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PubMed1985

Plasmapheresis in severe drug-induced toxic epidermal necrolysis.

Five patients with severe drug-induced toxic epidermal necrolysis improved rapidly after one to two plasma exchanges. The improvement of all five patients treated with plasmapheresis contrasts with the disease's mortality rate of up to 50%, as reported in the literature and as observed among our previously treated patients. Since there is no effective treatment for toxic epidermal necrolysis, a controlled clinical trial to evaluate the effectiveness of plasma exchange would seem worthwhile.

Adolescent↗
PubMed1985

Nasal symptoms in pseudoallergic reactions.

In a retrospective investigation 469 pseudoallergic reactions (analgesics asthma reactions) that emerged in 197 patients with analgesics intolerance have been analysed. Besides mostly severe asthma-attacks 26.5% of the reactions were sneeze-attacks and in 37.5% nasal secretion was found. 86% of the reactions emerged within a maximum of 45 minutes after oral application of the analgesic. About a third of the analgesics-asthma reactions occurs together with reactions of the nose mucous membrane. So the connection of analgesics-asthma and chronic hyperplastical changes of the mucous membrane of the upper respiratory tract is also reflected in the course of the pseudoallergic intolerance reaction.

Analgesics↗
PubMed1984

Rat neutrophil activation and effects of lipoxygenase and cyclooxygenase inhibitors.

Activation (defined as lysosomal enzyme secretion and generation of O(2) of rat neutrophils has been measured with the use of varying doses of soluble stimuli (phorbol myristate acetate (PMA); calcium ionophore A23187; and N-formyl-methionyl-leucyl-phenyl-alanine (FMLP] and particulate agents (immune complexes and zymosan particles). With either the calcium ionophore or the chemotactic peptide (FMLP), substantial enzyme release occurred, but the amount of O(2) produced was very small. Cytochalasin B greatly enhanced the enzyme release response to the chemotactic peptide but had little effect on neutrophil responses to other soluble stimuli. The cell response to PMA resulted in the greatest production of O(2) with significant enzyme secretion. When cell stimulation with insoluble stimuli (immune complexes or zymosan particles) was studied, significant amounts of enzyme release occurred in parallel with the generation of substantial amounts of O(2). The presence of cytochalasin B enhanced the cell responses to immune complexes but had an inhibitory effect on zymosan-induced responses. As expected, the amount of lysozyme secreted by stimulated rat neutrophils tended to exceed the amount of beta-glucuronidase released from the same cells. Neutrophil responses were investigated in the presence of drugs that were demonstrated in the rat neutrophil to inhibit either the lipoxygenase or the cyclooxygenase pathway. Inhibitors of the cyclooxygenase pathway (indomethacin, piroxicam, ibuprofen, BW755C), with few exceptions, consistently enhanced the enzyme secretion response, while effects on O(2) generation were less clear-cut but tended to be predominantly inhibitory. Drugs with inhibitory effects on the lipoxygenase pathway (nordihydroguaiaretic acid and nafazatrom) had significant inhibitory effects on both enzyme secretion as well as generation of O(2). These data suggest that activation responses (enzyme secretion and O(2) generation) of rat neutrophils may be dissociated (ie, one not always accompanying the other). Further, it appears that neutrophil activation, as defined by enzyme secretion, is enhanced by products of the lipoxygenase pathway and suppressed by products of the cyclooxygenase pathway. Generation of O(2) is not affected in such a clear-cut manner. Taken together the data suggest that enzyme release and O(2) production by activated rat neutrophils may be under separate control.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1982

[Detoxication of a drug-dependent patient (author's transl)].

Use of synthetic analgesics after pancreatectomy led the patient, a known alcoholic, to become drug-dependent (pethidine, dextromoramide). After four years the patient was hospitalized and given noramidopyrine injections twice daily with tiapride in the dose of three tablets per day, gradually increased to six tablets per day. As early as the second day noramidopyrine could be discontinued. Tiapride dosage was brought down to four tablets per day. The patient feels no need for analgesics.

Adult↗
PubMed1984

[Acute immunoallergic interstitial nephritis due to noramidopyrine].

A 46-year old patient under noramidopyrine treatment was admitted for acute renal failure. Renal biopsy was performed and showed acute interstitial nephritis without staining at immunofluorescent microscopy. In vitro and in vivo immunological tests using noramidopyrine as antigen were all negative. Abnormal serum creatinine levels were still present 4 months later. To our knowledge, noramidopyrine has rarely been the cause of interstitial nephritis (only one other case has been published), but it has frequently been responsible for drug-induced blood diseases, and noramidopyrine-related drugs have previously been involved in drug-induced nephritis. As the renal damage can probably be explained by a delayed hypersensitivity reaction, an early corticosteroid treatment would help in improving renal function.

