DOCSLIB.ORG

Current Recommendations for the Pharmacologic Therapy in Kawasaki Syndrome and Management of Its Cardiovascular Complications

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Current Recommendations for the Pharmacologic Therapy in Kawasaki Syndrome and Management of Its Cardiovascular Complications European Review for Medical and Pharmacological Sciences 2007; 11: 301-308 Current recommendations for the pharmacologic therapy in Kawasaki syndrome and management of its cardiovascular complications G. DE ROSA*, M. PARDEO*, D. RIGANTE *Section of Pediatric Cardiology; Department of Pediatric Sciences, Università Cattolica del Sacro Cuore – Rome (Italy) Abstract. – Kawasaki syndrome is a po- nign childhood disease: several years later, fatali- tentially life-threatening disease of early child- ties occurred in Japan among children with KS hood that untreated holds a risk of severe coro- nary involvement. Its diagnosis is made via a list younger than 2 years when they had apparently of clinical signs because etiology and patho- recovered. Post-mortem examinations revealed physiology are still unknown and no specific complete thrombotic occlusion of coronary artery laboratory tool is available. Appropriate therapy aneurysms with myocardial infarction as the im- with intravenous immunoglobulins and aspirin mediate cause of death. This syndrome has now reduces the incidence of coronary abnormalities surpassed rheumatic fever as the leading cause of to less than 5%. Immunoglobulins have been acquired heart disease in the developed countries shown to be highly effective in reducing disease 1 symptoms or their severity and chiefly in reduc- among children younger than 5 years . Although ing the rate of coronary artery aneurysm devel- its etiology is largely unknown, epidemiological opment. Aspirin is firstly used in high dose for findings suggest that genetic factors play a role in its anti-inflammatory properties and then in low the pathogenesis of KS: although KS has been re- dose for its anti-thrombotic effects. Timely diag- ported all over the world, it is overexpressed nosis and precociously administered treatment among Asian populations, especially in children are two crucial points in the definition of prog- nosis for Kawasaki syndrome. In this review of Japanese ancestry. KS results 10 times more heart complications are discussed and thera- prevalent in Japan, if compared with other na- peutic options stratified according to both tions, especially for infants with less than 2 years. severity of coronary involvement and grading of The proportions of KS Japanese patients with car- cardiovascular risk. diac sequels (such as dilation or stenosis of coro- nary arteries, myocardial infarction and valvular Key Words: lesions) 1 month or more after onset were ana- Kawasaki syndrome, Cardiovascular complications. lyzed using nationwide survey protocols: the prevalence of heart abnormalities was particularly high in males, infants younger than 1 year and children older than 5 years of age2. In the natural history of the disease three phases occur: we can Introduction distinguish an acute phase (in the first 2 weeks of illness), a subacute phase (including the 3th and 4th Kawasaki syndrome (KS) or muco-cutaneous- week of illness) and a phase of convalescence lymph node syndrome is an acute systemic vas- (lasting from the 5th to the 8th week since the on- culitis of unknown etiology that involves the set). The original guidelines for the diagnosis of walls of medium- and small-sized muscular arter- KS were created by a committee that was appoint- ies throughout the body in the pediatric age, ed by the Japanese Ministry of Health in 1970. In which was firstly described by Tomisaku the acute phase KS usually starts with more than Kawasaki in 1967. At that time, he reported 50 5 days of high fever followed by at least 4 of 5 children from 1961-1967 who presented with a main clinical features: non-exudative conjunctival distinctive clinical illness characterized by fever injection, polymorphous skin rash, reddening/fis- and skin rash, which was then thought to be a be- suring of lips and oral mucosa, abnormalities in- Corresponding Author: Donato Rigante, MD; e-mail: [email protected] 301 G. De Rosa, M. Pardeo, D. Rigante volving extremities of limbs and perineum and Table I. Criteria for the diagnosis of Kawasaki syndrome. cervical lymphadenitis (Table I). In the absence of specific diagnostic tests, pathognomonic features Fever persisting at least for 5 days (or more) plus at or evidence-based diagnostic algorithms, KS di- least 4 of the following 5 clinical main signs: agnosis remains basically clinical3. Laboratory Bilateral bulbar conjunctival injection without exudate findings are frequently helpful in confirming the Polymorphous skin rash correct diagnostic suggestion: inflammatory Changes in lips (reddened, dry or cracked) and oral markers as erythrocyte