Recognizing Rheumatologic Aspects of Cocaine Abuse

Cocaine has been implicated in many rheumatologic conditions. Recognition of these syndromes is important for appropriate diagnosis and management because they often are confused and misdiagnosis results. The principal effects of cocaine are seen in the CNS and the corticomesolimbic dopamine reward pathway. Whether cocaine itself or in combination with host proteins is immunogenic and whether such a phenomenon has clinical relevance is unclear. Levamisole was recently found to contaminate up to 70% of cocaine samples; it has been postulated to cause various cutaneous lesions. Cocaine-induced midline destructive lesions have been associated with cocaine. Cocaine may have deleterious effects on the cardiovascular system. Management strategies include making the diagnosis, gaining knowledge of the disorders that cocaine can mimic, and testing for cocaine and levamisole contaminant. (J Musculoskel Med. 2012;29:34-40) Thirty million Americans have used cocaine, making the United States the world’s largest consumer of the substance; there are about 5 million current users.1 More than 70% of cocaine samples have been contaminated with levamisole, an immunomodulatory agent associated with multiple medical complications. Cocaine, especially contaminated cocaine, has been implicated in many rheumatologic conditions, such as cutaneous vasculitis, midline granulomatous lesions, cerebral vasculitis, and coronary aneurysms. Prompt recognition of these syndromes is important for appropriate diagnosis and management because they often are confused and misdiagnosis results. In this article, we describe these syndromes and provide clues that help with early diagnosis and appropriate management of cocaine-induced rheumatologic mimics. Background and History Cocaine is a tropane ester alkaloid found in the leaves of Erythroxylum coca, a bush that grows in the Andes Mountains in South America.2 Its stimulant properties have been known to mankind for more than 2000 years. Cocaine has remained a vital part of the religious beliefs of the Andean peoples of Peru, Bolivia, Ecuador, Colombia, and northern Argentina and Chile from the pre-Inca period through the present. Key events in the history of cocaine include the following: • In 1596, cocaine was first used for medicinal purposes by a Spanish physician. • In 1860, cocaine was isolated from the coca leaf by a German graduate student, Albert Niemann, who also is credited with coining the word “cocaine.” • In 1884, Freud first reported the major effects of cocaine as a stimulant against hunger and fatigue, its efficacy in high-altitude sickness, and its effects as a local anesthetic and hemostatic agent. • In 1914, the Harrison Narcotic Act designated cocaine as a prescription drug and placed it under Schedule II of the Controlled Substances Act. A Global Menace There are a reported 14 million cocaine users worldwide.1 In 2002 and 2003, more than 5.9 million persons (2.5%) aged 12 years or older admitted to using cocaine within the previous year. In the United States, cocaine use rates ranged from 1.6% in Idaho to 3.9% in Colorado. The annual consumption of cocaine worldwide is about 600 tons; the United States consumes about 300 tons. Mechanism of Action The principal effects of cocaine, a monoamine neurotransmitter reuptake inhibitor, are seen in the CNS (vasoconstriction, tachycardia, hypertension, arrhythmias, seizures, mydriasis, hyperglycemia, and hyperthermia) and the corticomesolimbic dopamine reward pathway (acute use of cocaine elevates dopamine levels and causes euphoria; long-term use causes dopamine depletion, leading to dysphoria and craving). Cocaine also blocks sodium-gated ion channels, causing cardiac arrhythmias