ORIGINAL_ARTICLE
Indoor Air Quality and Severity of COVID-19: Where Communicable and Non-communicable Preventive Measures Meet
https://apjmt.mums.ac.ir/article_15312_c8be8fd6f2fa7a69583b7840b3c1c9ba.pdf
2020-03-01
1
2
10.22038/apjmt.2020.15312
Indoor Air Quality
Corona
COVID-19
Reza
Afshari
afsharireza@yahoo.com
1
Division of Occupational and Environmental Health, School of population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada
LEAD_AUTHOR
1. Mishra KP. Lead exposure and its impact on immune system: a review. Toxicol In Vitro 2009;23:969-72.
1
2. Carugno M, Dentali F, Mathieu G, Fontanella A, Mariani J, Bordini L, et al. PM10 exposure is associated with increased hospitalizations for respiratory syncytial virus bronchiolitis among infants in Lombardy, Italy. Environ Res 2018;166:452-7.
2
3. Billionnet C, Gay E, Kirchner S, Leynaert B, Annesi-Maesano I. Quantitative assessments of indoor air pollution and respiratory health in a population-based sample of French dwellings. Environ Res 2011;111:425-34.
3
4. McGrath M. Coronavirus: Air pollution and CO2 fall rapidly as virus spreads. BBC News. 2020 March 19. Available from: https://www.bbc.com/news/science-environment-51944780
4
ORIGINAL_ARTICLE
Oxidative DNA Damage and Pro-inflammatory Response In Chronic Exposure To Cement Dust
Background: Inflammatory cell activation, oxidative stress and oxidative DNA damage have been associated with exposure to cement dust. Biomarkers of oxidative stress, oxidative DNA damage, inflammation and heavy metals were estimated in cement loaders. Methods: Ninety men (45 cement loaders and 45 controls) were recruited into this comparative cross-sectional study. Total antioxidant capacity (TAC), total plasma peroxides (TPP), malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO) and uric acid (UA) were estimated by colorimetry, arsenic (As), chromium (Cr) and cadmium (Cd) by atomic absorption spectrophotometry and tumor necrosis factor alpha (TNF-α), 8-hydroxy-2-deoxyguanosine (8-OHdG) by enzyme linked immunosorbent assay. Results: Cement loaders had increased lipid peroxidation (MDA, TPP, OSI), inflammation (TNF-ɑ) and heavy metals (As, Cr) and lower antioxidants (UA, TAC, GSH) compared to controls (p<0.05). Increasing duration of exposure to cement dust was associated with higher lipid peroxidation, Cd, TNF-α and oxidative DNA damage (8-OHdG) (p<0.05). Negative correlation was observed between TAC and duration of exposure (r=-0.375, p=0.011) and positive correlations between TPP and duration of exposure (r=0.614, p=0.000), TNF-α and 8-OHdG (r=0.492, p=0.001) in cement loaders. Conclusion: Chronic exposure to cement dust is associated with depletion of antioxidants, increased lipid peroxidation, oxidative stress, inflammation and oxidative DNA damage. These may be implicated in the development of chronic lung conditions.
https://apjmt.mums.ac.ir/article_15313_4c78440dfb269187c5d7a86b30a8af22.pdf
2020-03-20
3
10
10.22038/apjmt.2020.15313
cement
Heavy metals
Inflammation Oxidative Stress
Lara
Obaji-Ogar
laraariye71@yahoo.com
1
Department of Medical Laboratory Science,University of Calabar, Nigeria
AUTHOR
Augusta
Nsonwu-Anyanwu
austadechic@yahoo.com
2
University of Calabar, Nigeria
LEAD_AUTHOR
Friday
Odum
destinedgodwins@gmail.com
3
Department of Medical Laboratory Science, University of Calabar, Nigeria
AUTHOR
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41
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42
ORIGINAL_ARTICLE
Lead Exposure Effect on Peripheral Blood Parameters among People around Bus Terminal in Yogyakarta
Background: Lead is a dangerous substance that can impact the blood components. Lead toxicity can cause imbalance in the homeostasis process of blood peripheral. The aim of this study is to search impact of lead exposure on peripheral blood parameter alterations among people around bus terminals in Yogyakarta. Methods: This study is a cross sectional research design with convenience sampling method. According to calculation of sample size, 72 respondents had fulfilled the inclusion criteria. The independent variable was lead exposure and dependent variables were peripheral blood parameters including leucocytes, erythrocytes, hemoglobin, and platelets. Lead exposure was measured by atomic absorption spectrophotometer (AAS) and peripheral blood parameters were measured by automatic hematology analyzer. Those variables were analyzed by linear regression. Results: Based on Independent T Test was found aged > 40 yo correlated with leukocyte (P =0.029), male workers correlated with leukocyte, erythrocyte, hemoglobin, and platelet (P =0.025,0.006, 0.000, and 0.031, respectively), smoking 1 packed per week associated with hemoglobin (P =0.006) and settlement 500 meter around terminal associated with leukocyte, erythrocyte, hemoglobin and platelet (P =0.025, 0.006, 0.000, and 0.031, respectively). Linear regression can predict level of leukocyte (β=0.32; CI 95= -0.207 to 0.643, P =0.006), erythrocyte (β=0.3; CI 95=-0.269 to 0.29; P =0.009), hemoglobin (β=0.33; CI 95=0.042 to 0.211; P =0.004), and platelet (β=0.25; CI 95=-0.548 to 0.73; P =0.029). Conclusion: Age > 40 years old associated with leukocyte; male gender associated with leukocyte, erythrocyte, hemoglobin, and platelet level, respectively; smoking 1 packed per week correlated with hemoglobin level; settlement 500 m around terminal associated with level leukocyte, erythrocyte, hemoglobin, and platelet level, respectively. Finally, level of lead can predict positively leukocyte, erythrocyte, hemoglobin, and platelet level respectively.
