[Effect of antipholigstics on the cell volume and volume distribution of in vitro grown Ehrlich ascites tumor cells].
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Animals↗
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Results for “Mefenamic Acid”
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The effects of anti-inflammatory and other agents on the rat dermal arthus reaction.
The inhibitory effects of selected drugs on the Arthus reaction, a model of immune-complex-induced tissue injury, were studied. The reverse passive Arthus reaction (RPAR) was elicited in the dorsal skin of rats, using bovine serum albumin and the gamma-globulin fraction of rabbit anti-BSA. The optimal amounts of antigen and antibody required to elicit the reaction, as well as the reaction kinetics, were examined. Chlorpheniramine, cyproheptadine, d-penicillamine, chloroquine, indomethacin, phenylbutazone, naproxen, and mefenamic acid were found to be inactive despite high doses; aspirin and ibuprofen were only weakly active. Hydrocortisone and colchicine were strong inhibitors of the RPAR: the calculated ED50 values were 13 mg/kg p.o. and 0.3 mg/kg i.v., respectively. The RPAR exhibits a different sensitivity to drug inhibition than conventional models of inflammation (e.g., carrageenin paw edema) end may be useful to detect new types of anti-inflammatory agents.
Animals↗
Histamine H2-receptors on guinea-pig ileum myenteric plexus neurons mediate the release of contractile agents.
Dimaprit, a highly selective H2-agonist, caused a multiphasic contraction of guinea-pig ileal segments and ileal myenteric plexus-longitudinal muscle preparations. The initial phase was characterized by a twitch which reached a maximum in 15 to 30 sec and was followed by a partial relaxation. The later phase was variable and consisted of a series of twitch responses or of a slowly developing contracture which sometimes was accompanied by oscillatory changes in tension. dose-response curves were generated for the initial response; for isolated ileal segments the EC50 was 5.1 +/- 1.8 micrometers (mean +/- S.D., N = 7) and the Hill coefficient was 1.1 +/- 0.2 and for longitudinal muscle strips the EC50 was 5.8 +/- 1.2 micrometer and the Hill coefficient was 1.2 +/- 0.1 (N = 7). Both the initial and secondary components of the contractile responses to dimaprit were prevented by 0.2 micron tetrodotoxin or 10 microns mefenamic acid and by the production of tachphylaxis to either substance P or serotonin. Scopolamine, 0.001 to 0.1 micron, insurmountably antagonized only the initial component of the response. Mepyramine (1.0 micrometer), hexamethonium (100 microns), bromolysergic acid (0.25 microns) and p-(imidazol-1-yl)phenyl (10 microns) were without effect on the response to dimaprit. The histamine H2-receptor antagonist, tiotidine, produced parallel dextral shifts in the dose-response curve for dimaprit. The apparent pA2 value for tiotidine was 7.65. The results suggest that dimaprit acts on H2-receptors located on myenteric plexus neurons to cause the release of contractile substances. The mediators of the contractile response are tentatively identified as acetylcholine, substance P, serotonin and a product(s) of the arachadonic acid cascade.
Animals↗
[Urticaria--angioedema induced by non-steroidal anti-inflammatory analgesics].
Forty-two adult patients had been evaluated with a history of Urticaria and Angioedema (U-AE) associated with ingestion of non-steroidal anti-inflammatory drugs (NSAID). None developed attacks of bronchospasm. None had chronic urticaria. The same reaction was repeated in 36 individuals on at least two different occasions following administration of these drugs. Based on patients'history we distinguished three groups: Group A: twenty-three patients who had presented U-AE with the administration of pyrazolone drugs. Thereafter, sixteen of them had taken aspirin without adverse reactions. Group B: Nine patients in whom aspirin caused U-AE, after three of them had taken pyrazolone drugs without intolerance. The remaining six had not taken analgesic drugs since the last reaction. Group C: Ten patients who had developed U-AE with aspirin as well as with pyrazolone drugs. The objective of our study was the following: 1) to observe tolerance level of these patients to other NSAID different from those which had produced the first reactions. 2) To test to see if the patients who had suffered U-AE by noramidopyrine and aminophenazone tolerated other pyrazolone drugs like sulfinpyrazone and phenylbutazone. 3) To see if reactions are produced with tartrazine in patients who had presented U-AE with pyrazolone drugs, given that this colouring (tartrazine) is a pyrazolone derivative. Skin test (prick and intracutaneous test) with noramidopyrine, phenylbutazone and noramidopyrine metasulphonate MG, were carried out on the patients in group A, group C and 30 normal controls. In all the groups oral challenge tests were performed with progressive doses of naproxen, indomethacin, paracetamol, ciclofenac, mefenamic acid, piroxicam and phenylbutazone. Oral challenge tests were accomplished with aspirin in group A and with propiphenazone in group B. Oral challenge tests with sulfinpyrazone and tartrazine were also performed on various patients in group A and group C. The interval between the administration of progressive doses of a drug was 3 and as half hours and were allowed to pass at least 24 hours before testing other different analgesics. The test was considered positive if cutaneous rash, wheals, AE or hypotension were produced. In this case, the test was halted and 7 days were allowed to pass before continuing the study with a new drug. Based on the oral challenge tests performed, three types of patients could be distinguished: 1) individuals sensitive only to the pyrazolone drugs and who can take with impunity other NSAID.(ABSTRACT TRUNCATED AT 400 WORDS)
Administration, Oral↗
The pathology of dysfunctional uterine bleeding.
