Diagnosis and Management of Idiopathic Drug-Induced and Severe

Total Page:16

File Type:pdf, Size:1020Kb

Diagnosis and Management of Idiopathic Drug-Induced and Severe Andrès E, Mourot-Cottet R, Maloisel F. J Lung Health Dis (2018) 1(1): 31-38 Minireview Open Access Diagnosis and management of idiopathic drug-induced and severe neutropenia and agranulocytosis: What should the lung specialist know? Emmanuel Andrès1*, Rachel Mourot-Cottet1, Frédéric Maloisel2 1Departments of Internal Medicine B, University Hospital of Strasbourg, Strasbourg 67000, France 2Department of Hematology, Saint Anne’s Clinic, Strasbourg 67000, France Article Info ABSTRACT Article Notes In this paper, we report and discuss the diagnosis and management of severe Received: August 16, 2017 neutropenia and agranulocytosis (neutrophil count of <0.5 x 109/L) related to Accepted: January 18, 2018 non-chemotherapy drug intake, called “idiosyncratic”. Lung specialists may *Correspondence: be faced with these events. In fact, all classes of drugs have been implicated Pr. E. ANDRÈS, Service de Médecine Interne, Clinique (“causative”) and clinical manifestations may include pneumonia or related Médicale B, Hôpital Civil, Hôpitaux Universitaires de disorders. Recently, several prognostic factors have been identified that may Strasbourg, 1 Porte de l’Hôpital, 67 091 Strasbourg Cedex, be helpful when identifying frailty patients. Old age (>65 years), septicemia or France; Telephone: 33-3-88-11-50-66; shock, metabolic disorders such as renal failure, and a neutrophil count below Fax: 33-3-88-11-62-62;; 0.1×109/L have been consensually accepted as poor prognostic factors for Email: [email protected] hematological recovery. In this potentially life-threatening disorder, modern © 2018 DAndrès E. This article is distributed under the terms of management with broad-spectrum antibiotics and hematopoietic growth the Creative Commons Attribution 4.0 International License. factors (particularly G-CSF), is likely to improve the prognosis. Thus, with appropriate management, the mortality rate of idiosyncratic drug-induced Keywords severe neutropenia and agranulocytosis is currently around 5%. Agranulocytosis Neutropenia Drugs Infections Pneumonia Introduction Antibiotics Hematopoietic growth factor Severe neutropenia is characterized by a profound decrease of circulating granulocytes, also called agranulocytosis in case of a neutrophil count of <0.5 x 109/L (associated or not with fever)1,2. cases of acute and severe pharyngeal infections, associated with a lackSchultz of granulocytes first introduced in the the blood term in “agranulocytosis”relation with drug inintake. 1922, Such for unpredictable event (named “idiosyncratic”)1,2. As in isneutropenia typically serious, related with around 50% of cases exhibiting severe sepsis and a mortality rate of 10-20% these twenty later years to chemotherapy, modern management of such event may reduce the infection-related mortality. All practitioners as the lung specialists may be informed and attentive of this potential life-threatening event, event in case of “daily” or “everyday” medication exposure, aggregationas: antibiotics inhibitors. (beta-lactams, cotrimoxazole), antithyroid drugs, neuroleptic, non-steroidal anti-inflammatory agents, and platelet In the present paper, we report and discuss the diagnosis and neutropenia and agranulocytosis. management of idiopathic drug-induced (or drug-associated) severe Page 31 of 38 Andrès E, Mourot-Cottet R, Maloisel F. J Lung Health Dis31-38 Journal of Lung Health and Diseases Search strategy I per year7. In our experience (observational study in a PubMed n the USA, reported ranges from 2.4 to 15.4 per million database of the US National Library of Medicine and on A literature search was performed on the Scholar Google. We searched for articles published between French hospital), from 1996 to 2017, the annual incidence [of8 symptomatic idiosyncratic agranulocytosis remained stable, with approximately 6 cases per million population January 2010 and February 2017, using the following key ]. It’s important to note that the incidence remains words or associations: “drug-induced neutropenia”, “drug- unchanged, despite the withdrawn 2of incriminated drugs induced agranulocytosis”, “idiosyncratic