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348 Allergic reactions to antimicrobial drugs in patient with a history of prior drug allergy
226
Abstracts
345
347 J. Stevens Ph.D., Antweqes~, BeIgium. The effect of local application of DSCG solution on the immediate skin prick test reactivity with histamine, codeine and house dust mite was studied in asthmatic children (n = 22) and in children with atopic dermatitis (n = 10). The design of the study was double-blind versus placebo (saline). DSCG or saline were applicated under plastic cover during 10 minutes before prick testing. DSCG had no effect upon histamine reactivity (5.34 mm + 2.12 versus 5.38 mm + 1.77, p = 0.906) but was found to inhibit code&e reactivity significantly (5.63 mm + 2.09 versus 4.72 mm + 1.55, p = 0.012). House dust mite reactivity tended so to inhibited by DSCG, but the difference was not statistically significant (7.07 mm + 4.06 versus 5.47 mm +. 3.74, p = 0.059). When the results of the asthmatic children were compared with the results of the children with atopic dermatitis, no major differences were found. This study shows that local application of DSCG solution inhibits codeine reactivity and tends to inhibit house dust mite skin reactivity.
346
Hamburg/*Munich,
FRG.
Between 1975 and 1985 24 patients >Nriith lbxic I+dental Necrolysis (TEN) have been seen at the Department of Dermatology in Munich. The retrospective study c+f the c%e histories showed that drug-induced TEN WA< more common in elderly individuals (age 4--X8 ), !I par :. .Sii 1. 13 > 60 y). The female/male ratio was 2. I /16/R). The data yielded a trend toward a higher prevalence ot ‘IXN m \ftc spring and summer pekd [ 15/22 pat.; predomkanrly 11:July (n=S) and in April (n=4jJ I n many cases thv first and/or most severe TEN-lesions occurred on the face and 011the extremities. 5 pat. developed TEN in connection wirh the administration of only one single drug. tvherez; ! pa!, contracted TEN after introduction of a new drug m addnion to a long term medication with some other drugs [r\iSAW (oxyphenbutazone, dipyrone, salicylamidj, antl-convulsive drugs (carbamazepine, phenytoin), other drugs (ailopnrb~oi. bromhexinbydrochloride) and herbal tea]. :X/24 pat. took more than one “culprit” dmg simultaneously ii. e. II! 7 pat. > 4 drugs); l/l 3 developed TEN aft?? a heavy sunburn. One patient had no history four administration rli a drug. 16 pat resolved. 5 pat. died and in ‘7 ales t?le WT. come remains unknown. All patients received corticosteroid therapy in a various manner (single and cumukmvr doses ranging from 60--S(K) mg and 280-4900 mg respectively). The data of this study are in good agreement with the literature. Our own data suggest a possible rofr tlf lJWight exposure in the pathosenesir of TEN in some patient:,
346
Austria. Exogenous contact to mercury can be demonstrated only in one third of patients sensitizised to mercury. Body storage mercury depots may be responsible for ineffective treatment despite allergen avoidance. Eight patients with chronic mercury contact dermatitis in whom an exogenous mercury source could not be demonstrated DMPS (chelating agent) were investigated for body mercury depots. After assessment Of baseline values of mercury in urine and blood 250 mg of DMPS were administered i.v. Urinary mercury was estimated at 1 hr, 3 6 hr and 24 hr after injection using hr, atomic absorbtion spectroscopy. Increased DMPS excretion after injection ( > 5 times of baseline level) of mercury 6 could be demonstrated patients. Mean value of mercury in ‘2”4 hr urine : 1.4 ug/l. Mean mercury excretion rates after DMPS injection: 1 hr: 102.5 ug/l 6 hr: 25.2 ug/l 3 hr: 91.2 ug/l 3.9 ug/l 24 hr: A slight decrease of mercury levels in blood (mean 4.6 ug/l) could be achieved in one patient. ( 11 ug/l before 250 DMPS, 8 ug/l after DMPS, normal: < 5 “g/o;) The increased mercury rates excretion after DMPS indicate presence of mercury depots ’ sensitive mercury patients. Three patfints reported decrease of their contact eczema after this single injection of 250 mg DMPS.
