COMPARING IMMUNOCYTOKINES LEVELS BETWEEN ALCOHOL- DEPENDENT PATIENTS WITH AND WITHOUT DELIRIUM TREMENS

Abstract Background Alcohol is a significant modulator of the immunocytokine system. Alcohol dependence (AD) can lead to a range of psychological and physical problems. Alcohol withdrawal syndrome (AWS) is a hallmark of AD and can manifest in various clinical phenotypes, including delirium tremens (DTs), which is considered the most severe and distinct form of AWS. Previous evidences suggest that AD is associated with dysregulation of immunocytokines such as Interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and tumor necrosis factor-alpha (TNF-α). However, whether there is a difference between patients with and without DTs was not known. Aims & Objectives This study aimed to investigate differences in IL-6, sIL-6R, and TNF-α levels between patients with AD who did and did not develop DTs. Method We enrolled 85 inpatients diagnosed with AD based on DSM-IV criteria and 49 health control (HC) participants. Among AD groups, 35 participants experienced DTs (classified as DTs group). Blood samples were collected from the AD group on the first and seventh days of withdrawal, as well as from the HC group. Serum levels of IL-6, sIL-6R, and TNF-α were measured using enzyme-linked immunosorbent assays. Results Patients with AD exhibited significantly elevated TNF-α levels and reduced sIL-6R levels at baseline compared to HCs. No significant differences in TNF-α and sIL-6R levels were observed between DTs and non-DTs groups. Moreover, the DTs group had the highest IL-6 levels, followed by the non-DTs group, then the HC group. After one week of alcohol withdrawal treatment, sIL-6R levels were normalized and comparable for the DTs and non-DTs groups. The levels of TNF-α remained elevated in the DTs group; however, the non-DTs group exhibited a significant decrease in TNF-α level. Additionally, IL-6 levels decreased significantly in the DTs group, while they remained unchanged in the non-DT group. Discussion & Conclusion Our findings suggest immunocytokines dysregulation may be associated with the pathophysiology of AD. The difference of IL-6 and TNF-α levels between DT and non-DT groups supports the potential role of immunocytokines in discriminating AD subgroups and highlights the potential clinical utility as a marker for DTs. Current evidence also suggests that convergent immune pathways may be involved in AUD and in these comorbid disorders.