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PubMed1995

[Mechanism of analgesic action of Y-23023, a new non-steroidal anti-inflammatory drug].

The analgesic mechanism of Y-23023, a new non-steroidal anti-inflammatory drug, was investigated in the writhing response induced by intraperitoneal injection of kaolin and captopril in mice. Y-23023 (0.1-1 mg/kg, p.o.) suppressed the writhing frequency in a dose-dependent manner. Y-23023 also significantly reduced the increased levels of prostaglandin (PG) and bradykinin (BK) in the peritoneal cavity. In contrast, indomethacin, diclofenac sodium, loxoprofen sodium and mefenamic acid inhibited the writhing response, but their efficacies were lower than that of Y-23023. The peritoneal PG levels were dose-dependently reduced to the same extent as Y-23023, whereas the BK levels were not. M1, an active metabolite of Y-23023, inhibited the cyclooxygenase from sheep vesicular gland in a concentration-dependent manner, and its potency was similar to that of indomethacin. These results suggest that in addition to the suppressive effect on PG production via inhibition of cyclooxygenase, the inhibitory effect on BK production is involved in the analgesic action of Y-23023, unlike indomethacin and diclofenac sodium.

Analgesics↗

PubMed1977

[Pharmacological studies on carprofen, a new non-steroidal anti-inflammatory drug, in animals (author's transl)].

The pharmacological profile of carprofen as a new non-steroidal anti-inflammatory drug has been established in various experimental inflammation models in animals. This compound possesses marked effects on prevention of adjuvant arthritis, cotton-pellet granuloma formation and hyperalgesic edema (scalding) and the extent is similar to that observed with indomethacin and piroxicam. The anti-inflammatory potency of carprofen is markedly stronger than those seen in cases of phenylbutazone, mefenamic acid, ibufenac and acetylsalicylic acid, almost equal to that of diclofenac and slightly lower than that of indomethacin in the following parameters: carrageenin-edema, granuloma-pouch, UV-erythema, and bradykinin and histamine-induced capillary permeability. As is the case with other non-steroidal anti-inflammatory drugs, carprofen has no inhibitory effect on lethal anaphylactic shock, passive cutaneous anaphylaxis and hyperuricemia. Carprofen induces ulcerogenicity and fecal occult bleeding to a extent markedly less than those seen with indomethacin and piroxicam. These investigations on anti-inflammatory drugs indicate a probable dissimilarity to the extent of anti-inflammatory effects and induction of gastrointestinal disturbances. Repeated administration of carprofen has no effect on spontaneous excretion of corticosterone and aldosterone into adrenal vein of rats.

Adrenal Cortex↗

PubMed1978

[Anti-inflammatory activity of SL-573 (author's transl)].

In the carrageenin-induced edema test in rats, the anti-inflammatory activity of SL-573 was 1.6 times as potent as those of phenylbutazone (PB) and ibuprofen (IP), 3.3 times as potent as that of mefenamic acid (MF) and 6.7 times as potent as that of mepirizole (MP). In the yeast-induced edema test in rats, SL-573 showed equipotent activity with IP, the activity of which was 4 times as potent as that of MP. In the dextran-induced edema test in rats, the anti-inflammatory activity of SL-573 was significantly higher than those of IP and MP. SL-573 showed no anti-inflammatory activity in the formalin-induced edema test in rats in the same way as seen with IP and MP. SL-573 markedly inhibited the increase in capillary permeability in mice induced by intraperitoneal administration of acetic acid, and its activity was 12 times as potent as that of PB and 17 times as potent as that of MF. SL-573 showed anti-granuloma activity neither systemically nor locally. SL-573 showed equi-potent activity with PB in the adjuvant arthritis test in rats and had little effect on the healing process of the skin wound in rats. The effect of SL-573 on the carrageenin-induced edema was not diminished in the adrenalectomized rats. The gastric bleeding effect of SL-573 was significantly weaker than that usually seen in nonsteroidal anti-inflammatory drugs. SL-573 did not induce intestinal perforation even at the high dose of 800 mg/kg. Additionally, SL-573 showed a protective effect on the indomethacin-induced intestinal lesions. These pharmacological profiles of SL-573 were considered to be quite characteristic as compared with those of known nonsteroidal anti-inflammatory agents.

