Glafenine-associated anaphylaxis as a cause of hospital admission in the Netherlands

Summary In 1981 generalized anaphylaxis was registered on 166 occasions in Dutch general and academic hospitals. Clinical details of 120 of those patients revealed that in 107 anaphylaxis was either probable (n=90) or possible (n=17), whereas in 13 cases some other reaction than anaphylaxis had occurred. The series of confirmed cases contained 46 men and 61 women, with mean ages of 47 y and 48 y, respectively.There was a complete recovery in 102 patients and two patients died. Hypotension was present in 79 cases (74%), dyspnoea in 34 cases (32%) and a skin reaction, mainly urticaria, erythema or angioedema, was mentioned in 62 cases (58%). Most cases of anaphylaxis were drug-induced (76%), the main causes being the analgesic glafenine and contrast media. Glafenine was mentioned as the cause in 36% of all admissions for drug-induced anaphylaxis. Only 3.7% of cases had been reported to the voluntary reporting scheme of the Netherlands Centre for Monitoring of Adverse Reactions to Drugs.On the basis of reimbursement data, the risk of developing severe anaphylaxis to glafenine was estimated at 11.7–19.3-fold relative to indomethacin, and 13.4–20.2-fold relative to oral penicillins.     

Auszüge und Besprechungen

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Medicinisch-naturwissenschaftlicher Nekrolog des Jahres 1870

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Dr. Ettner's medicinische Romane

Ohne ZusammenfassungEin Charakterbild aus der Geschichte der Medicin.     

Adverse reactions attributed to sumatriptan

There are several reports on cardiac adverse reactions attributed to the antimigraine drug sumatriptan in the recent literature. In order to assess the frequency and the character of adverse reactions to sumatriptan, a postmarketing cohort study was performed one year after registration of the drug in The Netherlands. With assistance of 86% of the drug dispensing general practitioners in The Netherlands, 1727 patients who had received sumatriptan were traced in July, 1992. Via their general practitioners, a questionnaire about use of sumatriptan, adverse reactions and other medication was sent to the patients in December 1992. During the study period, seven patients were lost to follow-up. Of the 1720 remaining patients, 1202 (70%) responded to the questionnaire, of whom 1187 had actually used sumatriptan. The most frequently reported suspected adverse reactions were paraesthesiae (139 patients, 95% CI 9.9%–13.5%) and dizziness (96 patients, 95% CI 6.5%–9.7%). Chest pain after use of sumatriptan was reported by 94 patients (7.9%, 95% CI 6.4%–9.4%), and according to the close temporal relationship with the intake of sumatriptan and a positive rechallenge, a causal relationship was probable in most of those patients. The frequency of chest pain attributed to sumatriptan was higher in females (9.0% vs 4.6%; relative risk 1.9, 95% CI 1.1–3.4). Age and hypertension were not associated with chest pain attributed to sumatriptan. Dyspnoea attributed to sumatriptan was reported by 26 patients (2.2%), and was associated with obstructive lung disease (relative risk 5.4 95% CI 1.7–16.9). Thus, in view of the high frequency of chest pain after use of sumatriptan and reports in the literature of cardiac disturbances, including myocardial infarction, cautious use of the drug is advised.     

Genetic polymorphisms and heart failure.

Heart failure is a complex clinical syndrome. There is evidence for a genetic contribution to the pathophysiology of heart failure. Considering the fundamental role of neurohormonal factors in the pathophysiology and progression of cardiac dysfunction and hypertrophy, variants of genes involved in this system are logical candidate genes in heart failure. In this report, genetic polymorphisms of the major neurohormonal systems in heart failure will be discussed. Studies on polymorphisms of the renin-angiotensin-aldosterone system (RAAS), adrenergic receptor polymorphisms, endothelin (receptor) polymorphisms, and a group of miscellaneous polymorphisms that may be involved in the development or phenotypic expression of heart failure will be reviewed. Research on left ventricular hypertrophy is also included. The majority of genetic association studies focused on the ACE I/D polymorphism. Initial genetic associations have often been difficult to replicate, mainly due to problems in study design and lack of power. Promising results have been obtained with genetic polymorphisms of the RAAS and sympathetic system. Considering the evidence so far, a modifying role for these polymorphisms seems more likely than a role of these variants as susceptibility genes. Besides the need for larger studies to examine the effects of single nucleotide polymorphisms and haplotypes, future studies also need to focus on the complexity of these systems and study gene-gene interactions and gene-environment interactions.