Lyndon E. Mansfield

Further investigation of the association between gastroesophageal reflux and bronchoconstriction

A double-blind modification of the intraesophageal acid perfusion challenge (Bernstein procedure) was performed in asthmatic subjects with and without gastroesophageal reflux, nonasthmatic subjects with reflux, and normal subjects. Conventional spirometric functions and total respiratory resistance (Rrs) were measured prior to and after the infusion. There were no changes in pulmonary functions except in the asthmatic subjects who had had a positive acid challenge. The greatest changes occurred in Rrs, which increased significantly with reflux symptoms (p less than 0.01) and decreased toward baseline (p less than 0.05) when these symptoms were relieved with antacids. The response was even greater in asthmatic subjects who associated reflux symptoms with attacks of asthma. These results support previous findings that acid reflux symptoms could cause a bronchoconstrictive response in certain asthmatic patients.

Sleep disordered breathing and daytime quality of life in children with allergic rhinitis during treatment with intranasal budesonide

BACKGROUND Nasal obstruction is recognized as an important cause of sleep disordered breathing. Congestion of the nasal mucosa and obstruction are common symptoms of allergic rhinitis. Daytime sleepiness is a common finding in symptomatic allergic rhinitis. Effective therapy of the nasal congestion of allergic rhinitis should alter sleep patterns in patients with symptomatic allergic rhinitis. OBJECTIVE To measure objective changes in polysomnograms (sleep studies) of children with allergic rhinitis before and after therapy with intranasal budesonide and to measure changes in the quality of life of these patients during treatment. METHODS Open clinical trial with objective measurements (polysomnography) and subjective data (Rhinitis Quality of Life Questionnaire [RQLQ]). Evaluations were performed before, during, and at completion of therapeutic intervention. RESULTS The 14 studied children tolerated the procedures and treatment without problems. The mean number of sleep arousals per hour (all apneas and hypopneas) decreased from a baseline of 8.4 to 1.2 (P = .005) after treatment. The change was mainly in hypopneic episodes (7.5-0.9, P = .003). Objective responses on the RQLQ showed improvements consistent with improved sleep and lessened rhinitis symptoms. CONCLUSIONS Decreasing the nasal congestion associated with allergic rhinitis can improve sleep measured by objective sleep studies and lead to improvement in daytime quality of life.

Oral Immunotherapy for Peanut Allergy: Multipractice Experience With Epinephrine-treated Reactions

BACKGROUND Peanut allergy creates the risk of life-threatening anaphylaxis that can disrupt psychosocial development and family life. The avoidance management strategy often fails to prevent anaphylaxis and may contribute to social dysfunction. Peanut oral immunotherapy may address these problems, but there are safety concerns regarding implementation in clinical practice. OBJECTIVE The purpose of this report is to communicate observations about the frequency of epinephrine-treated reactions during peanut oral immunotherapy in 5 different allergy/immunology practices. METHODS Retrospective chart review of peanut oral immunotherapy performed in 5 clinical allergy practices. RESULTS A total of 352 treated patients received 240,351 doses of peanut, peanut butter, or peanut flour, and experienced 95 reactions that were treated with epinephrine. Only 3 patients received 2 doses of epinephrine, and no patient required more intensive treatment. A total of 298 patients achieved the target maintenance dose for a success rate of 85%. CONCLUSION Peanut oral immunotherapy carries a risk of systemic reactions. In the context of oral immunotherapy, those reactions were recognized and treated promptly. Peanut oral immunotherapy may be a suitable therapy for patients managed by qualified allergists/immunologists.