Adrenalectomy↗

PubMed1986

[Studies of inflammatory pain response: related pain producing substance and endogenous opioid system].

A method for assessing inflammatory pain response was developed by modification of the formalin test. Formalin (0.5%, 25 microliters) was injected into the hindpaw of the mouse, and the durations spent in licking or biting response were measured as an indicator of pain response. The response curve was biphasic, having two peaks, from 0 to 5 min (first phase) and from 15 to 20 min (second phase). Morphine, ethylketocyclazocine, ketocyclazocine and pentazocine inhibited the response dose-dependently at the first and the second phases. Aspirin, oxyphenbutazone and dexamethasone inhibited only the second phase. Aminopyrine and mefenamic acid which acted at both central and peripheral sites inhibited both phases; however, the inhibition of the second phase was stronger than that of the first phase. Substance P (SP) antagonist inhibited only the first phase. Bradykinin (BK) inhibitor caused a inhibition of both first and second phases, and pretreatment of compound 48/80 and indomethacin inhibited only the second phase. From these facts, it was suggested that SP and BK played a role in the pain response at the first phase, and histamine, BK and PG were involved at the second phase. Naloxone produced hyperalgesia and bestatin produced analgesia at the second phase; then, it seems that the endogenous opioid system is activated by formalin stimulation and modulates the pain perception. Based on these findings, it is presumed that the pain of the first phase is evoked by the direct stimulation of the nerve fibers, and that of the second phase is due to the inflammatory reaction.

Analgesics↗

PubMed1990

[Pharmacological profile of mofezolac, a new non-steroidal analgesic anti-inflammatory drug].

Pharmacological activities of mofezolac were investigated in experimental animal models and compared with those of indomethacin, ibuprofen, mefenamic acid, aspirin and aminopyrine. Mofezolac showed a potent suppression of various writhing models in mice or rats; and its potency was slightly lower than that of indomethacin, but was higher than those of the other reference drugs. Thus, mofezolac was especially active against chemically induced writhing and also in the phenylquinone induced intraperitoneal dye leakage reaction in mice. Mofezolac also has a potent inhibitory activity on the algesic responses induced by the mechanical stimulus of the inflammed tissue. Mofezolac exhibited a therapeutic effect comparable to indomethacin in the urate synovitis in dogs. Considering the anti-inflammatory and antipyretic actions, mofezolac was obviously less effective than indomethacin, and its potency was similar to that of ibuprofen. The ulcerogenic effect of mofezolac on the gastric mucosa was far weaker than that of indomethacin. In in vitro studies, the prostaglandin biosynthesis and platelet aggregation were inhibited to the same extent by both mofezolac and indomethacin. Accordingly, it may be considered that the actions of mofezolac are due to the inhibition of cyclooxygenase. Our result suggest that mofezolac can be a useful drug that shows a rapid pain-relieving activity in acute inflammations.

Analgesics↗

PubMed1981

Pharmacological studies of the involvement of hypothalamic prostaglandins in the regulation of thyrotropin secretion.

