DOCSLIB.ORG

The Effect of Colestipol on Glycemic Control in Patients with Type 2 Diabetes

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Effect of Colestipol on Glycemic Control in Patients with Type 2 Diabetes The Effect of Colestipol on Glycemic Control in Patients With Type 2 Diabetes Elizabeth A. Sauter, PharmD; Sindhu Abraham, PharmD, BCPS; Tania G. John, PharmD; Seema Kapadia, PharmD, BCACP; and Judith A. Toth, PharmD, CGP, CDE Using an electronic chart review, the authors investigated the effect of colestipol, a bile acid sequestrant, on glycemic control in patients with type 2 diabetes. iabetes mellitus is a complex cations. In general, every percentage group and the placebo group of disease, characterized by hy- point drop in glycosylated hemoglo- − 0.5% (P = .007). Additionally, in perglycemia, and can be as- bin (A1C) can reduce the risk of mi- participants with a baseline A1C ≥ sociated with abnormalities crovascular complications (ie, eye, 8%, the difference in mean change in D 2 in fat, carbohydrates, and protein kidney, and nerve diseases) by 40%. A1C was − 1.0% (P = .002). Treat- metabolism that result from defects Improved control of LDL-C can re- ment with colesevelam was also in insulin secretion, insulin action, duce cardiovascular complications by associated with a reduction in post- or both. Type 2 diabetes is the most 20% to 50%.2 Current American Dia- prandial glucose (− 31.5 mg/dL, common form of diabetes in the betes Association (ADA) guidelines P = .026) and LDL-C (− 11.7%, United States, accounting for as many recommend an A1C of < 7% and an P = .007). The study authors con- as 90% to 95% of all cases.1 As of LDL-C < 100 mg/dL in patients with cluded that colesevelam may improve 2011, 25.8 million patients were di- diabetes.4 However, to achieve these both glycemic and lipid control in agnosed with diabetes, or 8.3% of the goals, patients with diabetes often patients with type 2 diabetes.5 Fol- U.S. population.2 Type 2 diabetes is need to use multiple medications.1,2 lowing the publication of this trial, more common in African Americans, As a result, recent attention has colesevelam received an FDA indica- Mexican Americans, Native Ameri- shifted to the use of single agents tion as an adjunctive treatment in pa- cans, Asian Americans, Native Ha- with both glucose and lipid-lowering tients with type 2 diabetes, in addition waiians, and other Pacific Islanders, effects. One such class of agents is the to its prior indication for hypercholes- as well as the elderly population.1,3 bile acid sequestrants. To date, both terolemia. Type 2 diabetes is characterized by colesevelam hydrochloride and cho- Another similar trial evaluated the insulin resistance and a relative lack lestyramine have demonstrated A1C use of cholestyramine for dyslipid- of insulin secretion. Insulin is neces- and glucose-lowering effects in clini- emia in patients with type 2 diabetes. sary for the breakdown of sugars and cal trials. The study researchers also examined carbohydrates in the body and plays The Glucose Lowering Effect the effect of cholestyramine on glu- a vital role in the uptake of glucose of Welchol Study (GLOWS) evalu- cose levels as a secondary endpoint. into cells for energy.1 ated the A1C lowering effect of co- This study was a randomized, dou- Uncontrolled diabetes is associ- lesevelam hydrochloride in subjects ble-blind, crossover study of 21 par- ated with numerous complications, with type 2 diabetes who were inad- ticipants receiving cholestyramine including blindness, kidney damage, equately controlled by oral antihyper- 8 g bid vs a placebo for 6 weeks heart disease, and lower-limb am- glycemic agents alone. Participants each. Study participants had type 2 putations. In patients with diabetes, were on a stable dose of metformin diabetes that was well controlled for optimal control of glucose and low- or a sulfonylurea for ≥ 90 days before at least 1 month prior to the initia- density lipoprotein cholesterol (LDL- the initiation of colesevelam. Sixty- tion of cholestyramine, using either C) has been shown to delay or even five study participants who had an insulin or glyburide therapy, and an prevent the development of compli- A1C of 7% to 10% were random- LDL-C of > 130 mg/dL. Addition- ized to receive either colesevelam ally, patients were on a stable dose of 3.75 g/d or placebo for 12 weeks. insulin or glyburide throughout the Dr. Sauter, Dr. Abraham, Dr. John, Dr. Kapadia, After 12 weeks, results demon- duration of the study. After 12 weeks, and Dr. Toth are all clinical pharmacy specialists in the Department of Pharmacy with the Jesse strated a difference in mean change results demonstrated that treatment Brown VA Medical Center in Chicago, Illinois. in A1C between the colesevelam with cholestyramine reduced total MAY 2012 • FEDERAL PRACTITIONER • 23 GLYCEMIC CONTROL Table 1. Data collected