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PubMed1989

[Allergic complications in patients with rheumatism].

The frequency and character of drug allergy was evaluated in 200 patients with rheumatism. Drug allergy was revealed in 60% of patients, in 62.5% of them to two and more drugs. Allergy was frequent in women and was influenced by concomitant lesions of the digestive and biliary organs, genetic factors (familial predisposition), presence of nondrug reactions. Most frequently allergic complications were observed due to use of antibiotics (37.5%), in particular, of the penicillin group; nonsteroid anti-inflammatory medicinal agents (13.5%) of all patients), primarily, the employment of pyrazolon drugs.

Adolescent↗
PubMed1989

[Aspirin. Pseudo-allergic reactions].

The author reviewed 2000 clinical records of his private allergy patients chosen at random. 197 records (9.7%) labeled "allergic to aspirin" were culled. 41 (2.1%) were acute cases and 153 (7.6%) had a history of "intolerance to aspirin". The main symptoms were angioedema or angioedema and urticaria in the majority of patients. No deaths were recorded. Each clinical record was surveyed and 61% of the acute cases and 72% of the patients with a history of intolerance to aspirin had a personal history of atopy. Family history of atopy was present in 63 and 73%, respectively. There was no history of atopy in 12% of the acute cases and in 7% of those with a history of intolerance to aspirin. 56 to 65% of these groups, respectively, had allergic rhinitis and 17 and 34%, had asthma. 23% of these patients showed allergic reactions simultaneously to Pyrazolones and between 12 and 22% showed allergy to Penicillin, and between 2 and 12%, to Acetominophene. The only food to which statistically significant allergy occurred was pancake, in 12%. 53% of the acute cases and 89% of those with a history of intolerance to aspirin showed a pseudoallergic reaction with products which contain aspirin or non steroidal antiinflamatory agents. 80% of the acute cases were treated with aqueous 1:1000 solution of epinephirine subcutaneously. 100% were given antihistaminics I.M. or orally and 61% were given steroids. Each patient was furnished with a list of the main aspirin containing products and non steroidal antiinflammatory agents, which cross react with aspirin.

Adolescent↗
PubMed1989

[The use of opiates in hospital practice].

We analyzed the type and dosage of opiates used for pain in a large general hospital from April to September 1985. Information was obtained from the computerized data base in 234 patients with a mean age of 49 years. Most patients came from the surgical service. The route of administration was intramuscular in 64% and not specified in 10% of patients. The most common drug was meperidine, the dose being 65 +/- 26 mg intramuscular and 39 +/- 26 intravenously. Methadone and morphine were used with less frequency. Good analgesic effect was recorded in 42 of 71 (59%) of patients, but the effect was not written down in the majority of subjects (70%). Other analgesics were associated in 73% of cases, most commonly a pyrazolone derivative. Nausea or vomiting was observed in only 12 patients; there were no instances of respiratory depression. We conclude that the dose of opiate used was frequently low and the associated drugs were not the best to obtain increased analgesic effect. Better recording of clinical effect of analgesics is needed in medical practice.

Analgesia↗
PubMed1985

[Combined propyphenazone and codeine poisoning in childhood (analysis of 6 patients with Spasmoplus poisoning)].

The case histories are presented of 6 patients with accidental poisoning by Spasmoplus suppositories. The main toxic constituents are codeine and the pyrazolone derivative, propyphenazone. All patients had symptoms of codeine intoxication with somnolence, miosis and oedema, 2 patients had also symptoms of prophyphenazone intoxication with hypotension, coma and convulsions. 1 patient died during the acute stage in a state of shock, with arrhythmia, and asystole.

Aminopyrine↗
PubMed1988

Involvement of prostaglandins in the inhibitory response of adrenoceptor agonists in the rat isolated uterus.

1. The possible involvement of intramurally generated prostaglandins in the responses produced by noradrenaline (NA), adrenaline (ADR) and salbutamol (SAL) has been investigated in the rat isolated uterus. 2. NA, ADR and SAL produced concentration-related inhibition of acetylcholine-induced tone in preparations from the proestrus, oestrus, metoestrus and dioestrus phases of the oestrous cycle, and from ovariectomized animals. 3. The cyclo-oxygenase inhibitor, flurbiprofen (FBF), enhanced uterine inhibitory response to all three agonists under the different hormonal conditions. 4. The dual inhibitor of cyclo-oxygenase and lipoxygenase, 3-amino-l-(m-trifluoromethyl)-phenyl-2-pyrazolone (BW 755C) also potentiated uterine response to NA, ADR and SAL, but the effect produced by BW 755C was similar to that achieved in the presence of FBF. 5. In contrast, the inhibition elicited by histamine and papaverine were unaffected by FBF treatment. 6. The above results provide pharmacological evidence that adrenoceptor agonists may influence prostaglandin production in the rat uterus both in the presence, and absence of the ovarian hormones.

