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[PMID]: 28701428
[Au] Autor:Carter M; Abdi A; Naz F; Thabet F; Vyas A
[Ad] Address:Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University, East Lansing, Michigan.
[Ti] Title:A Mercury Toxicity Case Complicated by Hyponatremia and Abnormal Endocrinological Test Results.
[So] Source:Pediatrics;140(2), 2017 Aug.
[Is] ISSN:1098-4275
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mercury (Hg) poisoning is considered a rare disease by the National Institutes of Health and the diagnosis can present great challenges to clinicians. Children who are exposed to Hg can present with a wide variety of symptoms, including acrodynia, tremor, excessive salivation, and psychiatric symptoms, including insomnia. However, endocrinologic manifestations from Hg exposure are less well known. This is a case report of a 12-year-old boy who presented with body rash, irritability, insomnia, and profuse sweating after returning from a summer camp. The child was initially managed in the outpatient setting, and the investigation was mainly targeted toward infectious etiology, including Rocky Mountain spotted fever and Lyme disease. He was eventually admitted to the hospital with altered mental status and was noted to have hyponatremia with serum sodium of 121 mEq/L. Thyroid studies also revealed elevated free thyroxine levels in the presence of normal triiodothyronine and thyrotropin. The patient developed hypertension and tachycardia, and was found to have elevated 24-hour vanillylmandelic acid and metanephrines. Finally, heavy metal measurements revealed a blood Hg level that was greater than the reference values of 0 to 9 ng/mL. Chelation treatment with 2,3-dimercaptopropane-1-sulfonate was subsequently initiated and over a period of 8 months his symptoms resolved and his thyroid function test returned to normal. This case highlights some of the challenges commonly encountered in identifying Hg exposure. More importantly, it illustrates that exposure to Hg should be considered in children who present with the symptoms and abnormal endocrinologic test results described in this report.
[Mh] MeSH terms primary: Hyperthyroxinemia/diagnosis
Hyponatremia/diagnosis
Mercury Poisoning/diagnosis
Metanephrine/blood
Rare Diseases
Vanilmandelic Acid/blood
[Mh] MeSH terms secundary: Chelation Therapy
Child
Diagnosis, Differential
Humans
Hyperthyroxinemia/etiology
Hyponatremia/etiology
Male
Mercury Poisoning/drug therapy
Patient Admission
Unithiol/therapeutic use
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:4076-02-2 (Unithiol); 5001-33-2 (Metanephrine); 55-10-7 (Vanilmandelic Acid)
[Em] Entry month:1708
[Cu] Class update date: 170828
[Lr] Last revision date:170828
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170714
[St] Status:MEDLINE

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[PMID]: 28472024
[Au] Autor:Tewell M; Spoto S; Wiese M; Aleguas A; Peredy T
[Ti] Title:Mercury Poisoning at a Home Day Care Center - Hillsborough County, Florida, 2015.
[So] Source:MMWR Morb Mortal Wkly Rep;66(17):433-435, 2017 May 05.
[Is] ISSN:1545-861X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:On November 12, 2015, the Florida Poison Information Center Tampa notified the Florida Department of Health in Hillsborough County of a boy aged 3 years with a urine mercury level of 79 µg/L (normal <10 µg/L). The patient had been admitted to the hospital on October 9, 2015 after a 3-4 week history of anorexia, weight loss, and lethargy. In the hospital, he developed a maculopapular rash, acrodynia (painful, pink discoloration of the hands and feet), tachycardia, hypertension, weakness, sweating, excessive salivation, and altered mental status. Subsequent investigation identified the source of the mercury exposure to be a broken sphygmomanometer (blood pressure monitor) at the home day care center attended by the child.
[Mh] MeSH terms primary: Child Day Care Centers
Mercury Poisoning/diagnosis
Mercury/urine
[Mh] MeSH terms secundary: Child, Preschool
Florida
Humans
Male
Public Health Practice
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:FXS1BY2PGL (Mercury)
[Em] Entry month:1705
[Cu] Class update date: 170516
[Lr] Last revision date:170516
[Js] Journal subset:IM
[Da] Date of entry for processing:170505
[St] Status:MEDLINE
[do] DOI:10.15585/mmwr.mm6617a1