SUCCESSFUL ORAL DESENSITIZATION FOR SYSTEMIC PEANUT ALLERGY

To the Editor: The present strategy of avoidance and epinephrine autoinjection for severe IgE-mediated food reactions is not always successful.1,2 This may be even truer for young children, who cannot read and have to depend on adults to administer the epinephrine. The following case report illustrates such a failure in a young child and describes a treatment that can be performed by an allergy specialist as an alternative to the avoidance-and-epinephrine strategy. The patient is a 6-year-old girl who had 2 systemic reactions to peanuts as a preschooler. The mother and child practiced avoidance measures. The mother provided an epinephrine autoinjector and instructions to the school nurse. While at school, another student was eating a peanut butter sandwich at the patient’s table. The child was touched by the other child. She denied eating any part of the sandwich. She complained to the teacher of shortness of breath, rash, and itching. The teacher tried to contact the school nurse; however, the nurse was not readily available. By the time the nurse came to administer the epinephrine, the child had collapsed. The emergency medical technician arrived and gave the child additional epinephrine. They started an intravenous infusion and transferred the child to the hospital. After an extended observation and treatment period, she was discharged. The parents were extremely distraught by the events, since they had done all they had been advised to do. There was a real risk of continuing emotional duress for the parents and the child. The child’s mother, who was so worried that she was considering quitting her job and keeping the child at home, asked if there were any alternatives. A review of the literature suggested that oral desensitization might offer a way to protect the child against unintentional exposures or ingestion.3–9 The process and procedure were explained to the parents. They were told that the goal was to ensure that the child would not have a reaction to unintentional modest exposures, not to make her eat peanuts as a normal food. They agreed and signed an informed consent form. The oral challenge and desensitization were performed with crushed peanuts in grape juice concentrate. The staff and equipment to treat an anaphylactic reaction were in place, including intravenous solutions and airways and pediatric manual resuscitators with oxygen. A staff member with extensive experience in intubation of children was available. Because of these unusual requirements, the procedure was performed in our office. The office is also one block from a fully equipped hospital emergency department. During the procedure, the child’s pulse rate, blood pressure, and oxygen saturation were monitored. Two placebo doses were given first. Doubling of peanut concentrations from 250 g to 8 g (4 whole kernels) every 15 minutes was planned. However, this goal was not achieved initially. After ingesting one peanut kernel, the child developed a small amount of rash and mild wheezing. Her blood pressure did not change. The wheezing was treated with a bronchodilator. The rash disappeared within 15 minutes, and she did not require epinephrine or antihistamines. The child’s mother was instructed to give a half kernel 3 times daily to the child. The first such dose was given 6 hours later in clinic. During an 8-week period, this amount of peanut was gradually increased in the clinic until the child tolerated 2 whole peanuts (4 whole kernels) 3 times daily. Subsequently, this was changed to ingesting 2 whole peanuts twice daily. She has been receiving this treatment for more than a year. There has been one contact with a schoolmate eating a peanut butter sandwich without a reaction. She has eaten a granola bar that was later shown to contain peanut flour without reaction. This clinical tolerance has been accompanied by immunologic changes. Her peanut specific IgE level was more than 100 IU at baseline, 74 IU at 6 months, and 42 IU at 12 months. Oral desensitization is a well-established procedure for severe IgE-mediated reactions to drugs, commonly performed by allergy specialists. Most often this is done correctly in an intensive care unit or similar facility. The staff skills and equipment in our office are not required for most allergy practices. We strongly suggest that the oral desensitization procedure only be done where complete ability to treat anaphylaxis exists. We intend to continue daily peanut therapy in this child and monitor levels of specific IgE and IgG for 24 to 36 months. At that time we plan to evaluate whether this therapy needs to be continued. Our experience concerns severe peanut allergy and may not be generalizable to all IgE-mediated food reactions. Oral desensitization for IgE-mediated food allergy has been previously reported.3–9 Currently, oral food desensitization may be useful in patients such as this one, for whom the situation had become dysfunctional. The procedure needs to be performed carefully in an adequate facility and with full understanding by the parents of what the goals and limitations of the treatment are. Although other approaches are being evaluated for severe food allergic reactions, such as sublingual food immunotherapy and monoclonal anti-IgE, further study of oral desensitization for food allergy in selected situations seems worthwhile given the magnitude of this vexing clinical problem and the need for better treatments.

Fexofenadine hydrochloride, 180 mg, exhibits equivalent efficacy to cetirizine, 10 mg, with less drowsiness in patients with moderate-to-severe seasonal allergic rhinitis

