ORIGINAL_ARTICLE
Qualitative versus Quantitative Evaluation of Scientists' Impact: A Medical Toxicology Tale
Evaluation of scientists working in a specific area of science is necessary, as they may strive for same limited resources, grants and academic promotions. One of the most common and accepted methods of assessing the performance and impact of a scientist is calculating the number of citations for their publications. However, such method suffer from certain shortcomings. It has become more and more obvious that evaluation of scientists should be qualitative in addition to quantitative. Moreover, the evaluation process should be pragmatic and reflective of the priorities of an institution, a country or an intended population. In this context, a scoring scale called "360-degree researcher evaluation score" is proposed in this paper. Accordingly, scientists are evaluated in 5 independent domains including (I) science development, (II) economic impact, (III) policy impact, (IV) societal impact and (V) stewardship of research. This scale is designed for evaluation of impacts resulted from research activities and thus it excludes the educational programs done by a scientist. In general, it seems necessary that the evaluation process of a scientist’s impact moves from only scintometric indices to a combination of quantitative and qualitative indices.
https://apjmt.mums.ac.ir/article_3729_0d06e1d33b7293b680330b3520103f7f.pdf
2014-12-01
134
140
10.22038/apjmt.2014.3729
Comparative Effectiveness Research
Cost-Benefit Analysis
Employee Performance Appraisal
Journal Impact Factor
Social Change
Reza
Afshari
afsharireza@yahoo.com
1
Addiction Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Seyed Mostafa
Monzavi
seyedmostafamonzavi@gmail.com
2
Addiction Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Kumar MJ. Evaluating Scientists: Citations, Impact Factor, h-Index, Online Page Hits and What Else? IETE Technical Rev 2009;26:165-8.
1
Van Houten BA, Phelps J, Barnes M, Suk WA. Evaluating scientific impact. Environ Health Perspect 2000;108:A392-3.
2
Hirsch JE. An index to quantify an individual's scientific research output. Proc Natl Acad Sci U S A 2005;102:16569-72.
3
Afshari R. What is the “Best Research” for Low Income Countries? Asia Pac J Med Toxicol 2013;2:1.
4
Krause ET. Impact: Take peer review into account. Nature 2013;503:198.
5
Stroobants K, Godecharle S, Brouwers S. Research evaluation: Flanders overrates impact factors. Nature 2013;500:29.
6
Jamali HR, Asadi S, Sedghi S. Research Outcome and Impact Assessment of Medical Research. 1st ed. Tehran: Iranian Academy of Medical Sciences; 2012.
7
Harzing AW. Publish or Perish [Internet]. 2007 [Cited 2014 November 5] Available from: http://www.harzing.com/pop.htm
8
Cellini SR, Kee JE. Cost-effectiveness and cost-benefit analysis. In: Wholey JS, Hatry HP, Newcomer KE, editors. Handbook of Practical Program Evaluation. 3rd ed. San Francisco, USA: Jossey-Bass; 2010. p.493-530.
9
Afshari R. Scientometric Analysis of Toxicology in Asia Pacific Region: Signs of Growth. Asia Pac J Med Toxicol 2014;3:92-6.
10
Rawat S, Meena S. Publish or perish: Where are we heading? J Res Med Sci 2014;19:87-9.
11
Afshari R. Empowerment of Medical Toxicology in Asia Pacific Region. Asia Pac J Med Toxicol 2013;2:36.
12
ORIGINAL_ARTICLE
Mortality Analysis of Patients with Paraquat Poisoning Treated at Two University Hospitals in Shiraz, Iran
Background: Poisoning with paraquat (PQ) is highly fatal. In this study; demographic and clinical characteristics of a series of patients with acute PQ poisoning treated at two university hospitals in Shiraz, Iran are presented and predictive factors for mortality are analyzed. Methods: This was an analytical cross-sectional study on consecutive PQ poisoned patients admitted to Shoushtari and Ali Asghar hospitals in Shiraz, Iran during 21st March 2012 to 20th March 2013. To find out predictive factors for mortality, independent variables were compared between death and survival using Fisher’s exact test. To determine the factors that had the strongest impact on mortality, logistic regression analysis was done. Results: Fifty-two patients (73.1% men) were included with mean age of 28.2 ± 10.3 years. The most common clinical findings were nausea and vomiting (88.5%), pharyngeal congestion (82.7%), epigastric pain (80.8%), increased creatinine (57.7%), increased liver enzymes (53.8%) and metabolic acidosis (53.8%). The volume of poison ingested was significantly higher in deceased compared to survived patients (P < 0.001). Death was significantly higher in patients with pharyngeal congestion (P = 0.001), respiratory distress (P < 0.001), loss of consciousness (P = 0.025), increased creatinine (P < 0.001), increased liver enzymes (P < 0.001), metabolic acidosis (P < 0.001), increased bilirubin (P < 0.001), respiratory acidosis (P = 0.001), increased INR (P = 0.023), suicidal intention (P < 0.001), and oral exposure (P = 0.047). After putting these factors to logistic regression model, only respiratory distress, increased bilirubin, increased liver enzymes and increased creatinine continued to be significantly associated with mortality. Conlcusion: PQ poisoning is associated with high mortality requiring an immediate assessment of patients and prediction of prognosis. Renal and hepatic failure in addition to respiratory distress can be the strongest risk factors for poor prognosis in acute PQ poisoning.
https://apjmt.mums.ac.ir/article_3730_4a62d9bbd320c65b8b8cb6a9eeab7f8b.pdf
2014-12-01
141
145
10.22038/apjmt.2014.3730
Mortality
Paraquat
Pesticides
Poisoning
Risk factors
Fazel
Goudarzi
goudarzi.fazel@gmail.com
1
Department of Medical Toxicology and Forensic Pathology, Ali-Asghar Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Jila
Armandeh
2
Trauma Research Center, Shahid Rajaee (Emtiaz) Trauma Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Kazem
Jamali
jamali.kazem@yahoo.com
3
Trauma Research Center, Shahid Rajaee (Emtiaz) Trauma Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
LEAD_AUTHOR
Hashem
Rahmati
4
Community Based Psychiatric Care Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Amirhosein
Meisami
5
Department of Emergency Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Hamidreza
Abbasi
6
Trauma Research Center, Shahid Rajaee (Emtiaz) Trauma Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Agarwal R, Srinivas R, Aggarwal AN, Gupta D. Experience with paraquat poisoning in a respiratory intensive care unit in North India. Singapore Med J 2006;47:1033-7.
1
Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol 2011;72:745-57.
2
Chen JG, Eldridge DL, Lodeserto FJ, Ming DY, Turner KM, Vanderford JL, et al. Paraquat ingestion: a challenging diagnosis. Pediatrics 2010;125:e1505-9.
3
Suntres ZE. Role of antioxidants in paraquat toxicity. Toxicology. 2002;180:65-77.
4
Somayajulu-Niţu M, Sandhu JK, Cohen J, Sikorska M, Sridhar TS, Matei A, et al. Paraquat induces oxidative stress, neuronal loss in substantia nigra region and parkinsonism in adult rats: neuroprotection and amelioration of symptoms by water-soluble formulation of coenzyme Q10. BMC Neurosci 2009;10:88.
