An attempted prospective testing of an asthma severity index and a quality of life survey for 1 year in ambulatory patients with asthma.

It has been recommended that allergist-immunologists use quality of life (QOL) surveys to document their "added value" in patient care. There are little cross-sectional or prospective data regarding longer term follow-up of patients using QOL assessments and none associated with prospective use of an asthma severity index (ASI). Our objective was to identify clinical and psychological correlates of adverse asthma outcomes as assessed using the ASI survey. A 12 item QOL and a nine item ASI survey, spirometry, and history and physical were obtained from patients initially and then every 3 months for a year. The ASI was calculated as follows: one point for each emergency treatment of asthma if not in status asthmaticus, three points for each hospitalization for status asthmaticus, and six points for each intensive care admission or intubation. Patients were 56 adults between ages 18 and 45 with asthma enrolled between May 1994 and February 1996 with the intention to be reassessed quarterly for a year. At enrollment the 56 patients had ASI scores for the previous 12 months ranging from zero to 30. The patient with an ASI of 30 did not return after the initial visit. Of the 13 patients who completed the study, 12 patients had a zero ASI score over a 12-month period; one patient who had an initial score of 26 finished with a score of one. There were no deaths throughout the follow-up period. Of the 43 patients who did not complete the study only six (13.9%) cited local managed care or primary care physician as taking over their care. Initial ASI scores were dichotomized (zero versus greater-than-zero) due to skewness. The forced expiratory volume in one second (FEV1), % predicted FEV1 and peak flow were not related significantly to the dichotomized ASI score. The strongest univariate predictor was the self-assessment of asthma burden using a 78 mm visual analog scale. A two variable model included a query about bodily pain in the last 4 weeks and a self-assessment of general health. The dropout rate was high but only 13.9% of such patients reported that managed care or primary care physicians were responsible. A two variable model was a strong predictor of asthma severity. The single best predictor of asthma severity was a visual analog scale based on the question "How do you think your asthma is?"

Pathophysiology and therapy for allergic and nonallergic rhinitis: an updated review.

Symptoms from rhinitis can be assessed to be more troubling to the patient than symptoms from asthma. Further, the array of bioactive mediators, cytokines, and cells in nasal mucosa suggests that rhinitis is a much more complex condition than formerly thought. The presence of allergic rhinitis is a risk factor for emergence of asthma. Topical nasal corticosteroids have a relatively flat dose-response curve and have onset of action within 1 to 2 days for some patients. Allergen immunotherapy remains the only immunomodulator for patients with allergic rhinitis, with the possible exception of long-term administration of nasal corticosteroids.

Cost-effective management of malignant potentially fatal asthma.

Asthma mortality is rising and noncompliance may be a contributing factor to asthma deaths. We have established a comprehensive treatment program for our most severe asthmatic patients, who are also noncompliant. The objective was to evaluate the effect of a treatment protocol for patients with malignant potentially fatal asthma on both clinical outcome and inpatient costs. A retrospective chart review of eight patients diagnosed with malignant potentially fatal asthma was conducted. Patients were initially evaluated in consultation either at Northwestern Memorial Hospital or in the Allergy-Immunology Clinic at Northwestern Medical Faculty Foundation. The patients all met at least one of the criteria for potentially fatal asthma and each patient was noncompliant with medical care, as they did not follow their doctor's instructions, did not keep scheduled appointments, and/or did not take prescribed medications. A treatment program that included regularly schedule visits with the same attending physician and physician in training, patient and family education, 24-hour telephone access, adequate doses of anti-inflammatory medication and psychiatric referral, if indicated, was instituted. The number of admissions to the hospital including intensive care unit admissions and emergency room visits was tabulated, as was the total cost per year per patient for hospital treatment of asthma before and after starting the treatment program. The number of hospitalizations markedly declined, with three of the eight patients requiring no further admissions to the hospital and three additional patients not requiring admission for at least 4 years. There were no fatal events and no further intensive care unit admissions. The mean cost per person per year for in-patient care before intervention was $22,999 +/- $20,639 and the mean postintervention cost per patient per year was $1107 +/- $1618. This was a statistically significant cost savings (P < 0.0017). We developed a comprehensive treatment program that has enabled us to successfully and cost effectively treat patients with malignant potentially fatal asthma.

Asthma deaths confounded by substance abuse. An assessment of fatal asthma.

