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...on Medical Aspects
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www.ProjectCork.org
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Spring 2004
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Alcoholism and obesity: Overlapping neuropeptide pathways? (review).
Thiele TE; Navarro M; Sparta DR; Fee JR; Knapp DJ; Cubero I.
Neuropeptides 37(6): 321-337, 2003. (250 refs.)
Ethanol is a caloric compound, and ethanol drinking and food
intake are both appetitive and consummatory behaviors. Furthermore, both
ethanol and food have rewarding properties. It is therefore possible that
overlapping central pathways are involved with uncontrolled eating and excessive
ethanol consumption. A growing list of peptides has been shown to regulate
food intake and/ or energy homeostasis. Peptides such as the melanocortins,
corticotropin releasing factor, and cholecystokinin promote reductions of
food intake while others such as galanin and neuropeptide Y stimulate feeding.
The present review highlights research aimed at determining if ingestive
peptides also regulate voluntary ethanol intake, with an emphasis on the
melanocortins and neuropeptide Y. It is suggested that research directed
at ingestive peptides may expand our understanding of the neurobiological
mechanisms that drive ethanol self-administration, and may reveal new therapeutic
candidates for treating alcohol abuse and alcoholism. Copyright 2003, Churchill
Livingstone.
Body packing: The internal concealment of illicit drugs. (review).
Traub SJ; Hoffman RS; Nelson LS. New England Journal of Medicine
349(26): 2519-2526, 2003. (50 refs.)
This article provides an overview of the history of body-packing,
and presentations to medical providers. They usually present to health
care providers for one of three reasons: drug-induced toxic effects, intestinal
obstruction, or medical assessment after detention or arrest. The circumstances
under which the patient presents will direct the clinical assessment, laboratory
evaluation, and subsequent management. Children should be evaluated in
a manner similar to that used for adults, although children's protective
services should immediately be consulted. It review history taking, physical
exam, and diagnostic testing. Management is also reviewed: symptomatic
heroin poisoning, and symptomatic poisoning with other drug, as well as
asymptomatic patients, and decontamination. The article concludes with
an overview of ethical issues. Copyright 2003, Massachusetts Medical Society.
Cannabinoids in multiple sclerosis: Do they have a therapeutic role?
Killestein J; Uitdehaag BMJ; Polman CH. Drugs 64(1): 1-11,
2004. (63 refs.)
This is an exciting time for cannabinoid research. Evidence
suggests that cannabis (marijuana) can alleviate symptoms like muscle spasticity
and pain in patients with multiple sclerosis (MS). Interest in the field
of cannabinoids has been strengthened by the identification and cloning
of cannabinoid receptors located in the central nervous system and the
peripheral immune organs, and by the discovery of the endogenous cannabinoid
ligands. Cannabinoids are also efficacious in animal models of MS. However,
there have been only ten published clinical reports on the use of cannabis
in MS, involving 78 individuals worldwide, and the results have been equivocal.
Researchers encounter a number of difficulties in designing clinical studies
that use cannabinoids. From the studies reporting the use of cannabinoids
in MS patients with spasticity, the somewhat better designed studies failed
to demonstrate objective improvement. Therefore, convincing evidence that
cannabinoids are effective in MS is still lacking. Copyright 2004, Adis
International Ltd.
Cannabis use and cerebrovascular disease.
Moussouttas M. Neurologist 10(1): 47-53, 2004. (42 refs.)
Background: Cannabis is the most commonly abused illicit drug
and is often considered innocuous. However, cases of acute onset neurologic
dysfunction occurring in relation to cannabis use have been described and
corresponding cerebral imaging studies have documented focal ischemic changes
and vessel abnormalities. Review Summary: This article reviews all reported
cases of presumed cannabis related cerebral ischemic events in the medical
literature, as well as pertinent human and animal experimental studies
on the cardiovascular and cerebrovascular effects of cannabis. Conclusions:
Cannabis use seems to have been causally related to several instances of
cerebral ischemia and infarction. Proposed etiologic mechanisms have included
cerebral vasospasm, cardioembolization, and systemic hypotension with impaired
cerebral autoregulation, but most of the available data points to a vasospastic
process. The exact relation of cannabis to cerebrovascular disease remains
to be determined. Copyright 2004, Lippibcott, Williams & Wilkins.
