BackgroundNSAIDs 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/MethodsThe 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.ResultsThe 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).ConclusionsAt 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.

Background: Sickle cell diseases (SCDs) are severe inflammatory processes on vascular endothelium, especially at the capillary level because the capillary system is the actual distributor of hardened red blood cells (RBCs) into the tissues. Methods: All cases with the SCDs were included. Results: We studied 222 males and 212 females with similar mean ages (30.8 vs 30.3 years, p>0.05, respectively). Disseminated teeth losses (5.4% vs 1.4%, p<0.001), ileus (7.2% vs 1.4%, p<0.001), cirrhosis (8.1% vs 1.8%, p<0.001), leg ulcers (19.8% vs 7.0%, p<0.001), digital clubbing (14.8% vs 6.6%, p<0.001), coronary heart disease (18.0% vs 13.2%, p<0.05), chronic renal disease (9.9% vs 6.1%, p<0.05), chronic obstructive pulmonary disease (25.2% vs 7.0%, p<0.001), and stroke (12.1% vs 7.5%, p<0.05) were all higher in males but not acute chest syndrome (2.7% vs 3.7%), pulmonary hypertension (12.6% vs 11.7), deep venous thrombosis and/or varices and/or telangiectasias (9.0% vs 6.6%), or mean age of mortality (30.2 vs 33.3 years) (p>0.05 for all). Conclusion: The hardened RBCs-induced capillary endothelial damage, inflammation, edema, and fibrosis are initiated at birth, and terminate with disseminated tissue hypoxia and multiorgan failures even at childhood in the SCDs. Although RBCs supports and corticosteroids in acute phase and aspirin plus hydroxyurea both in acute and chronic phases decrease severity of the diseases, survivals are still shortened in both genders, dramatically. Infections, medical or surgical emergencies, or emotional stresses-induced increased basal metabolic rate aggravates the sickling and capillary endothelial edema, and may terminate with acute painful crises, multiorgan failures, and sudden deaths. Key words: Sickle cell diseases, acute painful crises, sudden deaths, capillary endothelial inflammation, capillary endothelial edema, atherosclerosis, aging