BACKGROUND Previous studies have shown that fexofenadine and cetirizine effectively relieve symptoms of seasonal allergic rhinitis (SAR). OBJECTIVE To compare the effects of fexofenadine hydrochloride, 180 mg, and cetirizine, 10 mg, on symptoms, drowsiness, and motivation in patients with moderate-to-severe SAR. METHODS In this 2-week multicenter, double-blind, randomized study, 495 subjects with moderate-to-severe SAR received once-daily fexofenadine hydrochloride, 180 mg, or cetirizine, 10 mg, without regard to food intake. Daily 12-hour reflective (AM, PM) and instantaneous (AM) individual symptoms and total symptom score (TSS) were evaluated. Drowsiness and motivation were recorded daily using visual analog scale at 7 AM, 10 AM, and 3 PM. RESULTS Between-treatment differences in reduction from baseline in AM instantaneous and 24-hour reflective TSS were -0.18 [95% confidence interval (CI), -0.55 to 0.20) and -0.22 (95% CI, -0.59 to 0.15), respectively. Since CIs for reduction in TSS between treatments fell within a 0.7 margin (defined a priori), treatments were considered statistically equivalent. Patients receiving fexofenadine experienced significantly less overall drowsiness vs baseline than those receiving cetirizine [-2.33 (95% CI, -3.80 to 0.86) vs 0.37 (95% CI, -1.10 to 1.84), P = .0110]. There was a trend toward greater improvements in overall motivation with fexofenadine compared with cetirizine [-2.36 (95% CI, -3.83 to 0.90) vs -0.30 (95% CI, -1.76 to 1.17), P = .0504]. CONCLUSIONS Once-daily fexofenadine hydrochloride, 180 mg, given for 2 weeks caused statistically and clinically equivalent improvement in symptoms and significantly less drowsiness va baseline, compared with cetirizine, 10 mg, in patients with moderate-to-severe SAR.

Systemic reaction to papain in a nonoccupational setting

A patient experienced a severe systemic allergic reaction after ingesting meat tenderizer. Evaluation revealed that the reaction was mediated by IgE antibody to papain, an ingredient of the tenderizer. Papain hypersensitivity has been reported among pharmacists and factory workers exposed to the agent, but few nonoccupational cases have been described. The present case may be the first in which the sensitization appears to have occurred via the gastrointestinal route. Papain-containing products are commonly used throughout our society and papain hypersensitivity may represent an unrecognized cause of allergic symptoms.

Effects of Ascorbic Acid on Pulmonary Functions in Mild Asthma

Twenty subjects with mild asthma took a short course of moderately high doses of Vitamin C (500 mg four times daily for 3 days and 1 g prior to spirometric evaluation). There were no differences in pulmonary functions just prior to and after therapy. There were no adverse reactions noted. If, as reported, Vitamin C has a beneficial effect in asthma, it does not appear to be due to a bronchodilatory effect.

The role of antihistamine therapy in vascular headaches

Migraine (vascular) headache is a complex syndrome that involves vascular hyperreactivity. The functions of systemic mediators in migraine are not fully understood. It is unclear which mediators provoke this probably atopic disorder and which represent an attempt to correct an imbalance. However, it has been demonstrated fairly conclusively that increased histamine levels correlate with migraine attacks in susceptible persons. Recent studies showing that histamine seems to have many different receptors and to adopt different conformations for different receptors may serve as a useful guide to future scientific investigation. Further impetus may come from ongoing studies of H3 histamine receptors, which indicate that H3 agonists offer promise as prophylactic agents for people who suffer from vascular headaches.

Anaphylaxis Caused by the Sodium Succinate Ester of Hydrocortisone and Methylprednisolone

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Defense.

A comparative study of the effects of intranasal triamcinolone acetonide aerosol (ITAA) and prednisone on adrenocortical function

A comparison of adrenocortical function before and after treatment with either intranasal triamcinolone acetonide aerosol (ITAA), prednisone, or placebo was done. Sixty-two male subjects with allergic rhinitis were treated for 6 weeks with either ITAA (220 or 440 micrograms/day), oral prednisone (10 mg/day), or placebo in double-blind, parallel-group fashion. Adrenocortical function was assessed by 6-hour cosyntropin stimulation before and at the end of the treatment period. The placebo-treated and two ITAA-treated groups produced no changes in adrenocortical function with treatment, and the ITAA-treated groups were not different from the placebo-treated group with mean +/- SEM changes in stimulated plasma cortisol (micrograms per deciliter) as follows: placebo, -2.68 +/- 1.77; ITAA 220 micrograms, -2.69 +/- 1.18; ITAA 440 micrograms, -2.96 +/- 1.81. The prednisone-treated group had a mean reduction in adrenocortical function (mean +/- SEM change in stimulated plasma cortisol of -19.8 +/- 1.77 micrograms/dl) that was significant (p less than 0.0001) compared with that of the placebo-treated group. The results of this study indicate that 6 weeks of treatment with 220 micrograms/day or 440 micrograms/day of ITAA has no effect on adrenocortical function, but prednisone, at a dosage of 10 mg/day for 6 weeks, produces partial adrenocortical suppression.