Drinking pattern and risk of non-fatal myocardial infarction: A population-based
case-control study.
Trevisan M; Dorn J; Falkner K; Russell M; Ram M; Muti P et
al. Addiction 99(3): 313-322, 2004. (33 refs.)
Aims: Alcohol consumption has been associated with a reduced
risk of heart disease incidence and mortality. However, most studies have
focused on an average volume per specific time period and have paid little
attention to the pattern of drinking. The aim of this study was to examine
the association between various drinking patterns and myocardial infarction
(MI). Design: A population-based case-control study. Methods: Participants
were 427 white males with incident MI and 905 healthy white male controls
(age 35-69 years) selected randomly from two Western New York counties.
During computer-assisted interviews detailed information was collected
regarding patterns of alcohol consumption during the 12-24 months prior
to interview (controls) or MI (cases). Findings: Compared to life-time
abstainers, adjusted odds ratios (ORs) and 95% confidence interval (CI)
for non-current and current drinkers were 0.66 (0.31-1.39) and 0.50 (0.24-1.02),
respectively. Daily drinkers exhibited a significantly lower OR (0.41)
compared to life-time abstainers. Participants who drank mainly without
food had an OR of 1.49 (0.96-2.31) compared to those who drank mainly with
food and 0.62 (0.28-1.37) compared to life-time abstainers. Men who reported
drinking only at weekends had a significantly greater MI risk [1.91; (1.21-3.01)]
compared to men who drank less than once/week, but not compared to life-time
abstainers [0.91 (0.40-2.07)]. Conclusions: Our results indicate that patterns
of alcohol use have important cardiovascular health implications. Copyright
2004, Society for the Study of Addiction to Alcohol and Other Drugs.
Effect of alcohol consumption on diabetes mellitus: A systematic review.
(review).
Howard AA; Arnsten JH; Gourevitch MN. Annals of Internal Medicine 140(3): 211-219, 2004. (53 refs.)
Background: Both diabetes mellitus and alcohol consumption
are prevalent in the United States, yet physicians are poorly informed
about how alcohol use affects risk for or management of diabetes. Purpose:
To conduct a systematic review assessing the effect of alcohol use on the
incidence, management, and complications of diabetes mellitus in adults.
Data Sources: English-language studies in persons 19 years of age or older
that were identified by searching the MEDLINE database from 1966 to the
third week of August 2003 and the reference lists of key articles. Study
Selection: Two independent assessors reviewed 974 retrieved citations to
identify all experimental, cohort, or case-control studies that assessed
the effect of alcohol use on diabetes risk, control, self-management, adverse
drug events, or complications. Data Extraction: Two independent reviewers
extracted data and evaluated study quality on the basis of established
criteria. Data Synthesis: Thirty-two studies that met inclusion criteria
were reviewed. Compared with no alcohol use, moderate consumption (one
to 3 drinks/d) is associated with a 33% to 56% lower incidence of diabetes
and a 34% to 55% lower incidence of diabetes-related coronary heart disease.
Compared with moderate consumption, heavy consumption (>3 drinks/d)
may be associated with up to a 43% increased incidence of diabetes. Moderate
alcohol consumption does not acutely impair glycemic control in persons
with diabetes. Conclusions: Moderate alcohol consumption is associated
with a decreased incidence of diabetes mellitus and a decreased incidence
of heart disease in persons with diabetes. Further studies are needed to
assess the long-term effects of alcohol consumption on glycemic control
and noncardiac complications in persons with diabetes. Copyright 2004,
American College of Physicians.
Family history of alcoholism and response to sweets.
Kampov-Polevoy AB; Garbutt JC; Khalitov E. Alcoholism: Clinical
and Experimental Research 27(11): 1743-1749, 2003. (68 refs.)