neutropenia” and . This is in relation (which carry a high risk) and increased levels of medical “idiosyncratic agranulocytosis”; restrictions included: awareness and pharmacovigilance English- or French-language publications; published from induced by new drugs. trials, review articles or guidelines. All of the English and with the development of neutropenia and agranulocytosis Jan. 1, 2010, to Feb. 31, 2017; human subjects; clinical French abstracts were reviewed by at least two senior publishedDifferences1,2. Geographic in the observed variability incidence in incidence may beis relateddue to researchersAmerican from Society our workof Hematology group. educational books, different methods/inclusion criteria used in the studies could also suggest genetic differences in susceptibility. to both differences in reporting and medication usage but alsotextbooks used. of Hematology and Internal medicine, and information gleaned from international meetings were drug-induced neutropenia, probably because of increased Definition Older patients 2are. thought to be at greater risk for to Most, but not all cases of neutropenia and agranulocytosis medication use 9/L occur as a result of exposure to drugs [3 to educateAs we have all practitioners, shown below, including everyday thosemedication practicing can bein defined at least by a neutrophil count of <0.5 x 10 involved in such blood event. It is therefore very important ]. All drugs may be the hospitals or in the city. causative agents, particularly: chemotherapy, immune speciality as lung specialists, and pharmacists, those in modulator agents or biotherapies. Other daily drugs may Causative drugs be also more rarely incriminated. Such event1. Either is called the “idiosyncratic drug-induced” or “idiosyncratic drug- agent.associated” neutropenia and agranulocytosis For practitioners and pharmacists, it is important drug itself or one of its metabolites may be the causative to keep in mind that almost all classes1,2,9-11 of drugs. However, have forbeen drugsimplicated such (“causative”), as antithyroid but fordrugs, the majorityticlopidine, the The recommended criteria for diagnosing blood risk appears to be very small (table 2) cytopenias2,4. andThese for implicatingcriteria are a outlineddrug as a incausative table 1.agent As clozapine, phenothiazines, sulfasalazine,10,11 trimethoprim- idiosyncraticin neutropenia severe are derived neutropenia from an and international agranulocytosis consensus are sulfametoxazole (cotrimoxazole), and dipyrone or life-threateningmeeting conditions, no patient was re-challenged sulfasalazine,per 10,000 users the hasrisk beenmay reportedbe higher1 . For antithyroid drugs (propyl-thiouracil and méthimazole),9. Clozapine a risk induces of 3 with the incriminated drug (“theoretical method of . For ticlopidine, the reference”).Epidemiology risk is more than 100-fold higher agranulocytosis in almost 1%11 of patients, particularly in Idiosyncratic severe neutropenia or agranulocytosis is a . the first three months of treatment, with older patients and rare disorder. In Europe, the annual incidence of such events females being at a higher risk 2,5,6. In our single center cohort (n=203), the most frequent is between 1.6 and 9.2Table cases 1: Criteriaper million for idiosyncratic population drug-inducedcausative agranulocytosis drugs (adapted are: antibioticsfrom [1-3]). (49.3%), especially Definition of agranulocytosis Criteria of drug imputability • Onset of agranulocytosis during treatment or within 7 days of exposure to the drug, with a complete recovery in neutrophil count of more than 1.5 x 109/L within one month of discon- tinuing the drug Neutrophil count <0.5 x 109/L ± exis- • Recurrence of agranulocytosis upon re-exposure to the drug (this is rarely observed, as the tence of a fever and/or any signs of high risk of mortality contra-indicates new administration of the drug) infection • Exclusion criteria: history of congenital neutropenia or immune mediated neutropenia, recent infectious disease (particularly recent viral infection), recent chemotherapy and/or radiothera- py and/or immunotherapy* and existence of an underlying haematological disease *Immunoglobulins, interferon, anti-TNF antibodies, anti-CD20 (rituximab)… Page 32 of 38 Andrès E, Mourot-Cottet