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At least 109 records · Page 6Linked to original sources
PubMed1979

Antipyretic analgesics in patients on antiepileptic drug therapy.

The effect of administration for three days of acetylsalicylic acid (1500 mg/day), phenylbutazone (300 mg/day), paracetamol (1500 mg/day) and tolfenamic acid (300 mg/day) on serum concentrations of phenytoin and carbamazepine were studied in a group of patients on continuous antiepileptic therapy. When measured 10 h after the last dose of the analgesics, the only significant effect was a decrease in total serum phenytoin after three days of phenylbutazone. When six patients on continuous phenytoin therapy took phenylbutazone for two weeks there was at two days an initial decrease, followed by a signficiant increase in total serum phenytoin and a concomitant increase in free phenytoin in serum. Even phenylbutazone was well tolerated by most of the patients. However, its use had to be discontinued on one patient due to obvious signs of phenytoin intoxication, with concomitant increases in the serum free and total phenytoin concentrations.

Adult↗
PubMed1983

Gastrointestinal effects of antipyretic analgesics.

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. Aspirin is significantly associated with major upper gastrointestinal hemorrhage, whereas acetaminophen is not. Short-term use of aspirin produces erythema, erosions, and occasionally ulcers; acetaminophen use does not. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users; paradoxically, in only one epidemiologic study was a significant association found between acetaminophen intake and chronic gastric ulcer. Fecal occult blood loss is increased in most regular aspirin users but not in those taking acetaminophen. Although studies in children have not apparently been made, in isolated small clinical series it has been shown that gastrointestinal bleeding and anemia do occur in the pediatric age group following the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; acetaminophen has no effect on these parameters. Such changes correlate ultrastructurally with damage in surface epithelial cells and microerosions after the use of aspirin, but not after the use of acetaminophen. Aspirin causes a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, acetaminophen also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, bicarbonate output, and alteration of cell turnover. Because aspirin damage to gastric mucosa is often "silent," the clinician needs a high level of suspicion and awareness. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, acetaminophen is the drug of choice when a minor, noninflammatory problem requires an analgesic.

Acetaminophen↗
PubMed1983

Hematologic effects of antipyretic analgesics. Drug-induced agranulocytosis.

Drug-induced agranulocytosis may be type I (involving the drug, antibodies and neutrophils), type II (associated with accumulated drug toxicity in hypersensitive persons), or type III (representing different etiologies induced by immune and toxic mechanisms). The pyrazolones (amidopyrine, dipyrone and butazones), phenothiazine derivatives, antithyroid drugs, and antibiotics are thought to be causative agents in agranulocytosis. The symptoms may involve sudden onset of high fever, sore throat with ulcerative angina, or stomatitis. Diagnosis of agranulocytosis is confirmed by severe granulocytopenia (0-0.5 X 10(9)/l), but bone marrow examination is required to rule out aplastic anemia and cancer. Treatment of drug-induced agranulocytosis involves immediate withdrawal of the incriminated drug. In most patients, granulocyte, reticulocyte, and thrombocyte cell counts overshoot in the regenerative phase of drug-induced agranulocytosis.

Agranulocytosis↗
PubMed1983

Antipyretic analgesics and the allergic patient.

Recent studies of idiosyncratic reactions to analgesics have revealed several clinical patterns with different pathogeneses. In the common type of asthma precipitated by aspirin, inhibition of cyclooxygenase leads to disturbances in the metabolism of arachidonic acid. Drugs that precipitate possibly life-threatening bronchoconstriction and are absolutely contraindicated in patients with aspirin-induced asthma include indomethacin, mefenamic acid, flufenamic and meclofenamic acids, ibuprofen, fenoprofen, ketoprofen, naproxen, diclofenac, amidopyrine, noramidopyrine, phenylbutazone, flumizole, and ditazol. If necessary, patients with aspirin-induced asthma can safely take, even on a long-term basis, salicylamide, dextropropoxyphene, benzydamine, guaiacolic ester of salicylic acid, and chloroquine. In some patients with urticaria/angioedema, symptoms are due to inhibition of cyclooxygenase by analgesics; in others, the cause may be impurities in commercial preparations of aspirin; and in still others, the mechanisms remain unknown.