Background: The relationship between a hedonic response to
sweet tastes and a propensity to excessive alcohol drinking is supported
by both animal and human studies. This study was designed to test the hypothesis
that the genetic risk for alcoholism as measured by a paternal history
of alcoholism in young social drinkers is associated with sweet-liking,
defined as rating the strongest offered sucrose solution (i.e., 0.83 M)
as the most palatable during the standard sweet test. Methods: Participants
were 163 subjects (39% male) without a lifetime history of alcohol or drug
abuse or dependence. Eighty-one subjects had a paternal history of alcoholism
(FH+), and 82 did not (FH-). Each subject rated a series of sucrose solutions
for intensity of sweetness and palatability. Subjects were categorized
as sweet-likers if they rated the highest sucrose concentration as the
most pleasurable. Results: The estimated odds of being a sweet-liker were
2.5 times higher for FH+ than for FH- subjects. FH+ subjects disliked the
tastes of the two weakest offered sucrose concentrations (0.05 and 0.10
M), whereas FH- subjects reported these tastes to be neutral. Conclusions:
The results of this study support the hypothesis that sweet-liking is associated
with a genetic vulnerability to alcoholism. Copyright 2003, Research Society
on Alcoholism.
Fetal alcohol and drug effects. (review).
Chiriboga CA. Neurologist 9(6): 267-279, 2003. (130 refs.)
Background: Alcohol and drug use by pregnant women are harmful
to the developing embryo and fetus. Teasing apart the specific contributions
of each substance to adverse child outcome, however, proves difficult in
practice. The risks to the neonate include intrauterine growth retardation,
birth defects, altered neurobehavior, and withdrawal syndromes. Subsequent
behavior, development, and neurologic function may also be impaired. Review
Summary: Maternal cigarette smoking carries the greatest risk of impaired
fetal growth of any of the substances discussed herein and has been linked
to subsequent externalizing behaviors. Alcohol is a well-established teratogen.
Heavy exposure to alcohol in a subset of infants is associated with fetal
alcohol syndrome (FAS). Mental retardation is one of the main sequelae
of alcohol exposure in utero. Fetal marijuana exposure has no consistent
effect on outcome. Prenatal cocaine exposure has not been shown to have
any detrimental effect on cognition, except as mediated through cocaine
effects on head size. Although fetal cocaine exposure has been linked to
numerous abnormalities in arousal, attention, and neurologic and neurophysiological
function, most such effects appear to be self-limited and restricted to
early infancy and childhood. Opiate exposure elicits a well-described withdrawal
syndrome affecting central nervous, autonomic, and gastrointestinal systems,
which is most severe among methadone-exposed infants. Conclusion: Most
adverse effects of prenatal drug exposure are self-limited, with catch-up
growth and resolution of withdrawal and of prior neurobehavioral abnormalities
noted over time. The exception is alcohol, which is linked to life-long
impairments (i.e., mental retardation and microcephaly) and possibly cigarette-related
behavioral effects. The absence of tangible evidence of detrimental long-term
cocaine effects may reflect limitations in the methodology used to identify
children at greatest risk for adverse outcome. Copyright 2003, Lippincott,
Williams & Wilkins.
Marijuana withdrawal in humans: Effects of oral THC or divalproex.
Haney M; Hart CL; Vosburg SK; Nasser J; Bennett A; Zubaran
C; Foltin RW. Neuropsychopharmacology 29(1): 158-170, 2004. (39 refs.)
Abstinence following daily marijuana use can produce a withdrawal
syndrome characterized by negative mood (eg irritability, anxiety, misery),
muscle pain, chills, and decreased food intake. Two placebo-controlled,
within-subject studies investigated the effects of a cannabinoid agonist,
delta-9-tetrahydrocannabinol (THC: Study 1), and a mood stabilizer, divalproex
(Study 2), on symptoms of marijuana withdrawal. Participants (n=7/study),
who were not seeking treatment for their marijuana use, reported smoking
6-10 marijuana cigarettes/day, 6-7 days/week. Study 1 was a 15-day in-patient,
5-day outpatient, 15-day in-patient design. During the in-patient phases,
participants took oral THC capsules (0, 10 mg) five times/day, 1 h prior
to smoking marijuana (0,00, 3.04% THC). Active and placebo marijuana were
smoked on in-patient days 1-8, while only placebo marijuana was smoked
on days 9-14, that is, marijuana abstinence. Placebo THC was administered
each day, except during one of the abstinence phases (days 9-14), when
active THC was given. Mood, psychomotor task performance, food intake,
and sleep were measured. Oral THC administered during marijuana abstinence
decreased ratings of ''anxious', 'miserable', 'trouble sleeping', 'chills',
and marijuana craving, and reversed large decreases in food intake as compared
to placebo, while producing no intoxication. Study 2 was a 58-day, outpatient/in-patient
design. Participants were maintained on each divalproex dose (0, 1500 mg/day)
for 29 days each. Each maintenance condition began with a 14-day outpatient
phase for medication induction or clearance and continued with a 15-day
in-patient phase. Divalproex decreased marijuana craving during abstinence,
yet increased ratings of 'anxious', 'irritable', 'bad effect', and 'tired.'