https://apjmt.mums.ac.ir/article_15314_981263311dafafc5e512e5dbe18b2d58.pdf
2020-03-20
11
16
10.22038/apjmt.2020.15314
Bus Terminal
Lead exposure
Peripheral Blood Parameters
Sani
Soleman
sani.rachman@uii.ac.id
1
Department of Public Health, Faculty of Medicine, Islamic University of Indonesia, Indonesia
LEAD_AUTHOR
Shafira
Andini
alifianashafira@gmail.com
2
Professional Medical Doctor Program, Suroto General Hospital, Faculty of Medicine, Universitas Islam Indonesia, Indonesia
AUTHOR
Linda
Rosita
linda.rosita@uii.ac.id
3
Department of Clinical Pathology, Faculty of Medicine, Universitas Islam Indonesia, Yogyakarta, Indonesia
AUTHOR
1. Agency for Toxic Substances and Disease Registry. Toxicology profile of lead. 2019, available from https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=96&tid=22 (Accessed April 1, 2020)
1
2. Lange J. Lead: An environmental neurotoxic agent [editorial]. J Headache Pain Mngt 2017;2:1–2.
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3. Assi MA, Hezmee M, Haron A, Sabri M, Rajion M. The detrimental effects of lead on human and animal health. Vet world 2016;9:660–71.
3
4. Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger D, et al. Low-level environmental lead exposure and children’s intellectual function: An international pooled analysis. Environ Health Perspect 2005;113:894–9.
4
5. Harari F, Sallsten G, Christensson A, Petkovic M, Hedblad B, Forsgard N, et al. Blood lead levels and decreased kidney function in a population-based cohort. AJKD 2018;72:381–9.
5
6. Dongre N, Suryakar A, Patil A, Ambekar J, Rathi D, et al. Biochemical effects of lead exposure on systolic and diastolic blood pressure, heme biosynthesis an hematological parameters in automobile workers on North Karnataka India. India J Clin Biochem 2011;26:400-6.
6
7. Zeng Z, Huo X, Zhang Y, Zhehong X, Zhang Y, Xu X. Lead associated is associated with risk of impaired coagulation in preschool children from an e-waste recycling area. Environ Sci Pollut Res Int 2018;25:20670-9.
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8. Lorenzo L, Corfiati M. Evaluation of peripheral blood neutrophil leucocytes in lead exposed workers. Int Arch Occup Environ Health 2006,79:491-8.
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9. Aminzadeh Z, Parsa E. Relationship between age and peripheral white blood cell count in patients with sepsis. Int J Prev Med 2011;2:238-42.
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10. Lunzhen J, Altfed M. Sex differences in infectious diseases-common but neglected. J Infect Dis 2014;209:S79-S80.
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11. Malenica M, Prnjavorac B, Bego T, Dujic T, Sabina S, Skrbo S, et al. Effect of cigarette smoking on hematological parameters in healthy population. Med Arch 2017;71:132-6.
11
12. Shipa SA, Rana MM, Miah MF, Alam MJ, Mahmud MGR. Effect of Intensity of Cigarette Smoking on Leukocytes among Adult Men and Women Smokers in Bangladesh. Asia PacJ Med Toxicol 2017;6:12-7
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13. Leon O, Hernandez E, Juarez F, Rodriguez E, Alaniz F, Carrillo A, et al. Association between blood lead level and delta aminolevulinic acid dehydratase in pregnant women. Int J Environt Res Public Health 2017;14:432-8.
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15. Fujita H, Nishitani C, Ogawa K. Lead, chemical porphyria and heme as a biological mediator. Tohuku J Exp Med 2002;196:53-64.
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16. Jangid A, John P, Yadav D, Mishra S, Sharma P. Impact of chronic lead exposure on selected biological markers. Indian J Clin Biochem 2012;27:83-9.
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17. Nelson C, Chan N, Chan P. Coarse basophilic stippling in lead poisoning. Blood 2017;129:3270.
