 |
 |
|
Home |
Current Issue |
Past Issues |
In the Clinic |
ACP Journal Club |
CME |
Collections |
Audio/Video |
Mobile |
Subscribe |
Tools |
Help |
ACP Online
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 August 1993 | Volume 119 Issue 3 | Pages 226-235
Purpose: To discuss the forms of cocaine that are available and their methods of administration and to review the medical complications of cocaine abuse.
Data Sources: Pertinent articles were identified through a MEDLINE search of the English-language literature from 1986 to 1992 and through a manual search of bibliographies of all identified articles.
Study Selection: All articles describing complications of cocaine use were either case reports, review articles, or small series. No controlled studies on the subject were available.
Data Synthesis: A qualitative description of reported complications without the use of quantitative methods.
Results: Multiple complications of cocaine use have been described and are often related to the method of administration of cocaine. Since the introduction of freebase and "crack" cocaine, new complications have been noted, and nearly all organ systems have been affected. Indirect complications, related to violent behavior and infectious diseases, are also important consequences of cocaine use.
Conclusions: Adverse reactions to cocaine use should be considered in the differential diagnosis of various disorders, particularly ischemic events in young adults. The actual frequency of each complication is unknown.
REVIEW
Cocaine Abuse
In the last decade, cocaine use has increased dramatically, causing significant social, economic, and medical complications. As early as 1983, the medical community began to recognize the drastic escalation of hospitalizations due to cocaine abuse, starting in the Bahamas, at the approximate time that "crack" cocaine became available there [1]. Since then, the 1990 National Household Drug Survey found that 11% of Americans older than 12 years have used cocaine, and 7% of adults between 18 and 34 years old had used cocaine in the last year [2, 3] (Table 1). In a 1987 survey of primary-care practices, 35% of physicians saw at least one patient with cocaine-related problems in the month before the survey compared with 20% in 1982 [4]. Because of the increased frequency of cocaine use in our society, clinicians should learn to recognize the patterns of use and the potential risks associated with cocaine abuse.
|
This review examined English-language articles cited in MEDLINE from 1986 to 1992 as identified by the term cocaine and focused on toxicity, adverse effects, and poisoning. The bibliographies of all pertinent articles were also reviewed. This review presents an overview of the history of cocaine, the various forms of cocaine that are used today, the currently available tests for the diagnosis of cocaine use, and the medical complications associated with cocaine. The social and legal issues relating to cocaine use are not discussed here but have been reviewed elsewhere [5-7].
History
|
|---|
Chewing the coca leaf was the predominant mode of ingestion of cocaine until 1860, when the drug was isolated by Albert Niemann. The leaves have also been steeped into teas and incorporated into beverages, such as Coca Cola (which no longer contains cocaine.) In the United States, cocaine was once an ingredient in many patented medicines. In the late 1880s and 1890s, cocaine use became popular and many reports of addiction began to emerge, leading to the recognition of its potentially dangerous effects. The Harrison Narcotic Act of 1914, which was subsequently modified in 1922, prohibited the importation of cocaine and coca leaves, except for pharmaceutical purposes. The Controlled Substances Act of 1970 prohibits the manufacture, distribution, and possession of cocaine, except for limited medical purposes. The use of cocaine in the United States tapered in the 1920s, when amphetamines replaced cocaine as the most prevalent stimulant [8]. In the 1970s and 1980s, the development of "freebase" and "crack" cocaine revolutionized the use of the drug by providing a form that could be smoked.
Forms of Cocaine
|
|---|
Cocaine is found in all parts of the coca plant, comprising approximately 1% of the weight of the leaves. Chewing the leaves remains a frequent mode of administration in South America. Because of the limited gastrointestinal absorption of cocaine and because of the relatively low content of cocaine in coca leaves, the chewing of coca leaves does not produce the serious medical toxicity associated with purified forms of cocaine. The cocaine concentration in the leaves decreases with storage and is negligible within 6 months. To ensure more durable transportation, most cocaine is processed in South America into coca paste and then into cocaine hydrochloride (powder) before exportation.
Cocaine hydrochloride is a water-soluble powder and can be absorbed through the nasal mucosa or injected intravenously. It is often cut with adulterants, which may provide bulk (mannitol, lactose), or which imitate either its stimulant effects (caffeine) or its local anesthetic effect (procaine, lidocaine). Because of its high melting point, cocaine hydrochloride decomposes when burned; this form of cocaine is therefore not suitable for smoking.
Cocaine can be effectively smoked when it has been transformed into its alkaloid form, either "freebase" or "crack". The medical literature is often ambiguous when differentiating between freebase and crack cocaine. Freebase and crack are the same chemical form of cocaine but are made using different techniques. Freebase is made by dissolving cocaine hydrochloride in water, adding a base such as ammonia, and then a solvent such as ether. The cocaine base dissolves in the ether layer and can then be extracted by evaporation. By preparing freebase this way, many of the water-soluble adulterants may be removed. Because some of the highly volatile ether may remain after extraction, smokers of freebase cocaine are at risk for burns. With the increased availability of crack, freebase use has declined.
Crack cocaine is made by a simpler process. Cocaine hydrochloride is dissolved with water, mixed with baking soda, and heated. The cocaine base precipitates into a soft mass that becomes hard when dry [9]. The name "crack" is derived from the sound of cocaine crystals popping during preparation. Crack is typically sold premade, ready to smoke, without the danger of flammability. Crack and freebase melt at a much lower temperature (80 °C) compared with cocaine hydrochloride (180 °C). Experiments with human volunteers have shown that smoking cocaine can achieve blood levels comparable to those reached through intravenous injection [10]. Both crack and freebase cocaine can be smoked in pipes or mixed with marijuana or tobacco and smoked in a cigarette.
Coca paste, a crude extract of coca leaves mixed with water, kerosene, and sulfuric acid, is commonly smoked in South America. Sometimes called "bazooka," it is not widely used in the United States.
Physiologic Effects
|
|---|
The other major pharmacologic effect of cocaine is its local anesthetic action, which results from its ability to block the sodium channel in neuronal cells.
Pharmacokinetic Effects
The method of cocaine use affects its pharmacokinetics (Table 2 and Figure 1). Smoking cocaine provides the fastest route of entry into the cerebral circulation (approximately 6 to 8 seconds). When injected intravenously, the drug reaches the brain in approximately twice the time as when it is smoked, reflecting the longer transit time through the pulmonary and later the systemic circulation. Nasal insufflation (snorting) produces euphoria in 3 to 5 minutes, with peak cocaine levels achieved in 30 to 60 minutes [14]. The amount of cocaine that can be absorbed by the nasal mucosa is self-limited due the drug's concurrent vasoconstrictive properties. Estimates of the bioavailability of snorted cocaine range from 20% to 60% [14]. Much higher peak levels of cocaine can be achieved by smoking rather than snorting because smoking directs the drug into the vast pulmonary vascular bed, providing a larger surface area for absorption. The potency of a dose of cocaine that is smoked is equivalent to approximately 60% of the same dose given intravenously (that is, smoking 50 mg produces blood levels similar to those produced by an intravenous injection of 32 mg) [15].
|
|
Drug Testing
Testing for cocaine includes screening and confirmatory studies. The screening tests are designed to be relatively simple, rapid, and inexpensive and to have a high sensitivity rate. Confirmation tests may be more expensive and labor-intensive but are valuable because of their greater specificity [19]. Immunoassays are widely used for screening, with gas chromatography combined with mass spectroscopy being the main confirmatory procedure used in testing [20]. The combination of a screening immunoassay with a confirmatory gas chromatography and mass spectroscopy test is thought to be fully defensible in legal settings [21].