5
Afshari R, Mehrpour O. Pesticide Poisoning. In: Afshari R, Monzavi SM, editors. Afshari’s Clinical Toxicology and Poisoning Emergency Care. 2nd ed. Mashhad: Mashhad University of Medical Sciences Publication; 2012. p. 267-84.
6
Yoon SC. Clinical outcome of paraquat poisoning. Korean J Intern Med 2009;24:93-4.
7
Lin JL, Lin-Tan DT, Chen KH, Huang WH, Hsu CW, Hsu HH, et al. Improved survival in severe paraquat poisoning with repeated pulse therapy of cyclophosphamide and steroids. Intensive Care Med 2011;37:1006-13.
8
Chang MW, Chang SS, Lee CC, Sheu BF, Young YR. Hypokalemia and hypothermia are associated with 30-day mortality in patients with acute paraquat poisoning. Am J Med Sci 2008;335:451-6.
9
Afshari R, Majdzadeh R, Balali-Mood M. Pattern of acute poisonings in Mashhad, Iran 1993-2000. J Toxicol Clin Toxicol 2004;42:965-75.
10
Hassanian-Moghaddam H, Zamani N, Rahimi M, Shadnia S, Pajoumand A, Sarjami S. Acute adult and adolescent poisoning in Tehran, Iran; the epidemiologic trend between 2006 and 2011. Arch Iran Med 2014;17:534-8.
11
Sabzghabaee AM, Eizadi-Mood N, Montazeri K, Yaraghi A, Golabi M. Fatality in paraquat poisoning. Singapore Med J 2010;51:496-500.
12
Hwang KY, Lee EY, Hong SY. Paraquat intoxication in Korea. Arch Environ Health 2002;57:162-6.
13
Sandhu JS, Dhiman A, Mahajan R, Sandhu P. Outcome of paraquat poisoning-a five year study. Indian J Nephrol 2003;13:64-8.
14
Hsieh YW, Lin JL, Lee SY, Weng CH, Yang HY, Liu SH, et al. Paraquat poisoning in pediatric patients. Pediatr Emerg Care 2013;29:487-91.
15
Hong SY, Yang DH, Hwang KY. Associations between laboratory parameters and outcome of paraquat poisoning. Toxicol Lett 2000;118:53-9.
16
Lee EY, Hwang KY, Yang JO, Hong SY. Predictors of survival after acute paraquat poisoning. Toxicol Ind Health 2002;18:201-6.
17
Liu P, He YZ, Wang HC, Li G, Zhang CG, Zhang XG, et al. Study on the prognosis of patients with acute paraquat intoxication. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2011;29:212-5. (In Chinese)
18
Holubek WJ, Hoffman RS, Goldfarb DS, Nelson LS. Use of hemodialysis and hemoperfusion in poisoned patients. Kidney Int 2008;74:1327-34.
19
Pavan M. Acute kidney injury following Paraquat poisoning in India. Iran J Kidney Dis 2013;7:64-6.
20
Cherukuri H, Pramoda K, Rohini D, Thunga G, Vijaynarayana K, Sreedharan N, et al. Demographics, clinical characteristics and management of herbicide poisoning in tertiary care hospital. Toxicol Int 2014;21:209-13.
21
Bardin PG, Van Eeden SF. Organophosphate poisoning: grading the severity and comparing treatment between atropine and glycopyrrolate. Crit Care Med 1990;18:956-60.
22
Iseki K, Ozawa A, Seino K, Goto K, Tase C. The Suicide Pandemic of Hydrogen Sulfide Poisoning in Japan. Asia Pac J Med Toxicol 2013;3:13-7.
23
Senarathna L, Eddleston M, Wilks MF, Woollen BH, Tomenson JA, Roberts DM, et al. Prediction of outcome after paraquat poisoning by measurement of the plasma paraquat concentration. QJM 2009;102:251-9.
24
Jones AL, Elton R, Flanagan R. Multiple logistic regression analysis of plasma paraquat concentrations as a predictor of outcome in 375 cases of paraquat poisoning. QJM 1999;92:573-8.
25
ORIGINAL_ARTICLE
Outcome of Patients with Cholinergic Insecticide Poisoning Treated with Gastric Lavage: A Prospective Observational Cohort Study
Background: Gastric lavage (GL) is one of the most commonly used decontamination method for cholinergic insecticide ingestion in developing countries despite lack of supporting evidence. This study was designed to evaluate the outcome of patients with cholinergic insecticide poisoning treated with GL in regards to timing and frequency of the procedure. Methods: In this prospective observational cohort study, GL was planned to be administered to patients with cholinergic insecticide poisoning after initial stabilization irrespective of lavage given in peripheral hospitals. Therefore, some patients received one procedure (single GL) and some received more than one procedure (multiple GL). Early GL was defined as GL given within one hour of poison exposure and late GL was referred to performing the procedure after one hour. Results: During the study period, 238 patients with cholinergic insecticide poisoning received GL comprising of 93 who received early, 145 who received late, 127 who received single and 111 who received multiple GL. Seventy-six GL treated patients (31.9%) died. Mortality, early RF and duration of assisted ventilation were not significantly different between patients receiving early and late, or single and multiple GL. Patients receiving multiple GL compared to those who received single GL developed late RF (9.0% vs. 20.5%, P = 0.01) and IMS (9.9% vs. 23.6%, P = 0.005) in significantly lesser extents. In multiple logistic regression analysis, effect of multiple GL on IMS and late RF remained significant (P = 0.04). Conclusion: Number or timing of GL does not show any association with mortality while multiple GL had protective effect against development of late RF and IMS. Hence, GL might be beneficial in cholinergic insecticide poisoning.
https://apjmt.mums.ac.ir/article_3750_3825c21addc95f0388937dc203a8a4b5.pdf
2014-12-01
146
151
10.22038/apjmt.2014.3750
Gastric Lavage
Cholinesterase Inhibitors
Poisoning
Insecticides
Respiratory insufficiency
Mekkattukunnel
Andrews
anjulioness@gmail.com
1
Department of Medicine, Government Medical College, Thrissur, Kerala, India
LEAD_AUTHOR
Indira
Madhavan
drindirarun@yahoo.com
2
Department of Medicine, Government Medical College, Thrissur, Kerala, India
AUTHOR
Rakesh
Parakadavathu
rakeshtp@yahoo.com
3
Department of Medicine, Government Medical College, Thrissur, Kerala, India
AUTHOR
Hithesh Sanker Thottungal
Sankaranarayanan
4
Department of Forensic Medicine, Government Medical College, Thrissur, Kerala, India
AUTHOR
Gunnell D, Eddleston M. Suicide by intentional ingestion of pesticides: a continuing tragedy in developing countries. Int J Epidemiol 2003;32:902-9.
1
Dewan G. Analysis of Recent Situation of Pesticide Poisoning in Bangladesh: Is There a Proper Estimate? Asia Pac J Med Toxicol 2014;3:76-83.
2
Munidasa UA, Gawarammana IB, Kularatne SAM, Kumarasiri PVR, Goonasekera CDA. Survival pattern in patients with acute organophosphate poisoning receiving intensive care. J Toxicol Clin Toxicol 2004;42:343-7.
3
Due P. Effectiveness of High Dose Pralidoxime for Treatment of Organophosphate Poisoning. Asia Pac J Med Toxicol 2014;3:97-103.
4
Mahesh M, Gowdar M, Venkatesh CR. A Study on Two Dose Regimens of Pralidoxime in the Management of Organophosphate Poisoning. Asia Pac J Med Toxicol 2013;2:121-5.
