Facilitated referral to asthma specialist reduces relapses in asthma emergency room visits.

Facilitated asthma-specialist care delivered by allergists was compared to generalist care on the rate of relapse of asthma emergency room (ER) visits and hospitalizations and on asthma control in a prospective, controlled study of San Diego Kaiser Health Plan members with asthma. Subjects with asthma between the ages of 6 and 59 years presenting for acute ER care for asthma were systematically assigned by alternating, consecutively, the day of their ER visit to receive either (1) facilitated referral to an asthma specialist within the allergy department and concomitant comprehensive ongoing asthma care (intervention group, n = 149) or (2) continued outpatient management from generalist physicians (control group, n = 160). The course of their asthma was evaluated blindly during the subsequent 6 months by review of medical records, initial and follow-up questionnaires, and spirometry. Compared to the control group, the intervention group noted (1) a 75% reduction in the number of, and percent of, subjects with asthma awakenings per night (p less than or equal to 0.0001), (2) an almost 50% reduction in asthma ER relapses (p = 0.017) resulting from a reduction in the frequency of multiple relapse (p = 0.005), and (3) a greater use of inhaled corticosteroids (p less than 0.00001) and cromolyn (p = 0.002). Thus, facilitated referral of subjects with asthma to specialists in asthma therapy after acute ER therapy appears to reduce asthma ER relapses and to improve asthma outcome.

Effect of combined maternal and infant food-allergen avoidance on development of atopy in early infancy: a randomized study.

The effect of maternal and infant avoidance of allergenic foods on food allergy was examined in a prenatally randomized, controlled trial of infants of atopic parents. The diet of the prophylactic-treated group (N = 103) included (1) maternal avoidance of cow's milk, egg, and peanut during the third trimester of pregnancy and lactation and (2) infant use of casein hydrolysate (Nutramigen) for supplementation or weaning, and avoidance of solid foods for 6 months; cow's milk, corn, soy, citrus, and wheat, for 12 months; and egg, peanut, and fish, for 24 months. In the control group (N = 185), mothers had unrestricted diets, and infants followed American Academy of Pediatrics feeding guidelines. The cumulative prevalence of atopy was lower at 12 months in the prophylactic-treated (16.2%) compared to the control (27.1%) group (p = 0.039), resulting from reduced food-associated atopic dermatitis, urticaria and/or gastrointestinal disease by 12 months (5.1% versus 16.4%; p = 0.007), and any positive food skin test by 24 months (16.5% versus 29.4%; p = 0.019), caused primarily by fewer positive milk skin tests (1% versus 12.4%; p = 0.001). The prevalences of allergic rhinitis, asthma, and inhalant skin tests were unaffected. Serum IgE levels in the prophylactic-treated group were marginally lower only at 4 months. Thus, reduced exposure of infants to allergenic foods appeared to reduce food sensitization and allergy primarily during the first year of life.

Lack of pokeweed mitogen-induced IgE formation in vitro by human peripheral blood mononuclear cells: detection of cross-reacting idiotypic determinants on polyclonal Ig by antibodies to a single IgE myeloma protein.

The ability of human peripheral blood mononuclear cells to synthesize IgE in vitro in response to pokeweed mitogen (PWM) is controversial. To determine whether the conflicting results obtained by different laboratories could be due to inherent qualitative differences in the anti-IgE antibodies used to measure low concentrations of IgE in culture supernatants, we compared the specificities of anti-IgE reagents prepared by various methods. Immunoadsorbent-purified antibodies were isolated from a goat antiserum to the lambda, IgE myeloma protein PS and a rabbit antiserum to the kappa, IgE protein Bed in three ways: 1) antibodies to IgE PS (anti-PS) were isolated from the goat antiserum by affinity chromatography with PS coupled to Sepharose 4B; these antibodies consisted of anti-epsilon chain-specific and anti-idiotypic antibodies to protein PS; 2) antibodies specific for the epsilon-chain (anti-epsilon) were purified by affinity chromatography with IgE myeloma proteins that were not used for immunization; and 3) antibodies to idiotypic determinants of proteins PS (anti-id PS) and Bed (anti-id Bed) were isolated on affinity columns with the respective myeloma proteins after absorption of the epsilon-chain-specific antibodies. These three types of antibodies were then used in a solid phase radioimmunosorbent test to quantitate the amount of "IgE" synthesized by peripheral blood mononuclear cells from nonatopic and atopic donors cultured for 7 days in the presence and absence of PWM. ANTI-PS antibodies detected a PWM-induced "IgE formation" in cell culture supernatants of both non-atopic and atopic donors. (ABSTRACT TRUNCATED AT 250 WORDS)

Characterization with monoclonal antibodies of T lymphocytes bearing Fc receptors for IgE (T epsilon cells) and IgG (T gamma cells) in atopic patients.