R, Maloisel F. J Lung Health Dis31-38 Journal of Lung Health and Diseases Table 2: Drugs implicated in the occurrence of agranulocytosis [1-3]. Family drug Drugs Analgesics and nonsteroidal Acetaminophen, acid acetylsalicylic (aspirin), aminopyrine, benoxaprofen, diclofenac, diflunisal, dipyrone, anti-inflammatory drugs fenoprofen, indomethacin, ibuprofen, naproxen, phenylbutazone, piroxicam, sulindac, tenoxicam, tolmetin Amoxapine, chlomipramine, chlorpromazine, chlordiazepoxide, clozapine, diazepam, fluoxetine, haloperi- Antipsychotics, hypnoseda- dol, levopromazine, mirtazapine, imipramine, indalpin, meprobamate, mianserin, olanzapine, phenobarbi- tives and antidepressants tal, phenothiazines, risperidone, tiapride, ziprasidone Antiepileptic drugs Carbamazepine, ethosuximide, lamotrigine, phenytoin, trimethadione, valproic acid (sodium valproate) Antithyroid drugs Carbimazole, methimazole, potassium perchlorate, potassium thiocyanate, propylthiouracil Acid acetylsalicylic, amiodarone, aprindine, bepridil, captopril, coumarins, dipyridamole, digoxin, flurbipro- Cardiovascular drugs fen, furosemide, hydralazine, lisinopril,
Recommended publications
  • The Role of Histidine-Rich Proteins in the Biomineralization of Hemozoin Lisa Pasierb
    Duquesne University Duquesne Scholarship Collection Electronic Theses and Dissertations Fall 2005 The Role of Histidine-Rich Proteins in the Biomineralization of Hemozoin Lisa Pasierb Follow this and additional works at: https://dsc.duq.edu/etd Recommended Citation Pasierb, L. (2005). The Role of Histidine-Rich Proteins in the Biomineralization of Hemozoin (Doctoral dissertation, Duquesne University). Retrieved from https://dsc.duq.edu/etd/1021 This Immediate Access is brought to you for free and open access by Duquesne Scholarship Collection. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of Duquesne Scholarship Collection. For more information, please contact [email protected]. The Role of Histidine-Rich Proteins in the Biomineralization of Hemozoin A Dissertation presented to the Bayer School of Natural and Environmental Sciences of Duquesne University As partial fulfillment of the requirements for the degree of Doctor of Philosophy By Lisa Pasierb August 26, 2005 Dr. David Seybert, thesis director Dr. David W. Wright, advisor In memory of Anna Pasierb April 24, 1924 – May 31, 2005 ii Acknowledgements First and foremost, I would like to express my sincerest gratitude to my advisor, Dr. David W. Wright. His exuberating energy and conviction attracted me to his research group, while his unwavering faith in me taught me more than he could ever know. Secondly, of course, I would like to extend my appreciation to Glenn Spreitzer and James Ziegler, the other two original members of the Wright group, whom initially tried to exert male dominance, but eventually became very faithful friends and colleagues. Finally, to all the other members of the Wright group over the years, thanks for all of your help, suggestions, and camaraderie.
    [Show full text]
  • WO 2017/145013 Al 31 August 2017 (31.08.2017) P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2017/145013 Al 31 August 2017 (31.08.2017) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every C07D 498/04 (2006.01) A61K 31/5365 (2006.01) kind of national protection available): AE, AG, AL, AM, C07D 519/00 (2006.01) A61P 25/00 (2006.01) AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, (21) Number: International Application DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, PCT/IB20 17/050844 HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KH, KN, (22) International Filing Date: KP, KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, 15 February 2017 (15.02.2017) MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, (25) Filing Language: English RU, RW, SA, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, (26) Publication Language: English TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: 62/298,657 23 February 2016 (23.02.2016) US (84) Designated States (unless otherwise indicated, for every kind of regional protection available): ARIPO (BW, GH, (71) Applicant: PFIZER INC. [US/US]; 235 East 42nd Street, GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, New York, New York 10017 (US).
