Carl E. Arbesman

Cold urticaria: Immunologic studies

Four cases of primary acquired cold urticaria are described. In all four cases a serum factor was present which, when injected intradermally into normal human subjects, would cause localized urticaria at the sensitized sites after exposure to cold. In order to gain some insight into the pathogenesis of the cold urticarial reaction, attempts were made to characterize the factor in the serum of these four patients. The factor in the different serum specimens remained fixed to the skin of a recipient for periods of 7 to 28 days. The skin-sensitizing activity of the factor was destroyed by heating the serum at 56°C for varying periods. Reduction with 2-mercaptoethanol, followed by alkylation with iodoacetate also destroyed the activity. The cold urticaria factor was further analyzed by Sephadex ® G-200 gel filtration and DEAE-cellulose chromatography. It was not found in fractions containing only IgG and IgM but was eluted with the 0.025M and 0.035M phosphate buffers (where most IgE skin-sensitizing antibodies are found). Absorption studies showed that the passive transfer activity could be removed from the four serum specimens by monospecific antiserum to IgE but not by antiserum to any of the other immunoglobulins. All of these characteristics are quite similar to those of IgE skin-sensitizing antibodies.

Immunologic studies on aspirin: Clinical studies with aspiryl-protein conjugates

Abstract Aspiryl-chloride was conjugated with human serum albumin, human gamma globulin, rabbit gamma globulin, and poly- l -lysine. These conjugates were evaluated in skin tests, indirect hemagglutination, lymphocyte culture, and in an immunofluorescent test on tissues and sera of patients sensitive to aspirin. No evidence of specific immunologic reactions was found. Possible explanations for these results are discussed, and three possible nonimmunologic mechanisms for adverse reactions to aspirin are offered.

Unusual reactions following insect stings: Clinical features and immunologic analysis

Fifteen patients were studied who had unusual reactions following insect stings. These included serum sickness, neurologic disease, renal disease, and delayed hypersensitivity-type reactions. The clinical features are briefly outlined. Measurements were made of serum venom-specific IgE and IgG antibodies. These antibodies were present in some patients and in these instances suggested an immunologic pathogenesis for the reactions. Alternative etiologies for the unusual reactions are also discussed.

Clinical and immunological studies of beekeepers

Thirty‐four beekeepers were interviewed and their blood assayed for the presence of antibodies reacting with bee venom, bee venom phospholipase A (PLA), and whole bee body extract. Following a bee sting, most beekeepers experienced only minimal local tissue reaction. Their serum contained high levels of total antibodies (primarily IgG) reacting to bee venom and phospholipase A. These antibody titres correlated with the frequency of bee stings.

Local intranasal immunotherapy for grass-allergic rhinitis

In a double-blind controlled study, local intranasal immunotherapy was evaluated for the treatment of grass pollenosis. On the basis of serum grass-specific IgE levels, 50 grass-allergic patients were randomly divided into three groups and treated with either an aqueous solution of mixed-grass extract, a formaldehyde-modified mixed-grass extract (allergoid), or a histamine solution (placebo). Intranasal solutions were administered in gradually increasing doses over a preseasonal 10 wk period, adverse local reactions from the aqueous grass extract were frequent during treatment. Few adverse reactions occurred from the allergoid or histamine solutions. During the pollen season, patients receiving both grass extracts had much lower symptom/medication scores than patients receiving placebo. The severity of eye symptoms was the same in all groups. After treatment, serum grass-specific IgE rose in patients receiving aqueous and allergoid extract; no change was noted in patients receiving placebo therapy. Grass nasal secretory-specific IgA titers in each group did not change during the study. The results of this study suggest that local intranasal immunotherapy with either aqueous or allergoid grass extracts is clinically effective for the treatment of grass pollenosis. Adverse reactions associated with the aqueous extract may limit its usefulness. No correlation was present between the secretory immune response and clinical benefit.