A case is made for the involvement of pituitary prostaglandins (PGs) in the regulation of thyrotropin (TSH) secretion by citing recent evidence that TSH release in vivo and in vitro is enhanced by treatment with exogenous PGs and is inhibited by drugs (e.g., indomethacin) that block PG synthesis. Pharmacological studies were then performed to test the hypothesis that hypothalamic PGs also affect TSH secretion indirectly via the appropriate hypothalamic hormones that regulate pituitary secretion. The inhibition of thyroidectomy-induced TSH secretion was used as an endpoint in choosing the best of several drugs purported to inhibit PG synthesis. The established effectiveness of indomethacin and aspirin were used for reference in testing the following drugs: naproxen, mefenamic acid, tranylcypromine, and phenelzine. Only naproxen was found to be effective, but since it was no more potent than indomethacin, the latter drug was used for subsequent work. Indomethacin was stereotaxically implanted into several hypothalamic regions known to regulate TSH secretion, and sequential plasma samples were analyzed for TSH by radioimmunoassay. Bilateral implants of indomethacin in the anterior hypothalamic area increased TSH secretion throughout the 72 hr period of study. Sham inplants at this site and indomethacin implants in other nearby sites were ineffective. These findings suggest that endogenous PGs play an inhibitory role in the hypothalamic regulation of pituitary secretion.

Animals↗

PubMed1997

Indomethacin enhances the cytotoxicity of VCR and ADR in human pulmonary adenocarcinoma cells.

The ability of anti-inflammatory agents to modulate cellular sensitivity to anticancer drugs was investigated for pulmonary carcinoma cells in vitro. We examined the drug sensitivity of two pulmonary adenocarcinoma cell lines (76-2, 77-4) in the presence of two drugs, an anticancer drug and an anti-inflammatory agent, for 72 hr by the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay with 96 well plates. Anticancer drugs used for screening test were cyclophosphamide (CPM), mitomycin C (MMC), adriamycin (ADR), 5-fluorouracil (5FU), vindesine (VDS), cisplatin (CDDP), cytarabine (Ara C), methotrexate (MTX), etoposide (VP-16), and vincristine (VCR). Anti-inflammatory agents examined as modulators to anticancer drugs were aspirin, mefenamic acid, ibuprofen, sulindac, piroxicam, phenacetin, dicrofenac, ketoprofen, tolmetin and indomethacin. Screening tests showed indomethacin to be the most effective modulator, resulting in more than a 3-fold increase in cytotoxicity of VCR as compared with that produced by VCR alone. Study of each of the ten anticancer drugs in combination with indomethacin showed VCR to be the most effective anticancer drug in this combination. In 76-2 cells, the concentration of VCR producing 50% growth inhibition (IC50) for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 1.58 +/- 0.16 and 0.52 +/- 0.1 ng/ml respectively, which represents a 3-fold decrease. In 77-4 cells, the IC50 for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 2.86 +/- 0.2 and 0.52 +/- 0.11 ng/ml respectively, which represents a 3.8-fold decrease. Our studies indicate that clinically achievable concentrations of indomethacin may be useful in modulating VCR resistance in human pulmonary adenocarcinoma cells, so that combined use of VCR and indomethacin may be of potential clinical significance in the treatment of lung cancer.

Adenocarcinoma↗

PubMed1991

The problems and pitfalls of NSAID therapy in the elderly (Part I).

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly prescribed drugs worldwide when grouped by generic categories and account for 3 to 9% of total prescription numbers in various countries. While NSAIDs are responsible for approximately 25% of all reported adverse drug reactions, aging may substantially increase the risk of NSAID-induced reactions. Several factors may contribute to NSAID-related toxicity in the elderly. The increase in morbidity associated with aging may result in consumption of a wide range of potent drugs, while inappropriate drug therapy and aberrant compliance are also capable of contributing to adverse drug reactions in geriatric patients. Age-related alterations in pharmacokinetics may influence the handling of NSAIDs in the elderly; in particular, dosage reduction is appropriate for azapropazone (apazone), naproxen, ketoprofen and salicylates administered to healthy aged patients, whereas the presence of renal disease may also necessitate dosage reduction of diflunisal, indomethacin, sulindac and mefenamic acid. Changes in NSAID pharmacodynamics with aging, such as increased CNS sensitivity to NSAIDs and impaired homeostasis, also predispose the elderly to NSAID-related adverse effects. It is undisputed that gastrointestinal toxicity due to NSAID therapy is a class effect. A significant association has been found between aspirin and uncomplicated gastric, but not uncomplicated duodenal ulcer, while nonaspirin NSAIDs are significantly associated with both uncomplicated gastric and duodenal ulceration. The use of NSAIDs is accompanied by a 2- to 5-fold risk of serious complications of peptic ulcer disease, i.e. haemorrhage or perforation, which increases in the elderly, particularly women. A broad range of renal side effects has been ascribed to NSAIDs, of which acute renal impairment is the most common in the elderly. Although most NSAIDs have been reported to cause hepatotoxicity, serious abnormalities of liver function are rare and are largely unpredictable. Other adverse effects due to NSAIDs have also been described, some of which (e.g. cardiovascular, CNS and haematological effects) may be more common in the elderly.

