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Anti-Ige Autoantibodies in Systemic Sclerosis (Scleroderma)

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Anti-Ige Autoantibodies in Systemic Sclerosis (Scleroderma) Ann Rheum Dis: first published as 10.1136/ard.48.3.201 on 1 March 1989. Downloaded from Annals of the Rheumatic Diseases, 1989; 48, 201-205 Anti-IgE autoantibodies in systemic sclerosis (scleroderma) LEE D KAUFMAN,1 BARRY L GRUBER,1 MARY J MARCHESE,' AND JAMES R SEIBOLD2 From the 'Department of Medicine, Division of Allergy, Rheumatology, and Clinical Immunology, State University of New York at Stony Brook, Stony Brook, New York; and the 2Department of Medicine, Division of Rheumatology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, New Jersey SUMMARY An enzyme immunoassay was used to determine the prevalence of anti-IgE auto- antibodies in 66 patients with systemic sclerosis (scleroderma) stratified according to extent and duration of disease. Serum IgG anti-IgE antibodies were detected in 14 (21%) patients and IgM anti-IgE antibodies in nine (14%) patients. The overall prevalence of IgG or IgM isotypes was 21/66 (32%). Anti-IgE autoantibodies were not found in six patients with undifferentiated connective tissue disease or two patients with eosinophilic fasciitis. Attempts to demonstrate histamine release from basophils in vitro by using serum samples containing high titre anti-IgE antibody were unsuccessful. By multivariate analysis the presence of anti-IgE antibody was not copyright. associated with duration of systemic sclerosis; extent of scleroderma; specific visceral features, including heart, lung, renal, and gastrointestinal involvement; or mortality. Recent studies have focused attention on the poten- disorders,12-15 may represent an additional tial role of mast cells in the pathogenesis of systemic mechanism for activation of mast cells and their sclerosis (scleroderma) and other similar fibrosing subsequent interaction with fibroblasts in sclero- http://ard.bmj.com/ syndromes.1 An increased density of dermal mast derma. The current study sought to determine the cells has been described in patients with sclero- prevalence of anti-IgE autoantibodies in a group of derma,2 the toxic oil syndrome,3 graft versus host patients with scleroderma stratified according to disease,4 and in the tight skin mouse model of the extent and duration of disease as well as their scleroderma.5 Furthermore, the dermal mast cells of potential functional activity as determined by an in tight skin mice show massive degranulation,6 and vitro basophil release assay. disodium inhibitor treatment with cromoglycate (an on September 28, 2021 by guest. Protected of mast cell degranulation) has been observed to Patients and methods produce a marked decrease in skin fibrosis. Mast cells and circulating basophils may release PATIENTS their inflammatory mediators when activated by Sixty six patients fulfilled preliminary American lymphocyte products or histamine releasing factors Rheumatism Association criteria for classification as secreted from neighbouring mononuclear cells8 also definite systemic sclerosis16 and were selected to present in the dermis of patients with scleroderma.9 reflect a balanced stratification of disease extent and .After degranulation mast cell granules can be duration. Classification as generalised scleroderma intemalised by fibroblasts, and this interaction may required the presence of truncal skin thickening, then promote local fibrosis.10 Anti-IgE autoanti- whereas limited scleroderma described those bodies, previously reported in systemic lupus patients with skin involvement limited to the hands, erythematosus11 and other autoimmune and atopic forearms, face, and feet. Onset of systemic sclerosis was dated from the first non-Raynaud's clinical Accepted for publication 23 July 1988. manifestation, with three years' duration chosen as Correspondence to Dr Lee D Kaufman, HSC-T-16-040, Division of the divider between those patients with early and Allergy, Rheumatology, and Clinical Immunology, State Univer- sity of New York at Stony Brook, Stony Brook, New York those with late systemic sclerosis.'7 In addition, we 11794-8161, USA. studied six patients with undifferentiated connective 201 Ann Rheum Dis: first published as 10.1136/ard.48.3.201 on 1 March 1989. Downloaded from 202 Kaufman, Gruber, Marchese, Seibold tissue disease (defined as having at least four of the phosphate (100 ,g/well). The optical density (OD) following six features: late age of onset of Raynaud's at 405 nm was determined at 30 and 60 minutes on a phenomenon, finger oedema or sclerodactyly, or Dynatech ELISA reader. The relative quantity of both, abnormal nail fold capillaroscopic findings, bound IgG or IgM was calculated using standard serum anticentromere antibody with a titre >1/160, amounts of coupled purified IgG (Miles Laborator- and laboratory evidence of impaired maximal digital ies, Naperville, IL) or IgM (Calbiochem, Summer- arterial flow or of in vivo platelet activation18) and ville, NJ) ranging from 10 ng to 1 R,g. The data are two patients with recently diagnosed