DKUWNDUCED LYELL’S SYNDROME 0QXlC EPlDWSIS): AN AN&@S OF 24 CASES. JohannesR.ina. M. D. Ph. D., Dieter Vi&f. M. D.&im Wimschneickr. M. D. and Ber&-wrP.pQa.@ ,. .&I...-p..
ALLERGIC REACTIONS TO ANTIMICRQBIAL DRUGS IN PATIENTS’ WfFB A EISTORY OF PRIOR DRUG ALLERGY. J&p K. Mosolev. and m Sullivan. M.D- Da&as, Texas. We examined the hypothesis that a history of antimicrobial drug (AMD) allergy indicates an increased risk of reacting to another class of AMD in a A total of 2531 prospective case control study. hospitalized patients beginning a course of AMD therapy were screened, resuking in the identification of 149 (5.9%) with a documented history of AMD allergy and 37 of these 149 who were beginning a 7 day or more course of AMD therapy. Two matched control patients were selected for each allergic case. Five of 37 AMD allergic patients (13.2%) experienced an allergic reaction. Three developed pruritic rashes during therapy with mulitple AMD, one experienced fever and urticaria on erythromycin, and one patient on narfloxacin had a Stevens-Johnson (S-J) reaction. This is in keeping with our earlier retrospective study that detected a history of TEN/S-J/EM in 5 of 64 multiple AMD allergic patients. One of 74 control patients in this study (1.4%) developed a pruritic rash on ampicillin/ sulbactam. The increased risk associated with a history of prior AMD allergy was significant (P = O.OlS), with a relative risk of 9.4. The results of this prospective study provide direct evidence that AMD allegic subjects are at increased risk of reacting to drug haptens. This propensity involves a broad range of AMD haptens and a broad range of immunopathologic mechanisms.
Abstracts
345
347 J. Stevens Ph.D., Antweqes~, BeIgium. The effect of local application of DSCG solution on the immediate skin prick test reactivity with histamine, codeine and house dust mite was studied in asthmatic children (n = 22) and in children with atopic dermatitis (n = 10). The design of the study was double-blind versus placebo (saline). DSCG or saline were applicated under plastic cover during 10 minutes before prick testing. DSCG had no effect upon histamine reactivity (5.34 mm + 2.12 versus 5.38 mm + 1.77, p = 0.906) but was found to inhibit code&e reactivity significantly (5.63 mm + 2.09 versus 4.72 mm + 1.55, p = 0.012). House dust mite reactivity tended so to inhibited by DSCG, but the difference was not statistically significant (7.07 mm + 4.06 versus 5.47 mm +. 3.74, p = 0.059). When the results of the asthmatic children were compared with the results of the children with atopic dermatitis, no major differences were found. This study shows that local application of DSCG solution inhibits codeine reactivity and tends to inhibit house dust mite skin reactivity.
346
Hamburg/*Munich,
FRG.
