DOCSLIB.ORG

Review of the Comparative Effectiveness and Safety of Calcium Disodium Edetate and Penicillamine for the Treatment of Lead Poisoning in Children

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Review of the Comparative Effectiveness and Safety of Calcium Disodium Edetate and Penicillamine for the Treatment of Lead Poisoning in Children 18th Expert Committee on the Selection and Use of Essential Medicines (21 to 25 March 2011) Section 4.2 (Review) -- Children REVIEW OF THE COMPARATIVE EFFECTIVENESS AND SAFETY OF CALCIUM DISODIUM EDETATE AND PENICILLAMINE FOR THE TREATMENT OF LEAD POISONING IN CHILDREN Report October 2010 Brian M. Kaiser Pharm.D.; BCPS Clinical Pharmacist, Pediatrics University of California, San Francisco Medical Center The Benioff Children’s Hospital Assistant Clinical Professor University of California, San Francisco School of Pharmacy 521 Parnassus Ave, Rm. C‐152 San Francisco, CA 94143 UNITED STATES OF AMERICA Tel: +14154435046 Fax: +14153531305 1. Background In October 2007, the Expert Committee on the Selection and Use of Essential Medicines noted that lead poisoning was a significant public health problem in many developing countries. Treatment of lead poisoning, therefore, was considered essential to include on the Essential Medicines List for Children. While penicillamine and sodium calcium edetate are both licensed for this indication, there was no basis for the Subcommittee to determine which, if any, was superior. Both were therefore included, and a review of efficacy and safety was requested.i The Subcommittee of the Expert Committee on the Selection and Use of Essential Medicines reiterated the need for a synthesized or systemic review of the safety and effectiveness of penicillamine compared to sodium calcium edetate for the treatment of lead poisoning in the fall of 2008.ii The current document provides a review of the evidence to inform key stakeholders of the efficacy and safety or penicillamine and sodium calcium edetate in the treatment of lead poisoning in pediatric patients. 2. International Non­propriety Name (INN, generic name) of the medicine INN: Calcium disodium edetate Generic name: edetate calcium disodium Chemical name: [[N,N'‐1,2‐ethanediyl‐bis[N‐(carboxymethyl)‐ glycinato]](4‐)‐N,N',O,O',ON,ON']‐, disodium, hydrate, (OC‐6‐21)‐Calciate(2‐) INN: d‐penicillamine Generic name: penicillamine Chemical name: (2s)‐2‐amino‐3‐methyl‐3‐sulphanylbutanoic acid 3. Formulation Calcium disodium edetate: 200 mg calcium disodium edetate in 1 mL; vials of 2.5 mL and 5 mL Penicillamine: 250 mg penicillamine capsules; 30 capsules per package 250 mg penicillamine tablets, scores; 30 tablets per package A 50 mg/mL suspension may be made by mixing sixty 250 mg capsules with 3 g carboxymethylcellulose, 150 g sucrose, 300 mg citric acid, parabens (methylparaben 120 mg, propylparaben 12 mg, propylene glycol qs ad to 100 mL), and purified water to a total volume of 300 mL; cherry flavor may be added. Stability is 30 days refrigerated. (DeCastro Hosp Pharm 1977) 4. Global burden of disease It was estimated that in 2000, 120 million people worldwide had blood lead levels of 5‐10 mcg/dL and approximately the same number had levels above 10mcg/dL. About 40% of children had blood lead levels above 5mcg/dL and 20% above 10 mcg/dL, with 97% of these children living in developing regions. Less then 10% of children had levels above 20 mcg/dL but, 99% of those that did lived in developing regions.iii In the United States, the National Health and Nutrition Examination Survey has documented a steady decline in the number of children 1‐5 years old with blood lead levels > 10 mcg/dL 77.8% 2 (1976‐1980) down to 1.6% (1999‐2002).iv The dramatic decline has resulted in improved health and productivity, with an estimated averted health cost of $312 billion.v vi 5. Indications for use 5.1 