Acute Disease↗
PubMed1982

Study of platelet aggregation in vivo. IX. Effect of nafazatrom on in vivo platelet aggregation and spontaneous tumor metastasis.

Nafazatrom (Bay g 6575) was explored for its ability to inhibit platelet aggregation. In vitro, it had no effect on ADP, serotonin, epinephrine, or collagen induced platelet aggregation in platelet rich plasma of monkeys. On the other hand, in vivo it was a powerful inhibitor of ADP induced platelet aggregation as measured by the in vivo platelet aggregation recording instrument described previously (Ambrus et al., 1976). This effect was potentiated by dipyridamole. On the other hand, following parenteral administration of Bay g 6575, no ex vivo inhibition was noticed of ADP, serotonin, epinephrine, and collagen induced platelet aggregation. The hypothesis was presented that Bay g 6575 acts by increasing prostacyclin synthesis and/or release or interferes with its decomposition. This may explain in vivo activity; rapid decomposition may explain inability to demonstrate ex vivo activity. This also explains potentiation by the phosphodiesterase inhibitor dipyridamole. Bay g 6575 also was highly effective as a platelet aggregation inhibitor in monkeys after oral administration. In mice, Bay g 6575 increased circulation time of intravenously injected polyploid Ehrlich ascites tumor cells. In Furth-Wistar rats implanted with Furth-Columbia Wilms' tumor, in A/J mice implanted with C1300 neuroblastoma and in Wistar rats implanted with SMT-2A (Kim) breast cancer, Bay g 6575 significantly reduced spontaneous pulmonary metastasis. On the other hand, no effect was seen in the metastatic rate of NIH renal adenocarcinoma in BALB/cCr mice.

Adenocarcinoma↗
PubMed1984

On some presynaptic effects of meramyzole (analgine-pharmachim).

The effect of Analgine in different concentrations on the contractions of electrically stimulated isolated guinea-pig ileum and mouse vas deferens is studied and compared with the effect of morphine on the same isolated organs. Analgine causes morphine-like but weaker concentration-dependent inhibitory effect (IC50 = 5.75 X 10(-6) M) on guinea-pig ileum, which is completely eliminated by naloxon and 4-aminopyridine. Upon simultaneous administration of morphine analgine, potentiation of the effect of morphine is observed, which is also eliminated by naloxon and 4-aminopyridine. Analgine has a weaker inhibitory effect (IC50 = 1 X 10(-4) M) on the contractions of mouse vas deferens, compared with its effect on the ileum. The same is also valid for the independent and combined with analgine effect of morphine, completely eliminated only by 4-aminopyridine, but not by naloxon. In cases of reduced Na+-concentration in the medium, the effect of analgine on the contractions of the ileum is weaker (IC25 = 4.43 X 10(-5) M), while that of morphine is stronger compared with normal conditions. Increased Ca++-concentration is parallelled by a weaker effect of analgine (IC25 = 4.76 X 10(-5) M), unlike the effect of morphine which is potentiated. It is possible to assume some interaction of analgine with a definite type of presynaptic opiate receptors, similar or identical to these receptors which are responsible for the peripheral effects of the narcotic analgesics.

Aminopyrine↗
PubMed1983

[Modification of metastasis formation by inhibition of platelet aggregation. Experimental and clinical results].

Our clinical study to prevent relapse and metastases in several sarcomas and malignant lymphomas of the head and neck region with a long-term treatment with mopidamole was initiated in 1972 because the pyrimido-pyrimidine derivative was shown to inhibit platelet aggregation in vivo and to increase significantly the circulation time of intravenously injected, 32P-labelled Ehrlich ascites tumour cells in mouse blood. The aggregation of platelets to circulating tumour cells and their subsequent adhesion to vascular endothelium in turn appeared to be part of the early stages of the metastatic process. It seems, however, that other related mechanisms are also involved in the clinical results obtained. Mopidamole, as other related derivatives, probably inhibits platelet aggregation by inhibition of PDE-induced decomposition of cAMP and may stimulate the synthesis and/or release of prostacyclin from the vessel wall which in turn activates adenylate cyclase involved in cAMP synthesis. The latter mechanism was definitely shown only for the related pyrimido-pyrimidine derivative dipyridamole, the methyl-xanthine derivative pentoxifylline and the methyl-pyrazoline derivative nafazatrom. The increase of cAMP levels by mopidamole results in an inhibition of 3H-thymidine incorporation into human neoplastic cells and a direct inhibition of its mitotic rate. The adding of mopidamole to a culture of a human promyelocytic leukemic cell line promotes a reverse transformation of the malignant cells to normal which appears to be a permanent phenotypic change. Furthermore, mopidamole was shown to diminish significantly spontaneous lung metastases in syngenic Wilms' tumor (nephroblastoma) of the rat, the C1300-neuroblastoma of the mouse and the HM-Kim mammary carcinoma of the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Nafazatrom (BAY g 6575), a potent stimulator of prostacyclin release from cardiac and renal vessel wall.