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[PMID]: 27136627
[Au] Autor:Lai O; Parsi KK; Wu D; Konia TH; Younts A; Sinha N; McNelis A; Sharon VR
[Ti] Title:Mercury toxicity presenting as acrodynia and a papulovesicular eruption in a 5-year-old girl.
[So] Source:Dermatol Online J;22(3), 2016 Mar 16.
[Is] ISSN:1087-2108
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acrodynia is a reaction that occurs in children who have been exposed to mercury. Mercury toxicity has systemic manifestations as well as cutaneous manifestations, which can appear similar to those found in a number of other diseases. We present a case of acrodynia caused by mercury exposure in a previously healthy 5-year-old girl who developed hypertension, palmoplantar pruritus, and a papulovesicular eruption.
[Mh] MeSH terms primary: Acrodynia/diagnosis
Foot Dermatoses/diagnosis
Hand Dermatoses/diagnosis
[Mh] MeSH terms secundary: Acrodynia/complications
Acrodynia/pathology
Child, Preschool
Female
Foot Dermatoses/pathology
Hand Dermatoses/pathology
Humans
Hypertension/etiology
Mercury Poisoning/complications
Mercury Poisoning/diagnosis
Mercury Poisoning/pathology
Skin/pathology
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1704
[Cu] Class update date: 170425
[Lr] Last revision date:170425
[Js] Journal subset:IM
[Da] Date of entry for processing:160503
[St] Status:MEDLINE

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[PMID]: 26742052
[Au] Autor:Yeter D; Portman MA; Aschner M; Farina M; Chan WC; Hsieh KS; Kuo HC
[Ad] Address:Kawasaki Disease Center, Kaohsiung Chang Gung Memorial Hospital, Niaosong, Kaohsiung 83301, Taiwan. deniz.aydin.yeter@gmail.com.
[Ti] Title:Ethnic Kawasaki Disease Risk Associated with Blood Mercury and Cadmium in U.S. Children.
[So] Source:Int J Environ Res Public Health;13(1), 2016 Jan 05.
[Is] ISSN:1660-4601
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Kawasaki disease (KD) primarily affects children <5 years of age (75%-80%) and is currently the leading cause of acquired heart disease in developed nations. Even when residing in the West, East Asian children are 10 to 20 times more likely to develop KD. We hypothesized cultural variations influencing pediatric mercury (Hg) exposure from seafood consumption may mediate ethnic KD risk among children in the United States. Hospitalization rates of KD in US children aged 0-4 years (n = 10,880) and blood Hg levels in US children aged 1-5 years (n = 713) were determined using separate US federal datasets. Our cohort primarily presented with blood Hg levels <0.1 micrograms (µg) per kg bodyweight (96.5%) that are considered normal and subtoxic. Increased ethnic KD risk was significantly associated with both increasing levels and detection rates of blood Hg or cadmium (Cd) in a linear dose-responsive manner between ethnic African, Asian, Caucasian, and Hispanic children in the US (p ≤ 0.05). Increasing low-dose exposure to Hg or Cd may induce KD or contribute to its later development in susceptible children. However, our preliminary results require further replication in other ethnic populations, in addition to more in-depth examination of metal exposure and toxicokinetics.
[Mh] MeSH terms primary: Cadmium/blood
Cadmium/toxicity
Mercury/blood
Mercury/toxicity
Mucocutaneous Lymph Node Syndrome/blood
Mucocutaneous Lymph Node Syndrome/etiology
Seafood/toxicity
[Mh] MeSH terms secundary: African Continental Ancestry Group/statistics & numerical data
Asian Continental Ancestry Group/statistics & numerical data
Child, Preschool
Cohort Studies
European Continental Ancestry Group/statistics & numerical data
Female
Hispanic Americans/statistics & numerical data
Humans
Infant
Male
Mucocutaneous Lymph Node Syndrome/ethnology
Risk Factors
United States/ethnology
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:00BH33GNGH (Cadmium); FXS1BY2PGL (Mercury)
[Em] Entry month:1609
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:IM
[Da] Date of entry for processing:160108
[St] Status:MEDLINE