5
Benson BE, Hoppu K, Troutman WG, Bedry R, Erdman A, Höjer J, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila) 2013;51:140-6.
6
Dyas J, Krishna CV, Aldridge GL, Thompson JP. Gastric Lavage – An Audit of Current UK Practice. Clin Toxicol (Phila) 2010;48:646-7.
7
Okumura Y, Shimizu S, Ishikawa KB, Matsuda S, Fushimi K, Ito H. Comparison of emergency hospital admissions for drug poisoning and major diseases: a retrospective observational study using a nationwide administrative discharge database. BMJ Open 2012;2:e001857.
8
Bhattarai MD. Managing self poisoning. Gastric lavage is perhaps more important in developing countries. BMJ 2000;320:711.
9
Albertson TE, Owen KP, Sutter ME, Chan AL. Gastrointestinal decontamination in the acutely poisoned patient. Int J Emerg Med 2011;4:65.
10
Mircioiu C, Voicu VA, Ionescu M, Miron DS, Radulescu FS Nicolescu AC. Evaluation of in vitro absorption, decontamination and desorption of organophosphorous compounds from skin and synthetic membranes. Toxicol Lett 2013;219:99-106.
11
Eyer F, Meischner V, Kiderlen D, Thiermann H, Worek F, Haberkorn M, et al. Human parathion poisoning. A toxicokinetic analysis. Toxicol Rev 2003;22:143–63.
12
Kramer RE, Ho IK. Pharmacokinetics and pharmacodynamics of methyl parathion. Zhonghua Yi Xue Za Zhi (Taipei) 2002;65:187-99.
13
Liu YF, Fu FH, Zhang DY, Li XH, Han JT. The relationship between the concentration of blood and gastric contents and the activity of acetylcholinesterase enzyme in OP patients. Zhonghua Nei Ke Za Zhi 1997;36:478-9. (In Chinese)
14
Eddleston M, Haggalla S, Reginald K, Sudarshan K, Senthilkumaran M, Karalliedde L, et al. The hazards of gastric lavage for intentional self-poisoning in a resource poor location. Clin Toxicol (Phila) 2007;45:136-43.
15
Palaniappen V. Current Concepts in the Management of Organophosphorus Compound Poisoning. In: Muruganathan A, Geetha T, editors. Medicine Update. Mumbai, India: The Association of Physicians of India; 2013. p.427-33.
16
Benfenati E, Gini G, Piclin N, Roncaglioni A, Varì MR. Predicting logP of pesticides using different software. Chemosphere 2003;53:1155-64.
17
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.
18
Ahmed AS, Basher A, Amin MR, Faiz MA. Effect of Intensive Atropine Doses (Rapid Incremental Loading and Titration) for Management of Organophosphorus Pesticide Poisoning: a Case Series. Asia Pac J Med Toxicol 2014;3:23-6.
19
Senanayake N, Karalliedde L. Neurotoxic effects of organophosphorus insecticides. An intermediate syndrome. N Engl J Med 1987;316:761-3.
20
Indira M, Andrews MA, Rakesh TP. Incidence, predictors, and outcome of intermediate syndrome in cholinergic insecticide poisoning: a prospective observational cohort study. Clin Toxicol (Phila) 2013;51:838-45.
21
Li Y, Tse ML, Gawarammana I, Buckley N, Eddleston M. Systematic review of controlled clinical trials of gastric lavage in acute organophosphorus pesticide poisoning. Clin Toxicol (Phila) 2009;47:179-92.
22
Li Y, Yu X, Wang Z, Wang H, Zhao X, Cao Y, et al. Gastric lavage in acute organophosphorus pesticide poisoning (GLAOP)--a randomised controlled trial of multiple vs. single gastric lavage in unselected acute organophosphorus pesticide poisoning. BMC Emerg Med. 2006;6:10.
23
Merigian KS, Woodard M, Hedges JR, Roberts JR, Stuebing R, Rashkin MC. Prospective evaluation of gastric emptying in the self-poisoned patient. Am J Emerg Med 1990;8:479-83.
24
Jayawardane P, Senanayake N, Buckley NA, Dawson AH. Electrophysiological correlates of respiratory failure in acute organophosphate poisoning: evidence for differential roles of muscarinic and nicotinic stimulation. Clin Toxicol (Phila) 2012;50:250-3.
25
Jayasinghe SS, Pathirana KD. Slow Repetitive Nerve Stimulation in Patients with Acute Organophosphorus Poisoning after Clinical Recovery. Asia Pac J Med Toxicol 2013;2:14-18.
26
Paraiba LC, de Castro VLSS, Maia AHN. Insecticide distribution model in human tissues viewing worker's health monitoring programs. Braz Arch Biol Technol 2009;52:875-81.
27
Asari Y, Kamijyo Y, Soma K. Changes in the hemodynamic state of patients with acute lethal organophosphate poisoning. Vet Hum Toxicol 2004;46:5-9.
28
Eddleston M, Mohamed F, Davies JO, Eyer P, Worek F, Sheriff MH, et al. Respiratory failure in acute organophosphorus pesticide self-poisoning. QJM 2006;99:513-22.
29
Prasad DRMM, Jirli PS, Mahesh M, Mamatha S. Relevance of Plasma Cholinesterase to Clinical Findings in Acute Organophosphorous Poisoning. Asia Pacific J Med Toxicol 2013;2:23-7.
30
Bhardwaj UB, Subramaniyan A, Bhalla A, Sharma N, Singh S. Safety of gastric lavage using nasogastric ryle’s tube in pesticide poisoning. Health 2011;3:401-5.
31
Eddleston M, Juszczak E, Buckley N. Does gastric lavage really push poisons beyond the pylorus? A systematic review of the evidence. Ann Emerg Med 2003;42:359-64.
32
Mohanty MK, Pinnamaneni S, Arun M, Menezes RG, Palimar V. Correlation between postmortem diagnosis and survival time in poisoning deaths. J Indian Acad Forensic Med 2005;27:23-7.
33
Saetta JP, Quinton DN. Residual gastric content after gastric lavage and ipecacuanha-induced emesis in self-poisoned patients: an endoscopic study. J R Soc Med 1991;84:35-8.