Acetylcholine↗
PubMed1988

[Drug agents for the treatment of systemic connective tissue diseases].

Besides the steroids and the cytostatics used in the treatment of systemic connective tissue diseases, there are other drugs which could be also used in the treatment of these diseases. Of the so-called nonsteroidal anti-inflammatory and slow-acting antirheumatic drugs importance of the quinoline antimalarial drugs is pointed out. The action of the pyrazolone and indole derivatives is weaker. The action of some enzymic drugs in sclerodermia is pointed out as a novelty. The use of direct and indirect anticoagulants and of calcium antagonists is relatively limited but very important in the treatment of systemic vasculitis and lupus nephropathies.

Adrenal Cortex Hormones↗
PubMed1988

[Clinico-immunologic characteristics of acute toxic-allergic reactions to drugs and current methods for their treatment].

The paper is concerned with clinicoimmunological and allergological characterization of 29 cases of acute toxic allergic reactions (ATAR) to drugs. Four degrees of severity of disease were identified; the most severe form was toxic epidermal necrolysis caused by the use of sulfanilamides and pyrazolones in patients with acute respiratory virus and bacterial infections. Blood analysis in patients with III-IV degree of severity showed a sharp decrease in Ctot and C3 up to 0, an increase in the level of circulating immunocomplexes and "average molecules". Cellular immunity in III degree of severity was decreased. The main principles of therapy using extracorporeal immunocorrective methods were worked out. A leukocyte natural migration inhibition test was used for specific diagnosis of intolerance to medication.

Acute Disease↗
PubMed1987

Adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs (NSAID) are among the most frequent causes of adverse drug reactions. The clinical symptoms often resemble allergy and consist of anaphylactic shock, bronchospasm, urticaria, angioedema, and various skin eruptions. Patients with asthma or urticaria are particularly prone to these reactions. In about 10% of adult asthmatics, aspirin and several other NSAID precipitate open asthmatic attacks, most likely through inhibition of cyclooxygenase. This distinct clinical syndrome has a characteristic sequence of symptoms and clinical course. In 20% to 40% of patients with active urticaria, aspirin increases wheals and swelling. Pyrazolones might provoke two different types of clinical reactions, acting as allergens or interfering pharmacologically with cyclooxygenation of arachidonic acid. Other mechanisms might operate in some of the remaining adverse reactions to NSAID. Emerging clinical syndromes help to guide the clinicians through the maze of symptoms and often provide a unique insight into the mechanism of basic disease.

Anaphylaxis↗
PubMed1987

[The effect of metamizole on gastric emptying and small intestine transit in the rat].

The effect of the pyrazolone derivative metamizole on the motility of the upper gastrointestinal tract of the rat was investigated. An animal model for simultaneous quantification of gastric emptying and small intestinal transport was used. A test meal with different radioactive labels was administered by means of previously implanted tubes both to the stomach (1.0 ml; 51Cr) and to the duodenum (0.25 ml; 99mTc), and the spatial distribution of both isotopes in a gastrointestinal preparation was determined after a transport time of 30 min. It has been shown that intravenously administered metamizole reduces significantly the percentage of the test meal discharged by the stomach (control: 70.9 +/- 2.8; 50 mg/kg metamizole: 26.3 +/- 6.9, p less than 0.001; 250 mg/kg metamizole: 3.8 +/- 1.5, p less than 0.001); 1250 mg/kg metamizole: 1.1 +/- 0.3; p less than 0.001). The 50- and 250-mg/kg doses had no negative effect on the propulsion of the small intestine. A dose of 1250 mg/kg induced a significant reduction in small intestinal transport (p less than 0.001).

Aminopyrine↗
PubMed1986

Discharge characteristics of receptors with fine afferents from normal and inflamed joints: influence of analgesics and prostaglandins.