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18. Barman T, Kalahasthi R, Rajmohan H. Effects of lead exposure on the status of platelet indices in workers involved in a lead-acid battery manufacturing plant. J Exposure Sci Environ epidemiol 2014;24:629-33.
18
19. Farkhondeh T, Boskabady M, Kohi M, Hashjin G, Moin M. Lead exposure affects inflammatory mediators, total and differential white blood cells in sensitized guinea pigs during and after sensitization. Drug Chem Toxicol 2014;37:329–33
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20. Ragini S, Khushbu P, Mogra S. Effects of prenatal and neonatal exposure to lead on white blood cells in Swiss mice. J Cell Mol Biol 2011;10:33-40.
20
21. Grecka M, Dobrakowski M, Boron M, Lisowska G, Kasperczyk A, Kasperczyk S. The influence of occupational chronic lead exposure on the levels of selected pro inflammatory cytokines and angiogenic factors. Human Experimen Toxicol 2017;36:467-73.
21
22. Fenga C, Gangemi S, Salvatore V, Falzone L, Libra M. Immunological effects of occupational exposure to lead (review). Mol Med Report 2017;15:3355-60.
22
23. Barbara E, Ritschel K, Markowitz M. Lead poisoning. Acad Pathol 2017;4:1-3.
23
ORIGINAL_ARTICLE
Hydrocarbon Associated Toxicities: a Case Series and Review of Literature
Background: Hydrocarbon associated toxicity (HAT) is an emerging threat related to wide scale industrialization and easy access to hydrocarbon-containing chemical compounds. Hydrocarbons have a unique toxicological profile and the principles of managing related toxidromes are considerably different from other toxins. Case reports: Here, we present a case series and in-depth review of the existing literature to show the risks associated with these seemingly harmless chemicals, and the approved guidelines for treating exposed patients. In all three cases, the hydrocarbon was a diluent for a pesticide. The amount of pesticide ingested was nontoxic, while the hydrocarbons caused a dose-independent physical toxicity to the lungs. Discussion: Hydrocarbon associated toxicities often go unnoticed because of their usage as diluents for various other toxic chemicals. Their treatment usually differs from other toxins that may have been consumed with them, albeit in insignificant quantities. Conclusion: Recognition of a hydrocarbon diluent in a consumed toxin marks the first step in the correct treatment. Correct labeling of chemical solutions containing hydrocarbons would go a long way in identifying these toxins.
https://apjmt.mums.ac.ir/article_15315_0898411f496077f378db4a3ded4ee485.pdf
2020-03-20
17
20
10.22038/apjmt.2020.15315
Hydrocarbon Toxicity
Kerosene
Pesticide
Toluene
Turpentine
Ishan
Lamba
drishanlamba@yahoo.com
1
Assistant Professor, Dr DY Patil Medical College, India
AUTHOR
Dhiraj
Jadhav
jdhiraj2010@yahoo.com
2
Assistant Professor, Dr DY Patil Medical College, Sant Tukaram Nagar Pimpri, India
LEAD_AUTHOR
1) Carey F. Hydrocarbon. Encyclopedia Britannica. Available from: https://britannica.com/science/hydrocarbon 2) Gummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report. Clin Toxicol (Phila) 2018;56:1213-1415.
1
3) Al Hazmi AM. Patterns of accidental poisoning in children in Jeddah, Saudi Arabia. Ann Saudi Med 1998;18:457–9.
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4) All India Institute of Medical Sciences, New Delhi. National Poisons Information Centre. http://www.aiims.edu/en/departments-and-centers/central-facilities. html?id=167
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5) Malini SS, Maithily K. Analysis of oxidative stress in chronic exposure to petroleum hydrocarbons in Karnataka, India. Asia Pac J Med Toxicol 2017;6:6-11.
4
6) Asawari R, Atmaram P, Bhagwan K, Priti D, Kavya S, Jabeen GA. Toxicological Pattern of Poisoning in Urban Hospitals of Western India. J Young Pharm 2017;9:315-20.
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7) Das Adhikari D, Das S, Winston A B, et al. A retrospective study on non-drug related poisoning in the community among children from south India. Hosp Pract (1995) 2017;45:39-45.
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8) Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila) 2014;52:479-89.
7
9) Banerjee I, Tripathi SK, Sinha R, Sengupta P. Pesticide use pattern among farmers in a rural district of West Bengal, India. J Nat Sci Biol Med 2014;15:313-6.
8
10) Van Eijk, AM, Ramanathapuram L, Sutton PL, Peddy N, Choubey S, Mohanty S, et al. (2016). The use of mosquito repellents at three sites in India with declining malaria transmission: surveys in the community and clinic. Parasit Vectors 2016;9:418.