Because of the short half-life of cocaine, measurements of blood levels will only detect recent ingestion. Unlike ethanol, blood levels of cocaine do not predict toxicity [22]. In addition, cocaine undergoes continued hydrolysis in a test tube after the sample is drawn. Sodium fluoride can be added to the venipuncture tube to inhibit continued hydrolysis [16].
The duration of detection of urinary cocaine metabolites depends on two factors: the amount of cocaine absorbed or injected and the sensitivity of the drug assay used. Most assays for detecting cocaine abuse are designed to measure urinary benzoylecgonine levels. Thin-layer chromatography is an inexpensive method for detecting cocaine metabolites in urine specimens, but it is limited by its relatively poor sensitivity, requiring more than 1000 ng/mL of benzoylecgonine for detection. The enzyme-linked immunoassay technique is the most widely used mass screening test, with a threshold of 300 ng/mL for detection. Gas chromatography with mass spectroscopy is the "gold standard" for testing because it is the most sensitive and specific test for detection and because it can detect benzoylecgonine at concentrations of 1 to 10 ng/mL [17]. When used for drug abuse screening, it is recommended that positive test results be confirmed by gas chromatography with mass spectroscopy [22].
The sensitivity of cocaine detection depends on the cutoff level chosen to indicate a positive result. When lowering the cutoff for a positive immunoassay result from the conventional 300 ng/mL to 80 ng/mL and the gas chromatography plus mass spectroscopy limit from 100 ng/mL to 30 ng/mL, twice as many persons were found to have positive immunoassay results, all of which were confirmed by gas chromatography with mass spectroscopy [23]. Drano (S. C. Johnson, Racine, Wisconsin), bleach, and table salt, when added to urine specimens, have been found to cause false-negative results on immunoassays [24]. With the exception of prilocaine, compounds structurally or pharmacologically similar to cocaine and benzoylecgonine (including atropine and several local anesthetics) have not been found to cross-react with immunoassays for benzoylecgonine [25]. One study found a specificity of 100% using an enzyme-linked immunoassay for benzoylecgonine, testing 162 different drugs for cross-reactivity [26]. High proficiency can be achieved in commercial laboratories; one survey of 47 laboratories documented a 99.2% accuracy rate for testing cocaine metabolites in 376 specimens, with a sensitivity of 96% and a specificity of 100% [27].
The approximate time window for detection of cocaine metabolites is 1 to 2 days for the enzyme-linked immunoassay technique and 5 to 6 days for gas chromatography with mass spectroscopy [17]. The data on the yield of drug analysis are limited because most studies are done on persons after single, relatively low doses. With high-dose, long-term cocaine use, benzoylecgonine may be detected 10 to 22 days after cocaine use [28].
A new method of testing for cocaine use involves hair sampling [29]. Both cocaine and benzoylecgonine are deposited in the hair shaft. Using this method, one can estimate the duration and intensity of a person's cocaine use for the previous several months. Assuming an average hair growth of 0.5 inches in 30 days, samples can be taken for radioimmunoassay to determine whether cocaine or benzoylecgonine is present along the hair shaft at isolated times or in a steady pattern. The presence of benzoylecgonine in the hair shaft has been found to distinguish cocaine use from external contamination of hair with cocaine smoke [30]. Hair sampling does not give a precise measurement of the amount of cocaine used but provides a temporal pattern of its use.
Medical Complications Associated with Cocaine Use
|
|---|
|
Systemic Complications
Sudden Death
Cocaine use has been associated with sudden death, but the lethal doses and blood levels of persons dying suddenly have varied widely [33]. Several mechanisms may be responsible for sudden death, including arrhythmias, status epilepticus, centrally mediated respiratory arrest, and intracerebral hemorrhage. Sudden death may be preceded by an agitated delirium, hyperpyrexia, or generalized seizures [34]. Autopsy studies of victims of suspected cocaine-related sudden death must rely on the history and toxicology studies because no pathognomonic features of cocaine abuse exist [35].
Psychiatric
Cocaine addiction is a neurophysiologic process with prominent psychologic manifestations. Intoxication may produce psychological effects such as euphoria, poor judgment, psychomotor agitation, and physiologic effects such as tachycardia, hypertension, dilated pupils, nausea, and vomiting. High doses may also be associated with a transient psychosis, delirium, paranoid ideation, and bizarre behavior [36]. Tachyphylaxis to the euphoria produced by cocaine develops, requiring higher doses to achieve the same effect and leading to binges in which the user may readminister the drug repeatedly [7]. Binge use is thought to be a marker for "compulsive use" and cocaine addiction. Chronic users may exhibit symptoms suggestive of depression or an attention-deficit disorder [37].
Abstinence from cocaine has been divided into three phases, as described by Gawin and Kleber [12]. The "crash" is the immediate rebound effect after cessation of cocaine use, usually lasting a few hours. Dysphoria, cocaine craving, anxiety, depression, and profound exhaustion (leading to hypersomnolence) may follow. The hypersomnolence may last a few days and is often interrupted by periods of hyperphagia. The second phase is the "withdrawal" period, which is less dramatic than the crash. Psychological symptoms include anxiety, depression, anhedonia, with the major complication being suicide. Many users develop a "conditioned craving" in which the memories of cocaine smoking are so pleasurable that they tempt the user to resume drug use. Unlike withdrawal from other substances, no gross physiologic changes are associated with cessation of cocaine use [38]. The third phase, lasting months and possibly years, is called "extinction," in which bursts of craving may tempt persons to resume use.
Most persons who have used cocaine have not become addicted; it is not known why some persons become compulsive users [38].
Pulmonary
Most pulmonary complications resulting from cocaine use have been associated with smoking cocaine [39]. Users have found that having another person forcefully blow smoke into one's mouth augments the intensity of the drug's effect, probably by increasing the distribution of the cocaine in the pulmonary circulation. Mouth-to-mouth positive pressure by another person after smoking has been associated with barotrauma, including pneumothorax, pneumomediastinum, and pneumopericardium [40, 41].
Sporadic reports have described pulmonary edema associated with cocaine use [42, 43]. Many of these patients have resolution of the pulmonary edema without specific therapy [43]. The mechanism underlying the pulmonary edema is unclear, although transient left ventricular dysfunction or altered permeability in the pulmonary capillaries have been offered as possible causes. Chest radiographs of these persons have shown cardiac silhouettes of normal size [44]. No reports have given hemodynamic data for these patients with pulmonary edema. One patient underwent bronchoalveolar lavage and was found to have a protein level elevated to approximately four times the normal value, suggesting the possibility of altered capillary permeability [43].