sedimentation rate (ESR), cavity (strawberry tongue, diffuse oral and C-reactive protein (CRP), serum amyloid-A pharyngeal hyperemia) (SAA) are markedly elevated; neutrophil leuko- Changes in the extremities and in the perineum (erythema of palms or soles, indurative edema of cytosis (with toxic granulations and left shift), hands or feet, desquamation of perineal skin) mild-to-moderate normochromic anemia (with Acute cervical lymph node enlargement (with a haemoglobin levels < 2 SD for age), hypoalbu- diameter superior than 15 mm) minemia (< 3.5 g/dl), hyponatremia (< 135 mEq/L), elevated serum transaminases and sterile pyuria are typical of KS. In the subacute phase the vast majority of patients displays skin desqua- thrombosis. High-dose aspirin is administered to mation starting in the subungual regions of the reduce fever and KS inflammatory signs. The ef- fingers and spreading to palms and soles in com- ficacy of intravenous immunoglobulins is dose- bination with the increase of platelet count, some- depending: a randomized-controlled trial has times exceeding 1.000.000/mm3. In some patients demonstrated that a single infusion of 2 g/kg in- arthralgias or arthritides can appear in the suba- fused in a time of 10 hours has a higher efficacy cute phase. Incomplete and atypical forms of KS than a 4-day-infusion of 400 mg/kg/day5. There (with other vasculitic features as abdominal pain, is no evidence that immunoglobulin treatment on pneumonia, seizures, meningitis, urethritis, he- day 4 of fever or earlier has greater efficacy in patitis and gallbladder distention, parotitis, preventing cardiac complications than treatment uveitis, etc.) are more common in young infants on days 5 to 9. The mechanism of action of intra- with less than 1 year of age4. Characteristics sug- venous immunoglobulins is unknown, though it gesting disease other than KS include exudative might include neutralization of hypothetic infec- conjunctivitis, exudative pharyngitis, bullous, tious agents, inhibition of endothelial cell func- vesicular or exfoliating rash and generalized tions, non-specific anti-inflammatory effects by adenopathy. There is a great number of pathologic the down-regulation of proinflammatory cy- conditions mimicking KS which require to be con- tokines as tumour necrosis factor-α (TNF-α) and sidered attentively in the differential diagnosis as interferon-gamma, blockage of Fc-receptors on staphylococcal scalded skin syndrome, toxic shock macrophages, suppression of T and B cells and syndrome, Stevens-Johnson syndrome, scarlet blockage of complement cascade. Aspirin in- fever, measles, Epstein-Barr virus infection, Cyto- hibits prostaglandin synthesis and has been the megalovirus infection, tick-borne diseases, juve- first drug used in children with KS. High doses nile rheumatoid arthritis, reaction to drugs and are used only during the acute inflammatory mercury hypersensitivity (acrodynia). phase and vary across countries: 30-50 Therapeutical Approach in Kawasaki Syndrome A combination of a single dose of intravenous Table II. Standard treatment for Kawasaki syndrome. immunoglobulins (2 grams/kg of body weight in- fused over a period of 10-12 hours) and aspirin at Intravenous immunoglobulins: 2 g/kg of body weight (infused over a period of 10-12 hours) high doses (30 to 100 mg/kg/day in four divided Aspirin: 30-100 mg/kg orally, daily divided into 4 doses) are recommended when KS diagnosis is doses, until the normalization of inflammatory made during the first 10 days of illness. KS ther- parameters apy is schematized in the Table II. Treatment Subsequent antiplatelet treatment with aspirin: 3-5 with intravenous immunoglobulins is directed at mg/kg orally, once daily for 6-8 weeks (starting in reducing the inflammation in the vessel walls in- the subacute phase of the disease) or continued indefinitely if coronary abnormalities are volved by the disease, mostly in the coronary observed artery walls, and at preventing coronary artery 302 Pharmacologic therapy in Kawasaki syndrome and its cardiovascular complications mg/kg/day in the United Kingdom and 80-100 brachial arteries, with the exception of central mg/kg/day in Japan and in the United States6-8. nervous system arteries. The major sequels of Low-dose aspirin in the subacute phase inhibits KS are related to the cardiovascular district platelet aggregation and is aimed at the reduction which might be interested in all its structures: of the thrombotic risk which is higher in patients pericardium, myocardium, endocardium and showing coronary artery dilations. However, the above all coronary arteries. Myocardial disease occurrence of coronary abnormalities is not in- during the acute phase is commonly reported: fluenced by the association intravenous im- inflammation has been documented in 50-70% munoglobulins-aspirin, if compared with intra- of autoptic descriptions14-16. Its clinical find- venous immunoglobulins alone9.