9
11) Jain R. An Efficient Screening Method for Detection of Toluene-based Inhalant Abuse in Urine by Gas Chromatography-Nitrogen Phosphorous Detector. Addict Disorder Treat 2013;14:1. 12) Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila) 2014;52:1032-83. 13) Nelson ME, Nasr I. Parenteral hydrocarbon injection and associated toxicities: two case reports. West J Emerg Med. 2013;14(5):431-434. 14) Sanprasert K, Tangtrongchitr T, Krairojananan N. Dichloromethane Injection: Case Report. Asia Pac J Med Toxicol 2018;7:84-5.
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15) Khanna P, Devgan SC, Arora VK, Shah A. Hydrocarbon pneumonitis following diesel siphonage. Indian J Chest Dis Allied Sci 2004;46: 129.
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16) ) LoVecchio F, Fulton SE. Ventricular fibrillation following inhalation of Glade air freshener. Eur J Emerg Med 2001;8: 153. 17) Ford JB, Sutter ME, Owen KP, Albertson TE. Volatile substance misuse: an updated review of toxicity and treatment. Clin Rev Allergy Immunol 2014;46: 19-33. 18) Herskowitz A, Ishii N, Schaumburg H. N-hexane neuropathy. A syndrome occurring as a result of industrial exposure. N Engl J Med 1971;285:82-5.
12
19) Choi SH, Lee SW, Hong YS, Kim SJ, Moon SW, Moon JD. Diagnostic radiopacity and hepatotoxicity following chloroform ingestion: a case report. Emerg Med J. 2006;23(5):394-395.
13
20) Benson BE, Hoppu K, Troutman WG, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila) 2013;51:140-6. 21) The Royal Children’s Hospital. Clinical practice guideline; Hydrocarbon poisoning. The Royal Children’s Hospital; Melbourne: 2017.
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22) Heise CW, LoVecchio F. Hydrocarbons and volatile substances. Tintinalli’s Emergency Medicine: A comprehensive study guide. 9th edition.
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23) Chyka PA. Benefits of extracorporeal membrane oxygenation for hydrocarbon pneumonitis. J Toxicol Clin Toxicol 1996;34:357-63. 24) Mastropietro CW, Valentine K. Early administration of intratracheal surfactant (calfactant) after hydrocarbon aspiration. Pediatrics 2011;127:e1600-e1604. 25) Laurent Y, Wallemacq P, Haufroid V, Renkin J, Liolios A, Hantson P. Electrocardiographic changes with segmental akinesia after chloral hydrate overdose. J Emerg Med. 2006;30:179-82.
16
ORIGINAL_ARTICLE
Uric Acid Lowering Effects of Psyllium Seeds on a Hyperuricemic Patient: A Case Report and Review of Literature
Background: Psyllium seeds, produced from Plantago ovata Forsk, are an herbal treatment generally used as a laxative. They also reportedly have lowering effects on some metabolic parameters such as blood glucose, lipids and uric acid. In this paper, we report the effect of this herbal medicine in reducing serum uric acid levels, without major adverse effects, in a hyperuricemic patient. Case report: A 51-year-old patient with a history of hyperuricemia (10.5 mg/dL in a recent measurement) gave consent to undergo a 40-day treatment using psyllium seeds with dosage of 83.3 mg/kg. Treatment was given in two 20-day courses: During the first course, the seeds were given daily and during the second course, the same dosage was given every other day. Serum uric acid levels decreased to 8.1 mg/dL and 6.8 mg/dL on the 20th and 40th days, respectively. No major adverse effects were observed, such as skin rashes, digestive disorders, muscular pain, allergic manifestations, abnormalities in liver and kidney function tests, and abnormalities in blood parameters. Conclusion: Psyllium seeds may be effective in reducing serum uric acid levels in hyperuricemia patients, and major adverse effects are not expected to occur. These data can be used for further research and designing clinical trials.
https://apjmt.mums.ac.ir/article_16319_3f6345bcd0aa0b3cfbb873e4f404e4a4.pdf
2020-03-20
21
24
10.22038/apjmt.2020.16319
Hyperuricemia
Psyllium
Uric acid
Xanthine Oxidase
Alireza
Ebadollahi-Natanzi
alireza_ebad@yahoo.com
1
Assistant Professor of Toxicology & Pharmacology, Medicinal plants Department, Imam Khomeini Higher Education Center, Agricultural Research, Education and Extension Organization (AREEO), Karaj, Iran.
LEAD_AUTHOR
Gholamreza
Arabrahmatipour
arab.mplants@gmail.com
2
Laboratory Sciences Expert, Farabi Hospital Laboratory, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Strazzullo P, Puig JG. Uric acid and oxidative stress: relative impact on cardiovascular risk. Nutr Metab Cardiovasc Dis2007;17: 409- 14.
1
Liote F. Hyperuricemia and gout. Curr Rheumatol Rep 2003;5: 227-34.
2
Kunle OF, Egharevba HO, Ahmadu PO. Standardization of herbal medicines- A review. IntJ Biodvers Conserv 2012;4: 101-12.