Acute Disease↗
PubMed1975

Prostaglandins, antipyretic analgesics and adrenergic stimuli on the isolated artery.

In untreated, and cocaine- and DOCA-treated rabbit ear arteries, PGE2 and arachidonic depressed to responses to intramural sympathetic nerve stimulation. Constrictor responses to extraluminal NA in the treated arteries were also depressed. A comparison of its inhibitory potency on the two types of responses suggest that the effects of arachidonic acid, but not PGE2 on adrenergic nerve stimuli, were selectively blocked by aspirin 200 mug/ml and by indomethacin 3 mu/ml. In these concentrations, aspirin, but not indomethacin, enhanced the magnitude of the resoonses to the stimuli. Aspirin also selectively reduced the inhibition by arachidonic acid of the response to extraluminal NA (tested in cocaine0 and DOCA-treated arteries).

8,11,14-Eicosatrienoic Acid↗
PubMed1980

Influence of analgesic antipyretics on the central cardiovascular effects of clonidine in rats.

The centrally acting antihypertensive drug clonidine has been found to stimulate the synthesis of PGF2 alpha in the brain. Centrally administered PGF2 alpha, in turn, induces rises of blood pressure and heart rate. We therefore studied the influence of inhibitors of prostaglandin (PG) synthesis on the cardiovascular effects of clonidine in urethane-anaesthetised rats. Pretreatment with indomethacin or paracetamol (100 micrograms/rat into the fourth cerebral ventricle) antagonised the central hypotensive effect of clonidine (0.125-16.0 micrograms/rat into the fourth cerebral ventricle). The bradycardic effect of centrally administered clonidine was, however, enhanced by pretreatment with paracetamol but not influenced by indomethacin pretreatment. Sodium meclofenamate (100 micrograms/rat into the fourth cerebral ventricle) did not significantly affect the clonidine-induced changes in blood pressure and heart rate. These results suggest that the clonidine-induced hypotension on one hand and bradycardia on the other hand may be mediated by partly different mechanisms. An interference of the formation of PGF2 alpha with the cardiovascular effects of clonidine cannot be completely excluded since paracetamol pretreatment potentiated the bradycardic effect of clonidine. However, inhibitors of PG synthesis did not enhance but antagonised the hypotensive effect of clonidine. Therefore it is likely that the synthesis of PGF2 alpha does not interfere with the hypotensive effect of clonidine. Moreover, the antagonism of the hypotensive effect by inhibitors of PG synthesis suggests that some hypotensive metabolite of arachidonic acid in the brain could be involved in the central hypotensive effect of clonidine.

Acetaminophen↗
PubMed2002

Preparation of antipyretic analgesic by direct compression and its evaluation.

Direct compression is able to produce tablets at a lower cost than wet granulation and tableting method, due to a fewer items of process validation. In this study, acetaminophen was used as a medicine with various granular diameters to formulate tablets by direct compression, thus evaluating their physical properties. Consequently, direct compression was found effective in formulating tablets with excellent physical properties, with the granular diameter taken into account. It was confirmed that tablets produced by direct compression were similar in physical properties in tablets produced by wet granulation and tableting method. Further, it was suggested that use of a dry-type binder would make it possible to provide a tablet having higher content of the medicine with excellent physical properties.

Acetaminophen↗
PubMedDate not supplied

[A new anti-inflammatory-analgesic-antipyretic, morniflumate, in the treatment of chronic recurring bronchitis].

To assess the therapeutic effects of morniflumate, a new non-steroidal anti-inflammatory drug, a controlled study versus imidazole-2-hydroxybenzoate, both combined with amoxicillin, and antibiotic therapy alone was carried out on 60 patients, aged 18 to 60 with flare-ups of chronic bronchitis. After administering morniflumate, all the clinical parameters assessed (objective auscultation, cough, expectoration, exertional dyspnoea, chest pain, hyperthermia) had improved. The modifications observed in this group were greater and earlier when compared to those of the control groups. No significant variations of laboratory parameters nor any particular side-effects were reported.

Adolescent↗