Load more

Recommended publications
  • Mercury Poisoning Manifested Acrodynia, Reported in Four Old Boy in Michigan Ten Day After the Inside of His Heme Painted
    TOXIC INFECTIVE DISORDERS MERCURY POISONING AND LATEX PAINT Mercury poisoning manifested as acrodynia, reported in a four year old boy in Michigan ten day after the inside of his heme was painted with 64 liters of interior latex paint containing phenylmercurie acetate, prompted an investigation by the Division of Environmental Hazards and Health Effects, Centers for Disease Control, Atlanta, GA. Nineteen families were recruited from a list of more than 100 persons who called the Michigan Department of Public Health after a press release announced that some interior latex paint contained more than the recommended limit of mercury of 1.5 nmol per liter. Ihe median mercury content of the paint in 29 cans sanpled from the exposed households was 3.8 nmol per liter. Hie concentrations of mercury in the air sanples obtained from homes of exposed families were significantly higher than in the unexposed households. Urinary mercury concentrations were significantly higher among the exposed persons than among unexposed persons (4.7 nmol of mercury per millimole of creatinine compared to 1.1 nmol per millimole). These mercury concentrations in exposed persons have been associated with synptcmatic mercury poisoning. (Agocs MM, Etzel RA et al. Mercury exposure from interior latex paint. N Engl J Med Oct 18, 1990; 323:1096-1101). OCMVENT. Exposed children had the highest urinary mercury concentrations and young children may be at increased risk since vapors containing mercury are heavier than indoor air and tend to settle toward the floor. Individual exposure to mercury varies with the time spent in painted rooms, the depth and frequency of inhalation, the degree of ventilation in the room, and the likely decrease in mercury vapors over time.
    [Show full text]
  • Mercury Intoxication and Arterial Hypertension: Report of Two Patients and Review of the Literature
    Mercury Intoxication and Arterial Hypertension: Report of Two Patients and Review of the Literature Alfonso D. Torres, MD*; Ashok N. Rai, MD‡; and Melissa L. Hardiek, MD‡ ABSTRACT. Two children in the same household with evere systemic arterial hypertension in infants symptomatic arterial hypertension simulating pheochro- and children is usually secondary to an under- mocytoma were found to be intoxicated with elemental lying disease process. The most frequent causes mercury. The first child was a 4-year-old boy who pre- S of hypertension in this group include renal paren- sented with new-onset seizures, rash, and painful ex- chymal disease, obstructive uropathy, chronic pyelo- tremities, who was found to have a blood pressure of nephritis associated with reflux, and renal artery ste- 171/123 mm Hg. An extensive investigation ensued. Ele- vated catecholamines were demonstrated in plasma and nosis. Less frequent causes include adrenal tumors, urine; studies did not confirm pheochromocytoma. Mer- pheochromocytomas, neurofibromas, and an in- cury levels were elevated. These findings prompted an creasing number of familial forms of hypertension. evaluation of the family. A foster sister had similar find- Other causes are medications and drugs of ingestion ings of rash and hypertension. Both had been exposed to or abuse, especially cocaine and sympathomimetics. elemental mercury in the home. The family was tempo- Heavy metal intoxication is also implicated.1 We rarily relocated and chelation therapy was started. present 2 patients with an infrequent cause of hyper- A Medline search for mercury intoxication with hyper- tension. tension found 6 reports of patients ranging from 11 months to 17 years old.