Divalproex worsened performance on psychomotor tasks, and increased food
intake regardless of marijuana condition. Thus, oral THC decreased marijuana
craving and withdrawal symptoms at a dose that was subjectively indistinguishable
from placebo. Divalproex worsened mood and cognitive performance during
marijuana abstinence. These data suggest that oral THC, but not divalproex,
may be useful in the treatment of marijuana dependence. Copyright 2004,
Nature Publishing Group.
Maternal smoking in pregnancy, fetal development, and childhood asthma.
Jaakkola JJK; Gissler M. American Journal of Public Health 94(1): 136-140, 2004. (19 refs.)
Objectives. We examined the relationships among maternal smoking
in pregnancy, fetal development, and the risk of asthma in childhood. Methods.
We conducted a population-based cohort study, where all 58841 singleton
births were followed for 7 years using nationwide registries. Results.
Maternal smoking increased the risk of asthma (adjusted odds ratio = 1.35;
95% confidence interval = 1.13, 1.62 for high exposure). Low birthweight
and preterm delivery increased the risk of asthma at the age of 7, whereas
being small for gestational age did not. Conclusions. Maternal smoking
in pregnancy increases the risk of asthma during the first 7 years of life,
and only a small fraction of the effect seems to be mediated through fetal
growth. Copyright 2004, American Public Health Association.
Out-of-hospital care of critical drug overdoses involving cardiac arrest.
Paredes VL; Rea TD; Eisenberg MS; Cobb LA; Copass MK; Cagle
A et al. Academic Emergency Medicine 11(1): 71-74, 2004. (6 refs.)
Objectives: Death from acute drug poisoning, also termed drug
overdose, is a substantial public health problem. Little is known regarding
the role of emergency medical services (EMS) in critical drug poisonings.
This study investigates the involvement and potential mortality benefit
of EMS for critical drug poisonings, characterized by cardiovascular collapse
requiring cardiopulmonary resuscitation (CPR). Methods: The study population
was composed of death events caused by acute drug poisoning, defined as
poisoning deaths and deaths averted (persons successfully resuscitated
from out-of-hospital cardiac arrest by EMS) in King County, Washington,
during the year 2000. Results: Eleven persons were successfully resuscitated
and 234 persons died from cardiac arrest caused by acute drug poisoning,
for a total of 245 cardiac events. The EMS responded to 79.6% (195/245),
attempted resuscitation in 34.7% (85/245), and successfully resuscitated
4.5% (11/245) of all events. Among the 85 persons for whom EMS attempted
resuscitation, opioids, cocaine, and alcohol were the predominant drugs
involved, although over half involved multiple drug classes. Among the
11 persons successfully resuscitated, return of circulation was achieved
in six following EMS cardiopulmonary resuscitation alone, in one following
CPR and defibrillation, and in the remaining four after additional advanced
life support. Conclusions: In this community, EMS was involved in the majority
of acute drug poisonings characterized by cardiovascular collapse and may
potentially lower total mortality by approximately 4.5%. The results show
that, in some survivors, return of spontaneous circulation may be achieved
with CPR alone, suggesting a different pathophysiology in drug poisoning
compared with cardiac arrest due to heart disease. Copyright 2004, Hanley & Belfus,
Inc.
Surgical emergencies in the intravenous drug user. (review).
Calder KK; Severyn FA. Emergency Medicine Clinics of North
America 21(4): 1089-+, 2003. (105 refs.)
In 2000 it was estimated that approximately 6.3% of the population
aged 12 or older were using illicit drugs [1]. It is a common misconception
that drugs are a problem of unemployed ethnic minorities and less affluent
members of society, but this is clearly not the case. Illicit drugs know
no boundaries with respect to ethnicity, sex, race, or demographic group.