The mechanism of dysfunctional uterine bleeding remains unknown. Recent studies suggest that the majority of cases of dysfunctional uterine bleeding are due to local endometrial, or myometrial, dysfunction. Changes in the pattern of production of prostaglandins PGE2, PGF2 alpha, prostacyclin and thromboxane and increased fibrinolytic activity in the endometrium have been implicated in this disorder. Successful treatment of excessive menstrual bleeding with the prostaglandin synthetase inhibitor mefenamic acid and the fibrinolytic inhibitors epsilon amino caproic acid and tranexamic acid further substantiates the role of prostaglandins and fibrinolysis in pathological menstruation. The relationship between uterine mast cells, heparin-like activity and menstrual bleeding still needs to be elucidated. Further studies are required to improve our understanding of the pathogenesis of dysfunctional uterine bleeding, so that advances can be made in a specific treatment to restore normal menstrual function.
Blood Platelets↗
Inhibition of aminoacid decarboxylases by non-steroidal antiinflammatory drugs.
Several non-steroidal antiinflammatory drugs (NSAID) were shown to inhibit to various extents the decarboxylases of ornithine, lysine, histidine, arginine, and tyrosine. The most sensitive enzyme was ornithine decarboxylase, for which piroxicam, benoxaprofen and aminophenazone showed an IC50 of 0.007 mM; ibuprofen competitively inhibits the lysine decarboxylase. The most effective NSAID's in inhibiting histidine decarboxylase were mefenamic acid, ibuprofen and flufenamic acid. Arginine and tyrosine decarboxylase were inhibited by NSAID's only at high concentrations. None of the decarboxylase inhibitions were reversed by pyridoxal phosphate. Subplantar injection of the 5 amines formed by these aminoacid decarboxylases elicited a paw oedema in rat which was not antagonized by the various NSAID's. Some of the NSAID's stimulated all the decarboxylases and did not antagonize the carrageenin-induced paw oedema. With one exception, all the NSAID's tested in vivo inhibited the elimination of 14CO2 from labeled ornithine and lysine. The inhibition of certain aminoacid decarboxylases, particularly ornithine and lysine decarboxylase, appears to be a noteworthy mechanism of action for certain NSAID's.
Animals↗
Nonsteroidal anti-inflammatory agents in the treatment of primary dysmenorrhea.
The physiology of primary dysmenorrhea and its treatment with nonsteroidal anti-inflammatory agents are reviewed. Primary dysmenorrhea involves incapacitating pelvic pain associated with nausea, vomiting, and diarrhea. Currently, it is thought to be caused by an overproduction of prostaglandins that are released as the endometrium degenerates. Since the nonsteroidal anti-inflammatory agents are one class of antiprostaglandin agents, they are frequently prescribed for the relief of dysmenorrhea. Naproxen and naproxen sodium have both been shown to be superior to placebo in subjective and objective assessments of dysmenorrheic patients when administered at the onset of symptoms. Indomethacin studies demonstrate its efficacy over placebo, but the frequency of side effects at the doses used (25-50 mg t.i.d.) diminish its usefulness. Few placebo-controlled studies have been published on ibuprofen, but the studies that have been performed show that ibuprofen is more beneficial than placebo for treating dysmenorrhea with a low incidence of side effects. The fenamates appear to be effective in dysmenorrhea, although they were not studied extensively with placebo and previous experience with mefenamic acid has led to warnings about side effects. Phenylbutazone and oxyphenbutazone have been found to be effective; however, their use has been less frequent since the introduction of the newer less toxic nonsteroidal agents. Comparative studies of the nonsteroidal anti-inflammatory agents have not indicated that one agent is more effective than the others. Until further well-controlled comparative research is performed, any of the agents reviewed would be an appropriate choice in the treatment of primary dysmenorrhea.
