BC agonists Belladonna alkaloids, tertiary amines; Atropine A03BA; S01FA anticholinergics Benztropine N04AC Ethers of tropine or tropine derivatives Biperiden N04AA Tertiary amines Bornaprine N04AA Tertiary amines Bromocriptine G02CB; N04BC Prolactine inhibitors; dopamine agonists Budipine N04BX Other dopaminergic agents Cabergoline G02CB; N04BC Prolactine inhibitors; dopamine agonists Carbidopa N/A N/A Dexetimide N04AA Tertiary amines Dihydroergocryptine N04BC Dopamine agonists Entacapone N04BX Other
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 8,980,308 B2 Horstmann Et Al
    (12) United States Patent (10) Patent No.: US 8,980,308 B2 Horstmann et al. (45) Date of Patent: Mar. 17, 2015 (54) TRANSDERMAL PHARMACEUTICAL 5,877,173 A * 3/1999 Olney et al. ................... 514,217 PREPARATION CONTAINING ACTIVE 5,902,601 A 5/1999 Horstmann 6,193.992 B1* 2/2001 El-Rashidy et al. .......... 424/430 SUBSTANCE COMBINATIONS, FOR 2003, OO82214 A1 5, 2003 Williams TREATING PARKINSONS DISEASE 2003/01 19884 A1 6/2003 Epstein et al. 2004/OO13620 A1* 1/2004 Klose et al. ..................... 424,59 (75) Inventors: Michael Horstmann, Neuwied (DE); 2007/0225.379 A1* 9/2007 Carrara et al. ................ 514,756 Frank Theobald, Bad Breisig (DE) FOREIGN PATENT DOCUMENTS (73) Assignee: LTS Lohmann Therapie-Systeme AG, CA 2 383 509 3, 2001 Andernach (DE) DE 3710966 12/1987 EP O241809 B1 8, 1990 (*) Notice: Subject to any disclaimer, the term of this EP B-04O4807 6, 1993 patent is extended or adjusted under 35 EP 1254 661 11, 2002 EP A-1 256339 10, 2003 U.S.C. 154(b) by 1785 days. FR 2788.982 8, 2000 JP S611451 12 T 1986 (21) Appl. No.: 10/568,941 JP S61186.317 8, 1986 JP A S62-249923 10, 1987 (22) PCT Filed: Aug. 14, 2004 JP A HO2-503677 11, 1990 JP AH11-506744 6, 1999 PCT/EP2004/OO9136 JP H11506462 6, 1999 (86). PCT No.: JP AH11-209271 8, 1999 JP A 2000-514053 10, 2000 S371 (c)(1), JP A 2001-398.65 2, 2001 (2), (4) Date: Feb. 21, 2006 JP 2001518058 10, 2001 JP A 2002-97137 4/2002 (87) PCT Pub.
    [Show full text]
  • Management of Parkinson's Disease: an Evidence-Based Review
    Movement Disorders Vol. 17, Suppl. 4, 2002, p. i 2002 Movement Disorder Society Published by Wiley-Liss, Inc. DOI 10.1002/mds.5554 Editorial Management of Parkinson’s Disease: An Evidence-Based Review* Although Parkinson’s disease is still incurable, a large number tomatic control of Parkinson’s disease; prevention of motor com- of different treatments have become available to improve quality plications; control of motor complications; and control of non- of life and physical and psychological morbidity. Numerous jour- motor features. Based on a systematic review of the data, efficacy nal supplements have appeared in recent years highlighting one conclusions are provided. On the basis of a narrative non-system- or more of these and disparate treatment algorithms have prolifer- atic approach, statements on safety of the interventions are given ated. Although these are often quite useful, this “mentor analy- and finally, a qualitative approach is used to summarize the impli- sis” approach lacks the scientific rigor required by modern evi- cations for clinical practice and future research. dence-based medicine standards. The Movement Disorder Soci- This mammoth task has taken two years to complete and the ety, with generous but unrestricted support from representatives task force members, principal authors and contributors are to be of industry, have, therefore, commissioned a systematic review congratulated for their outstanding work. Physicians, the of the literature dealing with the efficacy and safety of available Parkinson’s disease research community and most of all patients treatments. The accompanying treatise is the result of a scrupu- themselves should welcome and embrace the salient findings of lous evaluation of the literature aimed at identifying those treat- this report as an effort to improve clinical practice.
    [Show full text]