The enhancement of prostacyclin (PGI2) formation in the cardiac and renal vessel wall by nafazatrom (BAY g 6575) and the vascular effects of this drug were studied in a series of experiments on perfused isolated rat hearts and kidneys. A dose-dependent increase of prostacyclin release (measured as 6-Keto-PGF1 alpha levels, delta % of control) from the vascular endothelium was achieved when nafazatrom was applied in concentrations ranging from 5 X 10(-7) to 10(-5) g/ml. In the heart, the minimal effective dose of nafazatrom was 5 X 10(-7) g/ml causing a 23 delta % increase of PGI2 release; maximal stimulation of PGI2 was 276 delta % at 5 X 10(-6) g/ml nafazatrom. In the kidney, only at the highest concentration of 10(-5) g/ml an increase of PGI2 to 192 delta % was found. Concomitant to the PGI2 release, in both organs, a reduction of perfusion pressure (delta % of control) was observed. Minimal vasodilation in the heart was - 9.6 delta % (5 X 10(-6) g/ml nafazatrom); the maximal effect was - 25.7 delta % (5 X 10(-6) g/ml nafazatrom). In the kidney, the only observed reduction of perfusion pressure was - 12 delta % at 10(-5) g/ml nafazatrom. The cyclooxygenase inhibitor indomethacin (10(-5) g/ml) blocked vasodilation produced by nafazatrom (5 X 10(-6) g/ml); delta P % was 0.5 + 1.

Animals↗
PubMedDate not supplied

The effect of prostaglandin modulators on prostate tumor growth and metastasis.

The purpose of this study was to investigate the effect of prostaglandin modulating drugs on the growth and metastasis of experimental prostate tumor. Nb rats bearing subcutaneous implants of an androgen-insensitive prostate adenocarcinoma were treated with indomethacin, a cyclooxygenase inhibitor, UK 38485, a thromboxane synthetase inhibitor, and nafazatrom, an antithrombotic agent which is thought to act by enhancing endogenous prostacyclin synthesis. Animals treated with these three drugs had significantly lower pulmonary metastasis than the untreated controls. The effect on primary tumor volume and mortality was variable. We conclude that shifting prostaglandin hemostasis in the tumor bearing animals in favor of prostacyclin, reduces pulmonary metastasis in this experimental tumor system.

Adenocarcinoma↗
PubMed1984

Antiaggregatory efficacy and its time-course after application of acetylsalicylic acid, prostacyclin and nafazatrom in vivo.

Antiaggregatory potency and time courses of their respective efficacy were assessed for acetylsalicylic acid, prostaglandin (PGI2) and nafazatrom, a stimulator of PGI2-release from endothelial cells, and were compared in vivo. Endothelial cell damage was induced by excitation of intravascular fluoresceinisothio-cycanate-dextran. Time from onset of the noxious stimulus to aggregate appearance (TAA) was assessed and dose-dependently delayed by antithrombotic compounds. PGI2 was two orders of magnitude more effective than nafazatrom, acetylsalicylic acid was three orders of magnitude less effective than nafazatrom. Whereas the antiaggregatory potency of PGI2 decreased after 3.1 min to 50%, the antithrombotic efficacy of both, ASA and nafazatrom, further increased after a single bolus injection.

Animals↗
PubMed1984

Platelet survival and function in animals with prosthetic mitral valve: the effect of nafazatrom.

Thromboembolism remains a serious problem in patients with prosthetic heart valves. Previous studies documented a number of platelet abnormalities in such patients and correlated the occurrence of thromboembolic complications with short platelet survival. We have studied platelet survival and platelet aggregation in eight goats fitted with prosthetic mitral valves and repeated the studies following treatment with nafazatrom, a potent antithrombotic agent. Eleven survival studies in eight animals showed a platelet survival not significantly different from control (6.52 +/- 0.72 vs. 6.94 +/- 0.81 days). Following seven to ten days of oral drug administration, platelet survival in the test animals was 7.34 +/- 0.96 days, significantly longer than pretreatment results (p less than 0.01). Animals with the shortest pretreatment platelet survival achieved substantial prolongation of platelet life span following drug treatment. The drug caused no change in ex vivo platelet aggregation.

Administration, Oral↗