Anti-Inflammatory Agents↗
[Effects of KB-1043 and some non-steroidal anti-inflammatory drugs on prostaglandin and SRS-A synthesis].
The effects of KB-1043, a new non-steroidal anti-inflammatory agent, on prostaglandin (PG) and SRS-A synthesis were investigated and compared with those of reference drugs. KB-1043 (3 X 10(-5) approximately 3 X 10(-4)M) inhibited the PG synthesis induced by PG synthetase prepared from bovine seminal vesicles. The IC50 value was 1.33 X 10(-4)M. The activity of KB-1043 was less than that of indomethacin, but was about 8 times stronger than that of aspirin. However, KB-1043 (10(-6) and 10(-5)M) did not increase the SRS-A released from sensitized guinea pig lung. With a concentration of 10(-4), KB-1043 decreased the SRS-A release. On the other hand, indomethacin (10(-6) and 10(-5)M), mefenamic acid (10(-6) and 10(-5)M), phenylbutazone (10(-5) and 10(-4)M) and aspirin (10(-4) and 10(-3)M) distinctly increased the SRS-A release from sensitized guinea pig lung.
Animals↗
Prostaglandin mediated histamine tachyphylaxis in subhuman primate tracheal smooth muscle.
The phenomenon of histamine tachyphylaxis previously observed in tracheal smooth muscle from canine species was investigated in isolated tracheal smooth muscle from subhuman primates. Tachyphylaxis to histamine was readily demonstrated by repetitive exposure to histamine. However, similar testing with acetylcholine did not indicate decreased responsiveness to this agent. The development of histamine tachyphylaxis could be prevented or reversed by inhibitors of prostaglandin synthesis (indomethacin, mefenamic acid, oxyphenbutazone). In indomethacin treated tissue, exogenous administration of prostaglandin E2 reduced the histamine response. It is concluded that the histamine tachyphylaxis which is present in subhuman primate tracheal smooth muscle is prostaglandin mediated.
Airway Resistance↗
Lipoxygenase inhibitor-provoked acute asthma in a patient with asthma relieved by aspirin.
BACKGROUND: A very small number of patients with asthma show symptomatic improvement after administration of aspirin and other cyclooxygenase inhibitors. The clinical features of such patients with so-called aspirin-relieved asthma are similar to those with aspirin-induced asthma, but the pathogenesis is unclear. METHODS: We encountered one confirmed aspirin-relieved asthma patient and investigated the effects of cyclooxygenase and lipoxygenase inhibitors on his condition. RESULTS: Our patient showed a marked improvement of the forced expiratory volume in one second (FEV1) after administration of aspirin and three other cyclooxygenase inhibitors (indomethacin, mefenamic acid, and ketoprofen). A 5-lipoxygenase inhibitor (AA861, Takeda, Japan), however, evoked acute asthma, and repeated administration of this drug resulted in some desensitization, but not complete tolerance. CONCLUSIONS: These results suggest an altered balance of arachidonic acid metabolism may play a critical role in the pathophysiology of aspirin-relieved asthma.
Acute Disease↗
The prescribing and adverse reactions of nonsteroidal antiinflammatory drugs in general practice: a Dunedin study.