Calcium disodium edetate The United States Food and Drug Administration (FDA) has approved calcium disodium edetate in both adults and children for the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy.vii 5.2 Penicillamine The indications for penicillamine are many and varied. In the case of adults, the FDA approved indications for penicillamine include: cystinuria, severe and active rheumatoid arthritis that has failed to respond to conventional therapy, and Wilson’s Disease. Penicillamine is not approved for the treatment of lead poisoning by the FDA, nor is there any approved indication for use in pediatric patients.viii 6. Treatment details (dosage regimen, duration; reference to existing WHO and other clinical guidelines; need for special diagnostic or treatment facilities and skills) 6.1 Dosage regimens Table 6.1: Indications and dose regimens for calcium disodium edetate and penicillamine in childrenix Indication(s) Dosage Duration of treatment Calcium disodium edetate Symptoms of lead 250mg/ m2/dose IM every 4 5 days, wait a minimum of 2 encephalopathy and/or blood hours days with no treatment before lead level >70 mcg/dL* 50mg/kg/day IV as a considering a repeat course continuous 24 hour infusion OR 1‐1.5gm/ m2 IV as either an 8 to 24 hour infusion or divided into 2 doses every 12 hours Symptomatic lead poisoning 167 mg/ m2/dose IM every 4 3‐5 days without encephalopathy or hours asymptomatic with blood lead 1gm/ m2 IV as an 8 to 24 hour level >70 mcg/dL† infusion or divided every 12 hours Asymptomatic children with 25mg/kg/day IV as an 8 to 24 5 days blood lead level 45‐69 mcg/dL hour infusion or divided every Depending upon the blood lead 12 hours level, additional courses may be necessary; repeat at least 2‐4 days, preferably 2‐4 weeks, apart Penicillamine Lead poisoning 20‐30 mg/kg/day orally in 3‐4 4‐12 weeks divided doses, maximum dose Depends upon pretreatment is 1.5gm/day blood lead level Start at 25% of total dose and increase gradually to full dose over 2‐3 weeks Moderate lead poisoning (blood 15mg/kg/day orally in 2 4‐12 weeks lead level 20‐40 mcg/dL) divided doses Depends upon pretreatment blood lead level Abbreviations: mg = milligram; gm = gram; kg = kilogram; m2 = meters squared; IM = intramuscular; IV = intravenous 3 * Use in conjunction with dimercaprol † Recommended to be used with dimercaprol until blood lead level is < 50mcg/dL 6.2 Reference to existing WHO and other clinical guidelines The United States Centers for Disease Control (CDC) recommends the following for children with confirmed elevated blood level concentrations. Table 6.2 CDC recommendations for children who have confirmed (venous) elevated blood lead concentrationsx Blood Lead Concentration Recommendation 10‐14 mcg/dL Lead education Follow‐up blood lead monitoring within 1 month 15‐19 mcg/dL Lead education Follow‐up blood lead monitoring within 1 month Proceed according to actions for 20‐44 mcg/dL if a follow‐ up blood lead concentration is in this range after at least 3 months; or blood level increases 20‐44 mcg/dL Lead education Follow‐up blood lead monitoring within 1 week Complete history and physical Laboratory work (hemoglobin, hematocrit, iron) Environmental investigation Neurodevelopmental monitoring Abdominal radiography (if particulate lead ingestion is suspected, with bowel decontamination if indicated) 45‐69 mcg/dL Lead education Follow‐up blood lead monitoring within 48 hours Complete history and physical Laboratory work (hemoglobin, hematocrit, iron, free erythrocyte protoporphyrin or zinc protoporphyin) Environmental investigation Lead hazard reduction Neurodevelopmental monitoring Abdominal radiography (if particulate lead ingestion is suspected, with bowel decontamination if indicated) Chelation therapy ≥ 70 mcg/dL Hospitalize and commence chelation therapy Follow‐up confirmation of blood level