This study was designed to characterize the clinical spectrum and course of tracheobronchial involvement in Wegener's granulomatosis (WG). Of the 51 patients with biopsy-proven WG who underwent bronchoscopy at least once at our institution between January 1982 and November 1993, 30 (59%) had endobronchial abnormalities due to WG. Initial findings included subglottic stenosis in five (17%), ulcerating tracheobronchitis with or without inflammatory pseudotumors in 18 (60%), tracheal or bronchial stenosis without inflammation in four (13%), and hemorrhage without identifiable source in two (4%) patients. Nine patients with ulcerating tracheobronchitis on initial study had subsequent bronchoscopies for continued symptoms, which in seven cases documented the progression from ulcerating tracheobronchitis to stenosis without inflammation. Bronchoscopic interventions included dilation by rigid bronchoscope in three, YAG-laser treatment in one, and placement of silastic airway stents in three patients. Only the stents provided persistent airway patency. Endobronchial biopsies were performed on 21 occasions in 17 patients. Half of the specimens were helpful in establishing the diagnosis and in all but three in assessing disease activity. While antineutrophil cytoplasmic antibody titers reflect overall disease activity, no correlation with endobronchial inflammatory activity was apparent.
Received I 3unc 1992: revised version rcccivcd 10 July I992Zymaian. which is composed primurily of 2.munnun i~nd/?~ylucan polymcn. is u well rccognnhcd netiwor of mxroph;lyc%. The type racptar by which unopronizrd rymosun inducts urarhidanic acid rclcm ws invcaliy;llcd. II WI bundthat partirulrtc~-&xan und x>moran stimulated an identical doss-dcpcndcnr rclcaric af unchidanis acid. This rclcac of trracbidunic ueid by xymonn wus blacked by rolublo&lucans whcrcar urlublc mannun hud na cffcct. Thiri iahibitbn WL not due IO a gr~\crd toxic effect al' the alublc&ylurrnx ;lr they h;ld no effect on alciutn ionophorcinduced rclmsc ofararhidonic arid. pl-ylucun-induced Tally ucid rclcnr from there cells ws shown to bc fairly rpccifrc for urachidonic acid. Thssc dlrli~ rcvcul that rymomn stimulatcr: lhc spccitlc rclcea of nrrrhidonic acid from rabbit ulvcalur mncrophuycs. UI Icast in part. vin H &uuwn receptor. is 51 well-recognized nctivtitor of olvcolar nxtcrophogcs (AMB). Alrl~oug!~ prrrticulntc zymostrn is tl potent stimulator of the altcrntltivc complement puthrray [I] and is therefore readily opsonizcd, unopsonizcd zymoran is also ti potent trctivutor of AM0. Unopsonizcd rymosun is phugocytoscd itnd stimulates the occrction of lysosomrr! enzymes [21 and rcuctivc oxygen intcrmcdiutcs [3] PS well us the rclcnsc of arachidonic acid (AA) from the mcmbrtrnt phorpholipids and its subscqucnt conversion to a variety of mct;tbolitcs [4.5]. Zymosun contrrins some prorcin and lipid but polysxchuridcs account for 73% of its dry weight. This carbohydrate consits entirely of 13.glucan and amtlnnan (74% and 26% of total polysxchnridc, rcspcctivcly) [6], BCGIUSC AM0 possess separate receptors for both tllc mannan and glucan components of zymosun [7]. it is not clear which receptor is involved in the stimulation of AA rclcasc from thcsc cells by zyrnosun. The purpose of this study was to dctcrminc which of thcsc two rcccptors mcdiatcti zymosun-induced AA rcIcnsc :n rsbbit AM0. AMQ urrc iralutcd from New Zetlnnd white rztbbits by branchoulvcolur Irvnyc its previously drscritxd [IO]. Cells isolated by thir proccdurc wcrc > 95% AM0 us dctcraincd by morpholoyy, Following isolation, the AM0 wcrc ullowcd to adhcrc IO Costar 6.~~11 or 24.well tivruc culture plaicr II ;1 conccntr~tion of 1.56 x IO' cellclcm:. After 60 min in u fully humidified almosphcrc of 95% air/S% CO.. 111~ wchs wcrc cxtcnrivclj wushcd IO rcmovc uny non-adhcrcnt cells.The udhcrcnt AM0 wcrc incubrtcd with 0. I PCi of "C-AA per well in II I:1 mixture of Medium 199 und RPM1 1640 ~upplcmcntcd with 2 mM glut;rminc. 100 U/ml penicillin and IOO~@ml arcptomycin nnd 0.1% fatty nsid&x bovine strum albumin (sulturc medium) for 2 h nt 37% in fully humidilird 95% air/S% CO:, Following incubation, the wcllr wcrc wushcd three timer with HBSS to rcmovc any unincorporutcd ["C]AA.2.4. n~,~-~c.~prrttrr,li,r 41 A rckfsr tttr&ttrtt fy :ytrtwtr or purticttlutc P-gfrtrutt
Importance. Medication-induced eosinophilia is an acknowledged, often self-limiting occurrence. Glatiramer acetate, a biologic injection used in the management of relapsing-remitting multiple sclerosis, is widely regarded as a safe and effective medication and lists eosinophilia as an infrequent side effect in its package insert. Contrary to reports of transient, benign drug-induced eosinophilia, we describe a case of probable glatiramer acetate-induced eosinophilia that ultimately culminated in respiratory distress, shock, and eosinophilic myocarditis. Observations. A 59-year-old female was admitted to the hospital after routine outpatient labs revealed leukocytosis (43,000 cells/mm3) with pronounced hypereosinophilia (63%). This patient had been using glatiramer acetate without complication for over 10 years prior to admission. Leukocytosis and hypereosinophilia persisted as a myriad of diagnostic evaluations returned negative, ultimately leading to respiratory depression, shock, and myocarditis. Glatiramer acetate was held for the first time on day 6 of the hospital stay with subsequent resolution of leukocytosis, hypereosinophilia, respiratory distress, and shock. Conclusions and Relevance. Glatiramer acetate was probably the cause of this observed hypereosinophilia and the resulting complications. Reports of glatiramer-induced eosinophilia are rare, and few case reports regarding medication-induced hypereosinophilia describe the severe systemic manifestations seen in this patient.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.