Peripheral toxicity in crack cocaine use disorders

Narvaez, Joana Corrêa de Magalhães; Magalhães, Pedro Vieira da Silva; Fries, Gabriel R.; Colpo, Gabriela D.; Czepielewski, Letícia Sanguinetti; Vianna, Priscila; Chies, José Artur Bogo; Rosa, Adriane Ribeiro; Diemen, Lísia von; Vieta, Eduard; Pechansky, Flávio; Kapczinski, Flávio

doi:10.1016/j.neulet.2013.03.045

Cited by 54 publications

(33 citation statements)

References 42 publications

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“…This finding corroborates previous studies that showed higher BDNF concentrations in CCD [9,25,37]. The increase of plasma BDNF levels during early abstinence might suggest a form of neuromodulation of the central nervous system in response to the crack/cocaine neurotoxicity [38], acting in an effort to recover the brain from the neuronal damage caused by chronic drug use [39].…”

Section: Discussionsupporting

confidence: 90%

Brain-Derived Neurotrophic Factor and Delayed Verbal Recall in Crack/Cocaine Dependents

et al. 2015

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Background/Aims: Considering the role of brain-derived neurotrophic factor (BDNF) in memory processes and its peripheral response during the detoxification of cocaine, the aim of this study was to investigate whether plasma BDNF levels could be related to memory performance in women with crack/cocaine dependence. Methods: Twenty-five abstinent female crack/cocaine users (CCD) and 25 unmedicated healthy women (HW), carefully matched for age and years of formal education, were assessed regarding memory performance. Logical Memory was used to assess the immediate verbal recall (IVR), delayed verbal recall (DVR) and memory retention. Plasma BDNF levels were measured by Elisa immunoassay. Beck Depression Inventory was used to assess the severity of depressive symptoms, and the Cocaine Selective Severity Assessment the severity of cocaine abstinence symptoms. Results: The CCD group had lower DVR scores and higher plasma BDNF levels when compared to HW group. In addition, a linear regression model showed that BDNF levels predicted DVR scores within CCD group independently of depressive symptoms (R = 0.51; R² = 0.26; t(22) = 4.025, p = 0.03). Conclusion: Despite higher plasma BDNF levels, crack users exhibited memory impairments when compared to healthy women. Specifically, peripheral BDNF levels predicted better cognitive performance only within individuals who already had cognitive impairment.

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Section: Discussionsupporting

confidence: 90%

Brain-Derived Neurotrophic Factor and Delayed Verbal Recall in Crack/Cocaine Dependents

et al. 2015

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“…Additionally, inflammation and atherosclerosis are substantial potentially lethal vascular effects of cocaine use that have acute and chronic systemic impact [2,4,10,13,16,23,35,37,38,42,50]. Cocaine creates an elevated immune system inflammatory state with decreased basal anti-inflammatory markers (e.g., interleukin-10) [42,51], and increased pro-inflammatory cytokines (e.g., tumor necrosis factor alpha, Interleukin 1β) [42,51], all contributing to vascular disease (e.g., endocarditis).…”

Section: Acute Effects Of Cocainementioning

confidence: 99%

Vascular disease in cocaine addiction

et al. 2017

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Cocaine, a powerful vasoconstrictor, induces immune responses including cytokine elevations. Chronic cocaine use is associated with functional brain impairments potentially mediated by vascular pathology. Although the Crack-Cocaine epidemic has declined, its vascular consequences are increasingly becoming evident among individuals with cocaine use disorder of that period, now aging. Paradoxically, during the period when prevention efforts could make a difference, this population receives psychosocial treatment at best. We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity. PubMed and Academic Search Complete were used with relevant terms. Findings consist of the major mechanisms of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine. The etiology underlying cocaine's acute and chronic vascular effects is multifactorial, spanning hypertension, impaired homeostasis and platelet function, thrombosis, thromboembolism, and alterations in blood flow. Early detection of vascular disease in cocaine addiction by multimodality imaging is discussed. Treatment may be similar to indications in patients with traditional risk-factors, with few exceptions such as enhanced supportive care and use of benzodiazepines and phentolamine for sedation, and avoiding β-blockers. Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction and employ preventive treatment to reduce silent disease progression.

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“…Increased BDNF in this scenario might represent as a compensatory search for neuroprotection. 10 However, this does not necessarily imply a better outcome for these children. In an animal model, the long-term effect of high BDNF levels has been suggested to affect neuronal migration and maturation through different developmental periods.…”

Section: Discussionmentioning

confidence: 98%

“…Blood collection and processing and BDNF and TBARS measurement were performed as usual in our laboratory. 10 The main outcome measure was assessed by generalized linear model (GLM) analyses (gamma distribution), while confounders were chosen on the basis of statistical criteria (association with both study factor and outcome measure at a significance level of p p 0.2). The accepted significance level was p p 0.05.…”

Section: Methodsmentioning

confidence: 99%

TBARS and BDNF levels in newborns exposed to crack/cocaine during pregnancy: a comparative study

Mardini

Rohde

Ceresér

et al. 2017

Rev. Bras. Psiquiatr.

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Objectives: To compare levels of a marker of lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and brain-derived neurotrophic factor (BDNF) in umbilical cord blood (UCB) between newborns exposed to crack/cocaine in utero (exposed newborns [EN], n=57) and nonexposed newborns (NEN, n=99), as well as in maternal peripheral blood at delivery. Methods: This was a cross-sectional study. Potential confounders, including perinatal parameters, psychopathology, and use of other substances, were assessed. Results: After adjusting for potential confounders, adjusted mean BDNF was significantly higher in EN (3.86 ng/mL, 95% confidence interval [95%CI] 2.29-5.43) than in NEN (0.85 ng/mL, 95%CI 0.47-1.23; p o 0.001; Cohen effect size: 1.12), and significantly lower in crack/cocaine mothers than in control mothers (4.03 ng/mL, 95%CI 2.87-5.18 vs. 6.67 ng/mL, 95%CI 5.60-7.74; p = 0.006). The adjusted mean TBARS level was significantly lower in EN (63.97 mM MDA, 95%CI 39.43-88.50) than NEN (177.04 mM MDA, 95%CI 140.93-213.14; p o 0.001; effect size = 0.84), with no difference between mother groups (p = 0.86). Conclusions: The changes in TBARS levels observed in EN suggest that fetuses exposed to cocaine mobilize endogenous antioxidant routes since very early stages of development. The increase in BDNF levels in EN might indicate changes in fetal development, whereas the changes in BDNF levels in mothers provide evidence of the complex metabolic processes involved in drug use during pregnancy.

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Peripheral toxicity in crack cocaine use disorders

Cited by 54 publications

References 42 publications

Brain-Derived Neurotrophic Factor and Delayed Verbal Recall in Crack/Cocaine Dependents

Brain-Derived Neurotrophic Factor and Delayed Verbal Recall in Crack/Cocaine Dependents

Vascular disease in cocaine addiction

TBARS and BDNF levels in newborns exposed to crack/cocaine during pregnancy: a comparative study

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