Aged↗

PubMed1976

Drugs and gastric damage.

The effects of aspirin, salicylate formulations and substitutes, smoking (nicotine), indomethacin, corticosteroids, phenylbutazone, ethanol, caffeine and reserpine on the gastric mucosa are discussed. The damaging effects of the drugs are considered in terms of the gastric mucosal barrier, gastric erosions, microbleeding and haematemesis and melaena and finally whether they cause peptic ulcer. There is suggestive evidence that unbuffered aspirin is a cause of haematemesis and melaena and of gastric ulcer but the incidence rates for hospital admission are low, being 10 to 15 per 100,000 heavy users per year. Aspirin in solution as acetylsalicylate buffered to maintain a neutral pH protects against gastric damage. Newer aspirin substitutes (mefenamic acid, fenoprofen, naproxen, tolmetin and ibuprofen) appear to cause less faecal blood loss than aspirin but their long-term effects have not been fully evaluated. Smoking is definitely associated with peptic ucler but the mechanism is unknown. Corticosteroids are probably not ulcerogenic despite clinical bias that they are. Indomethacin and phenylbutazone may be ulcerogenic but there is insufficient evidence to make firm judgements. Ethanol, caffeine and reserpine, on available evidence, are probably not ulcerogenic.

Adrenal Cortex Hormones↗

PubMed1985

Suprofen. A review of its pharmacodynamic and pharmacokinetic properties, and analgesic efficacy.

Suprofen (sutoprofen) is a non-steroidal anti-inflammatory analgesic, closely related structurally to drugs such as ibuprofen, ketoprofen and naproxen. In patients with acute pain, single oral doses of suprofen are at least as effective as: usual therapeutic doses of aspirin; codeine alone or combined with aspirin; dextropropoxyphene alone or in various combinations; oxycodone combined with aspirin; dipyrone; pentazocine; paracetamol (acetaminophen); diflunisal; ibuprofen; indomethacin; or mefenamic acid. In chronic pain due to osteoarthritis, suprofen is as effective as usual dosages of aspirin or dextropropoxyphene during long term therapy, and as effective as diclofenac, ibuprofen, indomethacin and naproxen during short term treatment. As with other non-steroidal anti-inflammatory drugs, gastrointestinal complaints are the most frequently reported side effects, although discontinuation due to gastrointestinal effects may be necessary less frequently with suprofen than with aspirin, dextropropoxyphene or combinations of the two. Suprofen appears to be a useful alternative to mild analgesics, analgesic combinations or the older more established non-steroidal anti-inflammatory drugs in the treatment of patients with acute or chronic pain. However, further definition of its efficacy and tolerability is required, especially in comparison with newer non-steroidal anti-inflammatory analgesics.

Acute Disease↗

PubMed1992

Management of dysfunctional uterine bleeding.

Dysfunctional uterine bleeding, although not usually life-threatening, can cause disruption and discomfort for many women. It has often been poorly researched in the past, possibly because of the difficulty in measuring menstrual blood loss. Several different therapies are available and individual women can choose from a number of options. Nonsteroidal anti-inflammatory drugs such as mefenamic acid or indomethacin will be the first choice for many women as they have few side effects and it is only necessary to take them when menstrual bleeding occurs. When contraception is also required, combined oral contraceptives are helpful. Progestogen and danazol therapy are also effective, although side effects do occur. A new development has been the levonorgestrel-containing intrauterine contraceptive device which has been shown to result in large decreases in menstrual blood loss. For those women who would like a surgical approach but do not want to undergo hysterectomy, the relatively new technique of endometrial resection results either in amenorrhoea or reduced menstrual blood loss in the majority of women.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2006

Inhibition of sulfotransferases by xenobiotics.