34
ORIGINAL_ARTICLE
Four-Year Study on Acute Poisoning Cases Admitted to a Tertiary Hospital in Bangladesh: Emerging Trend of Poisoning in Commuters
Background:The pattern of poisoning has a regional variability. This study was carried out to describe the epidemiological profile of acute poisoning in northeastern Bangladesh and to evaluate the mortality. Methods:In this retrospective cross-sectional study, medical records of poisoned patients treated at department of medicine of Sylhet M.A.G. Osmani Medical College Hospital, Sylhet, Bangladesh during 1st January 2008 to 31st December 2011 were reviewed. Patients aged 10 years and above with diagnosis of acute poisoning were included. Data collected were gender, age, place of residence, type of poison and intention of poisoning. Results:A total of 4435 (58.7% men) were included. Patients aged 21 to 30 years were the most common age group involved with poisoning (41.6%). The majority of patients (55.4%) lived in rural areas. Commuter poisoning (43.3%) was the most frequently occurring type of poisoning in both men and women in all 4 years followed by OP poisoning (25.7%). Men were found to be significantly more affected in commuter, organophosphate and alcohol poisoning (P < 0.001). Intention of poisoning in the greatest number of patients (54.5%) was suicidal followed by 1919 patients (43.3%) who were poisoned by homicidal/stupefying intents. Among the homicidal cases, men were significantly more victimized (67% vs. 33%, P < 0.001). Overall, 224 patients (5.1%) died. The highest number of deaths was due to OP poisoning (46.9%) followed by commuter poisoning (45.5%). Case fatality rate was the highest in the snakebite victims (23.3%) followed by alcohol poisoning (11.4%). Conclusion:Commuter or travel-related poisoning is an emerging public health threat in this part of Bangladesh. Public awareness should be raised and school-based educational programs should be emphasized regarding the commuter poisoning and the consequence of accepting and eating food from strangers.
https://apjmt.mums.ac.ir/article_3485_7c66c6386dbffc24e6ed806eb38f9c68.pdf
2014-12-01
152
156
10.22038/apjmt.2014.3485
Bangladesh
Chemically-Induced Disorders
Epidemiologic Studies
Poisoning
Travel
Mohammad Shafiqul
Bari
1
Department of Medicine, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
AUTHOR
Shishir Ranjan
Chakraborty
2
Department of Medicine, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
AUTHOR
Munsi Mohammad Jahangir
Alam
3
Department of Medicine, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
AUTHOR
Junaid Abdul
Qayyum
4
Department of Medicine, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
AUTHOR
Nazia
Hassan
5
Department of Gastroenterology, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
AUTHOR
Fazle Rabbi
Chowdhury
mastershakil@hotmail.com
6
Department of Medicine, Sylhet M.A.G. Osmani Medical College, Sylhet, Bangladesh
LEAD_AUTHOR
Kumar A, Verma A, Jaiswal K, Kumar S, Prasad R. Emergence of entirely new poisoning in rural India; An upcoming health hazard to the community health. Indian J Community Health 2012;24:248-51.
1
Afsari R, Majdzadeh SR, Balali-Mood M. Pattern of acute poisoning in Mashhad, Iran 1993-2000. J Toxicol Clin Toxicol 2004;42:965-75
2
Kerins M, Dargan PI, Jones AL. Pitfalls in the management of the poisoned patients. J R Coll Phys Edinburgh 2003;33:90-103.
3
Eddleston M, Sheriff MHR, Hawton K. Deliberate self-harm in Sri Lanka: an overlooked tragedy in the developing world. BMJ 1998;317:133-5.
4
Gunnell D, Eddleston M. Suicide by intentional ingestion of pesticides: a continuing tragedy in developing countries. Int J Epidemiol 2003;32:902-9.
5
Buckley NA, Karalliedde L, Dawson A, Senanayake N, Eddleston M. Where is the evidence for treatments used in pesticide poisoning? Is clinical toxicology fiddling while the developing world burns? J Toxicol Clin Toxicol 2004;42:113-6.
6
Chowdhury FR, Rahman AU, Mohammed FR, Chowdhury A, Ahasan HA, Bakar MA. Acute poisoning in southern part of Bangladesh - The case load is decreasing. Bangladesh Med Res Counc Bull 2011;37:61-5.
7
Dewan G. Analysis of Recent Situation of pesticide poisoning in Bangladesh: Is there a proper estimate? Asia Pac J Med Toxicol 2014;3:76-83.
8
Majumder MM, Basher A, Faiz MA, Kuch U, Pogoda W, Kauert GF, et al. Criminal poisoning of commuters in Bangladesh: prospective and retrospective study. Forensic Sci Int 2008;180:10-6.
9
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10
Amin MR, Awwal A, Sattar MA, Hasan R, Islam R, Jalil MA, et al. Pilot survey on cases of poisoning and its outcome in different category of hospitals in Bangladesh. J Medicine (Bangladesh) 2009;10:15-7.
11
Prajapati T, Prajapati K, Tandon R, Merchant S. Acute Chemical and Pharmaceutical Poisoning cases Treated in Civil Hospital, Ahmedabad: One Year study. Asia Pac J Med Toxicol 2013;2:63-7.
12
Patil A, Peddawad R, Verma VCS, Gandhi H. Profile of Acute Poisoning Cases Treated in a Tertiary Care Hospital: a Study in Navi Mumbai. Asia Pac J Med Toxicol 2014;3:36-40.
13
Sarkar D, Shaheduzzaman M, Hossain MI, Ahmed M, Nur M, Basher A. Spectrum of acute pharmaceutical and chemical poisoning in northern Bangladesh. Asia Pac J Med Toxicol 2013;2:2-5.
14
Howlader MAR, Sardar MH, Amin MR, Morshed MG, Islam MS, Uddin MZ, et al. Clinico-epidemiological pattern of poisoning in a tertiary level hospital. J Dhaka Med Coll 2008;17:111-5.
15
Howlader MAR, Hossain MZ, Morshed MG, Begum H, Sardar MH, Uddin MZ, et al. changing trends of poisoning in Bangladesh. J Dhaka Med Coll 2011;20:51-6.
16
Tufekci IB, Curgunlu A, Sirin F. Characteristics of acute adult poisoning cases admitted to a university hospital in Istanbul. Hum Exp Toxicol 2004;23:347-51.
17
Yamashita M, Matsuo H, Tanaka J. Analysis of 1000 consecutive cases of acute poisoning in the suburb of Tokyo leading to hospitalization. Vet Hum Toxicol 1996;38:34-5.
18
Mondal RN, Chowdhury FR, Rani M, Mohammad N, Islam MM, Haque MA, et al. Pre-Hospital and Hospital Management Practices and Circumstances behind Venomous Snakebite in Northwestern Part of Bangladesh. Asia Pac J Med Toxicol 2012;1:18-21.
19
Hameed FA, Ansari HK, Al-Najjar FJ. Prevalent Poisonings in Adults and Adolescents in Dubai: A Compendium from Rashid Hospital. Asia Pac J Med Toxicol 2014;3:115-9.
20
Ramesha KN, Rao KB, Kumar GS. Pattern and outcome of acute poisoning cases in a tertiary care hospital in Karnataka, India. Indian J Crit Care Med 2009;13:152-5.
21
Zaheer MS, Aslam M, Gupta V, Sharma V, Khan SA. Profile of poisoning cases at a North Indian tertiary care hospital. Health Popul Perspect Issues 2009;32:176-83.
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Uddin MJ, Shahed FH, Bhowmik SK, Rashid R, Ghose A, Rahman MR, et al. Transport related poisoning-an untapped public health problem. Healer 2003; 8:31-3.
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27
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28
Chowdhury FR, Bari MS, Alam J. Epidemiological Profile of Methanol Poisoning in Bangladesh (2008-2014) and Clinical Experience of a Single Outbreak. Asia Pac J Med Toxicol 2014;3:S6.
29
Lau FL. Emergency management of poisoning in Hong Kong. Hong Kong Med J 2000; 6:288-92.
30
Thomas SH, Bevan L, Bhattacharyya S, Bramble MG, Chew K, Connolly J, et al. Presentation of poisoned patients to accident and emergency departments in the North of England. Hum Exp Toxicol 1996; 15:466-70.
