[Pathogenesis of anaphylactic symptoms following an insect sting].
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Biomedical subjects
Publications and source records attributed to J C van der Zwan.
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We observed 3 patients with a severe falciparum malaria infection. Although the patients appeared not to be seriously ill on admission, severe complications occurred. Renal impairment was a prominent feature and haemodialysis was sometimes necessary. Many hypotheses have been proposed regarding the aetiology of renal failure in Plasmodium falciparum but cannot yet be fully substantiated. Whatever the aetiology of renal failure might be, we believe that treatment should not differ essentially from that of acute tubular necrosis after circulatory shock and early diagnosis and treatment is imperative in spite of an initially ostensibly good clinical condition.
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The generation of the anaphylatoxin C3a was measured after a wasp-sting challenge in eight patients with previous anaphylactic reactions to wasp stings. Whereas there was no change in C3a in one patient who showed no reaction and only a slight rise in three patients with mild reactions, C3a rose substantially in the four patients with severe anaphylactic reactions. This complement activation is the first in-vitro variable which correlates with the severity of wasp-sting anaphylactic reactions. A role for complement activation in the pathophysiology of wasp-sting anaphylaxis is therefore suggested.
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The use of the sting challenge (SC) in insect allergy has brought into doubt the widely held belief that clinical data, specific IgE and the skin test are reliable tools in diagnosis and decision making with regard to therapy. We subjected ninety patients, known to have a systemic reaction to SC, in the Intensive Care Unit. Of these patients, 28% once more showed a systemic reaction; 72% had only a local reaction. No statistically significant difference could be demonstrated between positive and negative SC patients with regard to age; sex; the presence of allergic disease(s)--other than allergy to insects--and the severity of the preceding systemic reaction; the sting site and the related time interval; or specific IgE, IgG1, IgG4, their ratios and the skin test. A negative skin test and/or specific IgE, however, does not exclude the possibility of a recurrent systemic reaction. The long-term value of the SC appeared to be good since the results of the revision SC remained unchanged. Skin test and specific IgE are useful as diagnostic tools in establishing the insect concerned. SC provides information on the likelihood of a recurrent systemic reaction.
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Eleven patients with a history of anaphylaxis, positive reactions to skin tests, and specific IgE antibody to wasp venom underwent hyposensitisation in a six hour procedure. No general reactions occurred. Complement activation and proteinuria could not be shown. The patterns of specific IgE, IgG1, and IgG4 were as described in other procedures--namely, IgE increased sharply and then decreased; IgG1 and IgG4 increased steadily and then decreased--but increase and decrease came earlier. Challenge by a stinging insect at least four weeks after treatment proved complete protection. The skin reactivity two years later showed an unpredictable pattern.
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After purifying a Haemophilus influenzae precipitinogen from endotoxic activity by means of ultracentrifugation, column chromatography (Sepharose 6B) and ion exchange chromatography (DEAE Sephadex A25) a fraction was obtained which still contained a specific precipitinogen that was virtually free of endotoxin. Furthermore, during the chromatographic procedures fractions with a high and a low molecular weight endotoxic activity were found. The limulus lysate test was more sensitive in the high molecular weight fractions and the LD50 in mice in the low molecular weight fractions with endotoxic activity.
In patients with chronic nonspecific lung disease (CNSLD), who had precipitins against Haemophilus influenzae (HI), a biphasic bronchial obstructive reaction is described after inhalation of killed HI bacteria. There was an early obstructive reaction, occurring immediately after the inhalation and lasting for 1 hr, followed by a late reaction, which started 5-6 hr after the inhalation and lasted for about 8 hr. The late reaction was accompanied by fever, malaise and leucocytosis. The difference in reaction after HI inhalation in five patients and two controls, and the effect of protection with sodium cromoglycate and prednisolone are discussed.