Comparison of the allergenicity and antigenicity of yellow jacket and hornet venoms

The immunologic properties of yellow jacket and hornet venoms were compared by measuring their reaction with rabbit antisera and human IgE and IgG antibodies. Anti-hornet venom rabbit serum showed precipitin bands unique to hornet venom and several bands crossreacting with yellow jacket venom. Anti-yellow jacket venom rabbit serum reacted with yellow jacket venom but failed to react with the hornet venoms. Most sera from patients who had had allergic reactions after vespid stings reacted with yellow jacket and hornet venoms in RAST analysis. A few sera reacted with only one of the venoms. RAST inhibition studies confirmed the crossreactivity of these IgE antibodies. The IgG antibody response of 14 patients was measured after yellow jacket venom immunotherapy. All had rising titers of yellow jacket venom-specific IgG. There was also an increase in the IgG antibody response measured with hornet venom in the majority of patients. The rise was significant with yellow hornet venom (p less than 0.02) but failed to reach significance with bald-faced hornet venom (p greater than 0.05). In IgG radioimmunoassay inhibition studies using yellow jacket venom-coupled discs, yellow jacket venom was considerably more potent than hornet venom. These studies indicate major crossreactivity between yellow jacket and hornet venoms. In this group of patients, yellow jacket venom appeared to be the primary allergen.

Measurement of serum IgE by a one-step single radial radiodiffusion method

Abstract A relatively simple, reproducible method for the measurement of serum IgE has been described. It is practical and could be performed inmost laboratories and the results obtained in a few days. A known reference serum, standard (such as the WHO standard) could be employed, and IgE myeloma protein would not be needed. The IgE values in serum may possibly be of diagnostic value in differentiating atopic dermatitis from other dermatoses and atapic versus nonatopic rhinitis and asthma. The studies presented confirm the work of previous investigators as to elevated IgE serum levels in atopic eczema, parasitic infestations, and, to a lesser degree, respiratory allergies. The additional (coincidental?) findings of increased serum IgE levels in patients with chronic infection, eosinophilia, and trichinosis need further elaboration.

IgE antibodies in nasal secretions of ragweed-allergic subjects.

Abstract Nasal washings from 50 ragweed-allergic and 10 normal individuals and parotid salivas from half of this group were studied for the presence of IgE antiragweed antibodies by means of radioimmunodiffusion (RID) and Prausnitz-Kustner (P-K) tests. Sixty per cent of the nasal washings from the group of allergic patients gave positive P-K reactions, but only 16 per cent were positive in the RID test. The nasal IgE antiragweed antibodies detected in RID showed reactions of identity with the IgE antibodies in the serum. The presence of nasal IgE antibodies as detected by RID did not seem to be related to the degree of chinical symptoms or immunotherapy but showed some correlation with P-K titers of the sera. The lower degree of sensitivity of RID, compared to that of the P-K test, accounted for the difference in the incidence of IgE antibodies in the nasal washings as detected by these two methods. Nasal washings from the control subjects and parotid salivas from both the allergic and normal individuals did not show reaginic antibody activity.

Local intranasal immunotherapy for ragweed allergic rhinitis II. Immunologic response

Local nasal immunotherapy (LNIT) was administered in a double-blind study to 67 subjects. Twenty-three received an unmodified ragweed extract (RW), 24 received a glutaraldehyde polymer of ragweed extract (PRW), and 21 received placebo. Serum ragweed-specific IgE (S-IgE), ragweed-specific nasal secretory (NS-) IgE, secretory IgA (SIgA) and IgG, and NS-albumin were measured. RW therapy caused a significant increase in ragweed-specific S-IgE (p less than 0.005) and NS-SIgA (p less than 0.05). PRW therapy caused a significant rise in ragweed-specific NS-SIgA (p less than 0.001). NS-IgE (p less than 0.05), and NS-IgG (p less than 0.01). Ragweed-specific S-IgG was not affected by any of the treatments. There was no consistent correlation between NS-antibody levels and symptom/medication scores.

Stinging insect allergy: Detection and clinical significance of venom IgE antibodies

Venom-specific IgE antibodies in 109 sera from patients who had had immediate systemic allergic reactions following insect stings were measured by the radioallergosorbent (RAST) procedure. The majority of sera contained IgE antibodies to either bee, yellow jacket, or hornet venoms. Some sera had positive RAST reactions with 2 or 3 venoms, but others contained single venom-specific IgE antibodies. Of 24 patients who had large local reactions, the sera of 12 contained venom IgE antibodies. The RAST procedure provides an accurate means of documenting IgE-mediated allergic sensitivity to stinging insects.