3
Ebadollahinatanzi A, Sabzevari O, Ghahremani MH. The effect of watercress on hepatic glutathione of intoxicated rats with acetaminophen. Toxicol Lett 2012;211S: 166.
4
Ebadollahinatanzi A, Arabrahmatipor G. The protective effects resulting from a combination of three medicinal plants on liver injury due to carbamazepine drug: A case report. Toxicol Lett 2016; 258S:105-6.
5
Ebadollahi - Natanzi A. Toxicity comparison of four Cruciferous plant extracts and evaluation of their cytotoxicity - radical scavenging correlations. Jundishapur J Nat Pharm Prod 2018;13: e13866.
6
Arabrahmatipour G, Ebadollahinatanzi A. The accelerated removal of kidney stones by concomitant use of camel thorn distillate and Rowatinex drug: A case report. Toxicol Lett 2018;295S: 265.
7
Zargari A. Medicinal plants. Volume 4, 6th ed. Iran: Tehran University Publication; 1997.
8
-Naghdi Badi H, Dastpak A, Ziai S. A review of Psyllium plant (Plantago ovata Forsk. and Plantago psyllium L.). J Med Plants 2004;1:1-14.
9
Ruiz-Ruiz JC, Matus-Basto AJ, Acereto-Escoffié P, Segura-Campos MR. Antioxidant and anti-inflammatory activities of phenolic compounds isolated from Melipona beecheii honey. Food Agr Immunol 2017;28: 1424-37.
10
Fang CH, Tsai CC, Shyong YJ, Yang CT, Li KY, LIn YW, et al. Effects of Highly oxygenated water in a hyperuricemia rat model. J Healthc Eng 2020;2020: 1323270.
11
World Medical Association Declaration of Helsinki. Ethical principles for medical research involving human subjects. Bull. World Health Organ 2001; 79:373-4. Available from: https://apps.who.int/iris/handle/10665/268312.
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Fallah Huseini H, Fakhrzadeh H, Dastpak A, Azarabadi M, Mohtashami Tokabny R. Review of antihyperlipedemic herbal medicine. J Med Plants 2005;3: 9-20.
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Diez R, Garcia JJ, Diez MJ, Sierra M, Sahagun AM, Calle AP, et al. Hypoglycemic and hypolipidemic potential of a high fiber diet in healthy versus diabetic rabbits. Biomed Res Int 2013;2013: 960568.
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Prasad C, Iqbal U, Westfall S, Prakash S. Management of hyperuricemia and gout by prebiotics and probiotics: potentials and limitations. Int J Probiotics Prebiotics 2017;12: 5-16.
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Day RO, Graham GG, Hicks M, McLachlan AJ, Stocker SL, Williams KM. Clinical pharmacokinetics and pharmacodynamics of allopurinol and oxypurinol. Clin Pharmacokinet 2007;46: 623–644.
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Hannan JMA, Ali L, Khaleque J, Akhter M, Flatt PR, Abdel-Wahab YHA. Aqueous extracts of husks of Plantago ovata reduce hyperglycaemia in type 1 and type 2 diabetes by inhibition of intestinal glucose absorption. Br J Nutr 2006;96: 131 –7.
17
-Ziai SA, Larijani B, Akhoondzadeh S, Fakhrzadeh H, Dastpak A, Bandarian F, et al. Psyllium decreased serum glucose and glycosylated hemoglobin significantly in diabetic outpatients. JEthnopharmacol 2005;102: 202 – 7.
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Ebadollahi-Natanzi A, Arab-Rahmatipour G. Psyllium together with allopurinol can efficiently reduce the increased serum level of uric acid, creatinine and urea: A case report. Iran J Toxicol 2017;11: 51-6.
19
Potapovich AI, Kostyuk VA. Comparative study of antioxidant properties and cytoprotective activity of flavonoids. Biochemistry (Mosc) 2003;68: 514-19.
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Kinoshita T, Lepp Z, Kawai Y, Terao J, Chuman H. An integrated database of flavonoids. Biofactors 2006;26: 179-88.
21
Ebadollahi Natanzi AR, Mahmoudian S, Minaeie B, Sabzevari O. Hepatoprotective activity of phloretin and hydroxychalcones against Acetaminophen induced hepatotoxicity in mice. Iran J Pharm Sci 2011;7: 89-97.
22
Scalbert A, Manach C, Morand C, Remesy C, Jimenez L. Dietary polyphenols and the prevention of diseases. Crit Rev Food Sci Nutr 2005;45: 287-306.
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Mo SF, Zhou F, Lv YZ, Hu QH, Zhang D, Kong LD. Hypouricemic action of selected flavonoids in mice: structure–activity relationships. Biol Pharm Bull 2007;30: 1551-6.
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Pacher P, Nivorozhkin A, Szabó C. Therapeutic effects of xanthine oxidase inhibitors: renaissance half a century after the discovery of allopurinol. Pharmacol Res 2006;58: 87–114.