An association has been described between asthma and smoking cocaine. Severe exacerbations of asthma in patients with long-term disease have been described [45, 46]. Inhaled or smoked cocaine may induce a nonspecific bronchial irritation. One study reported that one third of cocaine smokers noted wheezing during cocaine use [47].
Other findings associated with cocaine smoking include pulmonary hemorrhage [48, 49], the presence of alveolar macrophages laden with hemosiderin, bronchiolitis obliterans [50], and "crack lung" [51, 52]. "Crack lung" refers to the syndrome associated with chest pain, hemoptysis, and diffuse alveolar infiltrates. Whether this syndrome represents hypersensitivity to the cocaine itself or to an adulterant is unknown.
The long-term pulmonary effects of cocaine smoking have not been established. Pulmonary function tests have shown reductions in diffusing capacity of carbon monoxide in cocaine smokers [53], but definite abnormalities in spirometry have not been shown [42, 53]. Studies evaluating pulmonary dysfunction in cocaine users have been confounded by the inclusion of cigarette and marijuana smokers [54].
Cardiovascular
Cocaine use has been linked to heart disease. Many of the cardiac toxicities described with cocaine use can be related to the drug's physiologic effects. Cocaine can cause increased myocardial oxygen demand because of its association with tachycardia and hypertension, while also reducing coronary artery caliber and increasing coronary vascular resistance [55].
The first case report of myocardial infarction after cocaine use was published in 1982 [56]. Since then, more than 100 cases have been described. The average age for patients with myocardial infarction related to cocaine use is 31 years [57, 58], well below the usual age associated with coronary artery disease. Myocardial infarctions have been reported after smoking cocaine as well as after intravenous and intranasal use.
Angiographic studies in patients with cocaine-related myocardial infarctions show both diseased and normal coronary arteries [57, 59-63], with approximately one third of the patients having normal coronary arteries [55]. The mechanism for myocardial infarction in patients with normal coronary arteries is unknown. Theories include coronary vasospasm, enhanced platelet aggregation, and an increased myocardial oxygen demand due to the heightened sympathetic response after cocaine use. Unlike patients with Prinzmetal angina, those with cocaine-related myocardial infarction and normal coronary arteries have not developed vasospasm after intracoronary ergonovine injections [57, 61, 63]. Cold pressor testing failed to produce angina or electrocardiographic changes in patients with non-Q-wave myocardial infarctions [57]. Several angiographic studies have documented the narrowing of coronary arteries after intranasal administration of cocaine [64, 65].
An autopsy study of cocaine users found significant stenotic lesions in the coronary arteries, greater than that which would be expected in this fairly young population [66, 67]. Coronary angiograms from cocaine users with cardiac symptoms have shown atherosclerotic disease in about 60% of patients, despite their relatively young age [68]. Whether cocaine use actually triggers the atherosclerosis or simply acts as a marker to identify users with severe coronary artery disease is unknown. Animals fed a high-cholesterol diet along with repeated doses of cocaine have been shown to develop accelerated atherosclerosis [55].
The time course for myocardial ischemia associated with cocaine use varies. Some reports have described chest pain within minutes after cocaine use [62]; others have shown that the median time to the development of ischemic symptoms after cocaine use is 18 hours [59]. Nademanaee and colleagues [69] reported a high incidence of silent ischemia, as documented by ambulatory electrocardiographic monitors, in cocaine users during withdrawal. These electrocardiographic changes were most prominent during the first week after cessation of cocaine use. Only 1 of 20 patients with silent ischemia had an abnormal stress test result, suggesting the absence of fixed coronary disease.
In the last 10 years, the evaluation of chest pain related to cocaine use has become a significant management problem, particularly in emergency departments. Varying reports have described the incidence of myocardial infarctions associated with cocaine use. Considering the widespread use of cocaine, myocardial infarction is not a frequent event. Chest pain associated with cocaine use may not be the result of cardiac ischemia. Of 101 consecutive patients in Minnesota who were hospitalized with chest pain and a history of recent cocaine use, none proved to have a myocardial infarction. Forty percent of the patients had abnormal results of electrocardiograms, 32% of which were thought to be early repolarizations. None of these patients had elevations in the MB fraction of creatine kinase [70]. These authors warn against the use of thrombolytic agents in patients with chest pain associated with cocaine use, unless unequivocal evidence indicates myocardial injury. In a contrasting study from the Bronx, 31% of patients hospitalized with chest pains and a history of recent cocaine use were diagnosed with acute myocardial infarction [59]. The reason for the disparity in the frequency of myocardial infarction in these two studies is unclear.
Cocaine has been associated with various cardiac arrhythmias: accelerated ventricular rhythm [71], asystole [72], and ventricular fibrillation [73]. Cocaine use appears to be associated with cardiomyopathy [74, 75], myocarditis [76], and contraction band necrosis [77]. Because cocaine blocks reuptake of norepinephrine, cocaine users may have increased circulating norepinephrine. Elevated norepinephrine levels may cause myocardial damage similar to that seen with pheochromocytoma. Contraction band necrosis, a nonspecific finding related to "hypercontraction" and also seen with pheochromocytoma, has been reported in some autopsy studies of cocaine users. Some reports have described aortic rupture occurring after cocaine use [78].
Neurologic
Multiple acute and long-term neurologic complications have been reported with cocaine use [79], the most common being headaches. A telephone hotline for cocaine users showed that approximately two thirds of callers had intermittent headaches associated with cocaine use. Vascular headaches are most commonly reported; they may occur during cocaine use or during withdrawal [80, 81].
Seizures, both partial and generalized, have been reported with cocaine use. Cocaine is believed to lower the seizure threshold. Isolated seizures may be seen with cocaine use, or seizures may occur as a preterminal event. Most seizures occurring in cocaine users are associated with either smoking crack or with intravenous injection of cocaine. Nasal insufflation of cocaine is more likely to precipitate seizures in those patients with a previous history of a seizure disorder [82].
Strokes can be a devastating complication of cocaine use, particularly in young persons who have no other risk factors for cerebrovascular disease [83]. The use of cocaine hydrochloride is associated with hemorrhagic strokes [84]; many of these patients have underlying aneurysms or arteriovenous malformations. Cerebral infarctions are more common with crack than with cocaine hydrochloride [85, 86], possibly due to the higher serum concentrations obtained by smoking cocaine. High levels of cocaine may precipitate cerebral vasospasm. Most infarctions occur in the cerebral hemispheres, although brain stem and spinal cord infarctions have been reported [87]. Cocaine users who have dilated cardiomyopathies are at risk for embolic strokes.
Long-term, habitual cocaine users may develop cerebral atrophy, primarily in the frontal and temporal areas. Computed tomographic scans have shown a higher rate of cerebral atrophy in chronic compared with new cocaine users [88]. Neuropsychological testing in heavy cocaine users has shown mild impairment [89]. A few case reports have described cerebral vasculitis [90] in cocaine users; three such cases were confirmed histologically [91, 92].