using the electronic chart Demographic Age information Gender Race Baseline information A1C (within the 6 months Lipids (LDL-C, TGs, HDL-C) prior to initiation of LFTs (within normal limits [WNL] vs elevated) colestipol) After initiation of A1C (at least 3 months after starting colestipol) colestipol Lipids (LDL-C, TGs, HDL-C) (at least 4 weeks after starting colestipol) LFTs (WNL vs elevated) Any subsequent values for the above parameters following dose titration of colestipol for up to 6 months Adverse effects Medication intolerance as documented in the progress notes Medication Colestipol information • Initial dose • Maximum tolerated dose • Date of initiation • Date of discontinuation (if applicable) Concomitant oral antihyperglycemic medications (including sulfonylureas, biguanides, insulin, thiazolidinediones, α-glucosidase inhibitors, meglitinides, dipeptidyl pepti- dase-4 inhibitors, glucagon-like peptide-1 agonists, and dopamine agonists) • Dose when colestipol was started • Dosage changes since colestipol was started • Date of initiation • Date of discontinuation (if applicable) Concomitant lipid-lowering medications (including HMG-CoA reductase inhibitors, nicotinic acid, intestinal absorption inhibitors, fish oil, and fibric acid derivatives) • Dose when colestipol was started • Dosage changes since colestipol was started • Date of initiation • Date of discontinuation (if applicable) Medication Determined by the refill history in the electronic medical record and documentation compliance of nonadherence in the progress notes Patient education Counseling regarding the proper administration of colestipol in relation to other medications to minimize any possible interference with absorption (take other medications at least 1 hour before or 4 hours after colestipol) as documented in the progress notes or stated on the medication label cholesterol by 18% and LDL-C by that cholestyramine therapy effec- monotherapy, which does not com- 28%, when compared with placebo. tively reduced LDL-C and may also ply with the current clinical approach In addition, cholestyramine therapy improve glycemic control in patients in the United States of using bile acid improved glycemic control. Mean with diabetes.6 sequestrants as adjunctive therapy in plasma glucose levels decreased by It is important to note that there patients with diabetes. In other coun- 13%; a mean reduction in urinary glu- is 1 additional agent in this class of tries, colestilan has been proven effec- cose excretion of 0.22 g/d was noted, medications: Colestilan. However, this tive in reducing both A1C and fasting as well as a decrease in A1C values of agent is not approved in the United plasma glucose in patients with type 2 0.5%. The study authors concluded States and has been evaluated only as diabetes.7 Continued on page 27 24 • FEDERAL PRACTITIONER • MAY 2012 GLYCEMIC CONTROL Continued from page 24 Patient charts reviewed (239) Excluded Included (189) (50) Non- < 3 months No type 2 Antihyperglycemic No A1C adherence therapy diabetes changes (42) (8) (13) (30) (96) Figure 1. Study design. In general, bile acid sequestrants tory action increases LDL-C clearance demonstrated beneficial effects on act by binding bile acids, forming a from the blood, resulting in lowered both LDL-C and A1C in patients with complex that is then excreted in the LDL-C levels.8,9 type 2 diabetes, the specific effect of feces, thus preventing reabsorption The mechanism by which bile acid colestipol on glycemic control has yet in the intestines. This action also re- sequestrants exert their glycemic ef- to be evaluated. Currently, colestipol sults in partial removal of bile acids fects is not fully understood. One is FDA approved for the treatment of from the enterohepatic circulation, proposed mechanism is that bile acid primary hypercholesterolemia, and which prevents its reabsorption. This sequestrants cause a reduction in glu- it is the bile acid sequestrant that is leads to the depletion of serum bile cose absorption or a change in the currently on the formulary at Jesse acids, which activates cholesterol time course of glucose absorption in Brown VAMC. 7 alpha-hydroxylase to convert cho- the gastrointestinal tract. Another the- lesterol into bile acids. Consequently, ory is that by interrupting the entero- METHODS a demand for cholesterol in the liver hepatic pathway of bile metabolism, The purpose of this study was to is increased, resulting in increased bile acid sequestrants deactivate the evaluate the effect of colestipol on 3-hydroxy-3-methyl-glutaryl-CoA farnesoid X receptor. This receptor is glycemic control in patients with (HMG-CoA) reductase transcription a bile acid-activated nuclear receptor type 2 diabetes in a veteran popula- and activity, and an increased num- that plays a significant role in the me- tion. This study was an Institutional ber of LDL-C receptors.
