CASE REPORT
DOI 10.1111/J.1365-2133.2005.06340.X
Cannabis arteritis P. Combemale, T. Consort, L. Denis-Thelis, J-L. Estival, M. Dupin and J. Kanitakis* Department of Dermatology, Desgenettes Hospital, 108 Bd Pinel, 69003 Lyon, France *Department of Dermatology, Ed. Herriot Hospital, 5 Place d’Arsonval, 69003 Lyon, France
Summary Correspondence Patrick Combemale. E-mail:
[email protected]
Accepted for publication 5 August 2004
Key words: Buerger’s disease, cannabis, drug abuse, juvenile arteritis
Conflict of interest: None declared.
The main causes of arteriopathy in young patients include drugs, metabolic diseases, pseudoxanthoma elasticum and Buerger’s disease. Arteritis due to Cannabis indica was first reported in 1960, and the role of this drug as a risk factor for arteritis was confirmed in several subsequent publications. A 38-year-old smoker with no previous contributory medical history except for long-standing cannabis abuse developed a dry necrotic lesion of the left big toe. Imaging examinations revealed proximal arteriopathy of the lower limbs that predominated on the left side. He had no atherogenic or thrombogenic risk factors, and no signs of pseudoxanthoma elasticum were found. Remarkably, the development of arteritis paralleled cannabis abuse. The course was slowly favourable after weaning from the drug, vasodilator treatment and hyperbaric oxygen therapy. Despite some subtle clinical differences (more proximal than distal involvement), cannabis arteritis may be considered as a particular form of Buerger’s disease, where cannabis, along with tobacco, seems to cause arterial lesions. Along with the noxious effects of cannabis on vessels, a role for contaminating arsenic is also possible. Cannabis arteritis is not widely known, but may prove not to be so rare if one considers consumption of cannabis besides that of tobacco.
Juvenile arteritis (Buerger’s disease)1 is a well-known entity affecting young patients, and is caused by smoking. In 1960 the first cases of young cannabis abusers with arteritis were reported.2 These observations remained forgotten until 1999, when new similar cases were reported, and the triggering role of cannabis was reconsidered.3 We report a further case and review the relevant literature.
Case report A 38-year-old man consulted for a painful necrosis of the left big toe of some weeks’ duration. His past medical history was unremarkable: he did not have Raynaud’s syndrome or arterial hypertension, and had had no medical treatment. Notably, he had been smoking 20 cigarettes daily and three to five cannabis-containing cigarettes daily for over 20 years. He denied other drug intake (such as cocaine), as confirmed by toxicological analysis. Between June and November 2002 he had developed painful nodules of both legs that regressed within weeks but recurred regularly; a presumptive diagnosis of superficial migratory phlebitis was made. While incarcerated from November 2002 to May 2003 the patient continued tobacco (but not cannabis) smoking, and the development of nodules ceased. A fortnight before release from prison, he sustained traumatic injury on the left big toe; this seemed mild 166
and was neglected. After release the patient resumed cannabis abuse. Two weeks later his left big toe suddenly became bluish and extremely painful, and within days a necrotic lesion developed at the site of the wound. Because of the analgesic effect of cannabis he increased consumption up to eight cigarettes daily, but consulted because the necrotic lesion became extensive and the pain worsened, spreading to the whole foot. Examination revealed a dry necrotic lesion of the left big toe (Fig. 1). The left pedal and tibial pulses were not felt, and the right ones were very weak. Auscultation revealed a right femoral thrill. Peripheral pulses were felt on the upper limbs, but Allen’s manoeuvre was clearly positive with a delay of refilling of palmar arcades. No signs of local infection (cellulitis, purulent discharge or lymphadenopathy) were present. Examination was otherwise unremarkable: in particular, there were no signs of pseudoxanthoma elasticum (PXE). Doppler ultrasound examination showed arteriopathy predominating on the left leg, with disappearance of peroneal arteries; the left posterior tibial artery was atheromatous, partly calcified, narrowed and lacked pulsed flow. Lower limb arteriography showed proximal narrowing of the right iliac artery by 30% and the popliteal artery by 50%, occlusion of the left tibial– peroneal trunks, and 70% narrowing of the left anterior tibial artery at the level of the ankle. Neither corkscrew-like nor trapped popliteal arteries were observed (Fig. 2). Doppler
2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp166–169
