This study was undertaken to investigate the response of non-immunologic contact urticaria(NICU) test before and after ingestion of cyclo-oxygenase inhibitors such as naproxene, ibuprofen and mefenamic acid. Forty patients who showed positive reaction to 5% benzoic acid (BA) in petrolatum by 20 minutes closed patch test were chosen and divided into 3 groups. Group I was consisted of 13 patients who were taken naproxene 250mg bid, group II, 14 patients, taken ibuprofen 600mg bid, and group III, 13 patients, taken mefenamic acid 500mg bid. All the patients were tested with 5%, 2.5%, 1%, 0.5% and 0.1% BA in petrolatum using Finn chamber on Scanpor tape on the right arm before medication and next day on the left arm after medication of each day. Mefenamic acid did not show any significant differences before and after ingestion of drug. Naproxene reduced reaction about half of patients. Ibuprofen reduced reaction in almost all patients and blocked reaction completely in 9 of 13 patients. This results suggested that there was no correlation between blocking effect to BA induced contact urticaria and so called anti-inflammatory potencies of naproxene and ibuprofen, and that NICU by BA is partly mediated by prostaglandins(PG) or mediated by other mediators, which were potentiated by PG, except histamin.
Arm ; Benzoic Acid ; Cyclooxygenase Inhibitors ; Eating ; Humans ; Ibuprofen ; Mefenamic Acid ; Naproxen ; Patch Tests ; Petrolatum ; Urticaria*

This study was conducted to examine the effect of mefenamic acid for treatment of PDA in premature newborns. Ductus arteriosus is reopened by locally produced prostaglandin E2 in a premature newborn during hypoxia. Mefenamic acid is one of non-steroidal antiinflammatory drugs acting by inhibition of cyclo-oxygenase in the prostaglandin synthesis pathway. For three premature newborns with PDA, we administered mefenamic acid and evaluated them with echocardiography to study the effect of mefenmic acid for closure of PDA. In all three babies, ductus arteriosus was closed successfully. We feel that mefenamic acid is safe and effective medication for treatment of PDA in premature newborns, but further-study need to be conducted with larger numbers of cases to confirm this effect.
Anoxia ; Dinoprostone ; Ductus Arteriosus ; Echocardiography ; Humans ; Infant, Newborn* ; Mefenamic Acid* ; Prostaglandin-Endoperoxide Synthases

A 45-year-old woman presented with a generalized fixed drug eruption due to mefenamic acid, characterized by recurring erythematous patches with central bullae on the same sites of the whole body and leaving hyperpigmentation after each attack. Patch testing of a quiescent lesion with 50% mefenamic acid in vaselin revealed an eczematous reaction after 48 hours. The disease course was mild compared to the severe clinical manifestation. We here-in report a case of generalized fixed drug eruption due to mefenamic acid which is considered a rare occurrence.
Drug Eruptions* ; Female ; Humans ; Hyperpigmentation ; Mefenamic Acid* ; Middle Aged ; Patch Tests