31
Chowdhury FR, Ahasan HAMN, Rashid AKM, Mamun AA, Khaliduzzaman SM. Puffer fish (Tetrodotoxin) poisoning: A Clinical analysis, Role of Neostigmine and short-term outcome of 53 cases. Singapore Med J 2007;48:830-3.
32
ORIGINAL_ARTICLE
Genotoxic Effects of Tobacco on Buccal Epithelium: Cell Nuclear Anomalies as Biomarker
Background: Tobacco use has toxic effects on different organs. This study was carried out to assess the effect of indigenous tobacco both in smoking (bidi) and smokeless (gutkha, zarda and khaini) forms on buccal cells at chromosomal level, through assessment of different nuclear anomalies as biomarker. Methods:This study was done on people living in Durgapur and its adjacent areas, West Bengal, India during January to July 2011. The samples were collected from 50 smokers (case group), 50 smokeless tobacco consumers or chewers (case group) and 50 non-tobacco consumers (control group). Micronucleus assay was used to assess buccal cell nuclear changes. Buccal smears collected from study subjects were prepared on a grease free slide. Prepared slides were observed under light microscope and 2 to 5 fields were observed randomly for counting the different anomalies. In each field, the frequency of each anomaly was assessed in 100 cells and reported with percentage. Results:Chewers had significantly the highest frequency of all nuclear anomalies compared to smokers and healthy controls (HCs). Smokers also had significantly more anomalies compared to HCs. Condensed chromatin (CC), karyolysis (KL) and bi-nucleation (BN) in chewers and CC, pyknosis and BN in smokers were the most frequent anomalies. KL was significantly more frequent in chewers compared to smokers (59.8 ± 6.4 vs. 24.2 ± 12.4%, P < 0.001), however, the frequency of other nuclear anomalies were not significantly different in these two study groups. Presence of each nuclear anomaly was significantly greater in older ages in all study groups. Conclusion:Tobacco can cause and increase the rate of nuclear anomalies in both smoking and smokeless forms compared to HCs. The genotoxic effects of tobacco on buccal cells are partly age-related. Cell nuclear anomalies in buccal tissue can be used as biomarker indicating the detrimental effects of tobacco.
https://apjmt.mums.ac.ir/article_3843_26c32aaf98b5ef598b0e0852fb9edf34.pdf
2014-12-01
157
162
10.22038/apjmt.2014.3843
Micronucleus Tests
Mouth Mucosa
Smokeless tobacco
Tobacco Products
Toxicogenetics
Sohini Das
Biswas
1
Post Graduate Department of Conservation Biology, Durgapur Government College, Durgapur, India
AUTHOR
Babli
Garai
babli.india@rediffmail.com
2
Post Graduate Department of Conservation Biology, Durgapur Government College, Durgapur, India
AUTHOR
Moitreyee
Banerjee
miotreyeebanerjee@gmail.com
3
Department of Zoology, Durgapur Government College, Durgapur, India
LEAD_AUTHOR
World Health Organization (WHO). WHO Report on the Global Tobacco Epidemic, 2008: The MPOWER package. Geneva: WHO; 2008.
1
Levitz JS, Bradley TP, Golden AL. Overview of smoking and all cancers. Med Clin North Am 2004;88:1655-75.
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Johnson N. Tobacco use and oral cancer: a global perspective. J Dent Educ 2001;65:328-39.
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Nichter M, Cartwrigh E. Saving the children for the tobacco industry. Med Anthropol Q 1991;5;236-56.
4
World Health Organization (WHO). The global burden of disease: 2004 update. Geneva: WHO Press; 2008.
5
World Health Organization, Tobacco Free Initiative (TFI). Tobacco facts [Internet]. 2005 [cited 2014 Aug 10]. Available from: http://www.who.int/tobacco/mpower/tobacco_facts/en/
6
Centers for Disease Control and Prevention (US), National Center for Chronic Disease Prevention and Health Promotion (US), Office on Smoking and Heath (US). Nicotine addiction: past and present. In: How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Atlanta, USA: Centers for Disease Control and Prevention (US); 2010.
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De Silva WDAS. Effectiveness of Tobacco Control Measures in Reducing Tobacco Use among Adolescents and Young Adults in Anuradhapura, Sri Lanka. Asia Pac J Med Toxicol 2012;1:22-6.
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Saleheen D, Zhao W, Rasheed A. Epidemiology and public health policy of tobacco use and cardiovascular disorders in low- and middle-income countries. Arterioscler Thromb Vasc Biol 2014;34:1811-9.
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Agrawal S, Karan A, Selvaraj S, Bhan N, Subramanian SV, Millett C. Socio-economic patterning of tobacco use in Indian states. Int J Tuberc Lung Dis 2013;17:1110-7.
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Strickland SS. Anthropological perspectives on use of the areca nut. Addict Biol 2002;7:85-97.
11
Sapkota A, Gajalakshmi V, Jetly DH, Roychowdhury S, Dikshit RP, Brennan P, et al. Smokeless tobacco and increased risk of hypopharyngeal and laryngeal cancers: a multicentric case-control study from India. Int J Cancer 2007;121:1793-8.
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Hoffmann D, Hoffmann I, El-Bayoumy K. The less harmful cigarette: a controversial issue. a tribute to Ernst L. Wynder. Chem Res Toxicol 2001;14:767-90.
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Adak M. Effects of Smoking and Need for Cessation: Biochemical and Pharmacological Feedback. Biochem Pharmacol (Los Angel) 2014;3:145.
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Stewart BW, Kleihues P. World Cancer Report: Head and Neck Cancer. Lyon (France): IARC Press; 2003.
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DeMarini DM. Genotoxicity of tobacco smoke and tobacco smoke condensate: a review. Mutat Res 2004;567:447-74.
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Taybos G. Oral changes associated with tobacco use. Am J Med Sci. 2003;326:179-82.
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Silverman S. Oral Cancer. 5th ed. Atlanta, USA: American Cancer Society; 2003.
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Hecht SS. Tobacco carcinogens, their biomarkers and tobacco-induced cancers. Nat Rev Cancer 2003;3:733-44.
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Tolbert PE, Shy CM, Allen JW. Micronuclei and other nuclear anomalies in buccal smears: methods development. Mutat Res 1992;271:69-77.
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Kashyap B, Reddy PS. Micronuclei assay of exfoliated oral buccal cells: means to assess the nuclear abnormalities in different diseases. J Cancer Res Ther 2012;8:184-91.
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Proia NK, Paszkiewicz GM, Nasca MA, Franke GE, Pauly JL. Smoking and smokeless tobacco-associated human buccal cell mutations and their association with oral cancer--a review. Cancer Epidemiol Biomarkers Prev 2006;15:1061-77.
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Nersesyan A, Kundi M, Atefie K, Schulte-Hermann R, Knasmüller S. Effect of staining procedures on the results of micronucleus assays with exfoliated oral mucosa cells. Cancer Epidemiol Biomarkers Prev 2006;15:1835-40.
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Na H, Kim M, Chang S, Kim S, Park JY, Chung MW, et al. Tobacco smoking-response genes in blood and buccal cells. Toxicol Lett 2014;232:429-37.
25
Yao H, Rahman I. Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease. Toxicol Appl Pharmacol 2011;254:72-85.
26
Ramaesh T, Mendis BR, Ratnatunga N, Thattil RO. The effect of tobacco smoking and of betel chewing with tobacco on the buccal mucosa: a cytomorphometric analysis. J Oral Pathol Med 1999;28:385-8.