    [Show full text]
  • Dalbavancin • Oritavancin • Tedizolid • Ceftolozane/Tazobactam • Ceftazidime/Avibactam • Fecal Transplant
    What’s New in Infectious Diseases? Bruce L. Gilliam, M.D. Institute of Human Virology University of Maryland School of Medicine Baltimore, MD Topics New Antibacterial Therapeutics Emerging Pathogens HIV Hepatitis C Disclosures Research Studies Pfizer – Staph aureus Vaccine Trial TaiMed Biologics - Ibaluzimab Advisory Board Viiv Healthcare New Antibacterial Therapeutics • Dalbavancin • Oritavancin • Tedizolid • Ceftolozane/tazobactam • Ceftazidime/avibactam • Fecal Transplant Incidence of Staph aureus hospitalizations in U.S.A., 2001–2009 BMC Infect Dis 2014, 14:296 Dalbavancin (Dalvance) • Derived from Teicoplanin • ½ life – Effective: 8.5 days – Terminal: 346 hrs (14 days) • Bactericidal • Similar spectrum to Vancomycin, active against: – Staphylococci • MSSA, MRSA, CoNS – Streptococci • resistant pneumococci • anaerobic strep – Enterococci • VRE with van B, C but not A – Corynebacterium Dalbavancin Once Weekly Non- Inferior to Vanco/Linezolid N Engl J Med 2014;370:2169-79. Single-Dose (1.5 g) Non-Inferior to Weekly Dalbavancin for Treatment of Acute Bacterial Skin and Skin Structure Infection 100 90 80 70 60 50 Single Dose 40 Once Weekly 30 20 10 0 Overall Clinical Success Rate Success Rate Success Rate Response Day 14 Day 28 Day 14 MRSA Clin Infect Dis. 2015 Nov 26. pii: civ982. [Epub ahead of print] VA Experience with Dalbavancin • Background – Levels in bone > MIC for 14 days • 8 patients treated for osteomyelitis with IV Dalbavancin – Former IV drug users not eligible for home IV or unwilling to do home IV • Treated for up to 8 weeks • No adverse events • All with resolution of osteomyelitis • Cost savings vs. placement in facility Oritavancin (Orbactiv) • Derived from Vancomycin • ½ life – Terminal 245-393 hrs (10-16 days) • Bactericidal • Similar spectrum to Vancomycin, active against: – Staphylococci • MSSA, MRSA, CoNS – Streptococci • resistant pneumococci • anaerobic strep – Enterococci • VRE with van A, B, C – Corynebacterium Single Dose Oritavancin vs.
    [Show full text]
  • Jos Journal 2
    POST-OPERATIVE AUDIT OF G6PD-DEFICIENT MALE CHILDREN WITH OBSTRUCTIVE ADENOTONSILLAR ENLARGEMENT AT UNIVERSITY COLLEGE HOSPITAL, IBADAN, NIGERIA. John EN1, Totyen EL1, Jacob N2, Nwaorgu OGB1 1 .Department of ENT/Head and Neck Surgery, University College Hospital, Ibadan, Nigeria 2. Department of paediatrics, University College Hospital, Ibadan, Nigeria All correspondences and request for reprint to Dr John EN, Department of ENT/Head and Neck Surgery, University College Hospital, Ibadan, Nigeria Email: [email protected] Telephone: +2348036240109 Abstract Background: G6PD deficiency ranks among the commonest hereditary enzyme deficiency worldwide and notable as a predisposing condition to haemolyticcrises. The fear of possible untoward effects is often expressed by parents of G6PD deficient male children scheduled for surgery after obtaining an informed and understood consent. The parental perception of obstructive adenotonsillar enlargement in this condition was also appraised. Methods: A retrospective chart review of all G6PD deficient male children between ages 1 to 7years who had adenotonsillectomy over a 3year period at University college Hospital, Ibadan, Nigeria. Results: The patients comprised of 22 G6PD deficient male children diagnosed shortly after birth upon development of neonatal jaundice. Fifteen(68.2%) and 6(27.3%) of the patients subsequently developed episodes of drug- induced haemolysis and non-haemolytic drug reactions prior to undergoing adenotonsillectomy by the otolaryngologists. None of the patients was observed to develop haemolytic crises up to 2weeks post-adenotonsillectomy. From the parental perception and responses in the follow-up period,all 22(100%) patient had resolution of noisy breathing, 20(91%) had improvement of snoring and apnoeic spells. Only 15 (68%) were reported to stop mouth-breathing.