The sulfotransferase (SULT) family comprises important phase II conjugation enzymes for the detoxification of xenobiotics and modulation of the activity of physiologically important endobiotics such as thyroid hormones, steroids, and neurotransmitters. SULT enzymes catalyze the transfer of a sulfuryl group, donated by 3'-phosphoadenosine-5'-phosphosulfate (PAPS), to an acceptor substrate that may be a hydroxy group or an amine group in a process originally called sulfation, but more correctly referred to as sulfonation or sulfurylation. SULT activity may be inhibited when humans are exposed to certain xenobiotics including drugs (mefenamic acid, salicylic acid, clomiphene, danazol etc.), dietary chemicals (catechins, food colorants, flavonoids and phytoestrogens etc.), and environmental chemicals (hydroxylated polychlorinated biphenyls, hydroxylated polyhalogenated aromatic hydrocarbons, pentachlorophenol, triclosan and bisphenol A, etc.). Inhibition of individual SULT isoforms may cause adverse effects on human health. For example, hydroxylated polychlorinated biphenyls have been shown to interfere with the transport of thyroid hormones, inhibit estradiol sulfonation, and inhibit thyroid hormone sulfonation, thereby potentially disrupting the thyroid hormone system. Formation of sulfate conjugates of toxic xenobiotics usually decreases their toxicity, so inhibition of this pathway may lead to prolonged exposure to the compounds. Conversely, some sulfate conjugates are chemically reactive, inhibition of their formation may protect from toxicity. This manuscript will review the literature concerning the inhibition of SULTs by xenobiotics including isoform-selective effects, inhibition kinetics and health effects resulting from the inhibition.

Animals↗

PubMed1979

Suppression of uterine activity by prostaglandin synthetase inhibitors.

During hypertonic saline induction, the evolution of intrauterine pressure, the oxytocin response and abortion were delayed in naproxen-treated patients. The PG synthesis inhibitors naproxen, mefenamic acid and ibuprofen decreased the high uterine resting pressure ('tone'), the frequency of contractions but not always the active pressure ('amplitude') in dysmenorrheic patients, with a coincident decrease in pain. The naproxen-sodium treatment decreased prostaglandins F and E in menstrual blood and uterine jet washings by 60--80 per cent.

Abortion, Induced↗

PubMed1995

Renal impairment after acute diclofenac, naproxen, and sulindac overdoses.

Acute renal dysfunction has been described as a feature of acute overdoses of the nonsteroidal anti-inflammatory drugs benoxaprofen, fenoprofen, ibuprofen, mefenamic acid, piroxicam, suprofen, and zomepirac. The cases reported here include renal impairment after acute overdoses of another three nonsteroidal anti-inflammatory drugs: diclofenac (one case), naproxen (two cases), and sulindac (five cases). The eight patients presented with lumbar pain and oliguria and had protein and erythrocytes in the urine. Serum creatinine was increased to a maximum of 190-932 mumol/L. Renal impairment was generally transient but in one case was treated by hemodialysis and one by continuous arterio-venous hemofiltration dialysis. In all cases of significant acute overdose of nonsteroidal anti-inflammatory drugs, the risk of acute renal dysfunction must be considered.

Acute Kidney Injury↗

PubMed1999

[Drug-induced autoimmune hemolytic anemia].