27
Kallischnigg G, Weitkunat R, Lee PN. Systematic review of the relation between smokeless tobacco and non-neoplastic oral diseases in Europe and the United States. BMC Oral Health 2008;8:13.
28
Saranya RS, Sudha S. Cytomorphological changes in buccal epithelial cells of khaini chewers in different age groups. Asian J Biomed Pharm Sci 2014;4:43-7.
29
Abu Eid R, Sawair F, Landini G, Saku T. Age and the architecture of oral mucosa. Age (Dordr) 2012;34:651-8.
30
Thomas P, Harvey S, Gruner T, Fenech M. The buccal cytome and micronucleus frequency is substantially altered in Down's syndrome and normal ageing compared to young healthy controls. Mutat Res 2008;638:37-47.
31
Nersesyan A, Muradyan R, Kundi M, Knasmueller S. Impact of smoking on the frequencies of micronuclei and other nuclear abnormalities in exfoliated oral cells: a comparative study with different cigarette types. Mutagenesis 2011;26:295-301
32
Kausar A, Giri S, Mazumdar M, Giri A, Roy P, Dhar P. Micronucleus and other nuclear abnormalities among betel quid chewers with or without sadagura, a unique smokeless tobacco preparation, in a population from North-East India. Mutat Res 2009;677:72-5.
33
Sharma VL, Chowdhary DS, Agarwal SK, Aarushi J, Vijeta S, Shivani R. A comparative study of oral epithelium in tobacco and alcohol consumers in central Rajasthan population. Int J Biol Med Res 2013;4:3355-9.
34
Willis DN, Popovech MA, Gany F, Hoffman C, Blum JL, Zelikoff JT. Toxicity of gutkha, a smokeless tobacco product gone global: is there more to the toxicity than nicotine? Int J Environ Res Public Health 2014;11:919-33.
35
Ramaesh T, Mendis BR, Ratnatunga N, Thattil RO. The effect of tobacco smoking and of betel chewing with tobacco on the buccal mucosa: a cytomorphometric analysis. J Oral Pathol Med 1999;28:385-8.
36
Kallischnigg G, Weitkunat R, Lee PN. Systematic review of the relation between smokeless tobacco and non-neoplastic oral diseases in Europe and the United States. BMC Oral Health 2008;8:13.
37
Saranya RS, Sudha S. Cytomorphological changes in buccal epithelial cells of khaini chewers in different age groups. Asian J Biomed Pharm Sci 2014;4:43-7.
38
Abu Eid R, Sawair F, Landini G, Saku T. Age and the architecture of oral mucosa. Age (Dordr) 2012;34:651-8.
39
Thomas P, Harvey S, Gruner T, Fenech M. The buccal cytome and micronucleus frequency is substantially altered in Down's syndrome and normal ageing compared to young healthy controls. Mutat Res 2008;638:37-47.
40
ORIGINAL_ARTICLE
HPLC Measurement of MDMA Content in Ecstasy Tablets Available in the Black Market of West Azerbaijan Province, Northwestern Iran
Background:Ecstasy, mainly composed of 3,4-methylenedioxymethamphetamine (MDMA), is one of the most popular addictive synthetic drugs. This study was aimed to investigate the amount of MDMA in the ecstasy tablets seized in West Azerbaijan province, northwest Iran and also to assess the relationship between the physicochemical and morphological characteristics of the tablets. Methods: MDMA content of ecstasy tablets was analyzed using high-performance liquid chromatography method. Flow rate was 3 mL/min and mobile phase consisted of a mixture of acetonitrile and water containing triethylamine (pH = 3.2). The fluorescence spectrophotometer detector set at an excitation and emission wavelength of 220 and 306 nm, respectively. The retention time of ecstasy on this system was 2.2 minutes. The calibration curve was linear (R2= 0.999) over the concentrations ranging from 0.2 to 2 µg/ml. The limit of detection and the limit of quantitation were found to be 0.06 µg/L and 0.19 µg/L, respectively with six times repetition. Results: In this study, 85 ecstasy tablets were analyzed. Mean weight of the tablets was 275.6 ± 70.4 (range: 158.5-403.3) mg. Mean MDMA content of the tablets was 30.53 ± 23.23 (range: 0.05-70.7) mg. The tablets were classified into 8 groups based on their morphological features (color and logo). Considering the tablet groups, physicochemical features of the tablets (weight, MDMA content, and MDMA to weight ratio) were significantly different (P < 0.001). Correlation analysis showed that the MDMA content and weight of tablets were significantly correlated (P = 0.04). Conclusion: There is variability in the physicochemical properties of ecstasy tablets available in the black market for illicit drugs in northwest Iran. This variability may potentially put abusers at increased risk of overdose due to inadvertent excess ingestion of the tablets to achieve desired effects and also experiencing more harm due to tablets adulterants.
https://apjmt.mums.ac.ir/article_3844_d5eec4ed64e69bbaee0fdcb512495749.pdf
2014-12-01
163
168
10.22038/apjmt.2014.3844
Amphetamines
High Pressure Liquid Chromatography
Iran
N-Methyl-3,4-methylenedioxyamphetamine
Street Drugs
Reza
Ghafari
reza.moin1350@yahoo.com
1
Department of Basic Sciences, Science and Research Branch, Islamic Azad University, Hesarak, Tehran, Iran
AUTHOR
Amir
Heydari
heydari.866@gmail.com
2
Department of Pharmacology, Faculty of Pharmacy, Urmia University of Medical Science, Urmia, Iran
LEAD_AUTHOR
Mohammad Reza
Vardast
mrvardast@gmail.com
3
Department of Medicinal Chemistry, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Azam
Akbari
akbari.chem@gmail.com
4
Department of Medicinal Chemistry, Center for Cellular and Molecular Research, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Kulsudjarit K. Drug problem in southeast and southwest Asia. Ann N Y Acad Sci 2004;1025:446-57.
1
Amiri ZM, Shakib AJ, Moosavi AK. Prevalence and risk factors of ecstasy use among college students in Astara, Islamic Republic of Iran. East Mediterr Health J 2009;15:1192-200.
2
Kelleher C, Christie R, Lalor K, Fox J, Bowden M, O' Donnell C, et al. An Overview of New Psychoactive Substances and the Outlets Supplying Them. Dublin, Ireland: National Advisory Commitee on Drugs; 2011.
3
Maxwell JC, Rutkowski BA. The prevalence of methamphetamine and amphetamine abuse in North America: a review of the indicators, 1992-2007. Drug Alcohol Rev 2008;27:229-35.
4
Afshari R. Non-medical Use of Medications in Middle and Low Income Countries. Asia Pac J Med Toxicol 2014;3:49.
5
Afshari R, Monzavi SM. Poisoning with illegal substances and opioids. In: Afshari R, Monzavi SM, editors. Afshari’s Clinical Toxicology and Poisoning Emergency Care. 2nd ed. Mashhad: Mashhad University of Medical Sciences Publication; 2012. p.137-74.
6
Heydari A, Yeo KR, Lennard MS, Ellis SW, Tucker GT, Rostami-Hodjegan A. Mechanism-based inactivation of CYP2D6 by methylenedioxymethamphetamine. Drug Metab Dispos 2004;32:1213-7.