    [Show full text]
  • Annex 4: Drug Dosages for Children (Formulary)
    Medicines Dosage Form Dose according to body weight (calculate if weight is below or over) 3-6 kg 6-10 kg 10-15 kg 15-20 kg 20-29 kg albendazole 200 mg (half tablet) 12-24 months chewable tablet, 400mg 400 mg (one tablet) over 24 months amodiaquine 10 mg base/kg/3 days (total dose 30 mg base/kg) tablet, 200mg - - 1 1 1 amoxicillin 15 mg/kg/dose for 7 days tablet/capsule 250 mg ¼ ½ ¾ 1 1½ oral suspension, 125mg/5ml 2.5 ml 5 ml 7.5 ml 10 ml - non-severe pneumonia: 25 mg/kg 2 times per day for 3 days tablet/capsule 250 mg ½ 1 1½ 2 2½ oral suspension, 125mg/5ml 5 ml 10 ml 15 ml - - ampicillin IM 50 mg/kg/6 hours Vial of 500 mg mixed with 2.1 ml 1 ml 2 ml 3 ml 5 ml 6 ml sterile water to give 500 mg/2.5 ml artemether IM 3.2 mg/kg once on day 1 injection, 40mg/ml in 1ml ampoule then injection, 80mg/ml in 1ml ampoule see Chapter 5, management of the child with malaria IM 1.6 mg/kg daily until oral therapy is possible, total therapy one week artemether + fixed dose treatment (20+120 mg) twice daily for 3 days tablet 10+120 mg see Chapter 5, management of the child with malaria lumefantrine artesunate severe malaria: IV or IM 2.4 mg/kg over 3 minutes at 0, 12 and 24 vial of 60 mg in 0.6 ml with 3.4 ml hours on day 1.
    [Show full text]
  • Cytochrome P450 Oxidative Metabolism: Contributions to the Pharmacokinetics, Safety, and Efficacy of Xenobiotics
    1521-009X/44/8/1229–1245$25.00 http://dx.doi.org/10.1124/dmd.116.071753 DRUG METABOLISM AND DISPOSITION Drug Metab Dispos 44:1229–1245, August 2016 Copyright ª 2016 by The American Society for Pharmacology and Experimental Therapeutics Special Section on Emerging Novel Enzyme Pathways in Drug Metabolism—Commentary Cytochrome P450 and Non–Cytochrome P450 Oxidative Metabolism: Contributions to the Pharmacokinetics, Safety, and Efficacy of Xenobiotics Robert S. Foti and Deepak K. Dalvie Pharmacokinetics and Drug Metabolism, Amgen, Cambridge, Massachusetts (R.S.F.); and Pharmacokinetics, Dynamics, and Metabolism, Pfizer, La Jolla, California (D.K.D.) Downloaded from Received May 24, 2016; accepted June 10, 2016 ABSTRACT The drug-metabolizing enzymes that contribute to the metabolism this end, this Special Section on Emerging Novel Enzyme Pathways or bioactivation of a drug play a crucial role in defining the in Drug Metabolism will highlight a number of advancements that dmd.aspetjournals.org absorption, distribution, metabolism, and excretion properties of have recently been reported. The included articles support the that drug. Although the overall effect of the cytochrome P450 (P450) important role of non-P450 enzymes in the clearance pathways of family of drug-metabolizing enzymes in this capacity cannot be U.S. Food and Drug Administration–approved drugs over the past understated, advancements in the field of non-P450–mediated me- 10 years. Specific examples will detail recent reports of aldehyde tabolism have garnered increasing attention in recent years. This is oxidase, flavin-containing monooxygenase, and other non-P450 perhaps a direct result of our ability to systematically avoid P450 pathways that contribute to the metabolic, pharmacokinetic, or liabilities by introducing chemical moieties that are not susceptible pharmacodynamic properties of xenobiotic compounds.