Renal
Acute renal failure as a consequence of rhabdomyolysis is the most common renal complication of cocaine use. The patients often have no or relatively mild neuromuscular symptoms [93]. In one study, 24% of emergency department patients with complaints related to cocaine use were found to have rhabdomyolysis, as defined by elevations of creatine kinase levels to more than five times normal values [94]. In the largest series of cocaine-associated rhabdomyolysis, approximately one third of patients who had rhabdomyolysis developed acute renal failure, and one half of the patients with renal failure died [95]. The average creatine kinase level in that series of patients with rhabdomyolysis was 200 µkatal/L (12 000 U/L), and the value in those who developed renal failure was 467 µkatal/L (28 000 U/L). A low serum calcium level was predictive of more severe rhabdomyolysis. When associated with renal failure, rhabdomyolysis was sometimes accompanied by disseminated intravascular coagulation and elevated liver enzyme levels [95]. The mechanism of the rhabdomyolysis is unclear. It can be associated with hyperthermia and seizures [96]; however, many patients have neither been febrile nor had a seizure.
Gastrointestinal
Several intestinal disorders have been associated with cocaine use. Intestinal ischemia has been reported after oral, intravenous, and intranasal cocaine use [97-99]. Gastroduodenal perforations have been noted in young patients after using crack [100, 101]. A few cases of colitis have been reported in cocaine users. Colonoscopies have shown findings suggestive of pseudomembranous colitis or ischemic colitis [102, 103].
Persons wishing to smuggle or conceal cocaine may ingest packets of cocaine. If the wrapping of a packet deteriorates or is damaged, acute toxicity can result from exposure to large quantities of cocaine. The management of these "body packers" has been controversial; surgery and removal of the packets was initially thought to be the best treatment. More recently, conservative management has been recommended, reserving surgery only for those patients who developed obstruction or perforation [104].
Since 1967, it has been recognized that some cocaine and heroin users have abnormal liver enzyme levels; however, cocaine itself has not been determined to be a hepatotoxin. A mouse model of hepatic cocaine toxicity has been developed but whether this model applies to humans remains unclear. A small amount of cocaine is metabolized in the cytochrome p450 microsomal system to norcocaine, which is then transformed to N-hydroxynorcocaine. A byproduct of this chemical reaction may be nicotinamide-adenine dinucleotide phosphate depletion and depressed glutathione stores, which may also contribute to hepatotoxicity [105]. Of six cocaine users with abnormal liver enzyme levels and histologic findings, all also had elevated creatine kinase levels, myoglobinuria, or acute renal failure [106-108].
Endocrine
The adrenergic effects of cocaine use can mimic hyperthyroidism. Studies have shown a blunted thyroid-stimulating hormone response to thyroid-releasing hormone stimulation in chronic cocaine users [109]; however, routine thyroid function test results are normal in cocaine users [110]. Abnormalities of testosterone, cortisol, and luteinizing hormone have not been found in chronic cocaine users [111]. Dopamine, one of the neurotransmitters affected by cocaine use, inhibits prolactin secretion. Dopamine levels are increased during initial use of cocaine, resulting in decreased prolactin levels. During long-term use or withdrawal, dopamine levels become depleted, with resultant hyperprolactinemia [112].
Obstetric
The use of cocaine during pregnancy has been linked to an increased risk for placental abruption, lower infant weights, prematurity, and microcephaly [113] and possibly to congenital urologic abnormalities and neurobehavioral dysfunction [114]. Testing of infant hair by radioimmunoassay is more sensitive than testing of infant urine to determine fetal cocaine exposure [115].
Sexual Function
Long believed to have aphrodisiac properties, cocaine actually produces variable effects on sexual function. Reports of both enhanced and inhibited sexual function have been described with cocaine use [116]. Some cocaine users experience greater sexual arousal and prolonged stamina during intercourse while using cocaine [117]. Compulsive sexuality, defined by excessive preoccupation, loss of control, and continuation of sexual practices despite adverse effects, has been associated with cocaine use [118]. Sometimes referred to as "sexual addiction," compulsive sexuality may be related to the higher incidence of sexually transmitted diseases in cocaine users. As a form of barter, sexual activities may be performed in exchange for cocaine [119].
Erectile difficulties have also been associated with cocaine use. Perhaps the most commonly described effect on male sexual function is delayed or inhibited ejaculation. Small doses of cocaine may have a stimulant effect, whereas larger doses and long-term use cause sexual dysfunction. A few cases of priapism have been reported after cocaine use [120-122]. The route of administration may have some effect on sexual function; intravenous users commonly have the most negative sexual experiences [123].
Head and Neck
Oral complications of cocaine use include erosions of the dental enamel [124] and gingival ulceration at the site of application of oral cocaine [125]. Ocular complications reported with cocaine use include keratitis [126] and corneal epithelial defects [127]. Otolaryngologic complications include chronic rhinitis, a rhinitis similar to rhinitis medicamentosa, perforated nasal septum, aspiration of the nasal septum [128], midline granuloma [129], altered olfaction [130], optic neuropathy, and osteolytic sinusitis [131].
Indirect Complications
Infectious
In addition to the direct toxicity associated with cocaine, some infectious diseases are increased in cocaine users, due in part to the setting in which cocaine is used. Because of increased sexual activity, cocaine users may be at an increased risk for sexually transmitted diseases, such as the acquired immunodeficiency syndrome, gonorrhea, and syphilis [132]. The practice of exchanging drugs for sex with a prostitute or having sex in a "crack house" is associated with an increased risk for syphilis [133]. Serologic testing in Philadelphia found that 27% of clients at a crack house had positive rapid plasma reagin test results [134]. Pregnant women who tested positive for cocaine at the time of delivery were more likely to have positive rapid plasma reagin test results (18.7% compared with 2.4%) and to test positive for antibodies to human immunodeficiency virus (HIV) (7.6% compared with 1.4%) [135]. Intravenous use of cocaine has been associated with HIV transmission [136].
Because crack is often smoked in crowded, poorly ventilated rooms, the potential for transmission of respiratory infections exists. One report described a tuberculosis epidemic associated with a crack house in California [137].
Homicides
Cocaine use has been associated with violent behavior. The most common forms of death associated with cocaine use are homicide, suicide, or accidental causes. In 1989, 40% of homicide victims in Fulton County, Georgia tested positive for cocaine metabolites in their blood [138]. Firearm-related homicides are more common in persons testing positive for cocaine metabolites at autopsy [138, 139]. In 1985, 21% of suicide victims younger than 60 years in New York City tested positive for cocaine at autopsy [140].