AIMS: The aims of this study were to describe the prescribing of nonsteroidal antiinflammatory drugs (NSAIDs) by some general practitioners and to assess the information recorded on computer records on their use in individual patients so that techniques could be developed for a broader investigation of the topic in general practice. METHODS: All prescribing and consulting data from five Dunedin practices was reviewed for a 6 month period. From all consultations generating a prescription for NSAIDs, data was collected relating to the name of the drug, dosage, strength and length of treatment and patient demographic and morbidity details. Recorded adverse drug reactions were classified into six groups and four age groups were used for the analysis. RESULTS: Prescriptions for NSAIDs accounted for 2.6% of all items prescribed. Diclofenac was the most commonly prescribed NSAID, for most conditions, but menstrual problems were more likely to be treated with mefenamic acid. Coprescription of possibly contraindicated medications (usually antihypertensive medicines) occurred for 20.8% of patients. Gastric adverse reactions were reported in 3% of cases while 0.9% of prescriptions resulted in no change in condition, leading to a change in therapy. Aspirin, fenbufen, ketoprofen, sulindac and flurbiprofen were never prescribed for patients under 20 years old. CONCLUSION: Routinely recorded patient and prescribing information from general practice permits an assessment of the use of NSAIDs which includes the conditions for which they are prescribed, the total numbers prescribed, concurrent medications prescribed and their recorded adverse effects. This is not possible from any other source. Data from clinical trials provides an incomplete assessment of the use of these medications in general practice.
Adult↗
[Pharmacotherapy of headache with special reference to migraine].
Drug therapy is only one possibility to treat headache or migraine. In a migraine attack aspirin, acetaminophen, non-steroidal antiinflammatory drugs like ibuprofen, naproxen and mefenamic acid are used. Further more weak opiates, caffeine, metoclopramide and the new 5-HT1-receptor agonist sumatriptan are effective in the attack. Ergotamine and dihydroergotamine are probably the most effective though their side effects are troublesome. For prophylactic treatment, the beta-adrenergic receptor blockers propranolol, metoprolol and atenolol are the drugs of first choice. Also calcium channel antagonists like flunaricine and antidepressant drugs like amitryptiline and doxepine are used.
Analgesics↗
Potential strategies for circumventing myeloperoxidase-catalyzed degradation of vinca alkaloids.
Myeloperoxidase (MPO) has recently been shown in an in vitro, cell-free system to catalyze the peroxidative degradation of vincristine (VCR). Oxidation of VCR involves a ring fission between positions 20' and 21', and is thought to be facilitated by the presence of an hydroxyl (-OH) group at position 20'. We report here two different approaches, both with potential clinical application, to decrease MPO-catalyzed vinca degradation. Firstly, we tested the hypothesis that -OH substitution at position 20' increases vinca susceptibility to peroxidation by comparing the relative extent of degradation of vinorelbine (Navelbine or NVB), which lacks a 20' hydroxyl substitution, with that of VCR. As anticipated, NVB was significantly less susceptible to MPO-catalyzed peroxidation than was VCR (p < 0.01). Secondly, we screened an array of compounds that are in current clinical use for their ability to inhibit MPO. Acetaminophen, N-acetylcysteine, propylthiouracil, D-penicillamine, mefenamic acid, dapsone, and methimazole all inhibited MPO at clinically achievable concentrations. Insofar as increased MPO activity has been observed in patients with acute myeloid leukemia, these findings suggest potential strategies for improving the activity of vinca alkaloids in this disease.
Antineoplastic Agents↗
Pharmacology of the human gamma-aminobutyric acidA receptor alpha 4 subunit expressed in Xenopus laevis oocytes.
