Severe delayed-onset hypersensitivity reactions to amoxicillin in children.
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Amoxicillin, a semisynthetic aminopenicillin, has achieved widespread use in recent years for the treatment of respiratory tract and otic infections. Serious reactions have been relatively infrequent. From July 1986 to June 1987, 11 children aged 6 months to 10 years presented with delayed-onset hypersensitivity reactions. In 10 the symptoms were consistent with a serum-sickness-like illness, including urticaria, angioedema, arthritis and arthralgia. Radioallergosorbent testing for IgE antibodies to penicillin yielded negative results, and lymphocyte transformation testing gave a positive result in only one patient. Because of the negative immunologic test results and the occurrence of reactions only in children, who had received an amoxicillin solution, the reactions may have been caused by the excipient. (+info)
Purified equine rabies immune globulin: a safe and affordable alternative to human rabies immune globulin.
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Reported are the results of a retrospective study of 3156 patients who were treated at the Queen Saovabha Memorial Institute, Bangkok, with equine rabies immune globulin (ERIG). Only 51 patients (1.6%) exhibited serum-sickness-like reactions, none of which persisted for more than a week, and only 8 of these patients (15%) were treated with a short course of steroids. One patient, whose skin test was negative, had an immediate anaphylactic reaction to ERIG that responded to parenteral therapy with epinephrine and hydrocortisone sodium succinate. Serum-sickness-like reactions were more frequent among females and over 21-year-olds but were exceedingly rare (0.086%) among children under 10 years of age. (+info)
Drug-associated glomerulopathies.
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The renal glomeruli are vulnerable to injury by a number of drugs and other toxic agents. These agents may lead to damage by one of two basic mechanisms: direct, dose-related toxic injury; indirect, immunologically mediated injury, largely dose-independent. Proteinuria is the simplest and most important functional indicator of glomerular injury. It occurs almost immediately in direct toxic injury, but there is a latent period of weeks to months with immunologically mediated processes. Of the two mechanisms, the second is by far the more common in clinical settings. The best studied experimental agent causing direct toxic injury is the aminonucleoside of puromycin. Clinically, perhaps the most important agent is Cyclosporine A. Although this agent is usually thought of primarily as a tubular toxin, it is capable of giving rise to a microangiopathic glomerular lesion similar to that in the hemolytic uremic syndrome. The classic model for immunologic glomerular lesion is Heymann nephritis, which produces a membranous glomerulopathy. Clinically, most drug mediated glomerulopathies also take the form of a membranous nephropathy, usually with a frank nephrotic syndrome. Among the more common offenders are penicillamine, gold salts used in rheumatoid arthritis, and captopril used in hypertension. The other common type of drug-related glomerulopathy occurs as part of a lupus-like syndrome induced by a variety of drugs, including hydralazine, procainamide, and penicillamine. All of these give rise to a variety of antibodies, most prominently antinuclear antibodies, and in the more severe cases there may be lupus-like glomerular lesions as well. (+info)
Effects of sheep digoxin-specific antibodies and their Fab fragments on digoxin pharmacokinetics in dogs.
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Intact sheep antidigoxin antibodies and their Fab fragments have both been found to exert profound effects on digoxin pharmacokinetics in [3H] digoxin-treated dogs. Both classes of molecule remove digoxin from the extravascular space and sequester it in the circulation in protein-bound form, a form in which the digoxin is presumably inactive. These two classes of molecule differ, however, in that the intact antibody molecules interfere with digoxin excretion, thereby promoting the retention of the glycoside; this retained digoxin is eventually released in free, active form when the administered antibody is metabolically degraded. In contrast, urinary excretion of digoxin continues in Fab-treated dogs, with significant quantities of digoxin being excreted promptly in the urine in complex with Fab fragments. These differences in urinary excretion, together with the probable decreased immunogenicity of sheep antidigoxin Fab fragments, suggest that such fragments possess potential advantages over intact antibody molecules for use in the therapy of life-threatening digoxin intoxication in man. (+info)
Antinephritic effect of prostaglandin E1 on serum sickness nephritis in rats (5). Effect of PGE1 on disposal of heat-aggregated bovine serum albumin in the glomerulus.