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Gerdan V, Akkoc N, Ucan ES, Bulac Kir S. Paradoxical increase in uric acid level with allopurinol use in pyrazinamide-induced hyperuricemia. Singapore Med J 2013;54: e125-6.
26
Salem CB, Slim R, Fathallah N, Hmouda H. Drug-induced hyperuricaemia and gout. Rheumatology 2017;56: 679-88.
27
ORIGINAL_ARTICLE
Severe Calcium Channel Blocker Overdose and Successful Management: a Case Report and Literature Review
Background: Calcium channel blocker (CCB) toxicity is one of the most lethal and common drug overdoses encountered in the emergency department (ED). The toxicity of these drugs results from blockade of L-type calcium channels in smooth cells, myocardial cells, and beta cells of the pancreas. Severe toxicity can result in bradycardia, hypotension, hyperglycemia, metabolic acidosis, shock, cardiac arrest and death. According to the American Association of Poison Control Centers’ National Poison Data System’s annual report in 2015, cardiovascular medications were the fourth most common adult poisoning exposure and second most common cause of adult poisoning fatality in the USA. CCBs are responsible for a substantial portion of the mortality associated with cardiovascular medication overdose cases. Understanding the emergent management of CCB toxicity is essential. Treatment of patients with CCB overdose remains challenging especially in those with refractory hypotension and end organ dysfunction. Case Presentation: A 45-year-old male with massive amlodipine overdose presented to ED with syncope and severe hypotension. Intensive medical therapy (fluid resuscitation, inotropes, calcium gluconate, and hyperinsulinemia euglycemia therapy [HIET]) was initiated in the ED and continued in the Intensive Care Unit (ICU), and resulted in the patient’s total recovery, without any major complications. Fortunately, ECMO implantation (extracorporeal membrane oxygenation) was not required in this patient. Conclusion: Urgent administration of fluids, calcium, vasopressors, and HIET therapy seem to be the most well validated initial approaches to CCBs overdose treatment. Our successful management strategy should serve as a good learning experience as well as a recommendation for managing such patients.
https://apjmt.mums.ac.ir/article_15317_1b18c7c4459533644170fd8d05252819.pdf
2020-03-20
25
28
10.22038/apjmt.2020.15317
Amlodipine
Calcium Channel Blockers Overdose
Emergency Department
Hong Khai
Lau
lhongkhai@gmail.com
1
Department of Emergency Medicine, Sengkang General Hospial & Singapore General Hospital, Singapor
LEAD_AUTHOR
Kenneth
Boon Kiat Tan
kenneth.tan.b.k@singhealth.com.sg
2
Department of Emergency Medicine, Singapore General Hospital, Singapre
AUTHOR
Ponampalam
R
ponampalam@singhealth.com.sg
3
Department of Emergency Medicine, Singapore General Hospital, Singapore
AUTHOR
1). Jang DH, Nelson LS, Hoffman RS. Methylene blue in the treatment of refractory shock from an amlodipine overdose. Ann Emerg Med 2011; 58:565-7.
1
2). St-Onge M, Anseeuw K, Cantrell FL, Gilchrist IC, Hantson P, Bailey B., et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med 2017; 45: e306-e315.
2
3) Rana C, Das M, Traficante D, Kashani J. Massive Overdose of Calcium Channel Antagonist and Successful Management: A Case Report and Review of Management. J Clin Toxicol 2016; 6:319.
3
4) Burkes, R, Wendorf G. A multifaceted approach to calcium channel blocker overdose: A case report and literature review. Clin Case Rep 2015; 3: 566-9.
4
5) St-Onge M, Dubé PA, Gosselin S, et al. Treatment of calcium channel blocker poisoning: A systematic review. Clin Toxicol 2014; 52:92644.
5
6) Kanagarajan K, Marraffa JM, Bouchard NC, Krishnan P, Hoffman RS, Stork CM. The use of vasopressin in the setting of recalcitrant hypotension due to calcium channel blocker overdose. Clin Toxicol (Phila). 2007;45:56-9.
6
7) Sebe A, Dişel NR, Açıkalın Akpınar A, Karakoç E. Role of intravenous lipid emulsions in the management of calcium channel blocker and β-blocker overdose: 3 years experience of a university hospital. Postgrad Med 2015;127:119-24.
7
8) Doepker B, Healy W, Cortez E, Adkins EJ. High-dose insulin and intravenous lipid emulsion therapy for cardiogenic shock induced by intentional calcium-channel blocker and Beta-blocker overdose: a case series. J Emerg Med 2014;46:486-90.
8
9) Bekjarovski NG. Lipid Rescue Therapy and High-Dose insulin Euglycemic Therapy are Effective for Severe Refractory Calcium Channel Blocker Overdose: Case Report and Review of Literature. Asia Pac J Med Toxicol 2013; 2:114-6.
9
10) Bozkurt FT, Izdes S, Demir HO, Kayar Calili D, Hosgun D. Intravenous Lipid Emulsion Treatment and High-Dose Amlodipine Intoxication: A Case Report. Asia Pac J Med Toxicol 2019;8:140-3.