The human gamma-aminobutyric acidA (GABAA) receptor alpha 4 subunit was recently cloned and characterized pharmacologically using radioligand binding techniques. These studies suggested that alpha 4 subunits confer a novel diazepam-insensitive binding site. To further investigate the pharmacology of the alpha 4 subunit, we expressed human alpha 4 beta 2 gamma 2L subunit combinations in oocytes and compared the expression and pharmacology of these receptors with alpha 1 beta 2 gamma 2L, beta 2 gamma 2L, and other possible binary subunit combinations. Apparent GABA affinity was 2-3-fold higher for alpha 4 beta 2 gamma 2L than for alpha 1 beta 2 gamma 2L receptors. Functional modulation of receptors by benzodiazepine-site ligands and other classes of allosteric modulator were assayed over a broad concentration range (0.01-100 microM) on currents that were 10% of the maximum GABA response. Diazepam (0.01-1 microM) did not modulate GABA responses at alpha 4 beta 2 gamma 2L receptors, whereas it increased alpha 1 beta 2 gamma 2L responses by approximately 110%. Bretazenil (0.01-1 microM), a benzodiazepine partial agonist, induced higher efficacy modulation of alpha 4 beta 2 gamma 2L receptors (approximately 83%) than of alpha 1 beta 2 gamma 2L (approximately 25%). The benzodiazepine antagonist flumazenil (0.1-10 microM) unexpectedly potentiated alpha 4 beta 2 gamma 2L responses up to approximately 41%, and the benzodiazepine partial inverse agonist Ro15-4513 (1 microM) potentiated alpha 4 beta 2 gamma 2L responses by approximately 63%. Two other benzodiazepine-site ligands, CGS-9895 and methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate, had qualitatively similar effects at alpha 1 beta 2 gamma 2L and alpha 4 beta 2 gamma 2L. Modulators such as pentobarbital, 3 alpha-hydroxy-5 alpha-pregnan-20-one, mefenamic acid, and loreclezole also induced similar potentiation at both subtypes of receptor. The pharmacology conferred by the alpha 4 subunit was similar to that conferred by the alpha 6 subunit, to which it shows highest levels of homology, but the two subunits differ in sensitivity to the beta-carboline methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate. Properties of the alpha 4-containing receptors are consistent with diazepam-insensitive binding sites found in cerebral cortex and other forebrain structures. Characterization of these receptors should further our understanding of mechanisms underlying the behavioral effects of GABA modulators and help in the design of drugs with improved, or novel, therapeutic profiles.
Animals↗
[Emergency admission with suspected anemia-causing bleeding in the upper gastrointestinal tract].
The 33-year-old woman was violently beaten and suffered from concussion of the upper abdomen. Because of pain she took mefenamic acid for two days. Then she reported hematemesis, melena and vertigo. The value for hemoglobin was determined as 5.8 g/dl. Acute blood loss was suspected, but neither intraabdominal nor upper gastrointestinal hemorrhage could be detected. Further investigations revealed a Coombs-negative hemolytic anemia and thrombocytopenia, and microangiopathic hemolysis was suggested by the detection of fragmentocytes in a peripheral blood smear. The diagnosis of thrombotic thrombocytopenic purpura (TTP) was made, though the patient did not suffer from manifestations of impaired microcirculation like neurological symptoms or renal failure. The TTP was found to be associated with HIV infection. The hematological disease responded well to the treatment with fresh-frozen plasma.
Abdominal Injuries↗
[In vivo selectivity of nonsteroidal anti-inflammatory drugs on COX-1-COX-2 and gastrointestinal ulcers, in rats].
UNLABELLED: This work was aimed to study COX-1 and COX-2 selectivity in 16 non-steroidal anti-inflammatory drugs (NSAIDs), at ulcerogenic doses in 2 experimental models: 1) provided subcutaneously (sc), after solid food(SF), (antrum ulcers and intestinal erosions); and 2) orally (O) (fundic and intestinal erosions). METHODS: 17 groups of female Wistar rats (n = 7 each group), weighing 200 g, 36 h fasting with water ad libitum, were submitted to the following experiments: 1. SF (Cargill chow) during 1 h, and then sc: 1.1 ml saline; 2. diclofenac (Di); 3. indomethacine (Indo); 4. Ketorolac (Ke); 5. meloxicam (Mel); 6. Pyroxicam (P); 7. tenoxicam (T). The dose for the aforementioned drugs was 60 mg/kg; 8. aceclofenac (Ace); 9. 200 mg/kg nimesulide (Ni); 10. mefenamic acid (Mac); 11. aspirin (A); 12. etodolac (E); 13. ibuprophen (Ibu); 14. nabumetone (Na); 15. naproxene (Nap); 16. ketoprophen (Ket); 17. paracetamol (Pa), 500 mg/kg. II. The drugs where administered by orogastric tubing to the same groups of fasting animals. After 24 h the animals were killed by ether overdose. Laparotomy was performed and the stomach and the small intestine was removed. The percentage of antum ulcer, and fundic and intestinal erosion (mm2) was tabulated by planimetry. Blood and histological samples were obtained. RESULTS: The NSAIDs Indo, Ibu, Ke, Ket, P and Te yielded an antrum ulcer area: 5-29% and intestinal erosion, 101-395 mm2, similar to Indo (p > 0.50). In contrast there were neither ulcers nor intestinal erosions with Mac, A, Di, E and Nap (p > 0.50). While there were absence of ulcers with Ace, Me, Na, Ni and Pa and slight intestinal erosion (0-23 mm2; p < 0.01). II. There were differences in the following oral (NAIDs: Ace, Me, NA, Ni and Pa, yielding 0-5% fundic erosion and 0-22 mm2 intestinal erosion (p < 0.001). The other NSADs yielded 33-90% fundic erosion and 116-550 mm2 intestinal erosion, similarly to Indo (p > 0.50). HISTOLOGY: Leukocyte infiltrate in the gastrointestinal mucosa with all the NSADs, except Ibu and Pa. There was also neutrophilia (5000-20,000), but not with Ibu and Pa (700-1200). CONCLUSIONS: COX-2-COX-1 selectivity was demonstrated "in vivo" in aceclofenac, meloxicam, nabumetone, nimesulide and paracetamol.
