Comparison of the Effects of Piroxicam and Diclofenac Sodium as Treatments for Primary Dysmenorrhea.

BACKGROUND NSAIDs are the most common agents used in dysmenorrhea treatment. They reduce menstrual pain by reducing uterine pressure and PGF2alpha levels in the menstrual fluid. The aim of this study was to compare the effects of piroxicam and diclofenac sodium as treatments for primary dysmenorrhea. MATERIAL AND METHODS The study was conducted using a randomized and double-blind method. Patients with Visual Analogue Scale (VAS) scores greater than 5 were accepted into the study. The patients who were suitable for inclusion were randomized into 2 groups and received either intramuscular piroxicam or diclofenac sodium. The patients' pain levels were measured at baseline and at 15, 30, 45, and 60 min. A VAS of 10 cm, a numeric scale, a verbal scale, and additional symptoms, as well as pain relapse after 24 hours and required analgesics, were recorded. RESULTS The study included 400 patients. Overall, 200 patients (50%) were in the proxicam group, and 200 patients were in the diclofenac sodium group. The average decrease on the VAS after piroxicam or diclofenac administration was measured as 7.9±1.8 cm and 7.9±1.7 cm (median ± standard deviation), respectively. The pain-reducing efficiency of all the treatments was compared using the Mann-Whitney U test (p=0.929). Rescue medication was needed for 25 patients in the proxicam group (p=0.014). Overall, 30 patients in the proxicam group and 41 patients in the proxicam group needed analgesics again in the 24-hour period after treatment (p=0.150). CONCLUSIONS At the end of our study, it was observed that there was no difference in the results of primary dysmenorrhea treatment with 20 mg piroxicam or 75 mg diclofenac sodium.

Protective effects of minocycline, doxycycline and tetracycline on seizure and lethality in a mice cocaine toxicity model.

INTRODUCTION: Acute cocaine intoxication is one of the important causes of admission to emergency department, especially in western countries. We aimed to compare the efficacies of tetracycline, minocycline, doxycycline in the prevention of seizures and deaths in mice due to cocaine intoxication. METHODS: In the study, a total of 120 balb-c male mice weighing 25-30 g were randomized into 4 groups as tetracycline 255 mg/kg, minocycline 170 mg/kg, doxycycline 157 mg/kg, 0.5 ml saline (placebo). The doses of tetracycline, minocycline and doxycycline are the calculated ED50 values. The mice in the groups received 93 mg/kg cocaine intraperitoneally 10 min after drug administration. The dose of cocaine is 50% of the lethal dose. After cocaine injection, all mice were observed for 30 min in terms of cocaine toxicity findings. Mortality rates, death times, seizure activities, and seizure onset times of the mice were clinically evaluated in an observational way. RESULTS: There were significant differences among all the groups in terms of seizure and lethality (p < 0.001). The ratio of animals with seizures was significantly lower in the minocycline (73.3%), and doxycycline (73.3%) groups (all p = 0.040). The ratio of animals with lethality was significantly lower in the minocycline (23.3%) group compared with vehicle (p < 0.001). CONCLUSION: In our acute cocaine intoxication model, minocycline was effective in terms of lethality and preventing seizures, doxycycline was effective in preventing seizures.

A Comparison of Dexmedetomidine, Moxonidine and Alpha-Methyldopa Effects on Acute, Lethal Cocaine Toxicity.

BACKGROUND: The treatment of cocaine toxicity is an important subject for emergency physicians. We investigated the effects of dexmedetomidine, moxonidine and alpha-methyldopa on acute cocaine toxicity in mice. OBJECTIVES: The aim of this study was to evaluate the effects of dexmedetomidine, moxonidine and alpha-methyldopa in a mouse model of acute cocaine toxicity. MATERIALS AND METHODS: We performed an experiment consisting of four groups (n = 25 each). The first group received normal saline solution, the second group received 40 µg/kg of dexmedetomidine, the third group received 0.1 mg/kg of moxonidine and the fourth group received 200 mg/kg of alpha-methyldopa, all of which were intraperitoneally administered 10 minutes before cocaine hydrochloride (105 mg/kg). All animals were observed for seizures (popcorn jumping, tonic-clonic activity, or a loss of the righting reflex) and lethality over the 30 minutes following cocaine treatment. RESULTS: The ratio of animals with convulsions was lower in all treated groups when compared to the control (P < 0.001). Furthermore, 68% (n = 17) of animals in the dexmedetomidine group, 84% (n = 21) of the alpha-methyldopa group, 92% (n = 23) of the moxonidine group and 100% (n = 25) of the control group showed evidence of seizure activity (P = 0.009). Cocaine-induced lethality was observed in 12% (n = 3) of the dexmedetomidine group, 48% (n = 12) of the alpha-methyldopa group, 52% (n = 13) of the moxonidine group, and 72% (n = 18) of the control group (P < 0.001). All treatments prolonged the time to seizure, which was longest in the dexmedetomidine group (P > 0.05). In addition, the time to lethality was also longer in the same group (P < 0.001). CONCLUSIONS: The present study provides the first experimental evidence in support of dexmedetomidine treatment for cocaine-induced seizures. Premedication with dexmedetomidine reduces seizure activity in a mouse model of acute cocaine toxicity. In addition, while dexmedetomidine may be effective, moxonidine and alpha-methyldopa did not effectively prevent cocaine-induced lethality.