    [Show full text]
  • Evidence-Based Management of Kawasaki Disease in the Emergency Department
    January 2015 Evidence-Based Management Volume 12, Number 1 Authors Of Kawasaki Disease In The Kara K. Seaton, MD Fellow, Pediatric Emergency Medicine, Children’s Hospital and Clinics of Minnesota, Minneapolis, MN Emergency Department Anupam Kharbanda, MD Director of Research, Emergency and Trauma Services, Abstract Children’s Hospital and Clinics of Minnesota, Minneapolis, MN Peer Reviewers Kawasaki disease, also known as mucocutaneous lymph node syn- Catherine Sellinger, MD, FAAP Associate Director, Pediatric Emergency Services, Children’s drome, was first described in Japan in 1967. It is currently the leading Hospital at Montefiore; Assistant Professor of Pediatrics, Albert cause of acquired heart disease in children in the United States. Un- Einstein College of Medicine, Bronx, NY treated Kawasaki disease may lead to the formation of coronary artery Michael J. Stoner, MD Assistant Professor of Pediatrics, The Ohio State University aneurysms and sudden cardiac death in children. This vasculitis pres- College of Medicine; Attending Physician, Pediatric Emergency ents with fever for ≥ 5 days, plus a combination of key criteria. Because Medicine, Nationwide Children’s Hospital, Columbus, OH each of the symptoms commonly occurs in other childhood illnesses, CME Objectives the disease can be difficult to diagnose, especially in children who Upon completion of this article, you should be able to: present with an incomplete form of the disease. At this time, the etiol- 1. Describe the clinical features and risks associated with ogy of the disease remains unknown, and there is no single diagnostic Kawasaki disease. 2. Identify epidemiologic trends in Kawasaki disease in high- test to confirm the diagnosis. This issue reviews the presentation, diag- risk populations.
    [Show full text]
  • PINK DISEASE MENU Heather Thiele
    pink2a PINK DISEASE MENU most of these articles were gathered by Heather Thiele. http://www.users.bigpond.com/difarnsworth/pink2a.htm (1 of 2) [05/28/2000 1:42:05 AM] pink2a ACRODYNIA-Nelson's book of poisons & drugs. MERCURY & PINK DISEASE-Lancet 1951 THE MEDICAL JOURNAL OF AUSTRALIA (June 11-1960) MORTALITY FROM PINK DISEASE in 1923-1947 DISEASES KNOWN TO BE CAUSED BY THE DIET Dr. CHEEK...discoverer of possible CAUSE/linkage with Hg & Enzyme. PINK DISEASE-10 YEARS AFTER (The Epilogue) A LONG TERM STUDY OF 62 CASES YOUNG'S SYNDROME & PINK DISEASE. BMJ December 1993 Back to Top MAIN MENU http://www.users.bigpond.com/difarnsworth/pink2a.htm (2 of 2) [05/28/2000 1:42:05 AM] pink34 Acrodynia. Pink Disease, Swift Disease, Feer Disease, Erythodema, Dermatopolyneuritus Nelson’s Textbook Chemical and Drug Poisoning http://www.users.bigpond.com/difarnsworth/pink34.htm (1 of 4) [05/28/2000 1:42:21 AM] pink34 Acrodynia (the term derived from the Greek, denotes painful extremities) is principally a syndrome of chronic mercury poisoning in infants and young children consisting of many unusual symptoms which, in the well established cases, are so distinctive that there is practically no difficult diagnosis. In few other conditions is extreme and persistent misery such prominent part of the clinical picture. The condition was recognised in Australia as early as 1890 and established as a clinical entity in the British and American literature by Byfield and Bilderback in 1920. Etiology. Most and perhaps all cases of acrodynia represent the clinical response to repeated contact with or ingestion of mercury in products such as house paints, wallpapers, teething powders, vermifuges and diaper rinses.