Animals↗
Spectrofluorimetric determination of anthranilic acid derivatives based on terbium sensitized fluorescence.
Terbium sensitized fluorescence was used to develop a sensitive and simple spectrofluorimetric method for the determination of the anthranilic acid derivatives furosemide and mefenamic and tolfenamic acids. The method makes use of radiative energy transfer from anthranilates to terbium ions in alkaline methanolic solutions. Optimum conditions for the formation of the anthranilate-Tb3+ complexes were investigated. Under optimized conditions, the detection limits are 6 x 10(-9), 1.4 x 10(-8) and 9.0 x 10(-9) mol l-1 for furosemide, mefenamic acids and tolfenamic acid, respectively. The range of application is 2.5 x 10(-8)-5.0 x 10(-5) mol l-1 for all three drugs. The method was successfully applied to the determination of furosemide and mefenamic and tolfenamic acids in serum after extraction of the samples with ethyl acetate, evaporation of the organic layer under a stream of nitrogen at 40 degrees C and reconstitution of the residue with alkaline methanolic terbium solution prior to instrumental measurement. The mean recoveries from serum samples spiked with furosemide (5.0 x 10(-7), 2.0 x 10(-6) and 8.0 x 10(-6) mol l-1), mefenamic acid (3.0 x 10(-6), 9.0 x 10(-6) and 3.0 x 10(-5) mol l-1) and tolfenamic acid (3.1 x 10(-6), 12.5 x 10(-6) and 2.5 x 10(-5) mol l-1) were 96 +/- 8, 101 +/- 5 and 98 +/- 7%, respectively. The within-run precision (RSD) for the method for two serum samples of each drug varied from 2 to 8% and the day-to-day precision for two concentration levels varied from 2 to 13%.
Anti-Inflammatory Agents, Non-Steroidal↗
Capillary isotachophoretic determination of flufenamic, mefenamic, niflumic and tolfenamic acid in pharmaceuticals.
Anionic capillary isotachophoresis (ITP) with conductimetric detection has been used for determining selected non-steroid anti-inflammatory and analgesic drugs of the phenamate group, namely tolfenamic (I), flufenamic (II), mefenamic (III) and niflumic (IV) acid. Initially the pKa values (proton lost) of I-IV were determined as 5.11, 4.91, 5.39 and 4.31, respectively, by the UV spectrophotometry in aqueous 50% (w/w) methanol. The optimised ITP electrolyte system consisted of 10 mM HCl + 20 mM imidazole (pH 7.1) as the leading electrolyte and 10 mM 5,5'-diethylbarbituric acid (pH 7.5) as the terminating electrolyte. The driving and detection currents were 100 microA (for 450 s) and 30 microA, respectively (a single analysis took about 20 min). Under such conditions the effective mobilities of I-IV varied between 23.6 and 24.6 m2 V(-1) s(-1) (evaluated with orotic acid as the mobility standard). The calibration graphs relating the ITP zone length to the concentration of the analytes were rectilinear (r = 0.9987-0.9999) in the range 10-100 mg l(-1) of the drug standard. The R.S.D.s were 0.96-1.55% (n = 6) when determining 50 mg l(-1) of the analytes in pure test solutions. The method has been applied to the assay of the phenamates in six commercial mass-produced pharmaceutical preparations (Mobilisin gel and ointment, Lysalgo capsules, Nifluril cream, Niflugel gel, and Clotam capsules). According to the validation procedure based on the standard addition technique the recoveries were 98.4-104.3% of the drug and the R.S.D. values were 1.25-3.32% (n = 6).
Anti-Inflammatory Agents, Non-Steroidal↗