William F. Clayton

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.

Local Intranasal Immunotherapy with High-Dose Polymerized Ragweed Extract

Thirty-one ragweed-allergic patients received preseasonal local intranasal immunotherapy (LNIT) with high doses of gluteraldehyde-polymerized ragweed extract (average total dose 544 micrograms antigen E). Minimal side effects were reported during treatment and did not interfere with the dosing schedule. During the ragweed pollen season, LNIT-treated patients had lower symptom scores for sneezing, rhinorrhea and nasal congestion than a comparable group of untreated ragweed-allergic patients. There was no difference in ragweed-induced eye symptoms between the two groups. Secretory ragweed-specific IgA and IgG rose following LNIT treatment. Absolute antibody titers and changes in titers did not correlate with clinical improvement. LNIT with the polymerized ragweed did not block the seasonal rise in serum ragweed-specific IgE. These results suggest that LNIT with high-dose polymerized ragweed extract is a safe, simple and effective form of immunotherapy.

Further evaluation of local intranasal immunotherapy with aqueous and allergoid grass extracts

In a double-blind study, 45 grass-allergic patients received local nasal immunotherapy (LNIT) with either aqueous mixed-grass extract, formaldehyde-treated, mixed-grass extract (allergoid), or histamine placebo. Twenty-four patients received LNIT for a second successive year, and 21 patients received LNIT for the first year. The aqueous extract-treated patients had significantly lower symptom-medication scores than either allergoid- or placebo-treated subjects. There was no difference in symptom-medication scores in patients receiving allergoid and placebo treatment or in patients receiving 1 and 2 yr of LNIT. The aqueous extract stimulated a rise in serum grass-specific IgE. There was no serum or local antibody response after allergoid-extract treatment. Postseasonal rises in serum-IgE titers were observed in all three groups. These data suggest that LNIT with aqueous mixed-grass extract significantly reduces the symptoms of allergic rhinitis. The allergoid grass extract was ineffective in the second year of treatment. No cumulative effect of LNIT could be demonstrated in successive years of therapy.

Effect of prolonged venom immunotherapy on serum venom‐specific IgE and IgG

Serum venom‐specific IgE and IgG were monitored in twenty‐three patients receiving venom immunotherapy for more than 3 years. Two response patterns of IgE antibody were found. Following initiation of therapy, seven patients had a rise in serum venom‐specific IgE, peaking at one year, then decreasing. Sixteen patients had a persistent fall in IgE antibody titres following initiation of therapy. At the end of 3 years, levels of serum venom‐specific IgE in both groups were comparable. The presence of atopy may have influenced the rising IgE antibody response.

Insect sting anaphylaxis in patients without detectable serum venom‐specific IgE

Following insect sting anaphylaxis, twenty‐five patients of over 500 evaluated, did not have detectable serum venom‐specific IgE. Twenty‐two were evaluated within 1 year of the reaction, fifteen within 6 months. Anaphylaxis occurred in six patients after their first sting exposure. The clinical features of the sting reaction were typical of the reaction occurring in insect‐allergic patients with serum venom‐specific IgE. Eleven of the twenty‐five patients had negative venom skin tests. These observations suggest that a non‐IgE mechanism may be responsible for a minority of insect sting reactions.

Modified rapid venom desensitization

The clinical and immunologic response to a modified rapid (r) regimen of venom immunotherapy was evaluated and compared to a traditional (t) therapeutic regimen. Nineteen patients in the r group received a starting dose of 0.01 μg and reached a maintenance dose of 50 μg in 7 weeks. Twelve patients in the t group received an average of twenty‐one injections on a weekly basis, reaching the same maintenance dose. The age and sex distribution and pre‐treatment venom‐specific IgE titres (RAST) of both groups were comparable.