Load more

Recommended publications
  • Lipid Lowering Drugs and Inflammatory Changes: an Impact on Cardiovascular Outcomes?
    Annals of Medicine ISSN: 0785-3890 (Print) 1365-2060 (Online) Journal homepage: http://www.tandfonline.com/loi/iann20 Lipid Lowering Drugs and Inflammatory Changes: an Impact on Cardiovascular Outcomes? M. Ruscica, N. Ferri, C. Macchi, A. Corsini & C. R. Sirtori To cite this article: M. Ruscica, N. Ferri, C. Macchi, A. Corsini & C. R. Sirtori (2018): Lipid Lowering Drugs and Inflammatory Changes: an Impact on Cardiovascular Outcomes?, Annals of Medicine, DOI: 10.1080/07853890.2018.1498118 To link to this article: https://doi.org/10.1080/07853890.2018.1498118 Accepted author version posted online: 06 Jul 2018. Submit your article to this journal View Crossmark data Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iann20 LIPID LOWERING DRUGS AND INFLAMMATORY CHANGES: AN IMPACT ON CARDIOVASCULAR OUTCOMES? M. Ruscica1*, N. Ferri2*, C. Macchi1, A. Corsini1 and C. R. Sirtori3 1Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy; 2Dipartimento di Scienze del Farmaco, Università degli Studi di Padova, Padova, Italy; 3Centro Dislipidemie, A.S.S.T. Grande Ospedale Metropolitano Niguarda, Milan, Italy *Both authors contributed equally to this work Corresponding Author: Cesare R. Sirtori [email protected] Abstract Inflammatory changes are responsible for maintenance of the atherosclerotic process and may underlie some of the most feared vascular complications. Among the multiple mechanisms of inflammation, the arterial deposition of lipids and particularly of cholesterol crystals is the one responsible for activation of inflammasome NLRP3, followed by the rise of circulating markers, mainly C-reactive protein (CRP). Elevation of lipoproteins, LDL but also VLDL and remnants, associates with increased inflammatory changes and coronary risk.
    [Show full text]
  • Pharmacy Prior Authorization Non-Formulary and Prior
    Pharmacy Prior Authorization Non-Formulary and Prior Authorization Guidelines Scroll down to see PA Criteria by drug class, or Ctrl+F to search document by drug name PA Guideline Requirements Duration of Approval if Requirements Are Met Non-Formulary Requests for Non-Formulary Medications that do not have specific Prior Authorization Initial Approval: Medication Guidelines will be reviewed based on the following: • Minimum of 3 months, Guideline • An appropriate diagnosis/indication for the requested medication, depending on the • An appropriate dose of medication based on age and indication, diagnosis, to determine • Documented trial of 2 formulary agents for an adequate duration have not been effective or adherence, efficacy and tolerated patient safety monitoring OR • All other formulary medications are contraindicated based on the patient’s diagnosis, other Renewal: medical conditions or other medication therapy, • Minimum of 6 months OR • Maintenance medications • There are no other medications available on the formulary to treat the patient’s condition may be approved Indefinite Maryland Physicians Care determines patient medication trials and adherence by a review of pharmacy claims data over the preceding twelve months. Additional information may be requested on a case-by-case basis to allow for proper review. Medications Requests for Medications requiring Prior Authorization (PA) will be reviewed based on the PA As documented in the requiring Prior Guidelines/Criteria for that medication. Scroll down to view the PA Guidelines for specific individual guideline Authorization medications. Medications that do not have a specific PA guideline will follow the Non-Formulary Medication Guideline. Additional information may be required on a case-by-case basis to allow for adequate review.