This contribution presents several aspects of our work which are relevant in order to understand how pyrazolone drugs act. They include the discharge characteristics of individual fine afferent nerve fibres from the normal intact joint, the changes that acute experimental inflammation can induce in them, and the effects of prostaglandins and non-steroidal anti-inflammatory drugs.

Action Potentials↗
PubMedDate not supplied

[Rhinitis with intolerance to non-steroidal anti-inflammatory agents. Report of 3 cases].

Lumry described 6 patients who presented hypertrophic rhinosinusitis, positive nasal eosinophilia and intolerance to nonsteroidal antiinflammatory drugs, manifested exclusively with naso-ocular symptomatology. We present three patients with clinical manifestations of chronic rhinitis who had noticed before their first visit that several nonsteroidal antiinflammatory drugs precipitated their nasal symptomatology. None of them had ever presented with asthma symptoms. All of them had nasal polyps. The nasal smear showed eosinophilia of 20 to 45%. All three had sinusitis radiologically. The spirometric values were within normal limits (V.C., FEV1, MMEF25-75%). Skin tests with different inhalants antigens using the prick test technique as well as skin tests with pyrazolones (Phenyldimetrylpyrazolone: 25 and 250 mg./ml.; dipyrone: 4 and 44 mg./ml.; amidopyrine: 2.2 and 22 mg./ml.) using the intradermal technique were negative. Serum IgE (Phadezym IgE-Pharmacia) showed values of 23.9, 17.1 and 25.8 IU/ml. respectively. The bronchial inhalation challenge test with methacholine was positive with PD20FVE1 of 14 and 4.8 mg./ml. in two of our patients. Different nonsteroidal antiinflammatory drugs were administered to each patient in different days orally, with intervals of 7 and 25 days (aspirin 500 mg., dipyrone 575 mg., indomethacin 25 mg., naproxen 500 mg.) as well as tartrazine (50 mg.), paracetamol (500 mg.) and lactose as placebo. With 30 minutes intervals and up to three hours after drug administration, the symptoms were observed and spirometry was carried out. Steroids and antihistamines were suspended at least 48 hours before the test. Acetyl-salicylic acid, dipyrone, indomethacin and naproxen produced naso-ocular symptomatology without any objective reduction of FEV1; but paracetamol and tartrazine were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Disorders of the functional properties of thrombocytes causing thromboembolism in acute suppurative destructive diseases of the lungs and pleura].

An examination of 96 patients has established that the development of a pyo-destructive process in the lungs and pleura is accompanied by an increase of concentration of circulating thrombocytes as well as their adhesive-aggregating activity and degenerative-dystrophic alterations. These parameters were most pronounced in patients 1-3 days before their sudden death from thromboembolism of the pulmonary artery without a clinically detected source. Persantine, aspirin, pyrazolones and heparin in generally accepted therapeutic doses were shown not to possess evident anti-aggregative properties.

Acute Disease↗
PubMed1979

Drug therapy reviews: antirheumatic agents.

The pathophysiology, symptoms and drug treatment of rheumatic disease are reviewed. Antirheumatic drugs reviewed are salicylates (including aspirin, sodium salicylate, choline salicylate, choline magnesium salicylate, salsalate), phenylpropionic acid derivatives (fenoprofen, ibuprofen, naproxen), indole derivatives (sulindac, tolmetin and indomethacin), pyrazolone derivatives (phenylbutazone, oxyphenbutazone), gold compounds, penicillamine, antimalarials mefenamic acid, corticosteroids and immunosuppressives. Simple analgesic therapy (acetaminophen, aspirin, propoxyphene) is used in the early stage of the disease. As the disease progresses, aspirin remains the drug of choice for antiinflammatory activity but the phenylpropionic acid or indole derivatives may be preferred in patients unable to tolerate salicylates. If such nonsteroidal antiinflammatory agents are not effective, parenteral therapy with gold compounds or oral penicillamine usually is indicated. Indomethacin or phenylbutazone, then antimalarials, are resorted to next. Corticosteroids or immunosuppressives are reserved for patients who are unsuccessfully controlled or who have major side effects with the other drugs. Mefenamic acid occupies a very secondary place in rheumatoid arthritis treatment.

Anti-Inflammatory Agents↗
PubMedDate not supplied

[Factors regulating mono-oxygenase induction by phenobarbital xenobiotics].

