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PubMed1996

Drug related involvement of specific sites in fixed eruptions: a statistical evaluation.

Different drugs produce fixed eruptions over different parts of the body. However, the significance of preferential site involvement in fixed eruptions due to specific drugs has not been statistically evaluated. One hundred and twenty five patients of fixed drug eruption (FDE) were studied to examine this question. Different sites affected by individual drugs were classified as lips alone, genitalia alone, lips and genitalia together, trunk alone, trunk and limbs together, and generalized. Statistical analysis was carried out for 7 common drugs causing FDE in 5 or more patients. Cotrimoxazole, a combination of sulfamethoxazole and trimethoprim, was the most common offender for FDE (32.8%), followed by analgin (12%), tetracycline (8%), pyrazolones (8%), metronidazole (6.4%), ciprofloxacin (5.6%), and phenytoin sodium (4%). Major sites involved by FDE were trunk and limbs (24%), lips alone (20.8%), genitalia alone (20%), generalised (14.4%), lips and genitalia together (11.2%), and trunk alone (8.8%). Seventy-two (57.6%) patients had multiple lesions; 33 (42.4%) had single lesions. Involvement of mucocutaneous junctions of lips and genitalia by FDE was frequently caused by cotrimoxazole and tetracycline; trunk and limbs, by analgin and pyrazolones. Generalised eruptions were commonly caused by cotrimoxazole and phenytoin. The present statistical analysis confirms the clinical impression that genitalia alone are frequently involved in FDE due to tetracyclines (p < 0.001). FDE over trunk and limbs was significantly associated with analgin (p < 0.001), and generalised eruptions, with phenytoin sodium (p < 0.001). The association of FDE over lips with cotrimoxazole was statistically not significant.

Adolescent↗
PubMed1991

Drug-specific clinical pattern in fixed drug eruptions.

One hundred thirteen patients with fixed drug eruption (FDE) were studied for any drug-specific clinical pattern. The causative drugs were identified and confirmed by provocation tests. A trimethoprim-sulfamethoxazole combination caused maximum incidence (36.3%), followed by tetracycline (15.9%), pyrazolones (14.2%), sulfadiazine (12.4%), dipyrine (9.3%), acetaminophen (7.9%), aspirin (1.7%), thiacetazone (0.88%), and levamizole (0.88%). Sulfas, including trimethoprim-sulfamethoxazole, induced lesions on the lips (91%) and trunk and limbs (89%), with only minimal involvement of mucosae. Tetracycline caused lesions only on the glans penis, sparing other sites. Pyrazolones affected mainly the lips and mucosae, with a few lesions of the trunk and limbs. Dipyrine, aspirin, and acetaminophen caused lesions of the trunk and limbs, sparing the lips, genitalia, and mucosae. Levamizole caused associated constitutional disturbances with extensive skin lesions, as did thiacetazone. The current study indicates that the clinical pattern and distribution of lesions in FDE are influenced by the drug in question, and the study of the pattern may provide useful information in selecting the most likely causative drug, especially when the details of the drugs are unknown.

Adolescent↗
PubMed1985

Tolerance of carprofen in patients with asthma caused by non-steroidal anti-inflammatory drugs.

Eight asthmatics with respiratory intolerance to NSAIDs and two subjects (one asthmatic, one healthy) only sensitive (asthma) to pyrazolone drugs were challenged under single-blind conditions with a new NSAID, carprofen. No adverse effects were observed in patients sensitive to pyrazolones. Among the other patients, only three developed considerable bronchial obstruction which was rapidly reversed by inhalation of a beta 2-stimulant (fenoterol: 2 puffs). Two subjects developed nasal obstruction with rhinorrhoea: in conjunction with bronchoconstriction in one patient and alone in the other. In conclusion, acute administration of carprofen in patients with respiratory intolerance to NSAIDs, in contrast to most other NSAIDs, never creates a situation of real danger even though in some patients it may considerably increase nasal and bronchial resistance.

Adult↗
PubMed1997

4 Pro-R hydrogen of NADPH was abstracted for enzymatic hydride transfer by N-ethylmaleimide-reductase of Yarrowia lipolytica.