Peripheral blood T lymphocytes from nonatopic control donors, asymptomatic atopic donors, and patients with moderate to severe atopic dermatitis were analyzed for Fc receptors for IgE (T epsilon cells) and IgG (T gamma cells) by rosette assays and were characterized with monoclonal antibodies. The T cells were reacted first with monoclonal antibodies, followed by fluoresceinated F(ab')2 goat antimouse Ig; they were then rosetted, and subsequently the rosetting cells were examined for immunofluorescence. Seven nonatopic control donors had less than 0.1% T epsilon cells and a mean +/- SD of 10.5% +/- 4.1 T gamma cells. Seven asymptomatic atopic donors with low IgE levels (2 to 233 IU/ml) varied from less than 0.1 to 1.3% T epsilon cells and 7.2% +/- 3.7 T gamma cells. Six of seven patients with moderate to severe atopic dermatitis and IgE levels of 1339 to 24,261 IU/ml had less than 0.1% T epsilon cells and significantly fewer T gamma cells (3.1% +/- 2.7, p less than 0.01) than the nonatopic control donors and the atopic donors in remission. Both T epsilon and T gamma cells reacted with the pan-T cell antibody Lyt-3 (anti-sheep red cell receptor) but not with antibodies OKT3, OKT4, or OKT6. Subpopulations of both T epsilon and T gamma cells reacted with antibodies OKT8 and the antimonocyte antibody OKM1. The OKM1+ cells did not appear to be monocytes, however, because the T cells did not react with another antimonocyte antibody, BRL.2, and were negative for nonspecific esterase activity. (ABSTRACT TRUNCATED AT 250 WORDS)

Increased peripheral blood monocytes with Fc receptors for IgE in patients with severe allergic disorders.

Peripheral blood monocytes, defined as latex bead-ingesting mononuclear cells, from 15 healthy nonallergic donors and 22 patients with allergic disorders were analyzed for Fc receptors for IgE (Fc epsilon) by a rosette assay employing ox erythrocytes coated with IgE. The patients were divided into 3 groups. Group I: 12 patients with mild to moderate atopic disease and serum IgE levels up to 2300 IU/ml. Group II: 6 patients with severe generalized atopic dermatitis, allergic rhinitis, and asthma, of which 5 had IgE serum levels of 8000 to 77,500 IU/ml. Group III: 4 severely atopic patients with IgE levels greater than 10,000 IU/ml and receiving oral corticosteroids. The numbers of monocytes were similar in healthy donors and patients. In contrast, severely atopic patients (Group II) had significantly more (p less than 0.01) Fc epsilon + monocytes (107 +/- 42/mm3) than healthy donors (20 +/- 14/mm3) or patients of Group I (31 +/- 14/mm3). Patients of Group III had significantly fewer (p less than 0.05) Fc epsilon + monocytes (12 +/- 16/mm3) than controls and patients of Groups I and II. We conclude that patients with severe allergic disorders have a significant increase of peripheral blood monocytes with Fc receptors for IgE, which suggests that these cells may participate in the pathophysiology of atopic disease.

Increased IgE-dependent cytotoxicity by blood mononuclear cells of allergic patients.

Peripheral blood mononuclear cells from 14 healthy donors and 22 allergic patients were incubated with 51Cr-labelled chicken erythrocytes coated with an IgE myeloma protein or rabbit IgG antibodies. Mononuclear cells from patients with severe atopic disorders released a significantly greater percentage of 51Cr (P less than 0.001) from IgE-coated target cells than mononuclear cells from healthy controls, patients with mild atopic disease, or patients with severe atopic disease taking oral prednisone. Specific 51Cr-release from IgE-coated target cells was directly correlated to the percentage of monocytes (latex-ingesting cells) with Fc receptors for IgE (r = 0.87, P less than 0.01) as detected by a rosette assay employing ox erythrocytes coated with IgE. Mononuclear cells from patients and normals released similar amounts of 51Cr from IgG-sensitized target cells. Depletion of monocytes from mononuclear cell preparations from two severe atopic patients decreased 51Cr-release from IgE-coated target cells to levels seen in healthy donors or patients with mild allergic disease. These results demonstrate that mononuclear cells from severely allergic patients have a significantly increased cytotoxicity toward IgE-coated targets coated target cells and that this cytotoxicity correlates highly with the percentage of monocytes with Fc receptors for IgE in these mononuclear preparations.