Pattern of NSAID Poisoning in a Referral Poisoning Center of Iran: Solutions to Reduce the Suicide

Document Type : Research article


1 Department of Toxicology and Pharmacology, Islamic Azad University of Medical Sciences, Tehran, Iran.

2 Department of Clinical Toxicology, Loghman-Hakim Hospital, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.


NSAIDs are nonsteroidal anti-inflammatory drugs, thus, they will provide analgesic,
antipyretic, anti-inflammatory, antiplatelet effects. Severe poisoning and death because of acute
intoxication can occur by ingestions of more than 400 mg/kg. This cross-sectional retrospective
study was carried out in on all patients referred to Loghman Hakim Hospital from 2011 to 2016.
Grouping of our patients was based on the amount of NSAID ingestion, Type of NSAID, patient’s
conscious level according to Reed Scaling criteria, suicide attempt, and gender. Data were analyzed
using the SPSS software. A P-value of 0.05 or less was considered to be statistically significant.
The period prevalence of NSAID poisoning was 0.14% and the incidence was 3.816/100,000/
year. The uppermost number of poisoning were seen in 2012 (20.96%). Mean age was 23.75
± 9.76 years and most of the intoxications were seen in females (66.37%). Of the patients, 140
(61.13%) had ingested less than 200 mg/kg, and 9.17% committed suicide having a mortality rate
of 0.43%. The most common NSAIDs that had been used were Ibuprofen (73.79%). Of patients,
83.4% underwent through common complications of NSAID poisoning. We find significant
relationship between the type of NSAID and higher sodium, BUN, ALT, ALP, CPK levels in men,
and higher LDH level in women. Besides, we found substantial correlation between using shortacting
NSAIDs and female gender, suicide action, arrival to the hospital less than 12 h, amounts
under 200 mg/kg, hospitalization longer than 12 h, and presentation of loss of consciousness.


Main Subjects

(1) Morita I. Distinct functions of COX 1 and COX
2. Prostaglandins Other Lipid Mediat. (2002) 68:
(2) Saad J and Pellegrini MV. Nonsteroidal AntiInflammatory Drugs (NSAID) Toxicity. [Updated
2020 Jan 17]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2020 Jan.
Available from:
(3) Pereira Leite C, Nunes C, Jamal SK, Cuccovia
IM and Reis S. Nonsteroidal anti-inflammatory
therapy: a journey toward safety. Med. Res. Rev.
(2017) 37: 802–59.
(4) Volans G, Monaghan J and Colbridge M. Ibuprofen
overdose. Int. J. Clin. Pract. (2003) 135: 54–60.
(5) Levine M, Khurana A and Ruha AM. Polyuria,
acidosis, and coma following massive ibuprofen
ingestion. J. Med. Toxicol. (2010) 6: 315–7.
(6) Marciniak KE, Thomas IH, Brogan TV, Roberts JS
and Czaja Mazor SS. Massive ibuprofen overdose
requiring extracorporeal membrane oxygenation
for cardiovascular support. Pediatr. Crit. Care
Med. (2007) 8: 180–2.
(7) Wood DM, Monaghan J, Streete P, Jones AL and
Dargan PI. Fatality after deliberate ingestion of
sustained release ibuprofen: a case report. Crit.
Care (2006) 10: R44.
(8) Holubek W, Stolbach A, Nurok S, Lopez O, Wetter
A and Nelson L. A report of two deaths from
massive ibuprofen ingestion. J. Med. Toxicol.
(2007) 3: 52–5.
(9) Gambaro G and Perazella MA. Adverse renal
effects of anti-inflammatory agents: evaluation
of selective and nonselective cyclooxygenase
inhibitors. J. Intern. Med. (2003) 253: 643–52.
(10) McElwee NE, Veltri JC, Bradford DC and Rollins
DE. A prospective, population based study of acute
ibuprofen overdose: complications are rare and
routine serum levels not warranted. Ann. Emerg.
Med. (1990) 19: 657–62.
(11) Sanchez Hernandez MC, Delgado J, Navarro AM,
Orta JC, Hernandez M and Conde J. Seizures
induced by NSAID. Allergy (1999) 54: 90–1.
(12) Steinhauser HB and Hertting G. Lowering of
the convulsive threshold by non-steroidal antiinflammatory drugs. Eur. J. Pharmacol. (1981) 69:
(13) Robson RH, Balali M, Critchley J, Proudfoot AT
and Prescott L. Mefenamic acid poisoning and
epilepsy. Br. Med. J. (1979) 2: 1438.
(14) Risks of agranulocytosis and aplastic anemia.
A first report of their relation to drug use with
special reference to analgesics. The International
Agranulocytosis and Aplastic Anemia Study.
JAMA (1986) 256: 1749–57.
(15) Gummin DD, Mowry JB, Spyker DA, Brooks DE,
Fraser MO and Banner W. 2016 Annual Report
of the American Association of Poison Control
Centers’ National Poison Data System (NPDS):
34th Annual Report. Clin. Toxicol. (Phila) (2017)
55: 1072–254.
(16) Thomas S and Duarte Davidson R. National
Poisons Information Service Report 2017/18 
NSAID Poisoning
[Internet]. [2018] Available from: https://www.
(17) Thomsen RW, Riis A, Munk EM, Nørgaard M,
Christensen S and Sørensen HT. 30-day mortality
after peptic ulcer perforation among users of newer
selective COX 2 inhibitors and traditional NSAIDs:
a population based study. Am. J. Gastroenterol.
(2006) 101: 2704.
(18) Straube S, Tramèr MR, Moore RA, Derry S and
McQuay HJ. Mortality with upper gastrointestinal
bleeding and perforation: effects of time and
NSAID use. BMC Gastroenterol. (2009) 9: 41.
(19) Goodson NJ, Brookhart AM, Symmons DPM,
Silman AJ and Solomon DH. Non-steroidal antiinflammatory drug use does not appear to be
associated with increased cardiovascular mortality
in patients with inflammatory polyarthritis: results
from a primary care based inception cohort of
patients. Ann. Rheum. Dis. (2009) 68: 367–72.
(20) Conaghan PG. A turbulent decade for NSAIDs:
update on current concepts of classification,
epidemiology, comparative efficacy, and toxicity.
Rheumatol. Int. (2012) 32: 1491–502.
(21) Lanas A and Ferrandez A. Inappropriate prevention
of NSAID induced gastrointestinal events among
long term users in the elderly. Drugs Aging (2007)
24: 121–31.
(22) Schüssel K and Schulz M. Prescribing of COX 2
inhibitors in Germany after safety warnings and
market withdrawals. Int. J. Pharm. Sci. Rev. Res.
(2006) 61: 878–86.
(23) Greenberg JD, Fisher MC, Kremer J, Chang H,
Rosenstein ED, Kishimoto M, Lee S, Yazici Y,
Kavanaugh A and Abramson SB. The COX 2
inhibitor market withdrawals and prescribing
patterns by rheumatologists in patients with
gastrointestinal and cardiovascular risk. Clin. Exp.
Rheumatol. (2009) 27: 395.
(24) Hadgraft J. Formulation of anti-inflammatory
agents. In: Lowe NJ and Hensby C. Nonsteroidal
anti-inflammatory drugs. S Karger Publisher, New
York (1989) 21-43.
(25) Chen HW, Chen KC and Chen JS. Colchicine and
NSAID combination causing acute kidney injury.
J. Coll. Physicians Surg. Pak. (2012) 22: 737–9.
(26) Jones A. Over the counter analgesics: a toxicologic
perspective. Am. J. Ther. (2002) 9: 245–57