    [Show full text]
  • Implications for Inositol 1,4,5-Trip
    Review http://dx.doi.org/10.4070/kcj.2013.43.9.581 Print ISSN 1738-5520 • On-line ISSN 1738-5555 Korean Circulation Journal Mercury Promotes Catecholamines Which Potentiate Mercurial Autoimmunity and Vasodilation: Implications for Inositol 1,4,5-Triphosphate 3-Kinase C Susceptibility in Kawasaki Syndrome Deniz Yeter, MD1, Richard Deth, PhD2, and Ho-Chang Kuo, MD3 1Shawnee, KS, 2Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA 3Division of Allergy, Immunology and Rheumatology, Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose patients to mercury by increasing Ca2+ release. Hg2+ sensitizes inositol 1,4,5-triphosphate (IP3) receptors at low doses, which release Ca2+ from intracellular stores in the sarcoplasmic reticulum, resulting in delayed, repetitive calcium influx. ITPKC prevents IP3 from triggering IP3 receptors to release calcium by converting IP3 to inositol 1,3,4,5-tetrakisphosphate. Defective IP3 phosphorylation re- sulting from reduced genetic expressions of ITPKC in KS would promote IP3, which increases Ca2+ release. Hg2+ increases catecholamine levels through the inhibition of S-adenosylmethionine and subsequently catechol-O-methyltransferase (COMT), while a single nucleotide polymorphism of the COMT gene (rs769224) was recently found to be significantly associated with the development of coronary artery le- sions in KS. Accumulation of norepinephrine or epinephrine would potentiate Hg2+-induced calcium influx by increasing IP3 production and increasing the permeability of cardiac sarcolemma to Ca2+.
    [Show full text]
  • Forty Years Ago in the Late 1940S Hackney Hospital, a General Hos- Pital in East London, Had 700 Beds
    1182 Archives ofDisease in Childhood 1990;65:1 182 SISTER JOURNALS-EUROPE Arch Dis Child: first published as 10.1136/adc.65.10.1182 on 1 October 1990. Downloaded from European Journal of Pediatrics for their own chauvinist reasons. The effect is This is a well recognised journal which is now in its there is little in the European journal which is new 149th volume and is produced by Springer Inter- or revelatory. national. The texts are in English and are well pre- The acid test of any publication is whether one sented with good reproduction of graphs and would buy it. I feel this journal passes this test if photographs. for no other reason than with the approach of 1992 The content is widely varied covering most it is important that there is a increase in the inter- fields of paediatrics. Some are informative and change ofideas and scientific truths across national impart to the reader information which may be borders. In this regard it is interesting to see that useful in clinical practice. Unfortunately there is a in the references most authors have cited other considerable amount of 'paediatric philately' international workers and not just those of their which would be best reported in other subspecial- own nation. I feel this journal could be improved if ist journals or as short reports in this one. those of us who write regularly would seek to pub- It would appear possible that the journal suffers lish in these pages to the advantage of both from the fact that it would not be the first choice ourselves and our fellow Europeans.
    [Show full text]
  • Mercury Intoxication Presenting with Hypertension and Tachycardia 557
    556 Arch Dis Child 1999;80:556–557 Mercury intoxication presenting with Arch Dis Child: first published as 10.1136/adc.80.6.556 on 1 June 1999. Downloaded from hypertension and tachycardia Willi Wöâmann, Martina Kohl, Gunnar Grüning, Peter Bucsky Abstract excess but without cutaneous lesions or a An 11 year old girl presented with hyper- history of exposure to mercury. tension and tachycardia. Excess urinary catecholamine excretion suggested phaeo- Case report chromocytoma but imaging studies failed A Taiwanese girl was admitted to our institution to demonstrate a tumour. Other symp- because of hypertension (160/120 mm Hg) and toms included insomnia and weight loss, tachycardia (120 beats/min). She had suVered and she was found to have a raised from painful itching in her extremities but this concentration of mercury in blood and had resolved before admission. Oscillometric urine. Mercury intoxication should be 24 hour blood pressure monitoring revealed considered in the diVerential diagnosis of severe hypertension without nocturnal dipping hypertension with tachycardia even in (fig 1). Exposure to drugs and toxins was patients presenting without the skin le- denied, and there was no family history of sions typical of mercury intoxication and hypertension or malignant disease. Laboratory without a history of exposure. values showed normal thyroid and kidney func- (Arch Dis Child 1999;80:556–557) tion. Urinary concentrations of vanillylman- delic acid (VMA) were slightly raised (5.6–5.8 Keywords: hypertension; tachycardia; mercury nmol/µmol creatinine; normal < 4.7); homova- poisoning; phaeochromocytoma nillic acid (HMA) was within the normal range. Investigations including abdominal and cervical ultrasound, computed tomography scans, and The diVerential diagnosis of hypertension, an M-iodobenzylguanidine scan did not reveal a tachycardia, weight loss, and psychiatric symp- tumour.
