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Biomedical subjects

Eric C Kleerup

Publications and source records attributed to Eric C Kleerup.

6 recordsLinked to original sources
PubMed2006

Small airways response to naturalistic cat allergen exposure in subjects with asthma.

BACKGROUND: It is currently unclear whether the small airways (diameter <2 microm) contribute significantly to late asthmatic reactions to inhaled allergen. OBJECTIVES: We sought to determine whether naturalistic exposure to cat allergen induced late responses in the small airways as measured by pulmonary function testing and high-resolution computed tomography (HRCT) of the chest performed at end-expiration. METHODS: In a group of 10 subjects with cat-induced asthma, physiologic studies (spirometry and lung volumes, including closing volume) and HRCT were performed before and 6 and 23 hours after a cat room challenge that caused a 20% or greater acute fall in FEV(1). RESULTS: There was no significant decline in FEV(1) at 6 or 23 hours after cat exposure. Forced expiratory flow at 25% to 75% of forced vital capacity was significantly decreased at 6 hours after the challenge and returned to normal by 23 hours. HRCT image analysis as well as closing volume demonstrated increased air trapping from baseline at both 6 and 23 hours after the challenge. In addition, image analysis demonstrated a significant increase in small airways hyperresponsiveness to methacholine at 23 hours after the challenge. No significant mean changes were noted in lung volumes at either 6 or 23 hours or in PC(20) FEV(1) at 23 hours postchallenge. CONCLUSION: These findings demonstrate that naturalistic exposure to cat allergen results in significant small airways obstruction and hyperresponsiveness persisting for at least 23 hours, at which time these changes cannot be detected by conventional physiologic measures. CLINICAL IMPLICATIONS: Physiologically silent distal lung inflammation persists after an antigenic challenge.

Adult↗
PubMed2004

Regional differences in bronchoalveolar lavage and thoracic high-resolution computed tomography results in dyspneic patients with systemic sclerosis.

OBJECTIVE: Interstitial lung disease (ILD) is the leading cause of death in systemic sclerosis (SSc). Although early identification and treatment of alveolitis may prevent deterioration of lung function, the best approach for diagnosing active alveolitis remains controversial. This study was undertaken to investigate the utility of high-resolution computed tomography (HRCT) of the chest, in comparison with bronchoalveolar lavage (BAL), in the diagnosis of alveolitis in these patients. METHODS: Eighteen patients with SSc and dyspnea were evaluated for ILD by pulmonary function testing and bronchoalveolar lavage (BAL), and 15 of these patients underwent chest HRCT. BAL was performed in either the middle lobe or the lingula, and also in a lower lung segment. Differential cell counts were determined by clinical cytopathology, with retrospective recounting in a blinded manner by a single technician. Active alveolitis was defined as the presence of > or =3.0% polymorphonuclear cells and/or > or =2% eosinophils in BAL fluid. BAL fluids were cultured for bacteria, mycobacteria, and fungi. HRCT scans were evaluated in a blinded manner for ground-glass opacification and fibrosis in the lavaged lobes. RESULTS: Nine of the 18 patients had active alveolitis recorded in both lavaged segments, while in 4 patients it was recorded in only 1 segment (lower lobe in 3). Following repeat differential cell counting, 3 patients were reclassified as having active alveolitis and 1 as having no alveolitis. Culture of BAL fluid identified clinically unsuspected infection in 3 patients. For the right middle lung lobe or lingula there was excellent agreement between ground-glass opacification and the finding of alveolitis on BAL from segments in the same lung regions, but this was not observed for the lower lobes. The correlation between fibrosis on HRCT and the presence of alveolitis on BAL was significant for the lower lobes but not the middle lung fields. CONCLUSION: BAL of the middle lobe or lingula may underestimate the presence of active alveolitis. Similarly, while ground-glass opacification on HRCT accurately predicted alveolitis in the middle lung fields, HRCT did not detect all sites of inflammation and did not identify infectious etiologies. These data suggest that, in addition to HRCT, BAL with lavage, differential cell counting, and culture from at least 2 segments of lung be performed for diagnosing SSc alveolitis.

Adult↗
PubMed2004

Exhaled nitric oxide in the assessment of asthma.