PURPOSE: Nonsteroidal anti-inflammatory drugs inhibit the synthesis of prostaglandin(PG) through inhibition of the enzyme, cyclooxygenase. Some of the arachidonic acid metabolites may influence the spread of electrocortical activity, and delay the pentylenetetrazol(PTZ)-induced seizures. The purpose of the present study was to evaluate systematically the effect of pretreatment with PG synthetase inhibitors on PTZ-induced seizures. METHODS: To evaluate the effects of pretreatment with PG synthetase inhibitors on seizures produced by 30mg/kg, 60mg/kg PTZ, free-moving Sprague-Dawley rats weighing 250-300gm with chronically-implanted supracortical electrodes were used. Electrocorticogram was recorded for 1hr prior to pretreatment administration of either saline (control) or PG synthetase inhibitor and 1hr after administration of PTZ. RESULTS: 1) A 30mg/kg dose of PTZ produced bursts of high voltage activity after a latency of 616+/-72sec. Although the animals showed spontaneous movements throughout the test period, they were motionless or myoclonus. The number of high voltage bursts during the first hr of the test period was 368+/-31.2) A 30mg/kg of PTZ produced high voltage bursts after a latency of 1118+/-35sec which was significantly greater for the ibuprofen-pretreated groups receiving 90mg/kg when compared to the saline-pretreated group. In addition, the number of high voltage bursts(173+/-17) which occurred during the first hr of the test period was significantly smaller than that recorded from the saline-pretreated group. 3) After pretreatment with a 450mg/kg dose of paracetamol, a 30mg/kg of PTZ produced bursts of electrocortical activity with onset latencies of 665+/-112sec which were not significantly different than those recorded from the saline-pretreated group. The number of high voltage bursts during the first hr of the test period was 141+/-30 which was significantly smaller than that recorded from the saline-pretreated group. 4) A 50mg/kg dose of mefenamic acid pretreatment caused 30mg/kg PTZ-induced high voltage bursts after latency of 227+/-47sec which was significantly shorter than that recorded from the saline-pretreated group. The number of high voltage bursts during the first hr of the test period was 522+/-42 which was significantly greater than that recorded from the saline-pretreated group.5) A 60mg/kg dose of PTZ produced bursts of high voltage activity after a latency of 79+/-14sec. An electrocortical seizure with concurrent convulsions appeared subsequently by 129+/-30sec. 6) A 60mg/kg of PTZ produced high voltage bursts after a latency of 217+/-38sec which was significantly greater for the ibuprofen-pretreated groups receiving 90mg/kg when compared to the saline-pretreated group. An electrocortical seizure with concurrent convulsions appeared subsequently by 287+/-30sec.7) After pretreatment with paracetamol(450mg/kg), a 60mg/kg of PTZ produced bursts of electrocortical activity with onset latencies of 143+/-36sec which were significantly different than those recorded from the saline-pretreated group. There was no convulsive or no electrocortical seizure.8) A 50mg/kg mefenamic acid pretreatment caused 60mg/kg PTZ-induced high voltage bursts after latency of 35+/-5sec which was significantly shorter than that recorded from the saline-pretreated group. An electrocortical seizure appeared subsequently by 58+/-10sec which was significantly different than that recorded from the saline-pretreated group. CONCLUSION: It is possible that the delay and/or block of convulsions induced by the higher doses of PTZ was the result of PG synthesis inhibition. However, the PG synthetase inhibitors had a more differential effect on general PTZ-induced excitation of the CNS evidenced by changes in electrocortical activity. The mechanism underlying this action could be either through inhibition of the activity of cyclooxygenase in tissues which play a role in the manifestation of seizure activity or through an action not related to their common action on cyclooxygenase.
Acetaminophen ; Animals ; Arachidonic Acid ; Electrodes ; Ibuprofen ; Ligases ; Mefenamic Acid ; Myoclonus ; Pentylenetetrazole ; Prostaglandin-Endoperoxide Synthases* ; Rats, Sprague-Dawley ; Seizures*

PURPOSE: Mefenamic acid (MEF) as a non-steroidal anti-inflammatory drug is used as a medication for relieving of pain and inflammation. Radiation-induced inflammation process is involved in DNA damage and cell death. In this study, the radioprotective effect of MEF was investigated against genotoxicity induced by ionizing radiation in human blood lymphocytes. MATERIALS AND METHODS: Peripheral blood samples were collected from human volunteers and incubated with MEF at different concentrations (5, 10, 50, or 100 microM) for two hours. The whole blood was exposed to ionizing radiation at a dose 1.5 Gy. Lymphocytes were cultured with mitogenic stimulation to determine the micronuclei in cytokinesis blocked binucleated lymphocyte. RESULTS: A significant decreasing in the frequency of micronuclei was observed in human lymphocytes irradiated with MEF as compared to irradiated lymphocytes without MEF. The maximum decreasing in frequency of micronuclei was observed at 100 microM of MEF (38% decrease), providing maximal protection against ionizing radiation. CONCLUSION: The radioprotective effect of MEF is probably related to anti-inflammatory property of MEF on human lymphocytes.
Cell Death ; Cytokinesis ; DNA Damage ; Healthy Volunteers ; Humans* ; Inflammation ; Lymphocytes* ; Mefenamic Acid* ; Micronucleus Tests ; Radiation, Ionizing ; Radiation-Protective Agents