immediately Proceed according to actions for 45‐69 mcg/dL The American Academy of Pediatrics (AAP) makes specific recommendations for drug treatment based upon the CDC guidelines for venous blood lead level. If the blood lead level is greater than 45 mcg/dL and exposure source has been controlled, treatment should begin with oral succimer. Children with symptoms of lead poisoning or with a blood lead level greater than 70 mcg/dL or who are allergic or react to succimer should be hospitalized and receive treatment with calcium disodium edetate. The safety and efficacy of penicillamine has not been established and is reserved as a third line agent.xi 4 7. Summary of efficacy in the treatment of lead poisoning 7.1 Penicillamine 7.1.1 Literature search Medline (1950‐ September 2010), the Cochrane Database of Systematic Reviews and the World Health Organization website were searched to identify all published papers and trial reports that described the use of penicillamine for lead poisoning in children. Search terms used to identify studies included: penicillamine, lead, poisoning, infant, child, pediatrics, neonates and children. Medical subject headings (MeSH) were used when available or appropriate. Reference lists of retrieved articles were reviewed to identify any potentially relevant studies not identified during the database searches. The literature search did not identify any prospective randomized trials. Two prospective reports analyzed the use of penicillamine in children with small lead burdens.xii xiiiA retrospective cohort addressed the efficacy of penicillamine in children for lead poisoning; another retrospective analysis addressed adverse events.xiv xv 7.1.2 Efficacy Shannon et al studied the use of penicillamine in 27 children. The mean age was 33 months (range 14‐72). Patients received penicillamine as a crushed tablet or opened capsule dosed 15‐ 30 mg/kg daily. Clinic visits were made every two to four weeks for measurement of blood lead levels, erythrocyte protoporphyin levels, hematologic index and urinalysis. Mean treatment duration was 10 weeks (range, 4‐20 weeks). Results are shown
Load more

Recommended publications
  • Review of Succimer for Treatment of Lead Poisoning
    Review of Succimer for treatment of lead poisoning Glyn N Volans MD, BSc, FRCP. Department of Clinical Pharmacology, School of Medicine at Guy's, King's College & St Thomas' Hospitals, St Thomas' Hospital, London, UK Lakshman Karalliedde MB BS, DA, FRCA Consultant Medical Toxicologist, CHaPD (London), Health Protection Agency UK, Visiting Senior Lecturer, Division of Public Health Sciences, King's College Medical School, King's College , London Senior Research Collaborator, South Asian Clinical Toxicology Research Collaboration, Faculty of Medicine, Peradeniya, Sri Lanka. Heather M Wiseman BSc MSc Medical Toxicology Information Services, Guy’s and St Thomas’ NHS Foundation Trust, London SE1 9RT, UK. Contact details: Heather Wiseman Medical Toxicology Information Services Guy’s & St Thomas’ NHS Foundation Trust Mary Sheridan House Guy’s Hospital Great Maze Pond London SE1 9RT Tel 020 7188 7188 extn 51699 or 020 7188 0600 (admin office) Date 10th March 2010 succimer V 29 Nov 10.doc last saved: 29-Nov-10 11:30 Page 1 of 50 CONTENTS 1 Summary 2. Name of the focal point in WHO submitting or supporting the application 3. Name of the organization(s) consulted and/or supporting the application 4. International Nonproprietary Name (INN, generic name) of the medicine 5. Formulation proposed for inclusion 6. International availability 7. Whether listing is requested as an individual medicine or as an example of a therapeutic group 8. Public health relevance 8.1 Epidemiological information on burden of disease due to lead poisoning 8.2 Assessment of current use 8.2.1 Treatment of children with lead poisoning 8.2.2 Other indications 9.