AUTOANTIBODY PRODUCTION: The production of autoantibodies can only occur if immune tolerance is circumvented. Thus drug-induced autoimmune hemolytic anemia requires that the drug have an effect on both autoantigens and on the immune system. AN EXAMPLE, METHYLDOPA: Methyldopa is a hypotensive agent which induces major production of anti-Rh IgG anti-erythrocyte autoantibodies, anti-nuclear antibodies and anti-actin antibodies. These autoantibodies generally appear 6 months after treatment onset and are observed in 20% of treated patients. Hemolysis is however exceptional and is only clinically or biologically perceptible in 1 to 2% of the patients who become immunized. Induced lupus has been reported as have been several dozen cases of drug-induced hepatitis with anti-actin autoantibodies. DRUGS INDUCING HEMOLYTIC ANEMIA: Besides methyldopa, other drugs known to induce hemolytic anemia include levodopa used for Parkinson's disease, mefenamic acid, a nonsteroidal antiinflammatory drug, interferon-alpha, used in chronic viral hepatitis, cyclosporin used for the prevention of graft rejection and the treatment of certain autoimmune diseases, and fludarabin, used in chronic lymphoid leukemia. THERAPEUTIC STRATEGY: If there is no clinical or biological expression, the drug can be continued, excepting fludarabin where regular controls are needed. If hemolytic anemia is patent, the drug must be discontinued, transfusion and corticosteroid therapy should be envisaged.

Adrenal Cortex Hormones↗

PubMed1976

Activity of nonsteroid anti-inflammatory drugs in immunologically specific and nonspecific cellular responses.

The influence of nonsteroid anti-inflammatory drugs on immunologic reactions of the humoral type (agglutinins, hemolysins) and of the cellular types (blast test, transplantation test), and on the course of immunologically nonspecific inflammatory reactions(xylene inflammation, pleurisy, granulation test) has been studied. Virtually regardless of chemical structure (indomethacin, mefenamic acid, acetylsalicylic acid, chloroquine), the drugs of this group had no influence on humoral responses, but a distinct influence on the delayed type of cellular responses and on immunologically nonspecific reactions. The investigated drugs had quantitatively varying modes of action, and only chloroquine showed a qualitatively different mode of action. It was concluded that nonsteroid anti-inflammatory drugs ace on a common link in inflammatory processes involving the immunologic system, as well as without such an involvement. The mechanism of their effect was considered to consist in stabilization of cell membranes, inhibition of proliferation and cellular transformation, and inhibition of the lymph node permeability factor (LNPF).

Agglutinins↗

PubMed1979

Correlation between antiinflammatory activity and inhibition of prostaglandin biosynthesis induced by various non-steroidal antiinflammatory agents.

The effect of several non-steroidal antiinflammatory agents (some of them original from our laboratory) on prostaglandin biosynthesis in guinea pig lung (biological method) and in bovine seminal vesicles (spectrophotometric method) has been studied. When this effect is compared with the in vivo antiinflammatory activity determined in the rat carragenin foot edema and with the recommended clinical daily dose in rheumatoid arthritis, a good correlation between these properties was observed. Only mefenamic acid showed a clear discordance. The experience shows that inhibitory effect of antiinflammatory drugs on prostaglandin synthetase in vitro may be used to predict, in most cases, their antiinflammatory activity in vivo in the pharmacological screening of the new compounds. Structure-activity relationship in the UR-series is also discussed.

Animals↗

PubMed2001

The first world report of botulinum A toxin injection for status migrainosus.

The author reports the first ever documented publication in the world concerning the use of botulinum toxin A (BTX-A) injection for status migrainosus. A 58-year old man had been suffering from migraine without aura for 20 years. This last attack (a very severe throbbing headache) started over the left side of his head and he had tried several medications (paracetamol, aspirin, ergotamine, mefenamic acid, and diazepam) during the attack to no vail. Physical examination revealed an acutely ill patient with an agonizing pain condition. General and neurological examinations were normal. BTX-A solution was then injected into the Fung Chou point (classical Chinese acupuncture point for migraine) in the total amount of 25 international unit. Dramatic response was observed within 1 hour of injection and status migrainosus was abort within 10 hours. He was headache-free and had no further attack of migraine for another 2 months.

Acupuncture Points↗