Between 1975 and 1985 24 patients >Nriith lbxic I+dental Necrolysis (TEN) have been seen at the Department of Dermatology in Munich. The retrospective study c+f the c%e histories showed that drug-induced TEN WA< more common in elderly individuals (age 4--X8 ), !I par :. .Sii 1. 13 > 60 y). The female/male ratio was 2. I /16/R). The data yielded a trend toward a higher prevalence ot ‘IXN m \ftc spring and summer pekd [ 15/22 pat.; predomkanrly 11:July (n=S) and in April (n=4jJ I n many cases thv first and/or most severe TEN-lesions occurred on the face and 011the extremities. 5 pat. developed TEN in connection wirh the administration of only one single drug. tvherez; ! pa!, contracted TEN after introduction of a new drug m addnion to a long term medication with some other drugs [r\iSAW (oxyphenbutazone, dipyrone, salicylamidj, antl-convulsive drugs (carbamazepine, phenytoin), other drugs (ailopnrb~oi. bromhexinbydrochloride) and herbal tea]. :X/24 pat. took more than one “culprit” dmg simultaneously ii. e. II! 7 pat. > 4 drugs); l/l 3 developed TEN aft?? a heavy sunburn. One patient had no history four administration rli a drug. 16 pat resolved. 5 pat. died and in ‘7 ales t?le WT. come remains unknown. All patients received corticosteroid therapy in a various manner (single and cumukmvr doses ranging from 60--S(K) mg and 280-4900 mg respectively). The data of this study are in good agreement with the literature. Our own data suggest a possible rofr tlf lJWight exposure in the pathosenesir of TEN in some patient:,
346
Austria. Exogenous contact to mercury can be demonstrated only in one third of patients sensitizised to mercury. Body storage mercury depots may be responsible for ineffective treatment despite allergen avoidance. Eight patients with chronic mercury contact dermatitis in whom an exogenous mercury source could not be demonstrated DMPS (chelating agent) were investigated for body mercury depots. After assessment Of baseline values of mercury in urine and blood 250 mg of DMPS were administered i.v. Urinary mercury was estimated at 1 hr, 3 6 hr and 24 hr after injection using hr, atomic absorbtion spectroscopy. Increased DMPS excretion after injection ( > 5 times of baseline level) of mercury 6 could be demonstrated patients. Mean value of mercury in ‘2”4 hr urine : 1.4 ug/l. Mean mercury excretion rates after DMPS injection: 1 hr: 102.5 ug/l 6 hr: 25.2 ug/l 3 hr: 91.2 ug/l 3.9 ug/l 24 hr: A slight decrease of mercury levels in blood (mean 4.6 ug/l) could be achieved in one patient. ( 11 ug/l before 250 DMPS, 8 ug/l after DMPS, normal: < 5 “g/o;) The increased mercury rates excretion after DMPS indicate presence of mercury depots ’ sensitive mercury patients. Three patfints reported decrease of their contact eczema after this single injection of 250 mg DMPS.
DKUWNDUCED LYELL’S SYNDROME 0QXlC EPlDWSIS): AN AN&@S OF 24 CASES. JohannesR.ina. M. D. Ph. D., Dieter Vi&f. M. D.&im Wimschneickr. M. D. and Ber&-wrP.pQa.@ ,. .&I...-p..
ALLERGIC REACTIONS TO ANTIMICRQBIAL DRUGS IN PATIENTS’ WfFB A EISTORY OF PRIOR DRUG ALLERGY. J&p K. Mosolev. and m Sullivan. M.D- Da&as, Texas. We examined the hypothesis that a history of antimicrobial drug (AMD) allergy indicates an increased risk of reacting to another class of AMD in a A total of 2531 prospective case control study. hospitalized patients beginning a course of AMD therapy were screened, resuking in the identification of 149 (5.9%) with a documented history of AMD allergy and 37 of these 149 who were beginning a 7 day or more course of AMD therapy. Two matched control patients were selected for each allergic case. Five of 37 AMD allergic patients (13.2%) experienced an allergic reaction. Three developed pruritic rashes during therapy with mulitple AMD, one experienced fever and urticaria on erythromycin, and one patient on narfloxacin had a Stevens-Johnson (S-J) reaction. This is in keeping with our earlier retrospective study that detected a history of TEN/S-J/EM in 5 of 64 multiple AMD allergic patients. One of 74 control patients in this study (1.4%) developed a pruritic rash on ampicillin/ sulbactam. The increased risk associated with a history of prior AMD allergy was significant (P = O.OlS), with a relative risk of 9.4. The results of this prospective study provide direct evidence that AMD allegic subjects are at increased risk of reacting to drug haptens. This propensity involves a broad range of AMD haptens and a broad range of immunopathologic mechanisms.