Treatment
|
|---|
Frequent urine testing is important to confirm abstinence. Under investigation is the role of pharmacotherapy to relieve the symptoms of cocaine withdrawal and to prevent relapse. A controlled study of desipramine has shown less cocaine use and craving in the early withdrawal period [144], but long-term relapse prevention has not been documented. Other drugs, such as bromocriptine and amantadine, have been studied and have produced variable results. Practical measures to remove access to cocaine may help to prevent early relapse. Long-term relapse prevention involves training to ignore "conditioned cues" and to avoid situations in which cocaine is used. An individual's personal resources correlate with rates of abstinence [141]. Unlike the treatment for alcohol or opiate dependence, no equivalent of disulfiram or naltrexone exists to deter relapse. Cocaine Anonymous, a 12-step support group modeled after Alcoholics Anonymous, has been established for cocaine users.
Conclusions
|
|---|
Author and Article Information
|
|---|
 Top Author & Article Info References |
|---|
References
|
|---|
|
TopAuthor & Article InfoReferences |
|---|
1. Jekel JF, Allen DF, Podlewski H, Clarke N, Dean-Patterson S, Cartwright P. Epidemic free-base cocaine abuse. Case study from the Bahamas. Lancet. 1986; 1:459-62.
2. National Institute on Drug Abuse. National Household Survey on Drug Abuse: Main Findings 1990. Washington, DC: U.S. Department of Health and Human Services. DHHS publication no. (ADM)91-1788; 1991.
3. National Institute on Drug Abuse. National Household Survey on Drug Abuse: Population Estimates 1990. Washington, DC: U.S. Department of Health and Human Services. Publication no. (ADM)91-1732; 1991.
4. Weinstein SP, Gottheil E, Sterling RC. Cocaine users in medical practice: a five-year follow-up. Am J Drug Alcohol Abuse. 1992; 18:157-66.
5. Schober S, Schade C; eds. The Epidemiology of Cocaine Use and Abuse. NIDA Research Monograph. 1991; 110:DHHS publication no. 91-1787.
6. Johnson BD, Williams T, Sanabria H, Dei K. Social impact of crack dealing in the inner city. In: Harris LS; ed. Problems of Drug Dependence, 1989. Washington, DC: U.S. Department of Health and Human Services. 1990; 95:326-7. DHHS Publication no. (ADM)90-1663.
7. Schroeder EP. Legal aspects of urine screening. In: Harris LS; ed. Problems of Drug Dependence, 1989. Washington, DC: U.S. Department of Health and Human Services. 1990; 95:218-24.
8. Kennedy J. Coca Exotica: The Illustrated Story of Cocaine. Rutherford, New Jersey: Fairleigh Dickinson University Press; 1985.
9. Smart RG. Crack cocaine use: a review of prevalence and adverse effects. Am J Drug Alcohol Abuse. 1991; 17:13-26.
10. Cook CE, Jeffcoat AR. Pyrolytic degradation of heroin, phencyclidine, and cocaine: identification of products and some observations on their metabolism. NIDA Res Monogr. 1990; 99:97-120.
11. Lathers CM, Tyau LS, Spino MM, Agarwal I. Cocaine-induced seizures, arrhythmias and sudden death. J Clin Pharmacol. 1988; 28:584-93.
12. Gawin FH, Ellingwood EH Jr. Cocaine and other stimulants. Actions, abuse, and treatment. N Engl J Med. 1988; 318:1173-82.
13. Jones RT. The pharmacology of cocaine smoking in humans. NIDA Res Monogr. 1990; 99:30-41.
14. Jatlow PI. Drug of abuse profile: cocaine. Clin Chem. 1987; 33(11 Suppl):66B-71B.
15. Foltin RW, Fischman MW. Self-administration of cocaine by humans: choice between smoked and intravenous cocaine. J Pharmacol Exp Ther. 1992; 261:841-9.
16. Karch SB. Introduction to the forensic pathology of cocaine. Am J Forensic Med Pathol. 1991; 12:126-31.
17. Verebey K. Cocaine abuse detection by laboratory methods. In: Washton AM, Gold MS. Cocaine: A Clinician's Handbook. New York: Guilford Press; 1987:214-28.
18. Hoffman RS, Henry GC, Howland MA, Weisman RS, Weil L, Goldfrank LR. Association between life-threatening cocaine toxicity and plasma cholinesterase activity. Ann Emerg Med. 1992; 21: 247-53.
19. Scientific issues in drug testing. Council on Scientific Affairs. JAMA. 1987; 257:3110-4.
20. Saxon AJ, Calsyn DA, Haver VM, Delaney CJ. Clinical evaluation and use of urine screening for drug abuse. West J Med. 1988; 149: 296-303.
21. Hoyt DW, Finnigan RE, Nee T, Shults TF, Butler TJ. Drug testing in the workplace—are methods legally defensible? A survey of experts, arbitrators, and testing laboratories. JAMA. 1987; 258: 504-9.
22. Jatlow P. Cocaine: analysis, pharmacokinetics, and metabolic disposition. Yale J Biol Med. 1988; 61:105-13.
23. Soldin SJ, Morales AJ, D'Angelo LJ, Bogema SC, Hicks JM. The importance of lowering the cut-off concentration for urine screening and confirmatory tests for benzoylecgonine/cocaine. Clin Chem. 1991; 37:993.
24. Mikkelsen SL, Ash KO. Adulterants causing false negatives in illicit drug testing. Clin Chem. 1988; 34:2333-6.
25. Baselt RC, Baselt DR. Little cross reactivity of local anesthetics with abuscreen, EMIT d.a.u., and TDX immunoassays for cocaine metabolite (Letter). Clin Chem. 1987; 33:747.
26. Allen LV Jr, Stiles ML. Specificity of the EMIT drug abuse urine assay methods. Clin Toxicol. 1981; 18:1043-65.[Medline]
27. Frings CS, White RM, Battaglia DJ. Status of drugs-of-abuse testing in urine: an AACC study. Clin Chem. 1987; 33:1683-6.
28. Weiss RD, Gawin FH. Protracted elimination of cocaine metabolites in long-term high-dose cocaine abusers. Am J Med. 1988; 85: 879-80.
29. Mieczkowski T, Barzelay D, Gropper B, Wish E. Concordance of three measures of cocaine use in an arrestee population: hair, urine, and self-report. J Psychoactive Drugs. 1991; 23:241-9.
30. Koren G, Klein J, Forman R, Graham K. Hair analysis of cocaine: differentiation between systemic exposure and external contamination. J Clin Pharmacol. 1992; 32:671-5.
31. Rubin RB, Neugarten J. Medical complications of cocaine: changes in pattern of use and spectrum of complications. J Toxicol Clin Toxicol. 1992; 30:1-12.
32. Derlet RW, Albertson TE. Emergency department presentation of cocaine intoxication. Ann Emerg Med. 1989; 18:182-6.
33. Wetli CV, Wright RK. Death caused by recreational cocaine use. JAMA. 1979; 241:2519-22.
34. Mittleman RE, Wetli CV. Death caused by recreational cocaine use. An update. JAMA. 1984; 252:1889-93.
35. Karch SB, Stephens BS. When is cocaine the cause of death? (Editorial) Am J Forensic Med Pathol. 1991; 12:1-2.
36. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Third edition, revised. Washington, DC: American Psychiatric Association; 1987.