It has been focused on the importance of the host inflammatory response in periodontal pathogenesis and progression, treatment has been introduced to control the host response and the method, which diminishes production and activity of MMP by doxycycline, has been used in periodontal field. MMP is a proteolytic enzyme which plays a major role in tissue destruction and MMP-1 is secreted in the periodontally healthy tissue, while MMP-8, 9, 13, etc in the inflammatory state. Among these, MMP-13 has been discovered lately and reported to degrade primarily type II collagen. Periodontal ligament (PDL) cell plays a role in destruction of periodontal tissue. This study was to evaluate the effect of doxycycline and mefenamic acid, non-steroidal antiinflammatory drug on MMP-13 mRNA expression in the rat PDL cell. Doxycycline concentration of 1~100 microgram/ml was added rat PDL cell and cell activity was measured by MTT assay at day 1 and 3. MMP-13 gene expression was evaluated by RT-PCR after PDL cells were pre-treated for 1 hour with doxycycline (50 microgram/ml) alone or with mefenamic acid (10(-6)M), then added IL-1beta(1.0 ng/ml) and incubated for 16 -18 hours. The results are as follows: 1. Cell activity decreased significantly at 24 and 72 hours in 100 microgram/ml (p<0.05). 2. Level of MMP-13 mRNA was in 202% increase by IL-1beta and in pre-treating doxycycline group, expression of IL-1beta induced MMP-13 mRNA was inhibited by 31% than IL-1beta treated only. 3. Mefenamic acid did not inhibit on the expression of IL-1beta induced MMP-13 mRNA, while mefenamic acid in combination with doxycycline inhibited the expression by 41% compared to only IL-1beta stimulation. These results suggest that doxycycline synergistically inhibit the expression of IL-1beta induced MMP-13 mRNA in combination with mefenamic acid.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Collagen Type II ; Doxycycline* ; Gene Expression ; Mefenamic Acid* ; Periodontal Ligament* ; Rats* ; RNA, Messenger*

Osteonecrosis of the femoral head (ONFH) can cause femoral head depression and cortical discontinuity. Treatment for ONFH remains challenging. We performed botulinum toxin type A injection to psoas major muscle in five patients with radiological femoral head collapse (Association Research Circulation Osseus classification stage III) who were non-responsive after two years of conservative treatment (tramadol 200 mg/day, mefenamic acid 1,000 mg/day). At two weeks after the procedure, their mean hip pain was decreased from 88 ± 0.4/100 mm to 22 ± 0.4/100 mm based on visual analogue scale (VAS). The pain was maintained at a minimum of 20/100 mm and a maximum of 30/100 mm in VAS for at least six weeks after the procedure. These values were mean ± SD. These patients were followed-up for 6 months. There was no exacerbation of pain from repeated (three times) botulinum toxin type A injection to the psoas major muscle.
Botulinum Toxins* ; Botulinum Toxins, Type A* ; Classification ; Depression ; Femur Head Necrosis ; Head* ; Hip ; Humans ; Mefenamic Acid ; Osteonecrosis* ; Psoas Muscles*

Mefenamic acid is a potent analgesic possessing both anti-inflammatory and antipyretic properties. It is completely absorbed one to two hours after intake. Majority of patients however, expect relief of pain within 15 minutes. A new oral mefenamic acid containing sodium lauryl sulfate with a dissolution rate of 98 per cent in 15 minutes has been introduced. This phase 4 clinical trial was conducted to evaluate the onset of pain relief upon administration of mefenamic acid 500 mg combined with sodium lauryl sulfate. The study was an open, noncomparative clinical trial. Physicians all over the Philippines were asked to fill up a standard 3-page case report form. A total of 2,617 patients with a mean age of 36 years were enrolled. Forty two per cent were males and fifty eight per cent were females. Seventy per cent of patients took the drug every 6-8 hours. Majority (78.38%) reported complete resolution of pain (54.3%) of which occurred within 15 minutes, increasing to 84.93% within 30 minutes). Only 1.12 per cent showed no response. Forty one patients (1.57%) reported minor adverse reactions, majority of whose conditions improved with withdrawal of the drug. The overall assessment of clinical response was very good to excellent in 77.66 percent of patients.(Author)