We studied the steric course of the reaction catalyzed by the N-ethylmaleimide (NEM) reductase of Yarrowia (Candida) lipolytica (Y. lipolytica), using 4R-[4-2H1]NADPH and 4S-[4-2H1]NADPH as cofactors and N-ethylcitraconimide as substrate. Active substrates and inhibitors of NEM reductase and its subcellular distribution were also investigated to clarify the biochemical properties of this enzyme. NEM reductase catalyzes the reduction of N-ethylmaleimide to N-ethylsuccinimide with NAD(P)H as the cofactor. Several maleimide and cyclopentenone derivatives tested were also active substrates for NEM reductase of Y. lipolytica. Some pyrazolone derivatives, particularly 1-phenyl-5-pyrazolone, were found to be effective inhibitors of NEM reductase. Subcellular localization of NEM reductase was carried out using protoplast formation and differential centrifugation. Ninety-eight percent of the NEM reductase activity was recovered in the cytosolic fraction, indicating that NEM reductase in Y. lipolytica was the cytosolic enzyme. We also determined the stereochemical specificity of the reduction of N-ethylcitraconimide by NEM reductase in Y. lipolytica, showing that 4 Pro-R hydrogen of NADPH was abstracted for enzymatic hydride transfer by NEM reductase, and two hydrogen atoms from NADPH and H2O added to opposite faces of the double bond of N-ethylcitraconimide.

Candida↗
PubMed2000

[Metamizol--a new effective analgesic with a long history. Overview of its pharmacology and clinical use].

Metamizol is an effective, non-opioid analgesics which was originally introduced to the therapy in the year 1922. However, with the reference to the side effects of other related pyrazolone derivatives its administration, similarly as the usage of other pyrazolones, was significantly limited. Later, metamizol has been used, usually mixed, with spasmolytic agents and quite recently it has been introduced as a mono-component medicament. Metamizol proved to be a very effective analgesic. When administered in equipotent doses, it had its effects comparable to various opioid analgesics, such as tramadol, pentazocine and pethidine. Beside the strong analgesic effect, it produces also significant antipyretic and splasmolytic effects without the adverse, unpleasant anticholinergic impact. Its spasmolytic effect on the smooth muscle of the sphincter Oddi, urinary tract, and the gal bladder is comparable to the effects of buthylscopolamine. Unlike aspirin and other nonsteroidal antiinflammatory drugs it has, however, no antiinflammatory activity when administered in clinical doses. Similarly, metamizol has no effect on the CNS, cardiovascular system, renal and metabolic functions. On the other hand, metamizol, like aspirin, has got a significant effect on the aggregation of platelets. Metamizol is basically a prodrug. The parent substance is not effective before its conversion into two active metabolites (4-methylaninoantipyrine and 4-aminoantipyrine) in the body. Metamizol is well absorbed from the small intestine but only two above mentioned active metabolites and no parent drug can be detected in the blood. The active metabolites are consequently metabolised to ineffective metabolites including the relevant acetylderivatives, in which the acetylation phenotypes can be distinguished. In the therapy, metamizol can be used, as an analgesic, at post-surgical pain, patient's controlled analgesia (PCA), at the cancer's pain and in the pains of different origin (post-traumatic pain, the pain at myocardial infarction, craniocerebral trauma, and the invasive diagnostic interventions), as well as at he pain of neuromuscular origin, headache and migraine. Its spasmolytic effect in connection with a strong analgesic activity is very useful at various colic attacks. Further, metamizol is a useful antipyretic both in the adults and children. Its adverse effects are not pronounced and drug interactions are minimal. Only when metamizol is administered together with cyclosporine, the blood levels of the last substance should be regularly checked.

Analgesics↗
PubMed1992

[NSAIDs (non steroidal anti-inflammatory drugs) for the treatment of rheumatoid arthritis].

Non-steroidal anti-inflammatory drugs (NSAIDs) are often prescribed to patients with rheumatoid arthritis (RA), as the first line drugs, and are administered over a long term. NSAIDs are classified principally into acidic and basic preparations, and the former is more widely used for the treatment, since the latter possesses no anti-rheumatic effect. Moreover, the acidic NSAIDs are classified into salicylates, arylacetic acid, pyrazolone, fenamates and oxicams. Arylacetic acid has a strong analgesic effect. Pyrazolone is well balanced between analgesic, anti-inflammatory and antifebrile effects. The fenamates and oxicams are long acting. On the other hand, NSAIDs sometimes inhibit adverse reactions, such as gastroduodenal diseases and renal insufficiency, which are probably induced by the inhibition of cyclo-oxygenase to reduce prostaglandin content. Therefore, appropriate NSAIDs must be selected after consideration on the character, property and adverse reaction of each drug.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

[The determination of specific IgE in allergy diagnosis. The clinical significance of specific IgE in drug allergies].