    [Show full text]
  • Role of Bile Acids in the Regulation of Food Intake, and Their Dysregulation in Metabolic Disease
    nutrients Review Role of Bile Acids in the Regulation of Food Intake, and Their Dysregulation in Metabolic Disease Cong Xie 1,† , Weikun Huang 1,2,† , Richard L. Young 1,3 , Karen L. Jones 1,4 , Michael Horowitz 1,4, Christopher K. Rayner 1,5 and Tongzhi Wu 1,4,6,* 1 Adelaide Medical School, Center of Research Excellence (CRE) in Translating Nutritional Science to Good Health, The University of Adelaide, Adelaide 5005, Australia; [email protected] (C.X.); [email protected] (W.H.); [email protected] (R.L.Y.); [email protected] (K.L.J.); [email protected] (M.H.); [email protected] (C.K.R.) 2 The ARC Center of Excellence for Nanoscale BioPhotonics, Institute for Photonics and Advanced Sensing, School of Physical Sciences, The University of Adelaide, Adelaide 5005, Australia 3 Nutrition, Diabetes & Gut Health, Lifelong Health Theme South Australian Health & Medical Research Institute, Adelaide 5005, Australia 4 Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5005, Australia 5 Department of Gastroenterology and Hepatology, Royal Adelaide Hospital, Adelaide 5005, Australia 6 Institute of Diabetes, School of Medicine, Southeast University, Nanjing 210009, China * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: Bile acids are cholesterol-derived metabolites with a well-established role in the digestion and absorption of dietary fat. More recently, the discovery of bile acids as natural ligands for the nuclear farnesoid X receptor (FXR) and membrane Takeda G-protein-coupled receptor 5 (TGR5), and Citation: Xie, C.; Huang, W.; Young, the recognition of the effects of FXR and TGR5 signaling have led to a paradigm shift in knowledge R.L.; Jones, K.L.; Horowitz, M.; regarding bile acid physiology and metabolic health.
    [Show full text]
  • )&F1y3x PHARMACEUTICAL APPENDIX to THE
    )&f1y3X PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE )&f1y3X PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 3 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. Product CAS No. Product CAS No. ABAMECTIN 65195-55-3 ACTODIGIN 36983-69-4 ABANOQUIL 90402-40-7 ADAFENOXATE 82168-26-1 ABCIXIMAB 143653-53-6 ADAMEXINE 54785-02-3 ABECARNIL 111841-85-1 ADAPALENE 106685-40-9 ABITESARTAN 137882-98-5 ADAPROLOL 101479-70-3 ABLUKAST 96566-25-5 ADATANSERIN 127266-56-2 ABUNIDAZOLE 91017-58-2 ADEFOVIR 106941-25-7 ACADESINE 2627-69-2 ADELMIDROL 1675-66-7 ACAMPROSATE 77337-76-9 ADEMETIONINE 17176-17-9 ACAPRAZINE 55485-20-6 ADENOSINE PHOSPHATE 61-19-8 ACARBOSE 56180-94-0 ADIBENDAN 100510-33-6 ACEBROCHOL 514-50-1 ADICILLIN 525-94-0 ACEBURIC ACID 26976-72-7 ADIMOLOL 78459-19-5 ACEBUTOLOL 37517-30-9 ADINAZOLAM 37115-32-5 ACECAINIDE 32795-44-1 ADIPHENINE 64-95-9 ACECARBROMAL 77-66-7 ADIPIODONE 606-17-7 ACECLIDINE 827-61-2 ADITEREN 56066-19-4 ACECLOFENAC 89796-99-6 ADITOPRIM 56066-63-8 ACEDAPSONE 77-46-3 ADOSOPINE 88124-26-9 ACEDIASULFONE SODIUM 127-60-6 ADOZELESIN 110314-48-2 ACEDOBEN 556-08-1 ADRAFINIL 63547-13-7 ACEFLURANOL 80595-73-9 ADRENALONE
    [Show full text]
  • Pharmacological Agents Currently in Clinical Trials for Disorders in Neurogastroenterology