    [Show full text]
  • Unlicensed Medicines List for Suffolk D&T
    Unlicensed Medicines & Unlicensed Uses Doctors can prescribe unlicensed medicines, or licensed medicines for unlicensed uses (off-label/off license prescribing). In these situations the doctor is legally responsible for the medicine. They may be called upon to justify their actions in the event of an adverse reaction. Doctors are expected to take “reasonable care” in common law, and to act in a way which is consistent with the practice of a responsible body of their peers of similar professional standing. The General Medical Council guidance on Good Practice in Prescribing Medicines (January 2013) gives the following information for doctors (http://www.gmc-uk.org/guidance/ethical_guidance/prescriptions_faqs.asp) Prescribing unlicensed medicines You can prescribe unlicensed medicines but, if you decide to do so, you must: 1. Be satisfied that an alternative, licensed medicine would not meet the patient's needs. 2. Be satisfied that there is a sufficient evidence base and/or experience of using the medicine to demonstrate its safety and efficacy. 3. Take responsibility for prescribing the unlicensed medicine and for overseeing the patient's care, including monitoring and any follow up treatment. 4. Record the medicine prescribed and, where you are not following common practice, the reasons for choosing this medicine in the patient's notes. Prescribing medicines for use outside the terms of their licence (off-label) 1. You may prescribe medicines for purposes for which they are not licensed. Although there are a number of circumstances in which this may arise, it is likely to occur most frequently in prescribing for children. Currently pharmaceutical companies do not usually test their medicines on children and as a consequence, cannot apply to license their medicines for use in the treatment of children.
    [Show full text]
  • CAS Number Index
    2334 CAS Number Index CAS # Page Name CAS # Page Name CAS # Page Name 50-00-0 905 Formaldehyde 56-81-5 967 Glycerol 61-90-5 1135 Leucine 50-02-2 596 Dexamethasone 56-85-9 963 Glutamine 62-44-2 1640 Phenacetin 50-06-6 1654 Phenobarbital 57-00-1 514 Creatine 62-46-4 1166 α-Lipoic acid 50-11-3 1288 Metharbital 57-22-7 2229 Vincristine 62-53-3 131 Aniline 50-12-4 1245 Mephenytoin 57-24-9 1950 Strychnine 62-73-7 626 Dichlorvos 50-23-7 1017 Hydrocortisone 57-27-2 1428 Morphine 63-05-8 127 Androstenedione 50-24-8 1739 Prednisolone 57-41-0 1672 Phenytoin 63-25-2 335 Carbaryl 50-29-3 569 DDT 57-42-1 1239 Meperidine 63-75-2 142 Arecoline 50-33-9 1666 Phenylbutazone 57-43-2 108 Amobarbital 64-04-0 1648 Phenethylamine 50-34-0 1770 Propantheline bromide 57-44-3 191 Barbital 64-13-1 1308 p-Methoxyamphetamine 50-35-1 2054 Thalidomide 57-47-6 1683 Physostigmine 64-17-5 784 Ethanol 50-36-2 497 Cocaine 57-53-4 1249 Meprobamate 64-18-6 909 Formic acid 50-37-3 1197 Lysergic acid diethylamide 57-55-6 1782 Propylene glycol 64-77-7 2104 Tolbutamide 50-44-2 1253 6-Mercaptopurine 57-66-9 1751 Probenecid 64-86-8 506 Colchicine 50-47-5 589 Desipramine 57-74-9 398 Chlordane 65-23-6 1802 Pyridoxine 50-48-6 103 Amitriptyline 57-92-1 1947 Streptomycin 65-29-2 931 Gallamine 50-49-7 1053 Imipramine 57-94-3 2179 Tubocurarine chloride 65-45-2 1888 Salicylamide 50-52-2 2071 Thioridazine 57-96-5 1966 Sulfinpyrazone 65-49-6 98 p-Aminosalicylic acid 50-53-3 426 Chlorpromazine 58-00-4 138 Apomorphine 66-76-2 632 Dicumarol 50-55-5 1841 Reserpine 58-05-9 1136 Leucovorin 66-79-5