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In the present study, we investigated whether prostaglandin E1 (PGE1) could accelerate the disposal of heat-aggregated BSA (a-BSA) in the glomerulus by mesangial cells and/or resident mesangial cells. ICR mice were injected i.v. with 90 mg/100 g B.W. of a-BSA 3 times at 4-hr intervals. Kidneys were isolated at various times after the first injection of a-BSA. The location of a-BSA in the glomerulus was then detected by immunohistochemical staining and immunofluorescence. A-BSA was detected in the mesangium and along capillary walls by both techniques. The amount of glomerular a-BSA increased with time, attaining a peak about 12 to 14 hr after the first administration of a-BSA and then disappeared by 36 hr after. The mice injected with a-BSA 3 times received 150, 200, 300 and 400 micrograms/mouse of PGE1, s.c., and 200 and 400 micrograms/mouse of PGE2 or PGF2 alpha, s.c., at 12 hr; and their kidneys were isolated at 16 hr. The mice with 300 and 400 micrograms/mouse of PGE1 had 34.3% and 37.6% less a-BSA than the control mice, respectively. Additionally, the mice with 400 micrograms/mouse of PGE2 had 63.2% less a-BSA than the control mice. However, PGF2 alpha failed to reduce glomerular a-BSA to a level less than that of the control. In conclusion, we confirmed that PGE1 accelerates breakup of macromolecules by mesangial cells and/or resident mesangial cells in the glomerulus. (+info)
Three cases of illness during a drug trial in healthy volunteers.(38/78)
Serial study of phagocytic function in rat bovine serum albumin (BSA) nephritis.
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We have examined the in-vitro role of polymorphonuclear leucocytes (PMNs) and macrophages in the degradation of immune complexes (ICs) at various points during the induction of rat bovine serum albumin (BSA) nephritis. Two types of experiments have been used. In one set (experiment A) preformed 125I-BSA-anti-BSA complexes (which consisted of heterologous (rabbit) antibodies) were incubated with peritoneal macrophages and PMNs from normal and nephritic rats at 37 degrees C for between 1 h and 24 h and the degradation rates of ICs were studied. In the other set (experiment B), homologous ICs prepared from antibodies derived from the sera of nephritic rats were examined using macrophages and PMNs from normal rats. In experiment A, the degradation of heterologous ICs by macrophages was decreased but degradation by PMNs was not decreased if the assays were performed 8 or 9 weeks after injection. Degradation by both macrophages and by PMNs was increased at weeks 10 and 11. In experiment B, the degradation of homologous ICs from the nephritic rats was increased markedly at week 9 and a relationship was observed between both the degradation and antibody titre and the value of the antigen binding capacity of 33% (ABC-33) during the course of nephritis. There was no difference between PMNs and macrophages in their ability to degrade homologous ICs from the nephritic rats.(ABSTRACT TRUNCATED AT 250 WORDS) (+info)
Chronic serum sickness glomerulonephritis: removal of glomerular antigen and electron-dense deposits is largely dependent on plasma complement.
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Chronic serum sickness glomerulonephritis was induced in 20 rats, using radio-labelled cationised bovine serum albumin (BSA) as antigen. Four days after the last dose of antigen, half the rats were given cobra venom factor (CVF) in doses sufficient to render plasma complement activity undetectable. After ten days without circulating complement, the rats had significantly more antigen in glomeruli than the control group. Subepithelial and mesangial electron dense deposits are found in this model: morphometric analysis indicated that the elimination of plasma complement had slowed the removal of deposits at both of these sites. A second experiment studied the kinetics of this effect. CVF was again given four days after the last dose of antigen, but rats were killed in small groups at intervals thereafter. The results indicate that initially decomplementation had little effect, but after seven days without complement the removal of glomerular antigen had virtually ceased. The complement depleted rats had significantly lower levels of proteinuria, despite having more antigen and larger deposits in their glomeruli. In this model therefore, complement appears to be essential for the removal of deposits, and simultaneously contributes significantly to the induction of proteinuria. (+info)