PURPOSE: Asthma is now defined as a TH2-mediated inflammatory disease involving both large and small airways. However, assessment of airways inflammation is limited by techniques that are time consuming and possibly distressing to the patient. Exhaled nitric oxide, an easily and rapidly obtained noninvasive study, is a potential surrogate for measuring airways inflammation, but its clinical utility remains to be determined. This review examines the role of exhaled nitric oxide in assessing and directing therapy of asthmatic airways inflammation. RECENT FINDINGS: It is well established that exhaled nitric oxide is increased in patients with untreated asthma and decreases with corticosteroid treatment. Exhaled nitric oxide also generally correlates with eosinophilic inflammation in asthmatic patients. Recent studies show that this correlation is especially pronounced in atopic subjects with asthma when compared with nonatopic subgroups. Recent studies also show that exhaled nitric oxide may be useful in identifying subclinical inflammation, assessing the antiinflammatory effects of asthma medications other than inhaled or oral corticosteroids, and heralding an asthma exacerbation. A number of new studies assert the utility of exhaled nitric oxide as a diagnostic tool for asthma. SUMMARY: Exhaled nitric oxide may be a useful parameter for monitoring asthmatic inflammation, adjusting therapy, and diagnosing asthma, although prospective longitudinal trials investigating the correlation between exhaled nitric oxide and clinical outcomes are necessary to determine its utility.

Animals↗
PubMed2002

Evidence of chronic damage to the pulmonary microcirculation in habitual users of alkaloidal ("crack") cocaine.

STUDY OBJECTIVE: To evaluate BAL cells obtained from habitual users of alkaloidal ("crack") cocaine alone or in combination with tobacco, for evidence of cocaine-associated alveolar injury. DESIGN: Prospective cohort study. PATIENTS: A total of 36 healthy men and women (mean age [SD], 37.5 [7.5] years), including 10 cocaine-only smokers (CS), 6 cocaine-plus-tobacco smokers (CTS), 10 tobacco smokers (TS), and 10 nonsmokers (NS), underwent fiberoptic bronchoscopy and BAL. METHODS: Cytospins were prepared from BAL cells and stained with Wright-Giemsa for cell differentials and Gomori's stain for detection of hemosiderin. Endothelin (ET)-1 levels were determined from lavage fluid by enzyme-linked immunosorbent assay. RESULTS: None of the cocaine users reported episodes of hemoptysis or respiratory distress, and routine spirometry findings were within normal limits in all subjects. While there was little effect on total cell numbers or differential counts, the percentages of hemosiderin-positive alveolar macrophages (AMs) were markedly increased in CS (33.8 +/- 8.7% [SEM]) compared to TS and NS (< 2%; p < 0.05). The percentages of hemosiderin-laden AMs were also numerically increased in CTS (11.8 +/- 7.8%), but this value was not statistically significant from that of TS or NS. ET-1 levels were significantly increased in the fluid recovered from CS (6.2 +/- 0.8 pg/mL) when compared to NS (1.2 +/- 0.4 pg/mL) and TS (1.3 +/- 0.2 pg/mL) [p < 0.05], while ET-1 levels were elevated to a lesser extent in CTS (2.5 +/- 0.6 pg/mL). ET-1 levels correlated with the percentage of hemosiderin-positive AMs when CS were analyzed in conjunction with CTS (r = 0.64; p = 0.0004). CONCLUSION: Clinically inapparent alveolar hemorrhage occurs frequently in otherwise healthy crack cocaine smokers and is associated with elevated levels of ET-1, indicative of cocaine-induced pulmonary microvascular injury.

Adult↗
PubMed2002

Chronic and acute effects of "crack" cocaine on diffusing capacity, membrane diffusion, and pulmonary capillary blood volume in the lung.

STUDY OBJECTIVES: To evaluate possible alterations in the diffusing capacity of the lung for carbon monoxide (DLCO) or its components, membrane diffusing capacity of the lung for carbon monoxide (DMCO) and pulmonary capillary blood volume (Vc), in habitual smokers of "crack" cocaine (with or without tobacco) and following the short-term administration of inhaled cocaine base or IV cocaine HCl. DESIGN: Cross-sectional and longitudinal evaluation of DLCO and its components in smokers of cocaine alone, tobacco alone, and cocaine plus tobacco, and in nonsmokers and ex-smokers. Measurement of possible acute effects on DLCO and its components after experimental short-term administration of IV and smoked cocaine. SETTING: University and Veterans Affairs hospital research laboratories. PARTICIPANTS: Convenience sample of habitual smokers of crack cocaine with or without tobacco and matched control nonsmokers and ex-smokers, and smokers of tobacco only. MEASUREMENTS: DLCO, DMCO, and Vc. CONCLUSIONS: Neither habitual cocaine smoking in cross-sectional or longitudinal analysis nor the short-term administration of inhaled alkaloidal cocaine significantly affected DLCO or its component parts. In contrast, a clear cross-sectional effect of regular tobacco smoking was demonstrated.

Adult↗