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[PMID]: 26109979
[Au] Autor:Khodashenas E; Aelami M; Balali-Mood M
[Ad] Address:Department of Pediatrics, Sheikh Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.
[Ti] Title:Mercury poisoning in two 13-year-old twin sisters.
[So] Source:J Res Med Sci;20(3):308-11, 2015 Mar.
[Is] ISSN:1735-1995
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Mercury (Hg) is a toxic agent that evaporates in room temperature and its inhalation may cause poisoning. Due to the nonspecific symptoms, diagnosis is difficult in special circumstances with no initial history of Hg exposure. We report two such cases of Hg poisoning. The patients were two sisters, presenting with pain in extremities, itchy rashes, sweating, salivation, weakness, and mood changes. They have used a compound that contains mercury, for treatment of pedicullosis three months before admission. This compound was purchased from a herbal shop and was applied locally on the scalps for 2 days. Their urinary mercury concentrations were 50 and 70 mg/L. They were successfully treated by D-penicillamine and gabapentin. In a patient with any kind of bone and joint pain, skin rash erythema and peripheral neuropathy, mercury poisoning should be considered as a differential diagnosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1506
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:150626
[St] Status:PubMed-not-MEDLINE

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[PMID]: 25948960
[Au] Autor:Austin DW; Spolding B; Gondalia S; Shandley K; Palombo EA; Knowles S; Walder K
[Ad] Address:School of Psychology, Deakin University, Victoria.
[Ti] Title:Genetic variation associated with hypersensitivity to mercury.
[So] Source:Toxicol Int;21(3):236-41, 2014 Sep-Dec.
[Is] ISSN:0971-6580
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Very little is known about mechanisms of idiosyncratic sensitivity to the damaging effects of mercury (Hg); however, there is likely a genetic component. The aim of the present study was to search for genetic variation in genes thought to be involved in Hg metabolism and transport in a group of individuals identified as having elevated Hg sensitivity compared to a normal control group. MATERIALS AND METHODS: Survivors of pink disease (PD; infantile acrodynia) are a population of clinically identifiable individuals who are Hg sensitive. In the present study, single nucleotide polymorphisms in genes thought to be involved in Hg transport and metabolism were compared across two groups: (i) PD survivors (n = 25); and (ii) age- and sex-matched healthy controls (n = 25). RESULTS: Analyses revealed significant differences between groups in genotype frequencies for rs662 in the gene encoding paraoxanase 1 (PON1) and rs1801131 in the gene encoding methylenetetrahydrofolate reductase (MTHFR). CONCLUSIONS: We have identified two genetic polymorphisms associated with increased sensitivity to Hg. Genetic variation in MTHFR and PON1 significantly differentiated a group formerly diagnosed with PD (a condition of Hg hypersensitivity) with age- and gender-matched healthy controls.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:150508
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/0971-6580.155327

