The purpose of this paper was to revisit the old concept of cannabis arteritis first described in the 1960s and report 10 new cases. Ten male patients, with a median age of 23.7 years developed subacute distal ischemia of lower or upper limbs, leading to necrosis in the toes and/or fingers and sometimes to distal limb gangrene. Two of the patients also presented with venous thrombosis and three patients were suffering from a recent Raynaud's phenomenon. Biological test results did not show evidence of the classical vascular risk factors for thrombosis. Arteriographic evaluation in all cases revealed distal abnormalities in the arteries of feet, legs, forearms, and hands resembling those of Buerger's disease. A collateral circulation sometimes with opacification of the vasa nervorum was noted. In some cases, arterial proximal atherosclerotic lesions and venous thrombosis were observed. All patients were moderate tobacco smokers and regular cannabis users. Despite treatment with ilomedine and heparin in all cases, five amputations were necessary in four patients. The vasoconstrictor effect of cannabis on the vascular system has been known for a long time. It has been shown that delta-8- and delta-9-tetrahydrocanabinols may induce peripheral vasoconstrictor activity. Cannabis arteritis resembles Buerger's disease, but patients were moderate tobacco smokers and regular cannabis users. These cases show that prolonged use of cannabis could be an additive risk factor for juvenile and young adult arteritis. Cannabis arteritis is a forgotten and severe occlusive vascular disease occurring in young adults. Search for cannabis use may be an important tool for a better knowledge of arteritis in young smokers.
Commercial preparations of essences of sage, hyssop, thuja, and cedar have caused human intoxication in eight cases, from which tonico-clonic convulsions were the major symptom. The experimental study of the toxic properties of commercialized essential oils of sage and hyssop has revealed that their convulsant action was of central nervous system origin in unanesthetized rats, as proven by electrocortical records. The toxicity of the hyssop oil seems to be more powerful than that of sage, since the dose limit from which the cortical events are only subclinical is 0.08 g/kg for hyssop oil and 0.3 g/kg for sage oil. Above 0.13 g/kg for hyssop oil and 0.50 g/kg for sage oil, the convulsions appeared and became lethal above 1.25 g/kg with hyssop oil and 3.2 g/kg with sage oil. The daily repeated injection of subclinical doses revealed the cumulative toxic effect of hyssop oil, since the same low dose induced electrocortical clonic seizures. The toxicity of each oil appeared to be related to the presence of terpenic ketones, camphor in sage commercial oil, camphor and thujone in sage Dalmatian oil, thujone in thuja and cedar oils, and pinocamphone in hyssop oil. The convulsant properties of camphor are well known. The neurotoxicity of thujone and pinocamphone is demonstrated in rats for the first time.
The incidence of chronic methyl bromide intoxication is low. The risk for chronic exposure or persistent toxic effects may be masked by the severity of the acute toxic effects. The development of peripheral neuropathy immediately after the central neurological signs was noted in our two subjects. A dying back axonopathy may explain this unique chronological evolution.
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