eosinophilic expressed as a ratio as follows: fasciitis. All patients underwent a detailed clinical and OD 405 nm (sample) x ng of standard laboratory assessment as described by the sclero- OD 405 nm (standard) derma criteria cooperative study,16 which included Positivity was defined as a value greater than two chest radiograph, 12 lead electrocardiogram, cine- standard deviations from a control group of 22 oesophagography, pulmonary function testing, healthy, non-atopic individuals. The specificity of plasma renin activity, 24 hour urine collection for this assay has been previously confirmed." protein excretion and creatinine clearance, and a detailed serological profile. Serum samples were SERUM IgE CONCENTRATIONS collected and stored at -70°C until needed for Total serum IgE concentrations were measured by assay. a radioimmunosorbent (PRIST) assay (Pharmacia Data were entered on the Medlog clinical data Diagnostics, Piscataway, NJ). management system, and this system was used for statistical analysis. Fisher's exact and paired t tests BASOPHIL STUDIES were used for univariate analyses and linear regres- Leucocytes were separated from whole blood sion of least squares or stepwise linear regression obtained from non-atopic healthy volunteers and model procedures for multivariate analysis. Mean from selected patients with raised levels of anti-IgEcopyright. antibody titres among patient subgroups were antibodies after informed consent using dextran compared using Student's t distribution for two sedimentation (0.03% dextran, 0*3% glucose, 0-15 means (unpaired). M NaCl) by the method of Lichtenstein and Osler.'19 The leucocytes were washed in HEPES buffer ENZYME IMMUNOASSAY (N-2-hydroxyethylpiperazine-N'-2-ethanesulphonic Anti-IgE antibodies for both IgG and IgM isotypes acid) containing 0*03% human serum albumin and were determined by an enzyme linked immunosor- aliquots were incubated at 37°C for 30 minutes with http://ard.bmj.com/ bent assay (ELISA) as described by Nawata et al'5 serum containing anti-IgE antibodies in HEPES with minor modifications. Multiwell polystyrene buffer with 1.5 mM CaCl2 and 2-0 mM MgCl2. The plates (Dynatech Inc, Alexander, VA) were coated histamine released was measured in duplicate with myeloma IgE at 1 1tg/well in bicarbonate buffer samples by the double isotopic radioenzyme assay pH 9*6. Further blocking of any remaining reactive of Beaven et al.20 Commercially obtained goat sites to reduce background was not necessary and, in antihuman IgE (Kirkegaard and Perry Laboratories fact, created false positive reactivity directed against Inc, Gaithersburg, Maryland) was used as a positive the blocking reagents-for example, bovine serum control during each basophil release assay and on September 28, 2021 by guest. Protected albumin. The background in these unblocked plates consistently produced histamine release at dilutions remained less than 0-01 at optical density 405 nm. of both 1:100 and 1:1000. The plates were stored at 4°C and the assay was performed by diluting serum in phosphate buffered Results saline-Tween. The serum was diluted at 1:10 and 1:100 for the IgG anti-IgE and IgM anti-IgE Figure 1 shows the distribution of anti-IgE autoanti- ELISAs respectively and allowed to incubate on the bodies by isotype for patients and controls. The plates overnight at 4°C. (These dilutions were overall prevalence of IgG or IgM anti-IgE was 21 chosen as the approximate mean along the linear out of 66 patients (32%). Of these 66 patients, 14 slope of serum concentrations versus optical density (21%) had IgG anti-IgE and nine (14%) had IgM plotted in semilogarithmic form.) The plates were anti-IgE. Two patients had both IgG and 1gM then extensively washed with phosphate buffered isotypes. Anti-IgE antibodies were not found in the saline. Alkaline phosphatase labelled goat antihu- sera from six patients with undifferentiated connec- man IgG or IgM (Fc specific, Cappel Laboratories, tive tissue disease or two patients with eosinophilic Malverne, PA) at 1:1000 dilution was added for two fasciitis. Table 1 shows the prevalence of anti-IgE hours and allowed to react with p-nitrophenyl antibodies by isotype for each clinical subset of Ann Rheum Dis: first published as 10.1136/ard.48.3.201 on 1 March 1989. Downloaded from Anti-IgE autoantibodies in systemic sclerosis 203 0 IgG anti-IgE IgM anti-IgE 15.0 4 Fig. 1 Anti-IgE autoantibodies by IgG and 1gM isotype versus 10.0 non-atopic controls. *IgG versus controls p<O*02; *1gM versus * 0 controls p=NS. SS=systemic -- -- -----a Z-S1% & DF% - * 0 sclerosis. *0 0 *0 5.0 .. * 0 0 ---.---**-----0 -0-0- - - *--2SD- * 0 * 0.0 o.. * 0 * 0 * 0 00 0 000 040 0 0.0 0 ~~00 * ~ 0 0 0 .40 0 0 0. * 0' copyright. SS CONTROLS CONTROLS n-66 n 22 n 22 Table 1 Number (%) ofanti-IgE autoantibodies in There was a significant correlation between IgM systemic sclerosis anti-IgE and total serum IgE concentrations (R=04106; p<0.01), but no relation between IgG EG* (n=18) EL* (n=12) LG* (n=15) LL* (n=21) anti-IgE and total serum IgE concentrations http://ard.bmj.com/ IgG 4 (22) 3 (25) 1 (7) 6 (29) (p=NS).
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