BACKGROUND: The Chicago region has been identified as having a very high death rate from asthma in patients aged 5 to 34 years. We investigated circumstances surrounding the fatal attack to determine whether the death was from asthma, of indeterminate cause, or coincidental to asthma. METHODS: Cases of asthma deaths from the Office of the Medical Examiner, where the deceased were younger than 46 years of age, were used to determine clinical, toxicologic, and pathologic findings relevant to asthma. Toxicologic results were compared with homicide victims. RESULTS: From 102 cases of fatal asthma, 46 cases were classified as deaths from asthma and 17 cases were considered probably from asthma as toxicologic tests were negative. Twenty-three cases were of indeterminate cause in that the acute respiratory symptoms were accompanied by substance use or alcohol consumption. Fourteen cases were not caused by asthma but were substance related, primarily cocaine. Overall, 29 of 92 (31.5%) cases were confounded by substance abuse or alcohol ingestion, which is almost as high as in homicide victims (38/82 [46.3%]). Mucus plugging of bronchi and or hyperinflation in fatal asthma occurred in 65 of 93 (69.9%) cases. Anti-inflammatory medications were being utilized by just two patients. Sufficient information was available to identify potentially fatal asthma in 6 of 20 cases (30%). CONCLUSION: Some of the reported rise in asthma deaths is a reflection of substance use or alcohol consumption similar to that seen in victims of homicide. In that patients with asthma are hypersensitive to alpha-adrenergic agonists, the use of cocaine may be especially dangerous and induce fatal ventricular dysrhythmias.

Peripheral blood eosinophilia, hyperimmunoglobulinemia A and fatigue: possible complications following rupture of silicone breast implants.

BACKGROUND: Silicone breast implantation has been considered quite safe and of major cosmetic value. Immunologic sequelae such as collagen vascular diseases have not been confirmed in large studies. OBJECTIVE: We describe a 55-year-old woman who developed severe fatigue, peripheral blood eosinophilia, and hyperimmunoglobulinemia A after rupture of a silicone breast implant during closed manual manipulation to lyse fibrotic tissue. METHODS: We charted evidence for eosinophilia over a 19-year period and determined quantitative immunoglobulins, and lymphocyte subsets by FACS analysis. RESULTS: Peripheral eosinophilia in 1976 was 693/mm3 and increased to 1360/mm3 after rupture of the implant in 1992. Serum immunoglobulin A was 332 mg/dL in 1976 and ranged after rupture from 473 to 627 mg/dL without other cause. Fatigue was not reversed with a parenteral corticosteroid injection. CD4 and CD8 subsets were normal but 40% of CD3 cells were Ia positive although not CD25 positive (IL2 receptor). Only 5% of B cells were CD19 CD23 positive despite the high concentration of serum IgA. CONCLUSION: This case is an example of a previously unreported apparent adverse effect of silicone-breast implant rupture with persisting eosinophilia, hyperimmunoglobulinemia A, and fatigue.

Immunologic effects of intranasal corticosteroids.

Intranasally administered corticosteroids have a wide margin of safety and are the mainstay of treatment for patients with moderate to severe allergic rhinitis, nonallergic rhinitis, and nasal polyposis. Long term use in recommended dosages has not caused nasal mucosal atrophy or hypothalamic-pituitary-adrenal (HPA) suppression. In practice, although fluticasone propionate and flunisolide appear to be twice as potent as beclomethasone dipropionate, there is little, if any, difference in therapeutic effectiveness (maximum achievable effect) among any of the currently available preparations. Intranasally administered corticosteroids can 1) inhibit the early and late (3-11 hour) responses following experimental allergen challenge, 2) reduce the number of eosinophils and basophils in nasal lavage samples, and 3) decrease the number of activated (CD4+ CD25+) lymphocytes and presence of bioactive mediators. The number of interleukin 4 (IL-4) reactive cells is decreased in the nasal submucosa, which is of importance in that IL-4 participates in IgE synthesis, T cell activation, and vascular cell adhesion molecule (VCAM) upregulation. The beneficial immunologic actions and nasal protective properties of intranasal corticosteroids have resulted in widespread use and reduction in patient rhinitic symptoms. Nevertheless, intranasal corticosteroids are not a substitute for environmental control, cessation of smoking, or determination whether allergen immunotherapy is indicated.

Minocycline-induced serum sickness.

Minocycline, a semisynthetic derivative of tetracycline, has become a commonly prescribed medication for the treatment of persistent acne. It has been associated with a variety of adverse reactions, including one published case of serum sickness. We describe two additional cases of serum sickness reactions due to minocycline, characterized by erythematous rash, arthropathy, and in one case, angioedema. Both patients recovered fully after treatment with an antihistamine in combination with a brief course of corticosteroids. Although these represent only the second and third cases in the literature of minocycline-induced serum sickness, it may be reported more frequently in the future with the increased use of minocycline.