PDF(Pubmed)
Abstract：
BACKGROUND: Dual diagnosis in individuals with cocaine use disorders (CUDs) presents a mental health challenge marked by an increased susceptibility to disabling morbidities and premature mortality. Despite extensive research on depression and anxiety, other prevalent comorbidities, such as psychotic and personality disorders, have received less attention. This study explores inflammation-related mediators as potential biomarkers for CUD and dual diagnosis with schizophrenia (SCZ) or antisocial personality disorder (APD).
METHODS: This exploratory study included 95 participants, comprising 40 healthy subjects and 55 abstinent patients with CUD. Lifetime CUD was diagnosed either as single diagnosis (CUD group, N = 25) or as a dual diagnosis (DD group. N = 30) with SCZ (CUD+SCZ subgroup) or APD (CUD+APD subgroup). Participants were clinically assessed, and the plasma concentrations of growth factors (i.e., G-CSF, BDNF, and VEGF-A) and chemokines (i.e., CCL11/eotaxin-1, CCL2/MCP-1, and CXCL12/SDF-1) were determined and log(10)-transformed for analysis.
RESULTS: Growth factors and chemokines were dysregulated by CUD and psychiatric diagnoses. Specifically, patients in the CUD group exhibited significantly lower concentrations of G-CSF and CCL11/eotaxin-1 than the control group. In contrast, the DD group showed significantly higher concentrations of all analytes than both the CUD and control groups. Additionally, no differences in these analytes were observed between the CUD+SCZ and CUD+APD subgroups within the DD group. Regarding cocaine-related variables, significant associations were identified in the CUD group: an inverse correlation between the age at first cocaine use and the concentrations of BDNF and CCL2/MCP-1; and a positive correlation between the duration of the cocaine abstinence and the concentrations of BDNF and CCL11/eotaxin-1. Lastly, a logistic regression model incorporating all these analytes demonstrated high discriminatory power in distinguishing patients with CUD alone from those with dual diagnosis.
CONCLUSIONS: Individuals with dual diagnosis of CUD exhibit elevated concentrations of growth factors and chemokines, distinguishing them from those with CUD alone. It is unclear whether the differences in these inflammatory mediators are specific to the presence of SCZ and APD. The study highlights potential biomarkers and associations, providing valuable insights into the intricate interplay of CUD and psychiatric disorders to enhance clinical diagnosis and therapeutics.
METHODS: This exploratory study included 95 participants, comprising 40 healthy subjects and 55 abstinent patients with CUD. Lifetime CUD was diagnosed either as single diagnosis (CUD group, N = 25) or as a dual diagnosis (DD group. N = 30) with SCZ (CUD+SCZ subgroup) or APD (CUD+APD subgroup). Participants were clinically assessed, and the plasma concentrations of growth factors (i.e., G-CSF, BDNF, and VEGF-A) and chemokines (i.e., CCL11/eotaxin-1, CCL2/MCP-1, and CXCL12/SDF-1) were determined and log(10)-transformed for analysis.
RESULTS: Growth factors and chemokines were dysregulated by CUD and psychiatric diagnoses. Specifically, patients in the CUD group exhibited significantly lower concentrations of G-CSF and CCL11/eotaxin-1 than the control group. In contrast, the DD group showed significantly higher concentrations of all analytes than both the CUD and control groups. Additionally, no differences in these analytes were observed between the CUD+SCZ and CUD+APD subgroups within the DD group. Regarding cocaine-related variables, significant associations were identified in the CUD group: an inverse correlation between the age at first cocaine use and the concentrations of BDNF and CCL2/MCP-1; and a positive correlation between the duration of the cocaine abstinence and the concentrations of BDNF and CCL11/eotaxin-1. Lastly, a logistic regression model incorporating all these analytes demonstrated high discriminatory power in distinguishing patients with CUD alone from those with dual diagnosis.