    [Show full text]
  • Sodium Cellulose Phosphate Sodium Edetate
    Sevelamer/Sodium Edetate 1463 excreted by the kidneys. It may be used as a diagnostic is not less than 9.5% and not more than 13.0%, all calculated on supplement should not be given simultaneously with test for lead poisoning but measurement of blood-lead the dried basis. The calcium binding capacity, calculated on the sodium cellulose phosphate. dried basis, is not less than 1.8 mmol per g. concentrations is generally preferred. Sodium cellulose phosphate has also been used for the Sodium calcium edetate is also a chelator of other Adverse Effects and Precautions investigation of calcium absorption. heavy-metal polyvalent ions, including chromium. A Diarrhoea and other gastrointestinal disturbances have Preparations cream containing sodium calcium edetate 10% has been reported. USP 31: Cellulose Sodium Phosphate for Oral Suspension. been used in the treatment of chrome ulcers and skin Sodium cellulose phosphate should not be given to pa- Proprietary Preparations (details are given in Part 3) sensitivity reactions due to contact with heavy metals. tients with primary or secondary hyperparathyroidism, Spain: Anacalcit; USA: Calcibind. Sodium calcium edetate is also used as a pharmaceuti- hypomagnesaemia, hypocalcaemia, bone disease, or cal excipient and as a food additive. enteric hyperoxaluria. It should be used cautiously in pregnant women and children, since they have high Sodium Edetate In the treatment of lead poisoning, sodium calcium calcium requirements. Sodu edetynian. edetate may be given by intramuscular injection or by Patients should be monitored for electrolyte distur- intravenous infusion. The intramuscular route may be Эдетат Натрия bances. Uptake of sodium and phosphate may increase CAS — 17421-79-3 (monosodium edetate).
    [Show full text]
  • Uses and Administration Adverse Effects and Precautions Pharmacokinetics Uses and Administration
    1549 The adverse effects of dicobalt edetate are more severe in year-old child: case report and review of literature. Z Kardiol 2005; 94: References. 817-2 3. the absence of cyanide. Therefore, dicobalt edetate should I. Schaumann W, et a!. Kinetics of the Fab fragments of digoxin antibodies and of bound digoxin in patients with severe digoxin intoxication. Eur 1 not be given unless cyanide poisoning is confirmed and 30: Administration in renal impairment. In renal impairment, Clin Pharmacol 1986; 527-33. poisoning is severe such as when consciousness is impaired. 2. Ujhelyi MR, Robert S. Pharmacokinetic aspects of digoxin-specific Fab elimination of antibody-bound digoxin or digitoxin is therapy in the management of digitalis toxicity. Clin Pharmacokinet 1995; Oedema. A patient with cyanide toxicity developed delayed1·3 and antibody fragments can be detected in the 28: 483-93. plasma for 2 to 3 weeks after treatment.1 The rebound in 3. Renard C, et al. Pharmacokinetics of dig,'><i<1-sp,eei1ie Fab: effects of severe facial and pulmonary oedema after treatment with decreased renal function and age. 1997; 44: 135-8. dicobalt edetate.1 It has been suggested that when dicobalt free-digoxin concentrations that has been reported after edetate is used, facilities for intubation and resuscitation treatment with digoxin-specific antibody fragments (see P (Jrations should be immediately available. Poisoning, below), occurred much later in patients with r.�p renal impairment than in those with normal renal func­ Proprietary Preparations (details are given in Volume B) 1. Dodds C, McKnight C. Cyanide toxicity after immersion and the hazards tion.