10
11) Weinberg RL, Bouchard NC, Abrams DC, Bacchetta M, Dzierba AL, Burkart KM, et al. Venoarterial extracorporeal membrane oxygenation for the management of massive amlodipine overdose. Perfusion 2014; 29: 53–6.
11
12). Maskell KF, Ferguson NM, Bain J, Wills BK. Survival after cardiac arrest: ECMO rescue therapy after amlodipine and metoprolol overdose. Cardiovasc Toxicol 2017 ;17:223-5.
12
13) George M, I-wen W. Extra Corporeal Membrane Oxygenation (ECMO) review of a lifesaving technology. J Thorac Dis 2015; 7: E166–E176.
13
ORIGINAL_ARTICLE
Methadone Toxicity with Electrocardiographic Sodium Channel Blockade Changes in a Pediatric Patient Post-cardiopulmonary Arrest: a Case Report
Background: Cardiopulmonary arrest in the pediatric population due to methadone toxicity is not commonly reported. Severe methadone toxicity often involves respiratory depression with reports of orthostatic hypotension, due to vasodilation, and QTc prolongation. Case presentation: A pair of toddler siblings presented in cardiopulmonary arrest due to methadone ingestion. They were successfully resuscitated with no significant neurobehavioral deficits despite a suspected prolonged “downtime.” After return of spontaneous circulation, the older sibling, a four-year old male, had electrocardiographs (ECGs) that were suggestive of sodium channel blockade. These changes were reversed following bicarbonate therapy. The two-year old child’s ECGs did not show such changes. Discussion: There is no prior clinical literature on sodium channel blockade in methadone toxicity. The older sibling’s ECG findings and response to bicarbonate therapy appeared to be consistent with sodium channel blockade. There have been preclinical data that suggest methadone cardiotoxicity may involve cardiac sodium channels. Pharmacogenetic variations could also explain how these effects may selectively manifest. Conclusion: Physicians should be aware of the possible toxicologic causes of cardiopulmonary arrest in the pediatric population. Pharmacogenetic variations may contribute to different clinical manifestations in methadone cardiotoxicity.
https://apjmt.mums.ac.ir/article_15316_9aceddb870f6c181f1d952a743e9089a.pdf
2020-03-20
29
32
10.22038/apjmt.2020.15316
Electrocardiography
Heart Arrest
Pediatrics
toxicology
Gene
Ong
geneong@yahoo.com
1
KK Women's and Children's Hospital, Singapore
LEAD_AUTHOR
1. Paul ABM, Simms L, Mahesan AM. The Toxicology of Methadone-Related Death in Infants Under 1 Year: Three Case Series and Review of the Literature. J Forensic Sci 2017 ;62:1414-7.
1
2. Alinejad S, Kazemi T, Zamani N, Hoffman RS, Mehrpour O. A systematic review of the cardiotoxicity of methadone. EXCLI J 2015;14:577-600.
2
3. Lewington LE, Shaffer C, Ornstein AE. Pediatric methadone ingestions: An under-recognized form of child maltreatment? Paediatr Child Health 2014;19:139-40.
3
4. Ghaemi N, Alikhani S, Bagheri S, Sezavar M. A Cross Sectional Study of Opioid Poisoning in Children at a Tertiary Center. Asia Pac J Med Toxicol 2016; 5: 115-8.
4
5. Hamedi A, Ataei A, Balali M, Ghahremani S, Ghahremani S. A Cross Sectional Study on Pediatric Methadone Poisoning in Northeast of Iran. Asia Pac J Med Toxicol 2016; 5: 75-8.
5
6. Lund-Jacobsen H. Cardio-respiratory toxicity of propoxyphene and norpropoxyphene in conscious rabbits. Acta Pharmacol Toxicol (Copenh) 1978 ;42:171-8.
6
7. Whitcomb DC, Gilliam FR, Starmer CF, Grant AO. Marked QRS complex abnormalities and sodium channel blockade by propoxyphene reversed with lidocaine. J Clin Invest 1989;84:1629-36.
7
8. Stork CM, Redd JT, Fine K, Hoffman RS. Propoxyphene-induced wide QRS complex dysrhythmia responsive to sodium bicarbonate--a case report. J Toxicol Clin1995;33:179-83.
8
9. Ulens C, Daenens P, Tytgat J. Norpropoxyphene-induced cardiotoxicity is associated with changes in ion-selectivity and gating of HERG currents. Cardiovasc Res 1999 ;44:568-78.
9
10. Stoetzer C, Kistner K, Stüber T, Wirths M, Schulze V, Doll T, et al. Methadone is a local anaesthetic-like inhibitor of neuronal Na+ channels and blocks excitability of mouse peripheral nerves. Br J Anaesth 2015;114:110-20.