37. Gawin FH, Kleber HD. Abstinence symptomatology and psychiatric diagnosis in cocaine abusers. Clinical observations. Arch Gen Psychiatry. 1986; 43:107-13.
38. Gawin FH. Cocaine addiction: psychology and neurophysiology. Science. 1991; 1580-5.
39. Ettinger NA, Albin RJ. A review of the respiratory effects of smoking cocaine. Am J Med. 1989; 87:664-8.
40. Shesser R, Davis C, Edelstein S. Pneumomediastinum and pneumothorax after inhaling alkaloidal cocaine. Ann Emerg Med. 1981; 10: 213-5.
41. Adrouny A, Magnusson P. Pneumopericardium from cocaine inhalation (Letter). N Engl J Med. 1985; 313:48-9.
42. Allred RJ, Ewer S. Fatal pulmonary edema following intravenous "freebase" cocaine use. Ann Emerg Med. 1981; 10:441-2.
43. Cucco RA, Yoo OH, Cregler L, Chang JC. Nonfatal pulmonary edema after "freebase" cocaine smoking. Am Rev Respir Dis. 1987; 136:179-81.
44. Hoffman CK, Goodman PC. Pulmonary edema in cocaine smokers. Radiology. 1989; 172:463-5.
45. Rebhun J. Association of asthma and freebase smoking. Ann Allergy. 1988; 60:339-42.
46. Rubin RB, Neugarten J. Cocaine-associated asthma. Am J Med. 1990; 88:438-9.
47. Suhl J, Gorelick DA. Pulmonary function in male freebase cocaine smokers (Abstract). Am Rev Respir Dis. 1988; 137:488.
48. Murray RF, Albin RJ, Mergner W, Criner GJ. Diffuse alveolar hemorrhage temporarlly related to cocaine smoking. Chest. 1988; 93:427-9.
49. Godwin JE, Harley RA, Miller KS, Heffner JE. Cocaine, pulmonary hemorrhage, and hemoptysis (Letter). Ann Intern Med. 1989; 110:843.
50. Patel RC, Dutta D, Schonfeld SA. Free-base cocaine use associated with bronchiolitis obliterans organizing pneumonia. Ann Intern Med. 1987; 107:186-7.
51. Kissner DG, Lawrence WD, Selis JE, Flint A. Crack lung: pulmonary disease caused by cocaine abuse. Am Rev Respir Dis. 1987; 136:1250-2.
52. Forrester JM, Steele AW, Waldron JA, Parsons PE. Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. Am Rev Respir Dis. 1990; 142:462-7.
53. Itkonen J, Schnoll S, Glassroth J. Pulmonary dysfunction in "freebase" cocaine users. Arch Intern Med. 1984; 144:2195-7.
54. Tashkin DP, Simmons MS, Coulson AH, Clark VA, Gong H Jr. Respiratory effects of cocaine "freebasing" among habitual users of marijuana with or without tobacco. Chest. 1987; 92:638-44.
55. Kloner RA, Hale S, Alker K, Rezkalla S. The effects of acute and chronic cocaine use on the heart. Circulation. 1992; 85:407-19.
56. Coleman DL, Ross TF, Naughton JL. Myocardial ischemia and infarction related to recreational cocaine use. West J Med. 1982; 136:444-6.
57. Kossowsky WA, Lyon AF, Chou SY. Acute non-Q wave cocaine-related myocardial infarction. Chest. 1989; 96:617-21.
58. Pasternack PF, Colvin SB, Baumann FG. Cocaine-induced angina pectoris and acute myocardial infarction in patients younger than 40 years. Am J Cardiol. 1985; 55:847.
59. Amin M, Gabelman G, Karpel J, Buttrick P. Acute myocardial infarction and chest pain syndromes after cocaine use. Am J Cardiol. 1990; 66:1434-7.
60. Rod JL, Zucker RP. Acute myocardial infarction shortly after cocaine inhalation. Am J Cardiol. 1987; 59:161.
61. Zimmerman FH, Gustafson GM, Kemp HG Jr. Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. J Am Coll Cardiol. 1987; 9:964-8.
62. Smith HW 3d, Liberman HA, Brody SL, Battey LL, Donohue BC, Morris DC. Acute myocardial infarction temporally related to cocaine use. Clinical, angiographic, and pathophysiologic observations. Ann Intern Med. 1987; 107:13-8.
63. Cregler LL, Mark H. Relation of acute myocardial infarction to cocaine abuse. Am J Cardiol. 1985; 56:794.
64. Lange RA, Cigarroa RG, Yancy CW Jr, Willard JE, Popma JJ, Sills MN, et al. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med. 1989; 321:1557-62.
65. Flores ED, Lange RA, Cigarroa RG, Hillis LD. Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenoses. J Am Coll Cardiol. 1990; 16:74-9.
66. Dressler FA, Malekzadeh S, Roberts WC. Quantitative analysis of amounts of coronary arterial narrowing in cocaine addicts. Am J Cardiol. 1990; 65:303-8.
67. Simpson RW, Edwards WD. Pathogenesis of cocaine-induced ischemic heart disease. Autopsy findings in a 21-year-old man. Arch Pathol Lab Med. 1986; 110:479-84.
68. Om A, Warner M, Sabri N, Cecich L, Vetrovec G. Frequency of coronary artery disease and left ventricle dysfunction in cocaine users. Am J Cardiol. 1992; 69:1549-52.
69. Nademanee K, Gorelick DA, Josephson MA, Ryan MA, Wilkins JN, Robertson HA, et al. Myocardial ischemia during cocaine withdrawal. Ann Intern Med. 1989; 111:876-80.
70. Gitter MJ, Goldsmith SR, Dunbar DN, Sharkey SW. Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction. Ann Intern Med. 1991; 115:277-82.
71. Benchimol A, Bartall H, Desser KB. Accelerated ventricular rhythm and cocaine abuse. Ann Intern Med. 1978; 88:519-20.
72. Nanji AA, Filipenko JD. Asystole and ventricular fibrillation associated with cocaine intoxication. Chest. 1984; 85:132-3.
73. Isner JM, Estes NA 3d, Thompson PD, Costanzo-Nordin MR, Subramanian R, Miller G, et al. Acute cardiac events temporally related to cocaine abuse. N Engl J Med. 1986; 315:1438-43.
74. Chokshi SK, Moore R, Pandian NG, Isner JM. Reversible cardiomyopathy associated with cocaine intoxication. Ann Intern Med. 1989; 111:1039-40.
75. Wiener RS, Lockhart JT, Schwartz RG. Dilated cardiomyopathy and cocaine abuse. Report of two cases. Am J Med. 1986; 81:699-701.
76. Virmani R, Robinowitz M, Smialek JE, Smyth DF. Cardiovascular effects of cocaine: an autopsy study of 40 patients. Am Heart J. 1988; 115:1068-76.