    [Show full text]
  • An Oral Treatment for Lead Toxicity Paul S
    Postgrad Med J: first published as 10.1136/pgmj.67.783.63 on 1 January 1991. Downloaded from Postgrad MedJ (1991) 67, 63 - 65 D The Fellowship ofPostgraduate Medicine, 1991 Clinical Toxicology An oral treatment for lead toxicity Paul S. Thomas' and Charles Ashton2 'Northwick Park Hospital, Harrow, Middlesex HA] 3UJand2National Poisons Unit, Guy's Hospital, London SE], UK. Summary: Chronic lead poisoning has traditionally been treated by parenteral agents. We present a case where a comparison of ethylene diaminetetra-acetic acid was made with 2,3-dimethyl succinic acid (DMSA) which has the advantage oforal administration associated with little toxicity and appeared to be at least as efficacious. Introduction For many years the treatment of heavy metal ferase 112IU/I (normal<40). His electrolytes, poisoning has relied upon parenteral agents which urea, creatinine, clotting screening chest radio- themselves have a number of toxic side effects. We graph, computed tomographic head scan and lum- report a case ofplumbism which shows the benefits bar puncture were all normal. of using 2,3-dimethyl succinic acid (DMSA), a Re-evaluation revealed lead lines on his gingival treatment relatively new to Western countries. In margins and a urinary porphyrin screen was posi- by copyright. our case it was used in direct comparison to the tive indicating lead toxicity. Despite careful social, sodium-calcium salt of ethylene diaminetetra- occupational, and recreational history no cause for acetic acid, which has been the best available his excess lead intake could be found. As he was treatment. domiciled in India it was not possible to visit his home or workplace where he sold sarees.
    [Show full text]
  • Antidotes Atropine Calcium
    Version 2.9 Antidotes 4/10/2013 Atropine Indications AV conduction impairment: Cardiac glycosides , β-blockers , calcium channel blockers (CCBs) . Anticholinesterase inhibitors/Cholinergics: Organophosphates, carbamates Contraindications Relative: closed angle glaucoma, GIT obstruction, urinary obstruction Mechanism Competitive antagonist for ACh at muscarinic receptors. Pharmacokinetics Poor oral bioavailability, liver met, T ½=2-4hrs. Crosses BBB & placenta. 50% excreted unaltered. Administration AV conduction impairment: 0.6mg (20mcg/kg) IV repeated up to 3x Cholinergics: 1.2mg IV bolus, double dose q5mins until chest clear [also sBP>80mmHg, HR>80, dry axillae & no miosis]. Then infusion starting at ~10-20% of total loading dose (max 35mg/hr) Adverse Reactions Excessive dosage → Anticholinergic toxidrome. Calcium Indications CCB OD, HF exposure, hypocalcaemia, hyperkalaemia, iatrogenic hypermagnesaemia Contraindications Hypercalcaemia, ?digoxin toxicity - (contrary to traditional teaching, recently some evidence 2+ that Ca is not CI if on digoxin or even if digoxin toxic – however digoxin immune Fab & MgSO 4 10mmol might be preferred initially in the latter case) Mechanisms Restore low Ca2 + levels, binds F- ions, antagonises effects of high K + & Mg 2+ on heart. Administration Cardiac monitoring mandatory. CCBs: 20ml CaCl 2 IV (central line) or 60ml (1ml/kg) Ca gluconate IV (peripheral) over 5-10mins HF on skin: 2.5% Ca gel TOP OR local inj of 10% calcium gluconate (not fingers) OR Bier’s block with 2% Ca gluconate (i.e. 10ml of 10% in 40ml NS) for 20mins & release cuff OR same dose intra-arterially over 4 hrs & rpt prn. HF inhaled: Nebulised 2.5% Ca gluconate solution. HypoCa/HypoMg/HyperK: 5-10ml CaCl 2 or 10-20ml (1ml/kg) Ca gluconate IV over 5-10mins Adverse Reactions Transient hyperCa., vasodilatation, hypoBP, dysrhythmias, tissue damage from extravasated CaCl 2.