    Pharmacological agents currently in clinical trials for disorders in neurogastroenterology Michael Camilleri J Clin Invest. 2013;123(10):4111-4120. https://doi.org/10.1172/JCI70837. Clinical Review Esophageal, gastrointestinal, and colonic diseases resulting from disorders of the motor and sensory functions represent almost half the patients presenting to gastroenterologists. There have been significant advances in understanding the mechanisms of these disorders, through basic and translational research, and in targeting the receptors or mediators involved, through clinical trials involving biomarkers and patient responses. These advances have led to relief of patients’ symptoms and improved quality of life, although there are still significant unmet needs. This article reviews the pipeline of medications in development for esophageal sensorimotor disorders, gastroparesis, chronic diarrhea, chronic constipation (including opioid-induced constipation), and visceral pain. Find the latest version: https://jci.me/70837/pdf Review Pharmacological agents currently in clinical trials for disorders in neurogastroenterology Michael Camilleri Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER), Mayo Clinic, Rochester, Minnesota, USA. Esophageal, gastrointestinal, and colonic diseases resulting from disorders of the motor and sensory functions represent almost half the patients presenting to gastroenterologists. There have been significant advances in under- standing the mechanisms of these disorders, through basic and translational research, and in targeting the recep- tors or mediators involved, through clinical trials involving biomarkers and patient responses. These advances have led to relief of patients’ symptoms and improved quality of life, although there are still significant unmet needs. This article reviews the pipeline of medications in development for esophageal sensorimotor disorders, gastropa- resis, chronic diarrhea, chronic constipation (including opioid-induced constipation), and visceral pain.
    [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]
  • Does Your Patient Have Bile Acid Malabsorption?
    NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment.
    [Show full text]
  • Drugs That Require Prior Authorization
    Drugs That Require Prior Authorization (PA) Before Being Approved for Coverage You will need authorization by your HMSA Akamai Advantage (PPO) plan before filling prescriptions for the drugs shown in the chart below. The HMSA Akamai Advantage plan will only provide coverage after it determines that the drug is being prescribed according to the criteria specified in the chart. You, your appointed representative, or your prescriber can request prior authorization by calling HMSA at 1 (855) 479-3659, 24 hours a day, 7 days a week. Customer service is available in English and other languages. TTY/TDD users should call 711. PA Criteria Prior Authorization Group ACITRETIN Drug Names ACITRETIN, SORIATANE Covered Uses All FDA-approved indications not otherwise excluded from Part D, prevention of non-melanoma skin cancers in high risk individuals. Exclusion Criteria Required Medical Information Age Restrictions Prescriber Restrictions Coverage Duration Plan Year Other Criteria Prior Authorization Group ACTEMRA Drug Names ACTEMRA Covered Uses All FDA-approved indications not otherwise excluded from Part D, unicentric Castleman's disease, multicentric Castleman's disease. Exclusion Criteria Required Medical Information For moderately to severely active rheumatoid arthritis (new starts only): Inadequate response, intolerance or contraindication to a self-injectable tumor necrosis factor (TNF) inhibitor (e.g., adalimumab) or a targeted synthetic disease-modifying antirheumatic drug (DMARD) (e.g., tofacitinib). For active polyarticular juvenile idiopathic arthritis (new starts only): Inadequate response, intolerance or contraindication to a TNF inhibitor (e.g., adalimumab). For active systemic juvenile idiopathic arthritis (new starts only): Inadequate response to a corticosteroid monotherapy, methotrexate or leflunomide. Age Restrictions Prescriber Restrictions Coverage Duration Plan Year Other Criteria Prior Authorization Group ACTHAR HP Drug Names H.P.