    [Show full text]
  • Pink Ladies: Mercury Poisoning in Twin Girls
    PRACTICE C LINICAL V ISTAS Pink ladies: mercury poisoning in twin girls reviously well, developmentally nor- Pmal 20-month-old twin girls pre- sented with weakness, anorexia, a papular rash and increasingly swollen, red and painful hands and feet of 1 month’s dura- tion. They had no history of fever, con- junctivitis, lymphadenopathy or oral changes characteristic of Kawasaki dis- ease. The children appeared irritable and unwell and were diaphoretic but afebrile. Both had tachycardia, and one had an el- evated blood pressure of 130/90 mm Hg (95th percentile for age 108/62 mm Hg). Images courtesy Dr. Michael Weinstein Both children had reduced muscle power and diminished reflexes. Their dusky pink discolouration, swelling, agement of mercury poisoning is eli- palms and soles were erythematous and paresthesia and desquamation of the minating the source of exposure. The indurated with desquamation, judged to hands and feet. Symptoms of cate- effectiveness of chelation therapy in re- be acrodynia (Figs.1 and 2). cholamine excess such as sweating and versing symptoms is not entirely clear.9 Mercury toxicity was suspected, and hypertension occur because mercury Our case stresses the potential harm further questionning revealed that the blocks the degradation pathway of cate- of mercury. It reminds us to think of a infants had been given a mercury- cholamines. Other manifestations of toxic exposure when family members containing “teething powder” from India mercury toxicity include renal dysfunc- present with the same unusual constella- once or twice a week over the 4 preced- tion, peripheral neuropathy and neuro- tion of symptoms. It also highlights the ing months.
    [Show full text]
  • ED368492.Pdf
    DOCUMENT RESUME ED 368 492 PS 6-2 243 AUTHOR Markel, Howard; And Others TITLE The Portable Pediatrician. REPORT NO ISBN-1-56053-007-3 PUB DATE 92 NOTE 407p. AVAILABLE FROMMosby-Year Book, Inc., 11830 Westline Industt.ial Drive, St. Louis, MO 63146 ($35). PUB TYPE Guides Non-Classroom Use (055) Reference Materials Vocabularies/Classifications/Dictionaries (134) Books (010) EDRS PRICE MF01/PC17 Plus Postage. DESCRIPTORS *Adolescents; Child Caregivers; *Child Development; *Child Health; *Children; *Clinical Diagnosis; Health Materials; Health Personnel; *Medical Evaluation; Pediatrics; Reference Materials; Symptoms (Individual Disorders) ABSTRACT This ready reference health guide features 240 major topics that occur regularly in clinical work with children nnd adolescents. It sorts out the information vital to successful management of common health problems and concerns by presentation of tables, charts, lists, criteria for diagnosis, and other useful tips. References on which the entries are based are provided so that the reader can perform a more extensive search on the topic. The entries are arranged in alphabetical order, and include: (1) abdominal pain; (2) anemias;(3) breathholding;(4) bugs;(5) cholesterol, (6) crying,(7) day care,(8) diabetes, (9) ears,(10) eyes; (11) fatigue;(12) fever;(13) genetics;(14) growth;(15) human bites; (16) hypersensitivity; (17) injuries;(18) intoeing; (19) jaundice; (20) joint pain;(21) kidneys; (22) Lyme disease;(23) meningitis; (24) milestones of development;(25) nutrition; (26) parasites; (27) poisoning; (28) quality time;(29) respiratory distress; (30) seizures; (31) sleeping patterns;(32) teeth; (33) urinary tract; (34) vision; (35) wheezing; (36) x-rays;(37) yellow nails; and (38) zoonoses, diseases transmitted by animals.