    [Show full text]
  • Picture As Pdf Download
    NOTABLE CASES Succimer therapy for congenital lead poisoning from maternal petrol sniffing An infant, born at 35 weeks’ gestation to a woman who sniffed petrol, had a cord blood lead level eight times the accepted limit. Treatment with oral dimercaptosuccinic acid promptly reduced his blood lead levels. To our knowledge, this is the first reported case of congenital lead poisoning secondary to maternal petrol sniffing. We suggest that at-risk pregnancies should be identified, cord blood lead levels tested, and chelation therapy and developmental follow-up offered to affected infants. (MJA 2006; 184: 84-85) Clinical record therapy is recommended for any child with blood lead levels of μ 3 A 27-year-old Indigenous woman, who had sniffed petrol since 2.16 mol/L and over. Although chelation therapy in early child- childhood, presented for antenatal care during her first pregnancy. hood lowers blood levels, recent studies have not shown signifi- At the age of 14 years, she had severe lead encephalopathy that led cant improvement in cognitive and behavioural measurements 3,4,7 to chronic neurological deficits, including permanent ataxia and compared with untreated children. memory impairment. Her serum lead levels at 8 and 35 weeks’ There are a few case reports of neonatal lead intoxication that gestation were raised at 1.48 and 2.21 μmol/L, respectively (recom- occurred from maternal exposure to lead through pica, home 8-10 mended level, р 0.48 μmol/L1). renovation, or use of contaminated herbal medications. Petrol At 35 weeks’ gestation, she went into spontaneous labour and sniffing is a form of substance misuse that is widespread in some gave birth vaginally to a boy.
    [Show full text]
  • Oral Chelation Therapy for Patients with Lead Poisoning
    ORAL CHELATION THERAPY FOR PATIENTS WITH LEAD POISONING Jennifer A. Lowry, MD Division of Clinical Pharmacology and Medical Toxicology The Children’s Mercy Hospitals and Clinics Kansas City, MO 64108 Tel: (816) 234-3059 Fax: (816) 855-1958 December 2010 1 TABLE OF CONTENTS 1. Background of Lead Poisoning …………………………………………………………...3 a. Clinical Significance of Lead Measurements …………………………………….3 b. Absorption of Lead and Its Internal Distribution Within the Body ………………3 c. Toxic Effects of Exposure to Lead in Children and Adults ………………………4 d. Reproductive and Developmental Effects………………………………………...5 e. Mechanisms of Lead Toxicity ……………………………………………………6 f. Concentration of Lead in Blood Deemed Safe for Children/Adults………………6 g. Use of Blood Lead Measurements as a Marker of Lead Exposure ……………….7 2. Management of the Child with Elevated Blood Lead Concentrations …………………...8 a. Decreasing Exposure……………………………………………………………...8 b. Chelation Therapy…………………………………………………………………8 3. Oral Chelation Therapy …………………………………………………………………...8 a. Meso-2,3 dimercaptosuccinic acid (DMSA, Succimer) …………………………8 i. Pharmacokinetics………………………………………………………….9 ii. Dosing …………………………………………………………………….9 iii. Efficacy……………………………………………………………………9 iv. Safety…………………………………………………………………….11 b. Racemic-2,3-dimercapto-1-propanesulfonic acid (DMPS, Unithiol)……………11 i. Pharmacokinetics………………………………………………………...12 ii. Dosing ……………………………………………………………………12 iii. Efficacy…………………………………………………………………..12 iv. Safety…………………………………………………………………….12 c. Penicillamine……………………………………………………………………..12 i. Pharmacokinetics………………………………………………………...13
    [Show full text]
  • Other Data Relevant to an Evaluation of Carcinogenicity and Its Mechanisms
    P 201-252 DEF.qxp 09/08/2006 11:36 Page 249 INORGANIC AND ORGANIC LEAD COMPOUNDS 249 4. Other Data Relevant to an Evaluation of Carcinogenicity and its Mechanisms 4.1 Absorption, distribution, metabolism and excretion 4.1.1 Inorganic lead compounds (a) Humans (i) Absorption Absorption of lead is influenced by the route of exposure, the physicochemical charac- teristics of the lead and the exposure medium, and the age and physiological status of the exposed individual (e.g. fasting, concentration of nutritional elements such as calcium, and iron status). Inorganic lead can be absorbed by inhalation of fine particles, by ingestion and, to a much lesser extent, transdermally. Inhalation exposure Smaller lead particles (< 1 µm) have been shown to have greater deposition and absorption rates in the lungs than