CONCLUSIONS: Individuals with dual diagnosis of CUD exhibit elevated concentrations of growth factors and chemokines, distinguishing them from those with CUD alone. It is unclear whether the differences in these inflammatory mediators are specific to the presence of SCZ and APD. The study highlights potential biomarkers and associations, providing valuable insights into the intricate interplay of CUD and psychiatric disorders to enhance clinical diagnosis and therapeutics.
摘要：
背景：可卡因使用障碍（CUD）患者的双重诊断对心理健康提出了挑战，其特征是对致残发病率和过早死亡的易感性增加。尽管对抑郁和焦虑进行了广泛的研究，其他常见的合并症，比如精神病和人格障碍，受到的关注较少。这项研究探讨了炎症相关介质作为CUD和精神分裂症（SCZ）或反社会人格障碍（APD）双重诊断的潜在生物标志物。
方法：这项探索性研究包括95名参与者，包括40名健康受试者和55名患有CUD的戒断患者。终身CUD被诊断为单一诊断（CUD组，N=25）或作为双重诊断（DD组。N=30)与SCZ(CUD+SCZ亚组)或APD(CUD+APD亚组)。参与者进行了临床评估，和生长因子的血浆浓度(即，G-CSF,BDNF,和VEGF-A)和趋化因子(即，确定CCL11/eotaxin-1，CCL2/MCP-1和CXCL12/SDF-1），并转化log（10）进行分析。
结果：CUD和精神病诊断导致生长因子和趋化因子失调。具体来说,CUD组患者的G-CSF和CCL11/eotaxin-1浓度显著低于对照组.相比之下,DD组显示所有分析物的浓度显著高于CUD组和对照组。此外,在DD组内的CUD+SCZ和CUD+APD亚组之间没有观察到这些分析物的差异。关于可卡因相关变量，在CUD组中发现了显著关联:首次使用可卡因的年龄与BDNF和CCL2/MCP-1的浓度呈负相关;可卡因戒除时间与BDNF和CCL11/eotaxin-1的浓度呈正相关.最后,纳入所有这些分析物的逻辑回归模型在区分单纯CUD患者和双重诊断患者方面表现出很高的辨别能力.
结论：双重诊断为CUD的个体表现出升高的生长因子和趋化因子浓度，将它们与仅有CUD的人区分开来。尚不清楚这些炎症介质的差异是否对SCZ和APD的存在具有特异性。该研究强调了潜在的生物标志物和关联，为CUD和精神疾病的复杂相互作用提供有价值的见解，以增强临床诊断和治疗。
方法：这项探索性研究包括95名参与者，包括40名健康受试者和55名患有CUD的戒断患者。终身CUD被诊断为单一诊断（CUD组，N=25）或作为双重诊断（DD组。N=30)与SCZ(CUD+SCZ亚组)或APD(CUD+APD亚组)。参与者进行了临床评估，和生长因子的血浆浓度(即，G-CSF,BDNF,和VEGF-A)和趋化因子(即，确定CCL11/eotaxin-1，CCL2/MCP-1和CXCL12/SDF-1），并转化log（10）进行分析。
结果：CUD和精神病诊断导致生长因子和趋化因子失调。具体来说,CUD组患者的G-CSF和CCL11/eotaxin-1浓度显著低于对照组.相比之下,DD组显示所有分析物的浓度显著高于CUD组和对照组。此外,在DD组内的CUD+SCZ和CUD+APD亚组之间没有观察到这些分析物的差异。关于可卡因相关变量，在CUD组中发现了显著关联:首次使用可卡因的年龄与BDNF和CCL2/MCP-1的浓度呈负相关;可卡因戒除时间与BDNF和CCL11/eotaxin-1的浓度呈正相关.最后,纳入所有这些分析物的逻辑回归模型在区分单纯CUD患者和双重诊断患者方面表现出很高的辨别能力.
结论：双重诊断为CUD的个体表现出升高的生长因子和趋化因子浓度，将它们与仅有CUD的人区分开来。尚不清楚这些炎症介质的差异是否对SCZ和APD的存在具有特异性。该研究强调了潜在的生物标志物和关联，为CUD和精神疾病的复杂相互作用提供有价值的见解，以增强临床诊断和治疗。
