scholarly journals Plasma concentrations of granulocyte colony-stimulating factor (G-CSF) in patients with substance use disorders and comorbid major depressive disorder

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sandra Torres Galván ◽  
María Flores-López ◽  
Pablo Romero-Sanchiz ◽  
Nerea Requena-Ocaña ◽  
Oscar Porras-Perales ◽  
...  

AbstractGranulocyte colony–stimulating factor (G-CSF) has raised much interest because of its role in cocaine addiction in preclinical models. We explored the plasma concentrations of G-CSF in patients diagnosed with substance use disorder (SUD) and highly comorbid psychiatric disorders. In particular, we investigated the association between G-CSF concentrations and comorbid major depressive disorder (MDD) in patients with cocaine and alcohol use disorders (CUD and AUD, respectively). Additionally, patients with MDD but not SUD were included in the study. Three hundred and eleven participants were enrolled in this exploratory study: 136 control subjects, 125 patients with SUD (SUD group) from outpatient treatment programs for cocaine (N = 60, cocaine subgroup) and alcohol (N = 65, alcohol subgroup), and 50 patients with MDD but not SUD (MDD group) from primary-care settings. Participants were assessed based on DSM-IV-TR criteria, and a blood sample was collected to examine the plasma concentrations of G-CSF. G-CSF concentrations were negatively correlated with age in the entire sample (r = − 0.233, p < 0.001) but not in the patients with MDD. G-CSF concentrations were lower in patients with SUD than in controls (p < 0.05), specifically in the cocaine subgroup (p < 0.05). Patients with SUD and comorbid MDD had lower G-CSF concentrations than patients with SUD but not comorbid MDD or controls (p < 0.05). In contrast, patients with MDD but not SUD showed no differences compared with their controls. The negative association between G-CSF concentrations and age in the sample was not observed in patients with MDD. G-CSF concentrations were decreased in patients with SUD and comorbid MDD but not in patients with MDD. Therefore, G-CSF may be useful to improve the stratification of patients with dual diagnosis seeking treatment. Further investigation is needed to explore the impact of sex and type of drug on the expression of G-CSF.

2021 ◽  
Author(s):  
Sandra Torres Galván ◽  
María Flóres López ◽  
Pablo Romero Sanchíz ◽  
Nerea Requena Ocaña ◽  
Oscar Porras Perales ◽  
...  

Abstract Aims: Granulocyte colony–stimulating factor (G-CSF) has raised much interest due to its role to cocaine addiction in preclinical models. We analyzed the circulating expression of G-CSF in abstinent chronic users of alcohol and/or cocaine with or without comorbid major depressive disorders to investigate the role of this trophic factor with complicated substance use disorders.Methods: We recruited 176 patients and 136 controls. Patients were divided in 50 patients with major depressive disorder (MDD) and 126 abstinent substance use disorders (SUD) patients undergoing treatments for alcohol (N=66) or cocaine (N=60) addiction according to DSM-IV-TR criteria. A blood sample was collected to examine plasma concentrations of G-CSF.Results: The plasma concentrations of G-CSF were significantly decreased in the cocaine group compared with the SUD control group. There was a sex dimorphism in the alcohol group, with lower G-CSF concentrations in women compared with men. Plasma concentrations of G-CSF were associated with abstinence and with the length of alcohol problems. The decrease in G-CSF was associated with comorbid MDD, a finding specific for SUD patients since there were no alterations of G-CSF primary settings MDD outpatients.Conclusions: Circulating G-CSF is reduced in SUD patients, being associated to comorbid MDD. A sex-dependent effect was observed in female AUD. Plasma G-CSF concentrations might be used as a predictor of length of chronic alcohol use and as a stratification role in the dual diagnosis in SUD. Further investigation is needed to explore the role of G-CSF as potential biomarker of pathogenic/prognosis in SUD population.


2020 ◽  
pp. 070674372097482
Author(s):  
Shane J. McInerney ◽  
Trisha Chakrabarty ◽  
Malgorzata Maciukiewicz ◽  
Benicio N. Frey ◽  
Glenda M. MacQueen ◽  
...  

Objectives: Major depressive disorder (MDD) is associated with impairments in both cognition and functioning. However, whether cognitive deficits significantly contribute to impaired psychosocial and occupational functioning, independent of other depressive symptoms, is not well established. We examined the relationship between cognitive performance and functioning in depressed patients before and after antidepressant treatment using secondary data from the first Canadian Biomarker Integration Network in Depression-1 study. Methods: Cognition was assessed at baseline in unmedicated, depressed participants with MDD ( n = 207) using the Central Nervous System Vital Signs computerized battery, psychosocial functioning with the Sheehan Disability Scale (SDS), and occupational functioning with the Lam Employment Absence and Productivity Scale (LEAPS). Cognition ( n = 181), SDS ( n = 175), and LEAPS ( n = 118) were reassessed after participants received 8 weeks of open-label escitalopram monotherapy. A series of linear regressions were conducted to determine (1) whether cognitive functioning was associated with psychosocial and occupational functioning prior to treatment, after adjusting for overall depressive symptom severity and (2) whether changes in cognitive functioning after an 8-week treatment phase were associated with changes in psychosocial and occupational functioning, after adjusting for changes in overall symptom severity. Results: Baseline global cognitive functioning, after adjusting for depression symptom severity and demographic variables, was associated with the SDS work/study subscale (β = −0.17; P = 0.03) and LEAPS productivity subscale (β = −0.17; P = 0.05), but not SDS total (β = 0.19; P = 0.12) or LEAPS total (β = 0.41; P = 0.17) scores. Although LEAPS and SDS scores showed significant improvements after 8 weeks of treatment ( P < 0.001), there were no significant associations between changes in cognitive domain scores and functional improvements. Conclusion: Cognition was associated with occupational functioning at baseline, but changes in cognition were not associated with psychosocial or occupational functional improvements following escitalopram treatment. We recommend the use of more comprehensive functional assessments to determine the impact of cognitive change on functional outcomes in future research.


2021 ◽  
pp. 096032712110085
Author(s):  
EA Ahmed ◽  
AM Abd-Eldayem ◽  
E Ahmed

Acetaminophen (APAP) is often used as an antipyretic and analgesic agent. Overdose hepatotoxicity, which often results in liver cell failure and liver transplantation, is a severe complication of APAP usage. To save the liver and save lives from acute liver damage caused by APAP, the search for new strategies for liver defense is important. Wistar rats have been used for the induction of APAP hepatotoxicity. Elevated levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were evaluated for liver toxicity. In addition, the levels of hepatic tissue oxidative markers such as malondialdehyde (MDA), nitric oxide (NO) increased while glutathione (GSH) was depleted and catalase (CAT) activity was curtailed. The biochemical findings were consistent with the changes in histology that suggested liver damage and inflammation. Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high. After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity. Treatment with N-AC and G-CSF after administration of APAP has also attenuated inflammation and hepatocytes necrosis. The results of this study showed that G-CSF could be viewed as an alternative hepatoprotective agent against APAP-induced acute liver injury compared to N-AC.


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