Human ; Male ; Female ; Adult ; Mefenamic Acid ; Antipyretics ; Dodecyl Sulfate ; Sodium Dodecyl Sulfate ; Analgesics ; Pain ; Anti-inflammatory Agents ; Pain Management

Mefenamic acid and COX-2 selective inhibitor, Celecoxib in HN4 cell line. And then the cell line was evaluated with MTT assay and growth curve, the production of PGE2, total RNA extraction and RT-PCR analysis, and TEM The results were obtained as follows: 1. After administration of medication, in the result of MTT assay, Celecoxib inoculated group inhibit the cell growth rather than Mefenamic acid inoculated group. 2. The growth curve of cell line showed as time passes by there was a dramatic cell growth in the control group, and gradual growth inhibition was found in medication inoculated group and, in Celecoxib inoculated group there was more inhibition of cell growth. 3. After the administration of medication, Celecoxib tend to inhibit the synthesis of PGE2 more than Mefenamic acid. Mefenamic acid inhibit the synthesis of PGE2 more as the concentration gets high, but Celecoxib inhibited the synthesis of PGE2 even in low concentration. 4. After the administration of medication, the revelation of COX mRNA in cell line, there was a 50% decrease in COX-1, 60% decrease in COX-2 as in 50 micrometer Mefenamic acid, and in Celecoxib 50 micrometer there was not much difference in COX-1 and 90% decrease in COX-2 was found. 5. HN4 cell line showed broken nucleus and tangled cytoskeleton bundles in cytoplasm which meant apoptotic features after the treatment of Celecoxib in TEM view. Depending on the above results, we estimate that the inhibition of the expression of COX-2 cause the growth suppression of the oral squamous cell carcinoma, and it get achieved through pathway of reduced PGE2 production and increased apoptosis. In addition to, because COX-2 selective inhibitor specifically act to COX-2, it is considered that COX-2 selective inhibitor has the adequate potential as chemopreventive agent for oral squamous cell carcinoma.]]>
Apoptosis ; Carcinoma, Squamous Cell ; Cell Line ; Cytoplasm ; Cytoskeleton ; Dinoprostone ; Mefenamic Acid ; Mouth Neoplasms ; Pyrazoles ; RNA ; RNA, Messenger ; Sulfonamides ; Celecoxib

Vibrio vulnificus cytolysin caused platelet cytolysis and increased intracellular calcium concentration ((Ca2+))i) of rat platelets in a concentration-dependent manner. In the presence of V. vulnificus cytolysin (3 HU/ml), lactate dehydrogenase (LDH) activity was increased from 1.3+/-0.4% of control to 64.3+/-3.4% in platelet suspension buffer. In Ca2+-free platelet suspension buffer, however, V. vulnificus cytolysin did not induce (Ca2+)i increase and LDH release. Addition of EGTA (2 mM) to suspension buffer after the initial Ca2+ influx reversed (Ca2+)i to the control level. However, a Ca2+ channel blocker verapamil (20 muM) or mefenamic acid (20 muM) did not inhibit V. vulnificus cytolysin-induced (Ca2+)i increase and LDH release. Divalent cations such as Co2+, Cd2+ or Mn2+ (2 mM each) also did not alter V. vulnificus cytolysin-induced (Ca2+)i increase and LDH release. V. vulnificus cytolysin (3 HU/ml)-induced calcium influx was completely blocked by lanthanum (2 mM). Lanthanum (2 mM) also completely blocked V. vulnificus cytolysin (3 HU/ml)-induced LDH release. Osmotic protectants such as, raffinose, sucrose or PEG600 (50 mM each) did not inhibit the lytic activity of V. vulnificus cytolysin. In conclusion, lanthanum sensitive Ca2+ influx plays a significant role in Vibrio vulnificus cytolysin-induced platelet cytolysis and thrombocytopenia in V. vulnificus infection.
Animals ; Blood Platelets* ; Calcium ; Cations, Divalent ; Egtazic Acid ; Ethanol ; L-Lactate Dehydrogenase ; Lanthanum ; Mefenamic Acid ; Perforin* ; Raffinose ; Rats* ; Sucrose ; Thrombocytopenia ; Verapamil ; Vibrio vulnificus* ; Vibrio*