7
Gudelsky GA, Yamamoto BK. Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons. Pharmacol Biochem Behav 2008;90:198-207.
8
Kalant H. The pharmacology and toxicology of "ecstasy" (MDMA) and related drugs. CMAJ 2001;165:917-28.
9
Rogers G, Elston J, Garside R, Roome C, Taylor R, Younger P, et al. The harmful health effects of recreational ecstasy: a systematic review of observational evidence. Health Technol Assess 2009;13:1-315.
10
Taurah L, Chandler C, Sanders G. Depression, impulsiveness, sleep, and memory in past and present polydrug users of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy). Psychopharmacology (Berl) 2014;231:737-51.
11
Campbell GA, Rosner MH. The agony of ecstasy: MDMA (3,4-methylenedioxymethamphetamine) and the kidney. Clin J Am Soc Nephrol 2008;3:1852-60.
12
Raisjouyan Z, Talebi M, Ghasimi Shahgaldi F, Abdollahian E. Investigating the Effect of Emotional Intelligence on the Addiction Relapse after Quitting. Asia Pac J Med Toxicol 2014;3:27-30.
13
Wood DM, Stribley V, Dargan PI, Davies S, Holt DW, Ramsey J. Variability in the 3,4-methylenedioxymethamphetamine content of 'ecstasy' tablets in the UK. Emerg Med J 2011;28:764-5.
14
Sherlock K, Wolff K, Hay AW, Conner M. Analysis of illicit ecstasy tablets: implications for clinical management in the accident and emergency department. J Accid Emerg Med 1999;16:194-7.
15
Bell SE, Burns DT, Dennis AC, Matchett LJ, Speers JS. Composition profiling of seized ecstasy tablets by Raman spectroscopy. Analyst 2000;125:1811-5.
16
Cole JC, Bailey M, Sumnall HR, Wagstaff GF, King LA. The content of ecstasy tablets: implications for the study of their long-term effects. Addiction 2002;97:1531-6.
17
Khajeamiri AR, Kobarfard F, Ahmadkhaniha R, Mostashari G. Profiling of ecstasy tablets seized in Iran. Iran J Pharm Res 2011;10:211-20.
18
Shetab Boushehri SV, Tamimi M, Kebriaeezadeh A. Quantitative determination of 3,4-methylenedioxymethamphetamine by thin-layer chromatography in ecstasy illicit pills in Tehran. Toxicol Mech Methods 2009;19:565-9.
19
Palhol F, Lamoureux C, Chabrillat M, Naulet N. 15N/14N isotopic ratio and statistical analysis: an efficient way of linking seized Ecstasy tablets. Anal Chim Acta 2004;510:1-8.
20
Teng SF, Wu SC, Liu C, Li JH, Chien CS. Characteristics and trends of 3,4-methylenedioxymethamphetamine (MDMA) tablets found in Taiwan from 2002 to February 2005. Forensic Sci Int 2006;161:202-8.
21
Parrott AC. Is ecstasy MDMA? A review of the proportion of ecstasy tablets containing MDMA, their dosage levels, and the changing perceptions of purity. Psychopharmacology (Berl) 2004;173:234-41.
22
Tanner-Smith EE. Pharmacological content of tablets sold as "ecstasy": results from an online testing service. Drug Alcohol Depend 2006;83:247-54.
23
Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. Adulterants in illicit drugs: a review of empirical evidence. Drug Test Anal 2011;3:89-96.
24
Vogels N, Brunt TM, Rigter S, van Dijk P, Vervaeke H, Niesink RJ. Content of ecstasy in the Netherlands: 1993-2008. Addiction 2009;104:2057-66.
25
ORIGINAL_ARTICLE
Reversal of Cardiovascular Toxicity in Severe Organophosphate Poisoning with 20% Intralipid Emulsion Therapy: Case Report and Review of Literature
Background: Cardiac toxicity is one of the life-threatening effects of severe organophosphate (OP) poisoning. We presented a patient with severe OP poisoning, in cardiovascular shock poorly responsive to conventional treatments, who could be resuscitated successfully with intravenous lipid emulsion (ILE) therapy. Case report: A 26-year-old female was admitted to our emergency department who had ingested unquantifiable amount of parathion. On admission, she was tachycardic, tachypneic and hypotensive with pin-point pupils. Neurological examination revealed Glasgow coma scale (GCS) of 6. Immediately, she was admitted to intensive care unit, and was intubated and put under mechanical ventilation. Standard treatments including atropine and pralidoxime (according to WHO protocol) were given to the patient. However, the patient did not show favorable response to antidotes and supportive treatments and her condition continued to deteriorate. Because of bradycardia and hypotension, she was given noradrenaline vasopressor support. Due to failure of treatments in improvement of the patient's condition, a single 100 mL bolus (1.5 mL/kg) of 20% intralipid was administered intravenously and the same dose repeated 2 minutes later. Over 15 minutes, cardiovascular condition of the patient noticeably improved. ILE was continued up to a total dose of 300 mL when extrasystoles disappeared. The patient could be extubated from ventilator with GCS score of 15 on the 5th day of admission. Discussion: OPs are lipid soluble and ILE can move these kinds of compounds away from the site of toxicity and dissolve them in the plasma which will alleviate their toxic effects. Conclusion: This is the first human case report of OP poisoning which showed efficacy of intralipids as antidotal therapy outside the accepted setting of local anesthetic toxicity.
https://apjmt.mums.ac.ir/article_3487_36eb5aa5359e358a45e4fced7060568b.pdf
2014-12-01
169
172
10.22038/apjmt.2014.3487
Cardiotoxicity
Intravenous Fat Emulsions
Organophosphorus compounds
Parathion
Poisoning
Shafat Ahmad
Mir
mir.shafatahmad@gmail.com
1
Department of Anesthesiology and Critical Care, Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar, India
LEAD_AUTHOR
Rafia
Rasool
rasoolrafiya@gmail.com
2
Department of Biochemistry, Government Medical College, Srinagar, Kashmir, India
AUTHOR
Eddleston M. Patterns and problems of deliberate self-poisoning in the developing world. QJM 2000;93:715-31.
1
Dewan G. Analysis of Recent Situation of Pesticide Poisoning in Bangladesh: Is There a Proper Estimate? Asia Pac J MedToxicol 2014;3:76-83.
2
Peter JV, Cherian AM. Organic insecticides. Anaesth Intensive Care 2000;28:11-21.
3
Foxall G, McCahon R, Lamb J, Hardman JG, Bedforth NM. Levobupivicaine-induced seizures and cardiovascular collapse treated with intralipid. Anaesthesia 2007;62:516-8.
4
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.
5
Mégarbane B. Toxidrome-based Approach to Common Poisonings. Asia Pac J Med Toxicol 2014;3:2-12.
6
Roth A, Zellinger I, Arad M, Atsmon J. Organophosphates and the heart. Chest 1993;103:576-82.
7
Laudari S, Patowary BS, Sharma SK, Dhungel S, Subedi K, Bhattacharya R, et al. Cardiovascular Effects of Acute Organophosphate Poisoning. Asia Pac J Med Toxicol 2014;3:64-7.
8
Ludomirsky A, Klein HO, Sarelli P, Becker B, Hoffman S, Taitelman U, et al. Q-T prolongation and polymorphous ("torsade de pointes") ventricular arrhythmias associated with organophosphorus insecticide poisoning. Am J Cardiol 1982;49:1654-8.