The main nongenetic factors are revealed which regulate the catalytic activity and substrate specificity of microsomal monooxygenases preinduced by phenobarbital-type xenobiotics (barbituric acid and pyrazolone derivatives). It is shown that a blockage of the primary microsomal metabolism of an inducer is the obligate condition for its inductive effect on the content and activity of cytochrome P-450. On this basis it is practicable to convert the typical monooxygenase substrates into inducers of the enzyme biosynthesis by the blockage of the molecule site subjected to monooxygenation. A model is suggested which shows the phenobarbital participation in the formation of the specific configuration of the active site of cytochrome P-450 synthesized; the latter catalyzes the oxidation of a number of substrates by the way typical of inducer itself.

Aminopyrine↗
PubMed1979

[Pharmacologic remobilization of hyperadhesive granulocytes: a new principle in "anti-inflammatory" therapy].

It is thought that the nonsteroidal anti-inflammatory drugs act through inhibition of cyclooxygenase (CO). The authors show that the pyrazolon derivatives phenylbutazone (P) and sulfinpyrazone (S) affect PMN function in a manner independent of CO inhibition. During inflammation PMN often show increased adhesiveness. Such adhesiveness can be provoked in vitro by high concentrations of chemotaxins. Preincubation (10--20 minutes) of platelet-free human PMN suspensions in heat-inactivated plasma with 100 micrograms P or S per ml completely abolished a submaximal adherence induction on Petri dishes from 4% adherent cells in the absence, to 23% in the presence, of 10(-7) M of the chemotaxin N-f-Met-Leu-Phe (FP). In vivo, premedication of rabbits with P or S prevented the FP-induced neutropenia, e.g. 10 mg/kg of S blocked a 5-minutes agranulocytosis. P and S also abrogated adherence-induced lysosomal enzyme release and FP-stimulated hexose monophosphate pathway (HMP) activity. FP-induced hyperadhesiveness impedes PMN locomotion. Preincubation of PMN with P or S reestablished random motility and allowed chemotactic migration toward activated C (as C5a) in spite of the presence of 'adhesive' concentrations of FP. The potent CO inhibitors indomethacin and aspirin had no effect on FP-induced adherence, enzyme release, neutropenia and HMP stimulation. In 3 selected patients with PMN hyperadhesiveness, correction of this adhesiveness by P paralleled clinical remission. It is concluded that P and S exert their antiinflammatory action at least in part by interfering with PMN hyperadhesiveness and lysosomal enzyme release. These effects are independent of the prostaglandin-thromboxane system, since other CO inhibitors are uneffective.

Cell Adhesion↗
PubMed1979

Heterogeneity of anti-mitochondrial antibodies: characterization and separation of the antigen associated with the pseudolupus erythematosus syndrome.

It could be shown that anti-mitochondria antibodies (AMA) found in drug-induced pseudolupus erythematosus syndrome (PLE) had a different specificity from those found previously in primary biliary cirrhosis (PBC). The PLE antigen could be easily separated from the PBC antigen either by isopycnic sucrose density gradient centrifugation of cytoplasmic extracts (supernatant 40) or purified sonicated rat liver or kidney mitochondria. The PLE antigen was firmly membrane-bound and, in contrast to the PBC antigen, not solubilized by treatment with various salts or enzymes. The ATP-ase complex, the probable target antigen of PBC-specific antibodies, did not react with sera from patients with the PLE syndrome. There is evidence that the PLE-associated antibodies (M3) occur exclusively in patients who have been sensitized to derivatives of pyrazolone or their metabolites, indicating that PLE antibodies may be specific markers for this type of drug allergy.

Antibody Specificity↗
PubMed1977

[Drug-induced disorders of lupus erythematosus type (author's transl)].

Drug induced Lupus erythematosus (LE)-like syndromes are generally observed after long-term and/or high-dose therapy with so called "principal inducers" procainamide, hydralazine, isoniazide, chlorpromazine, anticonvulsives and possibly with D-penicillamine, too, and even so in some cases after some additional 26 drugs. The rare pseudo LE syndrome appears after combined drugs which usually contain pyrazolone derivatives used especially against venous diseases. The mechanism of induction of autoimmune reactions in these disorders varies and is after all still unknown. There are individual differences in drug metabolism, genetic disposition for increased autoantibody formation and sometimes humoral and cellular immune reactions against the drug itself. Essentially involved in the indication of autoimmune reactions is often the production of hapten carrier complexes between drugs and body constituents and drug induced changes of autoantigen elimination as well as drug mediated immunologic imbalance.

Animals↗