77. Peng SK, French WJ, Pelikan PC. Direct cocaine cardiotoxicity demonstrated by endomyocardial biopsy. Arch Pathol Lab Med. 1989; 113:842-5.
78. Barth CW 3d, Bray M, Roberts WC. Rupture of the ascending aorta during cocaine intoxication. Am J Cardiol. 1986; 57:496.
79. Lowenstein DH, Massa SM, Rowbotham MC, Collins SD, McKinney HE, Simon RP. Acute neurologic and psychiatric complications associated with cocaine abuse. Am J Med. 1987; 83:841-6.
80. Satel SL, Gawin FH. Migrainelike headache and cocaine use. JAMA. 1989; 261:2995-6.
81. Dhuna A, Pascual-Leone A, Belgrade M. Cocaine-related vascular headaches. J Neurol Neurosurg Psychiatry. 1991; 54:803-6.
82. Pascual-Leone A, Dhuna A, Altafullah I, Anderson DC. Cocaine-induced seizures. Neurology. 1990; 40:404-7.
83. Levine SR, Washington JM, Jefferson MF, Kieran SN, Moen M, Feit H, et al "Crack" cocaine-associated stroke. Neurology. 1987; 37:1849-53.
84. Lichtenfeld PJ, Rubin DB, Feldman RS. Subarachnoid hemorrhage precipitated by cocaine snorting. Arch Neurol. 1984; 41:223-4.
85. Levine SR, Brust JC, Futrell N, Brass LM, Blake D, Fayad P, et al. A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride—a review. Neurology. 1991; 41:1173-7.
86. Levine SR, Brust JC, Futrell N, Ho KL, Blake D, Millikan CH, et al. Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine. N Engl J Med. 1990; 323:699-704.
87. Mody CK, Miller BL, McIntyre HB, Cobb SK, Goldberg MA. Neurologic complications of cocaine abuse. Neurology. 1988; 38: 1189-93.
88. Pascual-Leone A, Dhuna A, Anderson DC. Cerebral atrophy in habitual cocaine abusers: a planimetric CT study. Neurology. 1991; 41:34-8.
89. O'Malley S, Adamse M, Heaton RK, Gawin FH. Neuropsychological impairment in chronic cocaine abusers. Am J Drug Alcohol Abuse. 1992; 18:131-44.
90. Kaye BR, Fainstat M. Cerebral vasculitis associated with cocaine abuse. JAMA. 1987; 258:2104-6.
91. Krendel DA, Ditter SM, Frankel MR, Ross WK. Biopsy-proven cerebral vasculitis associated with cocaine abuse. Neurology. 1990; 40:1092-4.
92. Fredericks RK, Lefkowitz DS, Challa VR, Troost BT. Cerebral vasculitis associated with cocaine abuse. Stroke. 1991; 22:1437-9.
93. Herzlich BC, Arsura EL, Pagala M, Grob D. Rhabdomyolysis related to cocaine abuse. Ann Intern Med. 1988; 109:335-6.
94. Welch RD, Todd K, Krause GS. Incidence of cocaine-associated rhabdomyolysis. Ann Emerg Med. 1991; 20:154-7.
95. Roth D, Alarcon FJ, Fernandez JA, Preston RA, Bourgoignie JJ. Acute rhabdomyolysis associated with cocaine intoxication. N Engl J Med. 1988; 319:673-7.
96. Merigian KS, Roberts JR. Cocaine intoxication: hyperpyrexia, rhabdomyolysis and acute renal failure. Clin Toxicol Clin Toxicol. 1987; 25:135-48.
97. Nalbandian H, Sheth N, Dietrich R, Georgiou J. Intestinal ischemia caused by cocaine ingestion: report of two cases. Surgery. 1985; 97:374-6.
98. Freudenberger RS, Cappell MS, Hutt DA. Intestinal infarction after intravenous cocaine administration. Ann Intern Med. 1990; 113: 715-6.
99. Mizrahi S, Laor D, Stamler B. Intestinal ischemia induced by cocaine abuse (Letter). Arch Surg. 1988; 123:394.
100. Lee HS, LaMaute HR, Pizzi WF, Picard DL, Luks FI. Acute gastroduodenal perforations associated with use of crack. Ann Surg. 1990; 211:15-7.
101. Abramson DL, Kral JG, Gertler JP, Lewis T. Gastropyloric ulcers related to "crack" (Letter). JAMA. 1989; 262:617-8.
102. Fishel R, Hamamoto G, Barbul A, Jiji V, Efron G. Cocaine colitis. Is this a new syndrome? Dis Colon Rectum. 1985; 28:264-6.
103. Yang RD, Han MW, McCarthy JH. Ischemic colitis in a crack abuser. Dig Dis Sci. 1991; 36:238-40.
104. Caruana DS, Weinbach B, Goerg D, Gardner LB. Cocaine-packet ingestion. Diagnosis, management, and natural history. Ann Intern Med. 1984; 100:73-4.
105. Kloss MW, Rosen GM, Rauckman EJ. Cocaine-mediated hepatotoxicity. A critical review. Biochem Pharmacol. 1984; 33:169-73.
106. Perino LE, Warren GH, Levine JS. Cocaine-induced hepatotoxicity in humans. Gastroenterology. 1987; 93:176-80.
107. Wanless IR, Dore S, Gopinath N, Tan J, Cameron R, Heathcote EJ, et al. Histopathology of cocaine hepatotoxicity. Report of four patients. Gastroenterology. 1990; 98:497-501.
108. Kanel GC, Cassidy W, Shuster L, Reynolds TB. Cocaine-induced liver cell injury: comparison of morphological features in man and in experimental models. Hepatology. 1990; 11:646-51.
109. Dackis CA, Estroff TW, Sweeney DR, Pottash AL, Gold MS. Specificity of the TRH test for major depression in patients with serious cocaine abuse. Am J Psychiatry. 1985; 142:1097-9.
110. Dhopesh VP, Burke WM, Maany I, Ravi NV. Effect of cocaine on thyroid functions. Am J Drug Alcohol Abuse. 1991; 17:423-7.
111. Mendelson JH, Teoh SK, Lange U, Mello NK, Weiss R, Skupny A, et al. Anterior pituitary, adrenal, and gonadal hormones during cocaine withdrawal. Am J Psychiatry. 1988; 145:1094-8.
112. Mendelson JH, Mello NK, Teoh SK, Ellingboe J, Cochin J. Cocaine effects on pulsatile secretion of anterior pituitary, gonadal, and adrenal hormones. J Clin Endocrinol Metab. 1989; 69:1256-60.
113. Volpe JJ. Effect of cocaine use on the fetus. N Engl J Med. 1992; 327:399-407.
114. Slutsker L. Risks associated with cocaine use during pregnancy. Obstet Gynecol. 1992; 79:778-89.
115. Callahan CM, Grant TM, Phipps P, Clark G, Novack AH, Streissguth AP, et al. Measurement of gestational cocaine exposure: sensitivity of infants' hair, meconium, and urine. J Pediatr. 1992; 120:763-8.