larger particles (Hodgkins et al., 1991; ATSDR, 1999). In adult men, approximately 30–50% of lead in inhaled air is deposited in the respiratory tract, depending on the size of the particles and the ventilation rate of the individual. The proportion of lead deposited is independent of the absolute lead burden in the air. The half- life for retention of lead in the lungs is about 15 h (Chamberlain et al., 1978; Morrow et al., 1980). Once deposited in the lower respiratory tract, particulate lead is almost completely absorbed, and different chemical forms of inorganic lead seem to be absorbed equally (Morrow et al., 1980; US EPA, 1986). In two separate experiments, male adult volunteers were exposed to aerosols of lead oxide (prepared by bubbling propane through a solution of tetraethyl lead in dodecane and burning of resulting vapour) containing 3.2 µg/m3 lead (15 subjects) or 10.9 µg/m3 lead (18 subjects) in a room for 23 h/day for up to 18 weeks (Griffin et al., 1975a).
    [Show full text]
  • The Selection and Use of Essential Medicines
    This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the World Health Organization WHO Technical Report Series 933 THE SELECTION AND USE OF ESSENTIAL MEDICINES Report of the WHO Expert Committee, 2005 (including the 14th Model List of Essential Medicines) World Health Organization Geneva 2006 i WHO Library Cataloguing-in-Publication Data WHO Expert Committee on the Selection and Use of Essential Medicines (14th : 2005: Geneva, Switzerland) The selection and use of essential medicines : report of the WHO Expert Committee, 2005 : (including the 14th model list of essential medicines). (WHO technical report series ; 933) 1.Essential drugs — standards 2.Formularies — standards 3.Drug information services — organization and administration 4.Drug utilization 5. Pharmaceutical preparations — classification 6.Guidelines I.Title II.Title: 14th model list of essential medicines III.Series. ISBN 92 4 120933 X (LC/NLM classification: QV 55) ISSN 0512-3054 © World Health Organization 2006 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 2476; fax: +41 22 791 4857; email: [email protected]). Requests for permission to reproduce or translate WHO publica- tions — whether for sale or for noncommercial distribution — should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; email: [email protected]). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.
    [Show full text]
  • Ed 092 563 Title Institution Report No Pub Date Note Available from Edrs Price Descriptors Identifiers Document Resume- Sp 008 1
    DOCUMENT RESUME- ED 092 563 SP 008 167 TITLE Poisoning and Intoxication by Trace Elements in Children. At Abstract Review of the Worldwide Medical. Literature 1966-1971. INSTITUTION Public Health Service (DREW), Washington, D.C. Bureau of Community Environmental Management. REPORT NO DREW-HSM-73-10005 PUB DATE 73 NOTE 104p. AVAILABLE FROM Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402 (No price quoted) EDRS PRICE MF-$0.75 HC-$5.40 PLUS POSTAGE DESCRIPTORS *Abstracts; Accidents; *Annotated Bibliographies; Clinical Diagnosis; *Health; Lead Poisoning; *Medical Case Histories; *Physiology; Safety IDENTIFIERS *Poisons ABSTRACT This annotated bibliography of 247 entries is divided into the following categories:(a) general aspects and reviews; (b) sources of poisoning, epideE-,..ology, and pica studies; (c) clinico-pathological studies;(d) diagnosis and screening; (e) laboratory methods; and (f) treatment and prevention. A subject and author index is included. (PD) ca° POISONING AND INTOXICATION BY TRACE ELEMENTS U.S. DEPARTMENT OF HEALTH. IN CHILDREN EDUCATICN IL WELFARE NATIONAL INSTITUTE OF EDUCATION THIS DOCUMENT HAS SEEN REPRO- DUCED EXACTLY AS RECEIVED FROM THE PERSON OR ORGANIZATION ORIGIN- ATING IT. POINTS OF VIEW OR OPINIONS STATED DO NOT NECESSARILY REPRE. SENT OFFICIAL NATIONAL INSTITUTE OF EDUCATION POSITION OR POLICY. an abstract review of the worldwide medical literature 1966-1971 DHEW Publication No. (HSM) 73-10005 U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE Public Health Service Health Services and Mental Health Administration Bureau of Community Environmental Management Division of Community injury Control For sale by the Superintendent ae Documents, U.S. Government Printing Office, Washington, D.C.