10
11. Schulze V, Stoetzer C, O'Reilly AO, Eberhardt E, Foadi N, Ahrens J, et al. The opioid methadone induces a local anaesthetic-like inhibition of the cardiac Na⁺ channel, Na(v)1.5. Br J Pharmacol 2014;171:427–37.
11
12. Elkalioubie A, Allorge D, Robriquet L, Wiart JF, Garat A, Broly F, et al. Near-fatal tramadol cardiotoxicity in a CYP2D6 ultrarapid metabolizer. Eur J Clin Pharmacol 2011;67:855-8.
12
13. Yiannakopoulou E. Pharmacogenomics and Opioid Analgesics: Clinical Implications. Int J Genomics 2015;2015:368979.
13
14. Kharasch ED, Regina KJ, Blood J, Friedel C. Methadone Pharmacogenetics: CYP2B6 Polymorphisms Determine Plasma Concentrations, Clearance, and Metabolism. Anesthesiol 2015;123:1142-53.
14
ORIGINAL_ARTICLE
Hepatic Failure in a Young Woman Following Ingestion of Tribulus Terrestris
Background: Plants have been used for the treatment of a wide range of conditions since ancient times but some have side effects and toxic effects that limit their use. Tribulus terrestris is traditionally used for lowering blood pressure, inhibiting kidney stone formation and inducing weight loss. In this case study, we present an Iranian woman who suffered from liver failure after using this plant. Case presentation: A 31-year-old Iranian woman was admitted to Emam-Reza hospital due to epigastric pain radiating to back and shoulders, and weakness, Malas,neusia and icterus. Upon admission,, her vital signs were normal. She had been consuming Tribulus terrestris as an herbal tea , several times a day for 2-3 months, in order to lose weight. Upon physical examination, the patient had generalized icterus and laboratory tests showed elevated transaminases, PT, and INR. Various causes of hepatic failure, such as viral hepatitis and autoimmune hepatitis, were ruled out and the only probable diagnosis was toxin-induced liver failure. Conclusion: Herbal plants may have some beneficial medical effects but they can also cause toxicity. Consistent use and high dose of Tribulus terrestris may cause hepatic failure and death.
https://apjmt.mums.ac.ir/article_15318_4b06e797463c17e43102cac907868730.pdf
2020-03-20
33
34
10.22038/apjmt.2020.15318
Acute Liver Failure
Icterus
Liver Function Tests
Tribulus terrestris
Zahra
Ataee
ataeez@mums.ac.ir
1
Medical Toxicology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Bita
Dadpour
dadpourb@mums.ac.ir
2
Bita Dadpour, MD. Assistant Professor, Toxicology Department, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Navarro VJ. Herbal and dietary supplement hepatotoxicity. Semin Liver Dis 2009; 29:373-82.
1
2. Al-Ali M, Wahbi S, Twaij H, Al-Badr A. Tribulus terrestris: preliminary study of its diuretic and contractile effects and comparison with Zea mays. J Ethnopharmacol 2003;85:257-60.
2
3. Joshi VS, Parekh BB, Joshi MJ, Vaidya AD. Inhibition of the growth of urinary calcium hydrogen phosphate dihydrate crystals with aqueous extracts of Tribulus terrestris and Bergenia ligulata. Urol Res 2005;33:80-86.
3
4.Paula-Lopes T.R.V,Souza M.A,Paz K,Lopes R.A,Sala M.A,Regalo S.C.H,Rodrigues E.R. Hepatotoxicity of medical plants. XXXIII. Action of Tribulus Terrestris L. in rats. Botucatu 2006;8:150-6 5. Weerasinghe WS, Gawarammana IB, Colambage A. Substituted urea herbicide (Diuron) induced haemolytic anemia: A case of unknown complication in humans. Asia Pac J Med Toxicol 2019;8:136-9. 6. SellahewaKH, Sivakumaran S, Ruwanpathiranage T, Halpe SM, Thampoe MS. Niyangala (Gloriosa superba) poisoning complicated with SIADH. Asia Pac J Med Toxicol 2018;7:114-7. 7. Essabar L, Meskini T, Ettair S, Erreimi N, Mouane N. Harmful Use of Veterinary Drugs: Blindness Following Closantel Poisoning in a 5-Year-Old Girl. Asia Pac J Med Toxicol 2014;3:173-5. 8. Prakash D,Singh PN,Wahi SP. An evaluation of Tribulus terrestris Linn(Chota Gokharu). Indian Drugs 1985; 22:332-3.
4
9. Aslani MR, Movassaghi AR, Mohri M, Pedram M, Abavisani A. Experimental Tribulus terrestris poisoning in sheep: clinical, laboratory and pathological findings. Vet Res Commun 2003;27:53-62.
5
10.Paula-Lopes TRV, Moreti DFLC, Paz K, Prado FO, Paz J, Baldochi MR, et al. Estudo hematologic em ratos sob acao de plantas medicinais. Jornada de biomedicine da unifran 2005;1-6:89-91 [In Portuguese].
6