IgE-mediated allergic reactions to drugs may be diagnosed on the basis of anamnestic criteria, clinico-pathological manifestations as well as by the measurement of allergen-specific IgE. The concordance of these diagnostic procedures was investigated in 50 patients with a history of sensitivity to penicillin (12), sulphamethoxazole (9) or both (14), aspirin (2) and pyrazolones (13). All subjects displayed chronic urticaria/angioedema syndrome. Optimal concordance values were observed for penicillin and sulphamethoxazole, while no specific IgE were detected in the ASA-sensitive group. False positive results were noted in pyrazolone-sensitive patients with high total IgE levels. Based on these results, serological methods that detect drug-specific IgE may be carefully used as complementary diagnostic procedure only in those patients in whom an adverse reaction to antibiotics is suspected.

Antibody Specificity↗
PubMed1985

Inhibitory action of dipyrone on rat thyroid peroxidase and lactoperoxidase activities.

Previous studies have shown that phenylbutazone, another pyrazolone, inhibits thyroid peroxidase activity and interferes with iodide organification. We have developed "in vitro" studies with rat particulated peroxidase and lactoperoxidase (LPO) to study the effects of dipyrone upon thyroid peroxidase and to determine the type of inhibition. The 3-monoiodothyrosine (MIT) and 3,5-diiodothyrosine (DIT) synthesis was markedly affected by 6 X 10(-4) M dipyrone with inhibitions of 59% and 30% respectively. No difference was observed with lower concentrations. Inhibition of peroxidase activity (Triiodide assay) was found when crude rat peroxidase preparations and LPO were incubated with dipyrone in concentrations ranging from 10(-3) M to 10(-8) M, with a Ki of 2.5 X 10(-5) M and 4 X 10(-5) M respectively. Guaiacol peroxidation was scarcely affected by the action of the drug; 10(-3) M produced inhibition of 50%. Line weaver-Burk: plots were used to investigate the inhibition of LPO activity by dipyrone. The inhibition by the drug was competitive with the iodide. We may conclude that dipyrone and other drugs of the pyrazolone group act upon peroxidase activity "in vitro", by an inhibition of competitive type and in presence of iodide.

Aminopyrine↗
PubMed1986

[Immediate-type reactions to pyrazole derivatives: results of skin tests and antibody determinations].

In a multicentric study by the European Study Group for Drug Allergy 58 patients suffering from an immediate type reaction after intake of pyrazol analgetics were examined with regard to allergy or pseudoallergy. Besides the scratch tests with the original substance we performed cutaneous tests with pyrazol conjugates and determined IgE and IgG antibodies by means of modified radioallergosorbent (RAST) method. Three groups could be distinguished: pseudoallergic reactions to nonsteroidal analgetics of the aspirin type (15 cases); IgE-mediated pyrazolone allergy verified by skin tests and/or IgE-RAST (21 cases), and pyrazolone idiosyncrasy (26 cases).

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Liver damage with non-narcotic analgesics.

Non-narcotic analgesics can produce a variety of hepatic lesions but clinically significant liver damage is uncommon with normal therapeutic use. The pattern of hepatotoxicity caused by the salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol (acetaminophen) and the pyrazolones differs but many of these drugs can cause generalised reactions which involve the liver. Depending on the drugs in question, the risks of liver injury may be conditioned by factors such as age, sex, dose and duration of treatment. Hepatotoxicity associated with the use of salicylates and most NSAIDs has been reported most often in females with collagen diseases but this may simply reflect the greater use of these drugs in such patients. Paracetamol-induced liver damage occurs almost exclusively as a result of overdosage. Except for the microvesicular fatty changes in hepatocytes in patients with Reye's syndrome attributed to salicylate, the acute centrilobular necrosis caused by paracetamol in overdosage and the marked cholestasis produced by benoxaprofen, the pathological changes in hepatic reactions to non-narcotic analgesics are rather variable and nonspecific. About 50% of patients given salicylate in full anti-inflammatory dosage develop minor abnormalities of liver function. There is usually a mild to moderate increase in plasma aminotransferase activity with patchy necrosis and degeneration of hepatocytes. These changes are related to plasma salicylate concentration and are usually rapidly reversible. In a small minority of patients, particularly the young, liver damage is more severe and may be associated with liver failure, acidosis, hypoglycaemia and encephalopathy. This picture closely resembles Reye's syndrome. In overdosage, paracetamol can cause acute hepatic necrosis. Without specific treatment, some 8% of adults suffer severe liver damage with plasma aminotransferase activity greater than 1000 U/L and about 1% die with hepatic failure and encephalopathy. The administration of sulfhydryl compounds such as N-acetylcysteine within 8 to 10 hours effectively prevents liver damage and death. Liver damage has been attributed to the therapeutic use of paracetamol. However, in most reports the dose was excessive and many patients were chronic alcoholics (who seem to be at increased risk). In these cases the features were typical of acute overdosage. A consistent and characteristic pattern of hepatotoxicity is evident with relatively few non-steroidal anti-inflammatory and pyrazolone analgesics. A rank order of relative risk cannot be established and the incidence in relation to use is not known.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetaminophen↗
PubMed1985

[Diagnostic and therapeutic methods in the asthmatic triad].