It is estimated that 77% of illicit drug users in 2000 continued to function
in the workplace [1].The economic and social sequelae of drug abuse are
immense. In 1992 drug abuse costs in the United States totaled nearly $100
billion [2], the majority of which came from public funds. These costs
are related not only to health care issues but to more global concerns
such as drug-related crime, motor vehicle accidents, interference with
family caregiving, incarceration, and loss of employment [2,3].Among illicit
drug users, those who inject are at particular risk for medical complications,
and many of these patients are frequent users of the local emergency department
(ED) [4]. These patients are not necessarily addicts; even infrequent injection
can result in severe sequelae [5]. There are a variety of proposed mechanisms
for disease including contaminated delivery mechanisms, injection technique,
poor hygiene, contaminated drug or drug diluents, needle sharing, impaired
cell-mediated immunity, sexual promiscuity, altered mental status with
impaired cough and gag reflexes, and direct toxic effects on local tissue
[6-10]. Drug users are also likely to self-prescribe antibiotics, which
results in alterations in their normal flora [11,12]. These patients sometimes
have multiple concurrent drug-related conditions that make diagnosis and
treatment more difficult. In addition, other special considerations make
therapy extremely challenging such as analgesic tolerance, lack of intravenous
access, poor social conditions, illiteracy, and a high likelihood of medical
noncompliance. This article focuses on some of the more commonly encountered
surgical complications seen in the intravenous drug user (IVDU; can mean
intravenous drug user or intravenous drug use), some of which have nonspecific
clinical presentations yet pose a risk for significant morbidity and mortality
if not diagnosed and treated without delay. The goal is to identify clinical
characteristics and laboratory and radiographic studies that are likely
to aid the emergency physician (EP) in the identification of patients who
warrant surgical evaluation. Copyright 2003, W.B. Saunders Co.
The effects of toluene on the central nervous system. (review).
Filley CM; Halliday W; Kleinschmidt-DeMasters BK. Journal of
Neuropathology and Experimental Neurology 63(1): 12-12, 2004. (67 refs.)
In recent decades the organic solvent toluene (methylbenzene)
has emerged as one of the best-studied neurotoxins. Long-term and intense
exposure to toluene vapors in humans who abuse spray paint and related
substances has led to the recognition that toluene has a severe impact
on central nervous system myelin. Chronic toluene abuse produces a devastating
neurological disorder, of which dementia is the most disabling component.
The clinical syndrome, toluene leukoencephal- opathy, can be detected by
a combination of characteristic symptoms and signs, detailed neurobehavioral
evaluation, and brain magnetic resonance imaging. In this paper, we consider
the impact of toluene abuse on our society, describe the specific neurobehavioral
deficits in toluene leuko-encephalopathy, review the spectrum of neuroimaging
findings in patients with this disorder, summarize the teratogenic effects
of toluene in both humans and animal models, and offer possible explanations
for the range of neuropathological damage seen in brains of individuals
who chronically abuse toluene. Copyright 2004, Journal of Neuropathologists
Inc.
Why is parkinsonism not a feature of human methamphetamine users?
Moszczynska A; Fitzmaurice P; Ang L; Kalasinsky KS; Schmunk
GA; Peretti FJ et al. Brain 127(Part 2): 363-370, 2004. (34 refs.)
For more than 50 years, methamphetamine has been a widely used
stimulant drug taken to maintain wakefulness and performance and, in high
doses, to cause intense euphoria. Animal studies show that methamphetamine
can cause short-term and even persistent depletion of brain levels of the
neurotransmitter dopamine. However, the clinical features of Parkinson's
disease, a dopamine deficiency disorder of the brain, do not appear to
be characteristic of human methamphetamine users. We compared dopamine
levels in autopsied brain tissue of chronic methamphetamine users with
those in patients with Parkinson's disease and in a control group. Mean
dopamine levels in the methamphetamine users were reduced more in the caudate
(-61%) than in the putamen (-50%), a pattern opposite to that of Parkinson's
disease. Some methamphetamine users had severely decreased dopamine levels,
within the parkinsonian range, in the caudate (up to 97% dopamine loss)
but not in the putamen. As the putamen and caudate subserve aspects of
motor and cognitive function, respectively, our data suggest that methamphetamine
users are not parkinsonian because dopamine levels are not sufficiently
decreased in the motor component of the striatum. However, the near-total
reduction in the caudate could explain reports of cognitive disturbances,
sometimes disabling, in some drug users, and suggests that treatment with
dopamine substitution medication (e.g. levodopa) during drug rehabilitation
might be helpful. Copyright 2004, Oxford University Press.
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