Thomas H. Kalb

Patterns of Asthma Death and Near-Death in an Inner-City Tertiary Care Teaching Hospital

Although the pathophysiology of asthma is increasingly understood, asthma deaths continue to increase, especially among non-Caucasians in inner-city urban areas including East Harlem, which has the highest mortality rate in the United States. The cause for this increase is uncertain, but several factors, including poor access to appropriate medical management, the overuse of beta agonists, environmental precipitants, or more severe disease, have been proposed as contributing factors. The Mount Sinai Hospital is a 1300-bed, tertiary care university hospital located at the juncture of East Harlem, an inner-city, predominantly Hispanic and African-American neighborhood, and Carnegie Hill, an affluent, predominantly Caucasian residential area. We examined asthma deaths (13) and near-deaths (20) at the Mount Sinai Hospital from 1986 to 1992 to determine risk factors and compared them to an age- and demographically matched control group. All of the information was based on retrospective patient chart reviews, and the parameters considered included ethnicity, insurance status, poverty level, and medications including the use of beta agonists. All of the asthma deaths and near-deaths except 1 occurred in low-income African-American and Hispanic patients (x = 16.9) However, steroid and beta-agonist usage were comparable in the adverse outcome group compared to the control group. Our results confirm that adverse outcome asthma in East Harlem occurred predominantly among non-Caucasians of low socioeconomic status. We conclude that ethnicity and socioeconomic status play an important role in asthma death and near-death at our institution.(ABSTRACT TRUNCATED AT 250 WORDS)

In vivo detection of a novel macrophage-derived protein involved in the regulation of nasal mucus-like glycoconjugate secretion

BACKGROUND We recently described a novel 68 kd mucus secretagogue (MMS-68) derived from human monocytes, pulmonary macrophages, and a macrophage hybridoma, clone 63. We detected MMS-68 in monocyte culture supernatants from patients with steroid-dependent asthma and in bronchoalveolar lavage fluid from patients with chronic bronchitis by antigen capture ELISA and in normal lung tissue by immunohistochemistry. METHODS To determine a role for MMS-68 in the regulation of nasal mucus, we labeled human nasal turbinates with tritiated glucosamine and assayed for the ability of the previously purified MMS-68 (stock solution) to induce mucus-like glycoconjugate release (MLGC). We also performed immunohistochemistry stains with an anti-MMS-68 antibody (1-D-10) on frozen sections (n = 5) of nasal turbinates from patients with allergic and nonallergic rhinitis who were undergoing rhinoplasty and measured MMS-68 levels in nasal lavages from patients who were undergoing topical nasal histamine or methacholine challenge. RESULTS MMS-68 is a potent nasal MLGC secretagogue causing a dose-dependent increase in MLGC release in vitro. Staining revealed a subepithelial distribution for MMS-68. Antigen capture ELISA of nasal lavages demonstrated mean MMS-68 levels from saline control challenge of 0.9 +/- 0.5 micrograms MMS-68 per milligram of protein (n = 5), 8.6 +/- 1.4 micrograms MMS-68 per milligram of protein from histamine challenge and 20.7 +/- 2.3 micrograms MMS-68 per milligram of protein (n = 5) after methacholine challenge. CONCLUSION Taken together these data suggest that MMS-68 may play a role in the normal regulation of mucus secretion.