ABSTRACT
Tramadol poisoning has increased in recent years. Seizure is one of the side-effects of tramadol toxicity. There is a controversy about possible preventive effect of naloxone in tramadol poisoning induced seizure. Therefore, this study was performed to compare seizure incidence in tramadol poisoning patients who received and did not receive naloxone, as an opioid antagonist. This study involved prospective data collection followed by retrospective analysis on 104 tramadol poisoning patients who were admitted in a referral poisoning center. The incidences of seizure were compared between patients received naloxone and those did not. Outcome was considered as survived without or with complications and death. Logistic Regression analysis was used to determine the effects of different variables on seizure incidence. 70 [67.3%] of the patients were men. The mean age of the patients was 26.3 +/- 9 years old. 18.3% of the patients received naloxone in their treatment period. Seizure incidence was significantly higher among tramadol poisoning patients who did not receive naloxone compare with those received naloxone [14.1% vs. 5.1%]. Among different variable studied, age had a significant effect on predicting of seizure [odds ratio = 2.09; 95% of confidence interval: 1.82-2.26; P value, 0.004]. Although the seizure incidence was lower in patients with tramadol poisoning who received naloxone, the logistic regression did not support the preventive effect of naloxone on seizure in tramadol poisoning cases
Subject(s)
Humans , Female , Male , Seizures , Tramadol/poisoningABSTRACT
OBJECTIVE@#To observe the expression of GABA(A) receptor alpha1 (GABA(A)alpha1) and GABA(B) receptor 1 (GABA(B)1) in human medulla oblongata solitary nucleus and ambiguous nucleus due to tramadol-induced death.@*METHODS@#GABA(A)alpha1 and GABA(B)1 were detected by immunohistochemical SP method in tramadol-induced death group and control group. All results were evaluated by images analysis system.@*RESULTS@#Low expression of GABA(A)alpha1 and GABA(B)1 were detected in solitary nucleus and ambiguous nucleus in the control brain tissue. In cases of tramadol-induced death, the expression of GABA(A)alpha1 and GABA(B)1 significantly increased.@*CONCLUSION@#The mechanism of tramadol intoxication death could be caused by respiratory depression induced by over-expression of GABA(A)alpha1 and GABA(B)1 in medulla oblongata solitary nucleus and ambiguous nucleus.
Subject(s)
Adult , Female , Humans , Male , Analgesics, Opioid/poisoning , Autopsy , Case-Control Studies , Cause of Death , Forensic Toxicology , Immunohistochemistry , Medulla Oblongata/metabolism , Receptors, GABA-A/metabolism , Receptors, GABA-B/metabolism , Respiration Disorders/etiology , Solitary Nucleus/metabolism , Staining and Labeling , Tramadol/poisoningABSTRACT
Tramadol is a centrally acting analgesic with a dual mode of action. Its analgesic efficacy is attributed to its partial affinity for the mu-opiate receptor and its inhibition of norepinephrine and serotonin reuptake. Acting in a synergistic manner and being more efficacious, tramadol is used worldwide for the treatment of moderate to severe acute or chronic pain. Abuse and dependence of tramadol as well as tramadol-related deaths have been increasingly reported, either ingested alone or taken in combination with other potentially interacting drugs. The possible toxic effect of tramadol was reviewed from aspects of its analgesic mechanisms, adverse effect, dependence, and abuse.