Comprehensive diagnostic methods used in 48 patients with the asthmatic triad made it possible to select diagnostic methods and means of control of treatment of such patients. Methods of specific diagnosis of the intolerance of pyrazolone drugs and some probable pathogenetic indicators of intolerance of acetylsalicylic acid, pyrazolone drugs and tartrazine containing substances in patients with different forms of bronchial asthma (atopic and infectious-allergic) in combination with nasal polyposis were evaluated. Basing on these materials conditions for specific immunotherapy were worked out.

Adolescent↗
PubMed1979

[Asthma caused by analgesics].

Asthma, caused by analgesics, a relatively frequent phenomenon in bronchial asthma conditioned by infection, often remains unrecognized and is then sometimes a danger of high degree for these patients. Pathogenetically, the asthma caused by analgesics perhaps does not underlie an immunological mechanism, but an induced by analgesics prostaglandin-E-synthesis inhibition. For this speak the results of skin tests, of the LTT with analgesics and of IgE concentration measurements. Concomitant phenomena of the asthma caused by analgesics are: initial rhinirrhoe, alcohol intolerance, polyposis nasi and NNH affections. Among the evoking noxae the pyrazolones (regard: pyrazolone containing asthma mixed preparations!) are of greatest importance. Since already the smallest doses of analgesics may evoke considerable asthmatic reactions the indication to the exposition test should be made cautiously. In an anamnestic suspicion on asthma caused by analgesics a strict avoidance of analgesics, antirheumatic drugs and antipyretic drugs is necessary. Salicyl amide does not cause in vitro a prostaglandin synthesis inhibition. Still further clinical examinations are necessary, whether it amy generally be recommended as a possible alternative of analgesics in asthma caused by analgesics.

Analgesics↗
PubMedDate not supplied

[Syndrome due to acetylsalicylic acid intolerance. What should be prescribed as substitutes for aspirin?].

In the daily practice of allergology, one of our commonest problems concerns the prescription of nonsteroidal anti-inflammatory drugs for our patients who are intolerant of acetylsalicylic acid, whose basic clinical expression of this intolerance is primary bronchial asthma. Our problem is the high frequency with which the syndrome appears after the administration of other analgesics chemically unrelated to acetylsalicylic acid. Most authors accept that derivatives of pyrazolones and indoles, and of phenylisopropionic and anthranilic acids must be avoided. This avoidance is based on collected clinical experience and the currently accepted hypothesis concerning the pathogenesis of the syndrome (pyrazolones, indoles, etc. are inhibitors of the byosynthesis of the E series of prostaglandins, particularly PG synthetase). On the other hand there is no agreement concerning what type of analgesics, anti-inflammatory drugs and antipyretics we should prescribe for these patients. The conclusions of the protocol which we carried out are as follows. Dextropropoxyphene chlorhydrate, diviminol, tilidine chlorhydrate, salicylamide, benzidamine, pentazocine, isonixine, hyoscine bromide and ergotamine tartrate can be prescribed safely for these patients in the usual therapeutic dosage. To the list of prohibitions should be added the derivatives of glaphenine and phenylacetic acid. As regards paracetamol, our opinion is that its use should be restricted to those cases in which the previously listed drugs cannot be substituted for it, and always after administration under medical supervision in a hospital setting.

Analgesics↗
PubMed1993

[Incidence of drug side effects by symptoms and syndromes. From the experiences of the Comprehensive Hospital Drug Monitoring and the Swiss Drug Side Effect Center. As an example: allergic and pseudo-allergic reactions with mild analgesics and NSAID].

From 1974 to 1989, 37,392 patients were admitted to the divisions of general internal medicine of the CHDM hospitals. 19,082 of them were treated with a minor analgesic or an NSAID. In 95 of the exposed patients, an allergic or a pseudoallergic reaction to one or two of these drugs was observed. From 1981 to 1990, general practitioners, hospitals and the pharmaceutical industry reported to SANZ 158 individual cases with comparable reactions to 175 exposures of the same kind. Of the 15 different syndromes and symptoms registered in both institutions, most were reactions of the skin, mainly the usual maculopapular exanthemas (rash), urticaria and angioedema. In the CHDM, allergic or pseudoallergic reactions were observed in 0.23% of patients exposed to minor analgesics (including ASA preparations on a daily dose up to 1.0 g and pyrazolones, mainly metamizole, propyphenazone) and in 0.81% of patients exposed to NSAIDs (including the pyrazolone oxyphenbutazone). In the experience of the Comprehensive Hospital Drug Monitoring in Berne and St. Gallen (CHDM) and the Spontaneous Adverse Drug Reactions Center of Switzerland (SANZ).

