Chest
Volume 121, Issue 4, April 2002, Pages 1231-1238
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Clinical Investigations
DRUGS
Evidence of Chronic Damage to the Pulmonary Microcirculation in Habitual Users of Alkaloidal (“Crack”) Cocaine

https://doi.org/10.1378/chest.121.4.1231Get rights and content

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.

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.

Section snippets

Subjects

A total of 36 subjects were evaluated (10 NS, 10 CS, 6 CTS, and 10 TS). All subjects were participants in an ongoing study evaluating the effects of habitual use of cocaine on the lung.23 Subjects were 23 to 50 years of age, with no known medical illnesses, and were selected for inclusion because they were either lifelong NS or habitual CS, TS, or CTS. Current cocaine use was verified by positive urine levels of cocaine metabolite. While most of the crack users had used marijuana in the past,

Subjects

Thirty-six subjects were studied (22 men and 14 women; mean age, 37.5 ± 7.5 years), including 10 NS, 10 CS, 6 CTS, and 10 TS. Subject characteristics are described in Table 1. Cocaine smokers (both CS and CTS) had a history of current or recent (within 6 months) smoking of alkaloidal cocaine on a regular basis for ≥ 8.1 years and an average of ≥ 1.0 g/wk during the past year. CS and CTS had last smoked cocaine between 1 h and 48 h before bronchoscopy, except for one CTS who had last smoked

Discussion

Diffuse alveolar hemorrhage associated with dyspnea and hemoptysis is believed to be a relatively common manifestation of cocaine abuse,3 although its occurrence has been underemphasized in the literature. Since the inception of the crack cocaine epidemic in the mid-1980s, several cases of acute pulmonary hemorrhage have been reported in temporal association with cocaine smoking.8,13,32,33 In some cases, diffuse alveolar hemorrhage has been associated with the acute crack lung syndrome,13 which

ACKNOWLEDGMENT

The authors thank Wendy Aft for manuscript preparation.

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