    [Show full text]
  • Appendix: Drug Dosing in Renal Failure
    44. Drug dosage in renal failure Appendix: Drug dosing in renal failure Abbreviations used: ACE: angiotensin-converting enzyme AV: atrioventricular BUN: blood urea nitrogen CCr: Creatinine clearance CAPD: continuous ambulatory peritoneal dialysis CHF: congestive heart failure CMV: cytomegalovirus CNS: central nervous system CRRT: continuous renal replacement therapy CSA/FK: cyclosporine A and tacrolimus CVD: cardiovascular disease CVVH: Continuous venovenous hemofiltration DVT: deep vein thrombosis ESRD: end-stage renal disease GI: gastrointestinal GFR: glomerular filtration rate HBV: hepatitis B virus HD: hemodialysis HDL: high-density lipoprotein HIT: heparin-induced thrombocytopenia HSV: herpes simplex virus INR: international normalized ratio IV: intravenous MI: myocardial infarction MMF: mycophenolate mofetil NA: not applicable NC: No data: no change required NSAIDs: nonsteroidal anti-inflammatory drugs TB: tuberculosis TDM: therapeutic drug monitoring VD: volume of distribution VZV: varicella zoster virus. 919 920 Table 2 . Antibacterial agents % of drug Dosage adjustment for renal failure with GFR Method of dosage adjustment Drug Normal dosage excreted (ml/min): Comments renally >50 10−50 <10 HD CAPD CVVH Aminoglycosides Group toxicity: all agents in this group are nephrotoxic and ototoxic; ototoxicity is worse when the patient is hyperbilirubinemic; measure serum levels for efficacy and toxicity; peritoneal absorption increases with presence of inflammation. V increases with edema, obesity, and ascites D Streptomycin 7.5 mg/kg q. 12 hr 60% q. 24 hr q. 24−72 hr q. 72−96 hr May be less nephrotoxic than other Half normal 20−40 mg/L/ Dose for GFR (1.0 g q. 24 hr members of class dose after day 10−50 ml/min; for TB) dialysis measure levels Kanamycin 7.5 mg/kg q.
    [Show full text]
  • From Mad Hatters to Thimerosal: the Truth About Mercury Poisoning
    From Mad Hatters to Thimerosal: the Truth about Mercury Poisoning Brian J Hall MD University of Utah CME Statement The University of Utah School of Medicine adheres to ACCME Standards regarding industry support of continuing medical education. Speakers are also expected to openly disclose intent to discuss any off-label, experimental, or investigational use of drugs, devices, or equipment in their presentations. This speaker has nothing to disclose. Goals for the talk 1. Understand common exposure sources of mercury 2. Appreciate some of the clinical features of acute and chronic mercury poisoning 3. Know the different tests available for mercury here at ARUP and other labs 4. Gain knowledge regarding treatments available for acute and chronic toxicity Mercury Chemical symbol is Hg Atomic number is 80 Also known as quicksilver or hydrargyrum hydr = water or runny argyros = silver At or near liquid at room temperature and pressure History Egyptian tombs - 1500 BC In China and Tibet thought to prolong life, heal fractures and maintain good health Qin Shi Huang died from drinking mercury taken to prolong his life Ancient Greeks, Egyptians and Romans Ointments and cosmetics History “Mad as a hatter” coined from mercury poisonings in the 18th and 19th centuries in the felt hat industry Hunter-Russel syndrome Mercury poisonings found among workers in a seed-packing factory in Norwich, England - late 1930s Forms of mercury Elemental Inorganic Mercury chloride and other salts Organic Methylmercury (MeHg) Dimethylmercury
    [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]