116. Meston CM, Gorzalka BB. Psychoactive drugs and human sexual behavior:the role of serotonergic activity. J Psychoactive Drugs. 1992; 24:1-40.
117. Wesson DR. Cocaine use by masseuses. J Psychoactive Drugs. 1982; 14:75-6.
118. Washton AM. Cocaine abuse and compulsive sexuality. Med Aspects Hum Sexuality. 1989; 23:32-9.
119. Carlson RG, Siegel HA. The crack life: an ethnographic overview of crack use and sexual behavior among African-Americans in a midwest metropolitan city. J Psychoactive Drugs. 1991; 23:11-20.
120. Mahler JC, Perry S, Sutton B. Intraurethral cocaine administration (Letter). JAMA. 1988; 259:3126.
121. Fiorelli RL, Manfrey SJ, Belkoff LH, Finkelstein LH. Priapism associated with intranasal cocaine abuse. J Urol. 1990; 143:584-5.
122. Rodriguez-Blazquez HM, Cardona PE, Rivera-Herrera JL. Priapism associated with the use of topical cocaine. J Urol. 1990; 143:358.
123. Macdonald PT, Waldorf D, Reinarman C, Murphy S. Heavy cocaine use and sexual behavior. Journal of Drug Issues. 1988; 18: 437-55.
124. Krutchkoff DJ, Eisenberg E, O'Brien JE, Ponzillo JJ. Cocaine-induced dental erosions (Letter). N Engl J Med. 1990; 320:408.
125. Quart AM, Small CB, Klein RS. The cocaine connection. Users imperil their gingiva. J Am Dent Assoc. 1991; 122:85-7.
126. Strominger MB, Sachs R, Hersh PS. Microbial keratitis with crack cocaine. Arch Ophthalmol. 1990; 108:1672.
127. McHenry JG, Zeiter JH, Madion MP, Cowden JW. Corneal epithelial defects after smoking crack cocaine. Am J Ophthalmol. 1989; 108:732.
128. Libby DM, Klein L, Altorki NK. Aspiration of the nasal septum: a new complication of cocaine abuse. Ann Intern Med. 1992; 116: 567-8.
129. Becker GD, Hill S. Midline granuloma due to illicit cocaine use. Arch Otolaryngol Head Neck Surg. 1988; 114:90-1.
130. Gordon AS, Moran DT, Jafek BW, Eller PM, Strahan RC. The effect of chronic cocaine abuse on human olfaction. Arch Otolaryngol Head Neck Surg. 1990; 116:1415-8.
131. Newman NM, DiLoreto DA, Ho JT, Klein JC, Birnbaum NS. Bilateral optic neuropathy and osteolytic sinusitis. Complications of cocaine abuse. JAMA. 1988; 259:72-4.
132. Marx R, Aral SO, Rolfs RT, Sterk CE, Kahn JG. Crack, sex, and STD. Sex Transm Dis. 1991; 18:92-101.
133. Rolfs RT, Goldberg M, Sharrar RG. Risk factors for syphilis: cocaine use and prostitution. Am J Public Health. 1990; 80:853-7.
134. Alternative case-finding methods in a crack-related syphilis epidemic—Philadelphia. MMWR. 1991; 40:77-80.
135. Minkoff HL, McCalla S, Delke I, Stevens R, Salwen M, Feldman J. The relationship of cocaine use to syphilis and human immunodeficiency virus infections among inner city parturient women. Am J Obstet Gynecol. 1990; 163:521-6.
136. Chaisson RE, Bacchetti P, Osmond D, Brodie B, Sande MA, Moss AR. Cocaine use and HIV infection in intravenous drug users in San Francisco. JAMA. 1989; 261:561-5.
137. Crack cocaine use among persons with tuberculosis: Contra Costa County, California, 1987-1990. MMWR. 1991; 40:485-9.
138. Hanzlick R, Gowitt GT. Cocaine metabolite detection in homicide victims. JAMA. 1991; 265:760-1.
139. Harruff RC, Francisco JT, Elkins SK, Phillips AM, Fernandez GS. Cocaine and homicide in Memphis and Shelby county: an epidemic of violence. J Forensic Sci. 1988; 33:1231-7.
140. Marzuk PM, Tardiff K, Leon AC, Stajic M, Morgan EB, Mann JJ. Prevalence of cocaine use among residents of New York City who committed suicide during a one-year period. Am J Psychiatry. 1992; 149:371-5.
141. Rawson RA, Obert JL, McCann MJ, Castro FG, Ling W. Cocaine abuse treatment: a review of current strategies. J Subst Abuse. 1991; 3:457-91.
142. Washton AM, Stone-Washton N. Outpatient treatment of cocaine addiction: suggestions to increase its effectiveness. Int J Addictions. 1990; 25:1421-9.
143. Wallace BC. Treating crack cocaine dependence: the critical role of relapse prevention. J Psychoactive Drugs. 1992; 24:213-22.
144. Gawin FH, Kleber HD, Byck R, Rounsaville BJ, Kosten TR, Jatlow PI, et al. Desipramine facilitation of initial cocaine abstinence. Arch Gen Psychiatry. 1989; 46:117-21.
This article has been cited by other articles:
 |
|
 |
|
  D. M. Fine, N. Garg, M. Haas, M. H. Rahman, G. M. Lucas, P. J. Scheel, and M. G. Atta Cocaine Use and Hypertensive Renal Changes in HIV-Infected Individuals Clin. J. Am. Soc. Nephrol., November 1, 2007; 2(6): 1125 - 1130. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. S. Restrepo, J. A. Carrillo, S. Martinez, P. Ojeda, A. L. Rivera, and A. Hatta Pulmonary Complications from Cocaine and Cocaine-based Substances: Imaging Manifestations RadioGraphics, July 1, 2007; 27(4): 941 - 956. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. D Treadwell and T. G Robinson Cocaine use and stroke Postgrad. Med. J., June 1, 2007; 83(980): 389 - 394. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Ulceronecrotic Nasoparanasal Lesion--Diagnosis Arch Dermatol, May 1, 2007; 143(5): 653 - 658. [Full Text] [PDF]
|
|
|
|
|
|
J. A. Jaffe and P. L. Kimmel Chronic Nephropathies of Cocaine and Heroin Abuse: A Critical Review Clin. J. Am. Soc. Nephrol., July 1, 2006; 1(4): 655 - 667. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Levine, M. E. Iliescu, H. Margellos-Anast, M. Estarziau, and D. A. Ansell The Effects of Cocaine and Heroin Use on Intubation Rates and Hospital Utilization in Patients With Acute Asthma Exacerbations Chest, October 1, 2005; 128(4): 1951 - 1957. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. C. Kleerup, S. N. Koyal, J. A. Marques-Magallanes, M. D. Goldman, and D. P. Tashkin Chronic and Acute Effects of "Crack" Cocaine on Diffusing Capacity, Membrane Diffusion, and Pulmonary Capillary Blood Volume in the Lung* Chest, August 1, 2002; 122(2): 629 - 638. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
|
Article