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[PMID]: 24995277
[Au] Autor:Hooker B; Kern J; Geier D; Haley B; Sykes L; King P; Geier M
[Ad] Address:Simpson University, 2211 College View Drive, Redding, CA 96001, USA.
[Ti] Title:Methodological issues and evidence of malfeasance in research purporting to show thimerosal in vaccines is safe.
[So] Source:Biomed Res Int;2014:247218, 2014.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:There are over 165 studies that have focused on Thimerosal, an organic-mercury (Hg) based compound, used as a preservative in many childhood vaccines, and found it to be harmful. Of these, 16 were conducted to specifically examine the effects of Thimerosal on human infants or children with reported outcomes of death; acrodynia; poisoning; allergic reaction; malformations; auto-immune reaction; Well's syndrome; developmental delay; and neurodevelopmental disorders, including tics, speech delay, language delay, attention deficit disorder, and autism. In contrast, the United States Centers for Disease Control and Prevention states that Thimerosal is safe and there is "no relationship between [T]himerosal[-]containing vaccines and autism rates in children." This is puzzling because, in a study conducted directly by CDC epidemiologists, a 7.6-fold increased risk of autism from exposure to Thimerosal during infancy was found. The CDC's current stance that Thimerosal is safe and that there is no relationship between Thimerosal and autism is based on six specific published epidemiological studies coauthored and sponsored by the CDC. The purpose of this review is to examine these six publications and analyze possible reasons why their published outcomes are so different from the results of investigations by multiple independent research groups over the past 75+ years.
[Mh] MeSH terms primary: Autistic Disorder/chemically induced
Preservatives, Pharmaceutical/adverse effects
Thimerosal/adverse effects
Vaccines/adverse effects
[Mh] MeSH terms secundary: Autistic Disorder/pathology
Humans
Infant
Preservatives, Pharmaceutical/administration & dosage
Thimerosal/administration & dosage
United States
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Name of substance:0 (Preservatives, Pharmaceutical); 0 (Vaccines); 2225PI3MOV (Thimerosal)
[Em] Entry month:1502
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:IM
[Da] Date of entry for processing:140705
[St] Status:MEDLINE
[do] DOI:10.1155/2014/247218

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[PMID]: 24174958
[Au] Autor:Yeter D; Deth R; Kuo HC
[Ad] Address:Shawnee, KS, USA.
[Ti] Title:Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome.
[So] Source:Korean Circ J;43(9):581-91, 2013 Sep.
[Is] ISSN:1738-5520
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract: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 Ca(2+) release. Hg(2+) sensitizes inositol 1,4,5-triphosphate (IP3) receptors at low doses, which release Ca(2+) 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 resulting from reduced genetic expressions of ITPKC in KS would promote IP3, which increases Ca(2+) release. Hg(2+) 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 lesions in KS. Accumulation of norepinephrine or epinephrine would potentiate Hg(2+)-induced calcium influx by increasing IP3 production and increasing the permeability of cardiac sarcolemma to Ca(2+). Norepinephrine and epinephrine also promote the secretion of atrial natriuretic peptide, a potent vasodilator that suppresses the release of vasoconstrictors. Elevated catecholamine levels can induce hypertension and tachycardia, while increased arterial pressure and a rapid heart rate would promote arterial vasodilation and subsequent fatal thromboses, particularly in tandem. Genetic risk factors may explain why only a susceptible subset of children develops KS although mercury exposure from methylmercury in fish or thimerosal in pediatric vaccines is nearly ubiquitous. During the infantile acrodynia epidemic, only 1 in 500 children developed acrodynia whereas mercury exposure was very common due to the use of teething powders. This hypothesis mirrors the leading theory for KS in which a widespread infection only induces KS in susceptible children. Acrodynia can mimic the clinical picture of KS, leading to its inclusion in the differential diagnosis for KS. Catecholamine levels are often elevated in acrodynia and may also play a role in KS. We conclude that KS may be the acute febrile form of acrodynia.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1406
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Da] Date of entry for processing:131101
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4070/kcj.2013.43.9.581