    [Show full text]
  • EDTA Chelation Therapy in the Treatment of Toxic Metals Exposure
    Original Article Spatula DD. 2011; 1(2):81-89 EDTA chelation therapy in the treatment of toxic metals exposure Toksik metallere maruz kalım tedavisinde EDTA şelasyon terapisi Nina Mikirova1, Joseph Casciari1, Ronald Hunninghake1, Neil Riordan1,2 1Riordan Clinic, Wichita, Kansas, USA. 2Medistem Inc, San Diego, California, USA SUMMARY BACKGROUND: Metal induced toxicity with wide range of physiological, biochemical and behavioral dysfunctions was reported in many studies. The chelation has been used for treatment to toxic metals’ exposure for many years. In our current clinical study, we compared different chelation protocols and two forms of EDTA (sodium calcium edetate and sodium edetate) in treatments of toxic metal exposure. METHODS: A 24 h urine samples were collected from each subject before and after treatment by Ca-EDTA or Na-EDTA. The levels of toxic and essential metals were measured by Atomic Absorption Spectrometer (AAS) with graphite furnace and by Inductively Coupled Plasma Atomic Emission Spectrometer (ICP-AES). The cellular levels of ATP were determined by ATP-bioluminescence assay. Mitochondrial potential was measured by fluorometer and flow-cytometer after cells’ staining by mitochondrial dye. RESULTS: Data from over 600 patients with a variety of complaints, but not acute toxic mineral exposure, given chelation therapy with sodium EDTA or calcium EDTA, were analyzed. Ca-EDTA and Na-EDTA at intravenous infusions of 3 g per treatment were equally effective in removing lead from the body, while Ca-EDTA was more effective in aluminum removal. The removal of lead was dose dependent but non-linear. Chelation by different doses of Na-EDTA (3 g and 1 g) resulted in mean difference in lead urine less than 50%.
    [Show full text]
  • Lead Poisoning
    LEAD POISONING An “Ethyl” petrol bowser, circa 1930. (From A Short History of Nearly Everything, Bill Bryson) In the late 1940s a young University of Chicago geology graduate named Clair Patterson (who incidentally was a male), was working on a project to accurately date the age of the Earth, a problem which had been the topic of intense debate for the previous one hundred years. He was using the newly developed and revolutionary technique of radiometric dating. He reasoned that by studying the radiometric decay of uranium to lead in meteorites he could arrive at a close figure for the age of the solar system and hence of the Earth. Something however seemed to be corrupting his results. Vastly and unexpectedly elevated levels of lead were interfering will his results. Patterson soon realized that the source of this lead was contamination from the atmosphere. Correcting for this he was eventually able to complete his work and announced to the world in 1952 from CALTECH where he was working, that the Earth was 4.55 billion years old, (give or take 70 million years or so), a figure still pretty much accepted today. Having achieved this Patterson turned his attention to the mystery of why atmospheric lead levels were so unexpectedly high. There was no known natural explanation for this. He was concerned as adverse effects of lead on the human body where strongly suspected at the time, although this still remained somewhat uncertain. By a further brilliant series of scientific investigations he began to study frozen ice cores form regions such as Greenland.
    [Show full text]