    [Show full text]
  • Digitalcommons@UNMC Granulocytopenia
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1936 Granulocytopenia Howard E. Mitchell University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Mitchell, Howard E., "Granulocytopenia" (1936). MD Theses. 457. https://digitalcommons.unmc.edu/mdtheses/457 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. G PA~lULOCYTOPENI A SENIOR THESIS By Howard E. Mitchell April 17, 1936 TABLE OF CONT'ENTS Introduction Definition • · 1 History . • • • 1 Nomenclature • • • • • 4 ClassificBtion • • • • 6 Physiology • • • • .10 Etiology • • 22 Geographic Distribution • 23 Age, Sex, and R9ce • • ·• 23 Occupation • .. • • • • .. • 23 Ba.cteria • • • • .. 24 Glandu18.r Dysfunction • • • 27 Radiation • • • • 28 Allergy • • • 28 Chemotactic and Maturation Factors • • 28 Chemicals • • • • • 30 Pathology • • • • • 36 Symptoms • • • • • • • 43 DiEtgnosis • • • • • .. • • • • • .. • 4'7 Prognosis 48 '" • • • • • • • • • • • • Treatment • • • • • • • • 49 Non"'specific Therapy • • • • .. 50 Transfusion • • • • .. 51 X-Ray • • • • • • • • • 52 Liver ·Extract • • • • • • • 53 Nucleotides • • • • • • • • • • • 53 General Ca.re • • • • • • • • 57 Conclusion • • • • • • • • • 58 480805 INTHODUCTION Although t~ere is reference in literature of the Nineteenth Century to syndromes similating the disease (granulocytopenia) 9.8 W(~ know it todes, it "vas not un­ til the year 1922 that Schultz 8ctually described his C8se as a disease entity and by so doing, stimulated the interest of tne medical profession to further in­ vestigation.
    [Show full text]
  • Chediak Higashi Syndrome Masquerading As Acute Leukemia / Storage Disorder - a Rare Case Report
    International Journal of Research in Medical Sciences Asif Baig M et al. Int J Res Med Sci. 2015 Jul;3(7):1785-1787 www.msjonline.org pISSN 2320-6071 | eISSN 2320-6012 DOI: http://dx.doi.org/10.18203/2320-6012.ijrms20150271 Case Report Chediak Higashi Syndrome masquerading as acute leukemia / storage disorder - A rare case report Mirza Asif Baig1,*, Anil Sirasgi2 1Former Asst. professor, BLDUs Shri B.M. Patil Medical College, Bijapure, Karnataka, India 2Associate professor, ESI Medical College, Gulbarga, Karnataka, India Received: 19 April 2015 Revised: 09 May 2015 Accepted: 23 May 2015 *Correspondence: Dr. Mirza Asif Baig, E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Chediak higashi Syndrome (CHS) is a rare autosomal recessive multisystem disorder with a defect in granule morphogenesis with giant lysosomes in leucocyte and other cells. CHS is a rare disease, approximately 200 cases have been reported so far. It was described in detail by Chediak in 1952 and Higashi in 1954. 1½ year old male child presented with multiple hypopigment patches on lower extremities, light colored hair, Hepatosplenomegaly and generalised Lymphadenopathy. PBS shows giant prominent liliac to purple granules in neutrophils, band forms, few lymphocytes and monocytes. Bone marrow is hypercellular showing giant prominent gray blue to purple heterogeneous granules often multiple seen in many myeloid precursors, Neutrophils, few lymphocytes and monocytes.