    [Show full text]
  • Major Products
    Data Section Major Products Innovative Pharmaceuticals Business Innovative Pharmaceuticals Business Brand Name (Generic Name) Efficacy Launched Remarks Brand Name (Generic Name) Efficacy Launched Remarks Japan [Daiichi Sankyo Co., Ltd.] US [Daiichi Sankyo Inc.] A first combination drug of the DPP-4 inhibitor teneligliptin and the SGLT2 inhibitor Opioid-induced First once-daily oral product approved by the FDA for the treatment of opioid-induced (teneligliptin / Type 2 diabetes mellitus MOVANTIK (naloxegol) 2015 CANALIA 2017 canagliflozin approved in Japan, which demonstrates blood glucose-lowering activity constipation treatment constipation (OIC) for adults with chronic non-cancer pain. canagliflozin) treatment through a complementary pharmacological effect. Orally active Factor Xa inhibitor. It is an anticoagulant that specifically, reversibly and directly inhibits the enzyme, Factor Xa, a clotting factor in the blood. Approved for indications to Sodium channel blocker. Suppresses the excessive excitation of nerves in the brain, and VIMPAT (lacosamide) Anti-epileptic agent 2016 SAVAYSA (edoxaban) Anticoagulant 2015 reduce the risk of stroke and systemic embolism (SE) in patients with non-valvular atrial reduces the occurrence of epileptic seizures. fibrillation (NVAF) and for the treatment of venous thromboembolism (VTE) (deep vein ADP receptor inhibitor. Inhibits platelet aggregation and reduces the incidence of artery thrombosis (DVT) and pulmonary embolism (PE)). Efient (prasugrel) Antiplatelet agent 2014 stenosis and occlusion due to thrombosis. Effient (prasugrel) Antiplatelet agent 2009 Inhibits platelet aggregation and reduces the incidence of artery stenosis and occlusion. Treatment for Benicar 2002 Benicar: Olmesartan osteoporosis / inhibitor Human monoclonal anti-RANKL antibody. Subcutaneous formulation which controls Benicar HCT 2003 Benicar HCT: A combination drug of olmesartan medoxomil and hydrochlorothiazide (diuretic) PRALIA (denosumab) for rheumatoid arthritis- 2013 bone resorption and bone destruction by specifically inhibiting RANKL.
    [Show full text]
  • 146 – March 2015 Produced by NHS Tayside Drug and Therapeutics Committee Medicines Advisory Group (MAG)
    TAYSIDE PRESCRIBER Tayside DTC Supplement No 146 – March 2015 Produced by NHS Tayside Drug and Therapeutics Committee Medicines Advisory Group (MAG) Special Points of Interest Drug Safety Updates for Primary Care Please follow link - Drug Safety Update Download - March 2015 Statin Update (page 2) Drug Driving SMC Advice - February: Abiraterone acetate (Zytiga®) The Drug Driving (Specified Limits)(England and Wales) Regulations 2014 came into effect in nd Bosutinib (Bosulif®) England and Wales on 2 March 2015. Similar legislation will be apply in Scotland, but the date on which it comes into effect has still to be set by the Scottish Parliament. It should be noted Colestilan (BindRen®) that patients may travel in England and Wales and be subject to the regulations at present. Follitropin alfa (Bemfola®) These regulations set maximum blood levels for several prescription medicines including Paclitaxel formulated as albumin diazepam, lorazepam, methadone, morphine, ketamine, and temazepam. bound nanoparticles (Abraxane®) ® Umeclidinium / vilanterol(Anoro ) The BNF already specifies the cautionary labels recommended for inclusion with the dispensed medicine. SMC Advice - March: The BNF specifies that patients should be advised if the treatment is likely to affect their ability Apixaban (Eliquis®) to drive (although it is not specified if this is the prescriber or pharmacist). ® Cabozantinib (Cometriq ) Dabrafenib (Tafinlar®) Further information is available using the links below: Fosfomycin (Fomicyt®) Information for Healthcare Professionals:
    [Show full text]
  • Ehealth DSI [Ehdsi V2.2.2-OR] Ehealth DSI – Master Value Set
    MTC eHealth DSI [eHDSI v2.2.2-OR] eHealth DSI – Master Value Set Catalogue Responsible : eHDSI Solution Provider PublishDate : Wed Nov 08 16:16:10 CET 2017 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 1 of 490 MTC Table of Contents epSOSActiveIngredient 4 epSOSAdministrativeGender 148 epSOSAdverseEventType 149 epSOSAllergenNoDrugs 150 epSOSBloodGroup 155 epSOSBloodPressure 156 epSOSCodeNoMedication 157 epSOSCodeProb 158 epSOSConfidentiality 159 epSOSCountry 160 epSOSDisplayLabel 167 epSOSDocumentCode 170 epSOSDoseForm 171 epSOSHealthcareProfessionalRoles 184 epSOSIllnessesandDisorders 186 epSOSLanguage 448 epSOSMedicalDevices 458 epSOSNullFavor 461 epSOSPackage 462 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 2 of 490 MTC epSOSPersonalRelationship 464 epSOSPregnancyInformation 466 epSOSProcedures 467 epSOSReactionAllergy 470 epSOSResolutionOutcome 472 epSOSRoleClass 473 epSOSRouteofAdministration 474 epSOSSections 477 epSOSSeverity 478 epSOSSocialHistory 479 epSOSStatusCode 480 epSOSSubstitutionCode 481 epSOSTelecomAddress 482 epSOSTimingEvent 483 epSOSUnits 484 epSOSUnknownInformation 487 epSOSVaccine 488 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 3 of 490 MTC epSOSActiveIngredient epSOSActiveIngredient Value Set ID 1.3.6.1.4.1.12559.11.10.1.3.1.42.24 TRANSLATIONS Code System ID Code System Version Concept Code Description (FSN) 2.16.840.1.113883.6.73 2017-01 A ALIMENTARY TRACT AND METABOLISM 2.16.840.1.113883.6.73 2017-01
    [Show full text]
  • Introduction Methods Results Conclusions
    133 Sebelipase Alfa Improves Atherogenic Biomarkers in Adults and Children With Lysosomal Acid Lipase Deficiency Don P Wilson,1 Sachin Marulkar,2 Radhika Tripuraneni,2 and Barbara K Burton3 1Cook Children’s Medical Center, Fort Worth, TX; 2Alexion Pharmaceuticals, Inc, New Haven, CT; 3Northwestern University Feinberg School of Medicine, Ann and Robert H. Lurie Children’s Hospital of Chicago, Chicago, IL • Management with lipid-lowering medications10: INTRODUCTION RESULTS Table 4. Effect of Sebelipase Alfa on Atherogenic Biomarkers in LAL-D Subjects – HMG CoA reductase inhibitors disrupt synthesis of FC, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors Stratified by Use of Lipid-Lowering Medication (LLM) at 20 Weeks of Treatment • Lysosomal acid lipase deficiency (LAL-D) is a rare, autosomal recessive lysosomal storage disorder (Online Mendelian prevent degradation of LDL receptors, and both types of lipid-lowering medications can markedly increase LDL uptake and increase lysosomal accumulation of LDL (Figure 2)2,10 Subject Characteristics Subjects Using LLM Subjects Not Using LLM Inheritance in Man [OMIM] #278000), historically called Wolman disease in infants and cholesteryl ester storage disease (n=24) (n=37) in older children and adults, that is associated with accumulation of cholesteryl esters and triglycerides in the liver and – Although statin therapy may improve lipid parameters, clinical reports have noted progression of liver disease in • Complete data on atherogenic biomarkers were available from 61 of 66 subjects
    [Show full text]