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[PMID]: 23183295
[Au] Autor:Rosenberg IH
[Ad] Address:Jean Mayer USDA Human Nutrition Research Center on Aging and Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA 02111, USA. irwin.rosenberg @ tufts.edu
[Ti] Title:A history of the isolation and identification of vitamin B(6).
[So] Source:Ann Nutr Metab;61(3):236-8, 2012.
[Is] ISSN:1421-9697
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:In the 1930s, Rudolf Peters showed that young rats kept on a semi-synthetic diet with added thiamin and riboflavin but no other supplement developed 'rat acrodynia', a condition characterized by severe cutaneous lesions. In 1934, Paul György showed that the factor which cured 'rat acrodynia' was vitamin B(6). Other studies soon showed that vitamin B(6) deficiency produced convulsions in rats, pigs, and dogs, and a microcytic anemia in certain animals. Samuel Lepkovsky isolated and crystallized vitamin B(6) in 1938. The following year, Leslie Harris and Karl Folkers, and Richard Kuhn and his associates independently showed that vitamin B(6) was a pyridine derivative, 3-hydroxy-4,5-dihydroxy-methyl-2-methyl-pyridine. György proposed the term pyridoxine for this derivative. Esmond Snell developed a microbiological growth assay in 1942 that led to the characterization of pyridoxamine, the animated product of pyridoxine, and pyridoxal, the formyl derivative of pyridoxine. Further studies showed that pyridoxal, pyridoxamine, and pyridoxine have largely equal activity in animals and owe their vitamin activity to the ability of the organism to convert them into the enzymatically active form pyridoxal-5-phosphate. Pyridoxal-5-phosphate plays a role in a wide variety of enzyme systems, especially in the metabolic utilization and transformation of amino acids.
[Mh] MeSH terms primary: Vitamin B 6/chemistry
Vitamin B 6/history
Vitamin B 6/isolation & purification
Vitamin B 6/pharmacology
[Mh] MeSH terms secundary: Animals
Dogs
History, 20th Century
Pyridoxal Phosphate/metabolism
Pyridoxamine/metabolism
Pyridoxine/metabolism
Rats
Swine
Vitamin B 6 Deficiency/drug therapy
Vitamin B 6 Deficiency/physiopathology
Vitamins/metabolism
[Pt] Publication type:HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Vitamins); 5V5IOJ8338 (Pyridoxal Phosphate); 6466NM3W93 (Pyridoxamine); 8059-24-3 (Vitamin B 6); KV2JZ1BI6Z (Pyridoxine)
[Em] Entry month:1304
[Cu] Class update date: 151119
[Lr] Last revision date:151119
[Js] Journal subset:IM
[Da] Date of entry for processing:121128
[St] Status:MEDLINE
[do] DOI:10.1159/000343113

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[PMID]: 22863825
[Au] Autor:Brannan EH; Su S; Alverson BK
[Ad] Address:Department of Pediatrics, Rhode Island Hospital, Providence, RI 02903, USA.
[Ti] Title:Elemental mercury poisoning presenting as hypertension in a young child.
[So] Source:Pediatr Emerg Care;28(8):812-4, 2012 Aug.
[Is] ISSN:1535-1815
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mercury intoxication is an uncommon cause of hypertension in children and can mimic several other diseases, such as pheochromocytoma and vasculitis. Mercury intoxication can present as a diagnostic challenge because levels of catecholamines may be elevated, suggesting that the etiology is a catecholamine-secreting tumor. Once acrodynia is identified as a primary symptom, a 24-hour urine mercury level can confirm the diagnosis. Inclusion of mercury intoxication in the differential diagnosis early on can help avoid unnecessary and invasive diagnostic tests and therapeutic interventions. We discuss a case of mercury intoxication in a 3-year-old girl presenting with hypertension and acrodynia, without a known history of exposure. Chelation therapy successfully treated our patient's mercury intoxication. However, it was also necessary to concurrently treat her hypertension and the pain associated with her acrodynia. Because there were no known risk factors for mercury poisoning in this case, and because ritual use of mercury is common in much of the United States, we recommend high clinical suspicion and subsequent testing in all cases of acrodynia.
[Mh] MeSH terms primary: Acrodynia/diagnosis
Hypertension/etiology
Mercury Compounds/adverse effects
[Mh] MeSH terms secundary: Abdominal Pain/etiology
Acrodynia/etiology
Acrodynia/therapy
Air Pollution, Indoor/adverse effects
Catecholamines/analysis
Chelating Agents/therapeutic use
Chelation Therapy
Child, Preschool
Environmental Exposure/adverse effects
Exanthema/etiology
Female
Humans
Hypertension/therapy
Mercury Compounds/urine
Succimer/therapeutic use
Tachycardia/etiology
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Catecholamines); 0 (Chelating Agents); 0 (Mercury Compounds); DX1U2629QE (Succimer)
[Em] Entry month:1305
[Cu] Class update date: 131121
[Lr] Last revision date:131121
[Js] Journal subset:IM
[Da] Date of entry for processing:120807
[St] Status:MEDLINE
[do] DOI:10.1097/PEC.0b013e3182628a05


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