    [Show full text]
  • Clozapine, Agranulocytosis, and Benign Ethnic Neutropenia
    EDITORIAL 545 Postgrad Med J: first published as 10.1136/pgmj.2004.031641 on 2 September 2005. Downloaded from Pharmacology and toxicology ethnic groups in the Middle East, ....................................................................................... including Yemenite Jews and Jordanians, have BEN.12 13 BEN has only been reported in ethnic groups that have Clozapine, agranulocytosis, and tanned or dark skin.13 Subjects with BEN do not show increased incidence of benign ethnic neutropenia infections, and their response to infec- tions is similar to those without BEN.13 S Rajagopal ................................................................................... CLINICAL IMPLICATIONS In the United Kingdom and Ireland, the Current knowledge and clinical implications Clozaril patient monitoring service (CPMS) supervises the prescribing of clozapine and the haematological test- lozapine is an atypical antipsycho- agranulocytosis, is more common in ing (Clozaril is the brand name of tic that is effective in treatment black people.6 A white cell count spike clozapine). The CPMS uses a lower cut resistant schizophrenia.1 The of 15% or more above the immediately C off point for patients with BEN than for National Institute for Health and preceding measurement may predict the general population (table 1). A Clinical Excellence (NICE) guidelines agranulocytosis within the next ‘‘green’’ alert indicates satisfactory for schizophrenia specify that ‘‘in indi- 75 days.7 However, as these differences count, an ‘‘amber’’ alert requires a viduals with evidence of treatment between the risk factors for agranulocy- repeat FBC test while clozapine can be resistant schizophrenia, clozapine tosis and neutropenia have been extra- should be introduced at the earliest polated primarily from epidemiological continued, and a ‘‘red’’ alert warrants opportunity’’.2 studies, they may be subject to change immediate cessation of clozapine.
    [Show full text]
  • Severe Agranulocytosis in Two Patients with Drug-Induced Hypersensitivity Syndrome/Drug Reaction with Eosinophilia and Systemic Symptoms
    Acta Derm Venereol 2016; 96: 842–843 SHORT COMMUNICATION Severe Agranulocytosis in Two Patients with Drug-induced Hypersensitivity Syndrome/Drug Reaction with Eosinophilia and Systemic Symptoms Miyuki Kato, Yoko Kano*, Yohei Sato and Tetsuo Shiohara Department of Dermatology, Kyorin University School of Medicine, 6-20-2 Shinkawa Mitaka, Tokyo 181-8611, Japan. *E-mail: [email protected] Accepted Mar 24, 2016; Epub ahead of print Mar 30, 2016 Drug-induced hypersensitivity syndrome/drug reac- No evidence was seen of lymphoma or other haematological tion with eosinophilia and systemic symptoms (DIHS/ malignancies. Granulocyte-colony stimulating factor (G-CSF) DRESS) is a life-threatening adverse reaction characteri- and intravenous immunoglobulin at 5 g/day were administered for 5 days. As high-grade fever continued, antibiotics were zed by skin rashes, fever, leukocytosis with eosinophilia started. During the appearance of agranulocytosis, atypical and/or atypical lymphocytosis, lymph node enlargement, lymphocytosis (2–11%) was detected. On day 24 after onset, and liver and/or renal dysfunctions (1, 2). A wide variety leucocyte count was normalized, but liver dysfunction ap- of other involvements have also been reported, including peared (aspartate aminotransferase (AST) 276 IU/l (normal limbic encephalitis, myocarditis, and gastrointestinal < 33 IU/l); alanine aminotransferase (ALT) 159 IU/l (normal < 30 IU/l)). Renal function was also exacerbated (BUN 86.6 disease, developing during the course of the disease mg/dl; Cr 2.8 mg/dl). Seven days later, leucocytes overshot (3–5). It has been demonstrated that human herpesvirus to 21.3 × 109/l (neutrophil 81.0%; eosinophil 0.5%; monocyte 6 (HHV-6), Epstein-Barr virus (EBV) and cytomegalo- 8%; lymphocyte 10%; atypical lymphocyte 0.5%).
    [Show full text]