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Letters to the Editor |
Thoracic Surgery – Second University of Naples, Italy
Received 3 March 2008; accepted 19 June 2008.
* Corresponding author. Address: Chirurgia Toracica – Seconda Università di Napoli, Piazza Miraglia, 2, I-80138 Naples, Italy. Tel.: +39 0815665228; fax: +39 0815665230. (Email: mario.santini{at}unina2.it).
Key Words: Marijuana smoke Lung bullae Emphysema Pneumothorax
We read with great interest the article by Beshay and colleagues [1] on the incidence of emphysema and secondary pneumothorax in young adults smoking cannabis. The link between cannabis and lung bullae is quite definite [2–4]. Retrospectively, Beshay compared the findings of 17 marijuana and nicotine smokers (4 of these added a sporadic use of cocaine, one LSD over 3 years, and one sporadic heroin abuse) affected by spontaneous pneumothorax for bullous lung emphysema (group I) with the findings of non-marijuana smokers affected by spontaneous pneumothorax in the same (group II) and in a different period (group III). The authors showed that the presence of lung emphysema on computed tomographic scan in group I was significantly different to groups II and III while no significant difference in the form of clinical, laboratory, histopathological findings and postoperative course was found. In the last 5 years at our institution, we observed seven Caucasian young male marijuana smokers affected by emphysema and secondary pneumothorax. All patients had a tobacco smoke history (mean 6 pack years): five patients were current smokers of marijuana only (MS) and two current smokers of cocaine plus marijuana (CMS) over 4 years. In all patients
1-antitrypsin serum levels were normal (median 1.6 g/l). High resolution CT-scan showed that the emphysema was paraseptal in distribution and hence quite distinct from the more uniformly distributed bullae of centrilobular emphysema, typical changes associated with a lifetime of tobacco smoking. However CMS had multiple and larger emphysematous bullae with pleural thickening (size 12 cm) than MS affected by small bilateral bullae (size from 0.5 to 7 cm). Spirometric tests of CMS confirmed reduced FVC and FEV1 value with a reduced FEV1/FVC ratio suggesting mild airways obstruction in contrast to normal values of MS. All patients were treated by VATS for prevention of relapsing pneumothorax. Bullectomy specimen of MS illustrated minor accumulation of pigmented histiocytes (smoker's macrophages) than of CMS where we found a coarser brown to black pigment [4]. The postoperative course of MS was unremarkable while CMS had prolonged air leaks and in one case was performed pleurectomy by thoracotomy. In contrast to Beshay who showed no difference among all patients of group I, we noted several differences for clinical, radiological and histopathological evaluation and in the postoperative course of CMS compared to MS. These observations suggest that cocaine, when smoked together with marijuana, might aggravate marijuana-induced lung injury. Is it coincidence? Fligiel and colleagues reported that the effects of cocaine and marijuana on the airway appear not to be additive [5]. However the authors report histopathologic features of mucosal biopsy but do not include alveolar lung tissue and bullous disease. Probably noxious components that are a mixture of cocaine smoke plus components included in marijuana smoke might stimulate an amplified inflammation response with a dramatic increase of injurious effects on the alveolar lung. Finally in the light of this hypothesis, further studies are required to assess the effects of marijuana when smoked by itself and in conjunction with other illicit substance on lung parenchyma.
References
This article has been cited by other articles:
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R. A. Schmid and M. Beshay Reply to Fiorello et al. Eur. J. Cardiothorac. Surg., September 1, 2008; 34(3): 707 - 707. [Full Text] [PDF] |
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