9
Mahesh M, Gowdar M, Venkatesh CR. A Study on Two Dose Regimens of Pralidoxime in the Management of Organophosphate Poisoning. Asia Pac J Med Toxicol 2013;2:121-5.
10
Ciechanowicz S, Patil V. Lipid emulsion for local anesthetic systemic toxicity. Anesthesiol Res Pract 2012;2012:131784.
11
Turner-Lawrence DE, Kerns Ii W. Intravenous fat emulsion: a potential novel antidote. J Med Toxicol 2008;4:109-14.
12
Cave G, Harvey M, Graudins A. Intravenous lipid emulsion as antidote: a summary of published human experience. Emerg Med Australas 2011;23:123-41.
13
Dunn C, Bird SB, Gaspari R. Intralipid fat emulsion decreases respiratory failure in a rat model of parathion exposure. Acad Emerg Med 2012;19:504-9.
14
Zhou Y, Zhan C, Li Y, Zhong Q, Pan H, Yang G. Intravenous lipid emulsions combine extracorporeal blood purification: a novel therapeutic strategy for severe organophosphate poisoning. Med Hypotheses 2010;74:309-11.
15
Kramer RE, Ho IK. Pharmacokinetics and pharmacodynamics of methyl parathion. Zhongua Yi Xue Za Zhi (Taipei) 2002;65:187-99.
16
Thunga G, Pandey S, Nair S, Mylapuri R, Vidyasagar S, Kunhikatta V, et al. harmacokinetic Studies on Oximes in Organophosphate Poisoning: A Mini Review. Asia Pac J Med Toxicol 2014;3:120-3.
17
Due P. Effectiveness of High dose Pralidoxime for Treatment of Organophosphate Poisoning. Asia Pac J Med Toxicol 2014;3:97-103.
18
Weinberg G. Lipid infusion resuscitation for local anesthetic toxicity: proof of clinical efficacy. Anesthesiology 2006;105:7-8.
19
Rothschild L, Bern S, Oswald S, Weinberg G. Intravenous lipid emulsion in clinical toxicology .Scand J Trauma Resusc Emerg Med 2010;18:51.
20
Weinberg GL, VadeBoncouer T, Ramaraju GA, Garcia-Amaro MF, Cwik MJ. Pretreatment or resuscitation with a lipid infusion shifts the dose-response to bipuvicaine-induced asystole in rats. Anesthesiology 1998;88:1071-5.
21
Moshiri M, Vahabzadeh M, Etemad L, Hosseinzadeh H. Failure of Intravenous Lipid Emulsion to Reduce Diazinon-induced Acute Toxicity: a Pilot Study in Rats. Iran J Pharm Res 2013;12:897-902.
22
Picard J, Harrop-Griffiths W. Lipid emulsion to treat drug overdose: past, present and future. Anaesthesia 2009;64:119-21.
23
ORIGINAL_ARTICLE
Harmful Use of Veterinary Drugs: Blindness Following Closantel Poisoning in a 5-Year-Old Girl
Background: Closantel is a veterinary drug used as anthelmintic for ruminants while it is contraindicated for humans. This report describes a rare case of blindness, increased liver enzymes and coagulopathy following closantel poisoning. Case report: A 5-year-old girl was presented with acute blindness following closantel poisoning. She was given mistakenly a dose of 500 mg/day (25mg/kg/day) for 8 days. Clinical examination revealed a well-appearing child with bilateral mydriasis, loss of pupillary light reflex and absence of blinking to threat. Fundoscopic exam revealed bilateral pre-atrophic papilledema. Electroretinogram showed a highly significant decrease in retinal activity. Laboratory examinations revealed 52% increase in prothrombin time, prolongation of activated partial thromboplastin time to 1.3 times the normal and rise of aspartate aminotransferase to 120 IU/L. In addition, creatine kinase peaked at 904 IU/L. Moreover, normocytic normochromic anemia with hemoglobin at 10.7 mg/L and leukocytosis with lymphocytic predominance was noted. The patient received glucocorticoids, vitamin B12 and vitamin K and was discharged after correction of blood and coagulation parameters and normalization of liver enzymes. Partial recovery in visual acuity was found two months after ingestion of the last dose. Discussion:Closantel can cause significant spongiform change (intra-myelin vacuolation) in the white matter of the cerebrum and the cerebellum. It can also induce optic nerve damage as a result of Wallerian degeneration, fibrosis and atrophy. On the retina, closantel leads to papilledema, necrosis of the outer layers, and retinal detachment. It can also cause fatty change and hydropic degeneration in the liver and hepatocellular degeneration. Conclusion: Closantel is a toxic drug for humans causing blindness, hematologic and hepatic disorders. Public awareness should be raised regarding the risks of use of unapproved drugs for human.
https://apjmt.mums.ac.ir/article_3486_d63488ac6e34b21f5ba7be7a11f49ba3.pdf
2014-12-01
173
175
10.22038/apjmt.2014.3486
Acute Liver Failure
blindness
Closantel
Poisoning
Salicylanilides
Laila
Essabar
1
Department of Pediatric Hepatology-Gastroenterology and Nutrition, Rabat Children’s Hospital, Mohammed V- Souissi University, Rabat, Morocco
AUTHOR
Toufik
Meskini
toufik.meskini@gmail.com
2
Department of Pediatric Hepatology-Gastroenterology and Nutrition, Rabat Children’s Hospital, Mohammed V- Souissi University, Rabat, Morocco
LEAD_AUTHOR
Said
Ettair
3
Department of Pediatric Hepatology-Gastroenterology and Nutrition, Rabat Children’s Hospital, Mohammed V- Souissi University, Rabat, Morocco
AUTHOR
Naima
Erreimi
4
Department of Pediatric Hepatology-Gastroenterology and Nutrition, Rabat Children’s Hospital, Mohammed V- Souissi University, Rabat, Morocco
AUTHOR
Nezha
Mouane
5
Department of Pediatric Hepatology-Gastroenterology and Nutrition, Rabat Children’s Hospital, Mohammed V- Souissi University, Rabat, Morocco
AUTHOR
Swan GE. The pharmacology of halogenated salicylanilides and their anthelmintic use in animals. J S Afr Vet Assoc 1999;70:61-70.
1
Sargison ND. Pharmaceutical control of endoparasitic helminth infections in sheep. Vet Clin Food Anim 2011;27:139-56.
2
Joint FAO/WHO Expert Committee on Food Additives. Evaluation of certain veterinary drug residues in food: thirty-sixth report of the Joint FAO/WHO Expert Committee on Food Additives. Geneva, Switzerland: WHO press; 1990.
3
Charlier J, Hostens M, Jacobs J, Van Ranst B, Duchateau L, Vercruysse J. Integrating fasciolosis control in the dry cow management: the effect of closantel treatment on milk production. PLoS One 2012;7:e43216.
4
Skuce PJ, Fairweather I. The effect of the hydrogen ionophore closantel upon the pharmacology and ultrastructure of the adult liver fluke Fasciola hepatica. Parasitol Res 1990;76:241-50.
5
Rassouli A, Arab H, Ghezelloo Y, Shams GR. A bioequivalence study on two closantel oral suspensions in sheep: an Iranian product (fascinil®) versus flukiver® as a reference product. Iran J Vet Med 2013;7:263-9.
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