Allelic association of the D2 dopamine receptor gene with cocaine dependence.

The objective of the present study was to examine allelic prevalence of the D2 dopamine receptor (DRD2) gene in male cocaine-dependent (CD) Caucasian (non-Hispanic) subjects and to determine the relationship of DRD2 alleles to family history and selected behavioral measures. The prevalence of the A1 allele in CD subjects (n = 53) was 50.9%. It was significantly higher than either the 16.0% prevalence (P < 10(-4)) in non-substance abusing controls (n = 100) or the 30.9% prevalence (P < 10(-2)) in population controls (n = 265) wherein substance abusers were not excluded. Similarly, a significantly higher prevalence (P < 10(-2)) of the B1 allele was found in CD subjects (n = 52) compared with non-substance abusing controls (n = 53); 38.5% vs. 13.2%. Logistic regression analysis of CD subjects identified potent routes of cocaine use and the interaction of early deviant behaviors and parental alcoholism as significant risk factors associated with the A1 allele. The cumulative number of these three risk factors in CD subjects was positively and significantly (P < 10(-3)) related to A1 allelic prevalence. The data showing a strong association of the minor alleles (A1 and B1) of the DRD2 with cocaine dependence suggest that a gene, located on the q22-q23 region of chromosome 11, confers susceptibility to this drug disorder.

Unrecognized cocaine use among schizophrenic patients.

OBJECTIVE: Unrecognized stimulant use could lead to the misdiagnosis of schizophrenia or the misunderstanding of its course and prognosis. This study was conducted to determine the prevalence of unrecognized stimulant use among patients with a clinical diagnosis of schizophrenia. METHOD: The subjects were 108 schizophrenic patients admitted consecutively to a Veterans Affairs psychiatric hospital. Admitting psychiatrists supplemented routine clinical evaluations with a semistructured interview regarding recent and lifetime use of alcohol, cocaine, amphetamine, marijuana, and opiates. A urine specimen was assayed for the four illicit drugs. RESULTS: Of the 103 patients who provided a urine specimen, 37 (36%) used cocaine during the 6 months before admission, including 31 who used the drug in the week before admission. Because of the poor reliability of negative self-reports of recent cocaine use, clinicians failed to recognize cocaine use in one-third of the patients with a urine toxicology positive for cocaine metabolites. Two other groups of patients were identified; schizophrenic patients without substance abuse (including alcohol) and schizophrenic patients with substance abuse other than stimulants. Both substance-abusing groups were younger than the nonabusing group, but the three groups had similarly high rates of recent psychotic symptoms, homelessness, and unemployment. CONCLUSIONS: Among schizophrenic patients who require hospitalization, clinicians should not rely solely on self-reported stimulant use. Recognition of stimulant use could be improved through routine urine toxicologies for all psychotic patients. The authors suggest that recognition of stimulant use among schizophrenic patients may identify a population with a better prognosis for schizophrenia and different treatment needs.

Smoked cocaine: patterns of use and pulmonary consequences.

This article offers a perspective on the use of volatilized alkaloidal cocaine in its freebase and crack forms and on the pulmonary consequences of such use. The inhalational route of administration of freebase and crack cocaine exposes the lung to their combustion products, raising concern about possible adverse pulmonary effects. A brief historical review of cocaine and its methods of use precedes the presentation of data concerning current modes and patterns of use and some pulmonary complications of crack and freebase use. Results from a systematic study of a large sample of cocaine users document a high frequency of occurrence of acute respiratory symptoms in temporal association with cocaine smoking. No relationship was detected between the prevalence of acute pulmonary symptoms and identifiable aspects of techniques of cocaine administration. These results suggest that the respiratory consequences of alkaloidal cocaine are most likely attributable to the inhaled cocaine itself, rather than to variable characteristics of usage.

Respiratory effects of cocaine freebasing among habitual cocaine users.

Smoking of alkaloidal cocaine ("crack") has become increasingly prevalent in our society. Recent evidence suggests that crack smoking can cause acute respiratory symptoms, abnormalities in lung function and, in some instances, severe, life-threatening acute lung injury. To evaluate further the relationship between frequent cocaine smoking and respiratory symptoms and lung dysfunction, we studied a sample of 177 heavy, habitual smokers of freebase cocaine (mean 6.6 gm/wk for an average of 27 months) with or without concomitant smoking of tobacco and/or marijuana. Results in this sample were compared with those in a control sample of 75 age-, sex- and race-matched nonsmokers of cocaine who did or did not also smoke tobacco and/or marijuana. After controlling for the use of other smoked substances, heavy, habitual cocaine smoking was associated with the following: (1) a high frequency of acute respiratory symptoms (cough, black sputum, chest pain) in temporal association with freebase use; (2) an obstructive ventilatory abnormality involving the large airways; and (3) a mild but significant impairment in the diffusing capacity of the lung. These findings suggest that heavy, habitual crack smoking produces (1) respiratory tract injury manifested by acute respiratory symptoms and evidence of chronic airflow obstruction in large airways, and (2) an abnormality in diffusion of gas at the alveolar-capillary level. The mechanism of the diffusion defect is unknown but could reflect damage to the alveolar-capillary membrane. Further study of the magnitude, persistence, reversibility, mechanism and clinical significance of the abnormality in diffusing capacity is needed.

Pulmonary status of habitual cocaine smokers.

We determined the prevalence of respiratory symptoms and lung dysfunction in a large sample of habitual smokers of freebase cocaine ("crack") alone and in combination with tobacco and/or marijuana. In addition, we compared these findings with those in an age- and race-matched sample of nonusers of crack who did or did not smoke tobacco and/or marijuana. A detailed respiratory and drug use questionnaire and a battery of lung function tests were administered to (1) a convenience sample of 202 habitual smokers of cocaine (cases) who denied intravenous drug abuse and (2) a reference sample of 99 nonusers of cocaine (control subjects). The cocaine smokers (85% black) included the following: 68 never-smokers of marijuana, of whom 43 currently smoked tobacco and 25 did not, and 134 ever-smokers of marijuana (42 current and 92 former), of whom 92 currently smoked tobacco and 42 did not. The control subjects (96% black) included the following: 69 never-smokers of marijuana, of whom 26 currently smoked tobacco and 43 did not, and 30 ever-smokers of marijuana (18 current and 12 former), of whom 21 currently smoked tobacco and 9 did not. Cases smoked an average of 6.5 g cocaine per week for a mean of 53 months. The median time of the most recent use of crack prior to study was 19 days (range less than 1 to 180 days). After controlling for the use of other smoked substances, frequent crack use was associated with: (1) a high prevalence of at least occasional occurrences of acute cardiorespiratory symptoms within 1 to 12 h after smoking cocaine (cough productive of black sputum [43.7%], hemoptysis [5.7%], chest pain [38.5%], usually worse with deep breathing, and cardiac palpitations [52.6%]) and (2) a mild but significant impairment in the diffusing capacity of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)