Adverse Drug Reaction Reporting Systems↗
PubMed1976

[Colorimetric cleck of the working dilutions of disinfectants on an aldehyde and phenol basis (author's transl)].

The applicability of 2 colour reactions were tested for the monitoring of the working concentration of disinfectant solutions containing aldehyde or phenol. The red coloration of Schiff's acid solution (Schiff's reagent to aldehydes) can be used with limitations. The formation of a red dye by the reaction of phenols with 1-phenyl-2,3-dimethyl-4-amino-pyrazolone-(5) in the p-esence of alkali and potassium hexacyano-ferrate (III) is unequivocal and is not influenced by contaminations in the water. Evaluation is made in either case by comparison with standard dilutions of the respective commercially available preparation. The samplest procedure for this a visual colour comparison in test tubes with calibration spectrum. Pyrazolone dye can be analysed photometrically. Thus this colour reaction can be regarded as an analytic method of satisfactory accuracy. A frequent monitoring of the disinfectant concentrations by means of simple chemical procedures is expected to help limit the improper use of disinfectants and to check hospital infections.

Aldehydes↗
PubMed1989

Trichosporon beigelii pneumonia in a neutropenic patient.

A case of pulmonary infection caused by Trichosporon beigelii is reported in an asthmatic patient undergoing steroid treatment who developed fever and lung infiltrates. Arthroconidia and blastoconidia were isolated from repeated sputum, bronchial aspirate and telescopic catheter samples. The infection coincided with neutropenia resulting from pyrazolone treatment. The response to amphotericin B treatment was favourable.

Agranulocytosis↗
PubMed2004

Structure-activity studies for a novel series of tricyclic dihydropyridopyrazolones and dihydropyridoisoxazolones as K(ATP) channel openers.

In search of a novel chemotype of K(ATP) channel openers a series of tricyclic dihydropyridopyrazolones and dihydropyridoisoxazolones was synthesized. It was found that cyclopentanone in the left hand portion of the molecule was 4-fold more potent than cyclohexanone. Introduction of gem-dimethyl groups as well as incorporation of oxygen in the cyclohexanone ring in the left hand portion of the molecule increased the potency 10-fold. In the right hand portion of the molecule, the NH-group of the pyrazolone can be effectively substituted by oxygen increasing the activity 5-fold. Incorporation of a methyl group adjacent to the dihydropyridine (DHP) nitrogen not only significantly boosted activity, but also provided an additional benefit of increased metabolic stability. In vitro tests on the tissue from pig bladder strips provided further confirmation of K(ATP) activity of these compounds.

Animals↗
PubMed2006

Lgf-YL-9 induces apoptosis in human epidermoid carcinoma KB cells and multidrug resistant KBv200 cells via reactive oxygen species-independent mitochondrial pathway.

Pyrazolon derivatives were reported to have cytotoxicity to some tumour cells. In the present study, we investigated the effect of Lgf-YL-9 on cytotoxicity and cell apoptosis in human epidermoid carcinoma drug-sensitive parental KB cells and multidrug resistant (MDR) KBv200 cells. Lgf-YL-9 exhibited potent cytotoxicity not only to KB cells but also to KBv200 cells, and the IC(50) were 3.81 and 3.45 microg/mL in KB cells and KBv200 cells, respectively. Importantly, Lgf-YL-9 effectively inhibited tumour growth of KB cell xenografts in nude mice. Lgf-YL-9-induced cell apoptosis was confirmed by chromatin condensation, DNA fragmentation, Annexin-V and propidium iodide (PI) double-staining assay and poly(ADP-ribose) polymerase (PARP) cleavage. Furthermore, Lgf-YL-9-mediated apoptosis in KB cells and KBv200 cells was accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)), the release of cytochrome c, and the activation of caspases-3, -7, and -9, but not by intercalating to DNA. Although Lgf-YL-9-induced apoptosis was associated with the decrease of DeltaPsi(m), reactive oxygen species (ROS) reduction was interestingly observed in both cell lines. The data suggest that Lgf-YL-9 has similar cytotoxicity to drug-sensitive parental KB cells and MDR KBv200 cells. Lgf-YL-9-induced apoptosis is involved in a new ROS-independent mitochondrial dysfunction pathway, but not in intercalating to DNA.

Animals↗