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There are currently no consistent objective biochemical markers of alcohol abuse and alcoholism. Development of reliable diagnostic biomarkers that permit accurate assessment of alcohol intake and patterns of drinking is of prime importance to treatment and research fields. Diagnostic biomarker development in other diseases has demonstrated the utility of both open, systems biology, screening for biomarkers and more rational focused efforts on specific biomolecules or families of biomolecules. Long-term alcohol consumption leads to altered inflammatory cell and adaptive immune responses with associated pathologies and increased incidence of infections. This has led researchers to focus attention on identifying cytokine biomarkers in models of alcohol abuse. Alcohol is known to alter cytokine levels in plasma and a variety of tissues including lung, liver, and very importantly brain. A number of cytokine biomarker candidates have been identified, including: tumor necrosis factor-alpha, interleukin (IL)-1-alpha, IL-1-beta, IL-6, IL-8, IL-12, and monocyte chemoattractant protein-1. This is an emerging and potentially exciting avenue of research in that circulating cytokines may contribute to diagnostic biomarker panels, and a combination of multiple biomarkers may significantly increase the sensitivity and specificity of the biochemical tests aiding reliable and accurate detection of excessive alcohol intake.
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... The explanation of why these biomarkers are insufficient in this population could be due to the influence of additional factors in cognitive dysfunction, such as other nutritional deficiencies (i.e., low BMI, ascorbic acid deficiency, or thiamine deficiency) [17,18], comorbid psychiatric disorders (i.e., affective disorders) [19], as well as inflammation and oxidative stress caused by chronic alcohol intake or alcohol withdrawal episodes per se [20]. Heavy alcohol consumption throughout life triggers a proinflammatory organic state that leads to neurocognitive alterations [21][22][23]. Alcohol can stimulate Toll-like receptor 4 (TLR4), which activates several signaling pathways (i.e., Nuclear Factor-κB, inducible Nitric Oxide Synthase), resulting in the release of cytokines, chemokines, and oxidative-nitrosative stress [24][25][26], associated with neuroinflammation and structural brain damage [27][28][29]. ...
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For a long time, Substance Use Disorders (SUDs) were not considered a component in the etiology of dementia. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders introduced substance-induced neurocognitive disorders, incorporating this notion to clinical practice. However, detection and monitoring of neurodegenerative processes in SUD patients remain a major clinical challenge, especially when early diagnosis is required. In the present study, we aimed to investigate new potential biomarkers of neurodegeneration that could predict cognitive impairment in SUD patients: the circulating concentrations of Neurofilament Light chain protein (NfL) and Brain-Derived Neurotrophic Factor (BDNF). Sixty SUD patients were compared with twenty-seven dementia patients and forty healthy controls. SUD patients were recruited and assessed using the Psychiatric Research Interview for Substance and Mental (PRISM) and a battery of neuropsychological tests, including the Montreal Cognitive Assessment test for evaluation of cognitive impairment. When compared to healthy control subjects, SUD patients showed increases in plasma NfL concentrations and NfL/BDNF ratio, as well as reduced plasma BDNF levels. These changes were remarkable in SUD patients with moderate–severe cognitive impairment, being comparable to those observed in dementia patients. NfL concentrations correlated with executive function and memory cognition in SUD patients. The parameters “age”, “NfL/BDNF ratio”, “first time alcohol use”, “age of onset of alcohol use disorder”, and “length of alcohol use disorder diagnosis” were able to stratify our SUD sample into patients with cognitive impairment from those without cognitive dysfunction with great specificity and sensibility. In conclusion, we propose the combined use of NfL and BDNF (NfL/BDNF ratio) to monitor substance-induced neurocognitive disorder.
... (46,47) Furthermore, TNF-α, IL-1β, and IL-6 are elevated in alcohol-induced liver disease. (48) Hence, although we observed increased TNF-α, IL-1β, and IL-6 in some patients, their liver disease status was unknown, preventing further interpretation of these findings. Our study findings supported the potential involvement of oxidative stress and inflammatory cytokine pathways in the development and clinical manifestations of gout and the associated comorbidities. ...
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Objective This single-center clinical study identifies clusters of different phenotypes and pathophysiology subtypes of patients with gout and associated comorbidities. Methods Patients clinically diagnosed with gout were enrolled between January 2018 and December 2019. Hierarchical cluster analyses were performed using clinical data or biological markers, inflammatory markers, and oxidative stress pathway metabolites assayed from serum and plasma samples. Subgroup clusters were compared using the analysis of variance (continuous data) and Chi-square tests (categorical data). Results Hierarchical cluster analysis identified three clusters—cluster 1 (C1; n = 24) comprising dyslipidemia, hypertension, and early onset of gout, without tophi; cluster 2 (C2; n = 25) comprising hypertension, dyslipidemia, nephrolithiasis, and obesity; cluster 3 (C3; n = 39) comprising multiple comorbidities and tophi. Post-hoc comparisons of data obtained from samples of patients in C1–C3 revealed significant differences in the levels of oxidative stress and inflammation-related markers, including 3-nitrotyrosine, tumor necrosis factor-α, C-reactive protein, interleukin (IL)-1β, IL-6, plateletderived growth factor (PDGF)-AA, and PDGF-BB. Re-clustering patients based on the biological markers that significantly differed among the initial clusters, and all markers, identified similar clusters. Conclusion Oxidative stress and inflammatory marker levels may affect the development and clinical manifestations (clinical phenotypes) of gout. Measuring oxidative stress and inflammatory cytokines is a potential adjunctive tool and biomarker for early identification and management of gout.
... While these findings suggest statistical interactions between marijuana and alcohol, the biological mechanism for this interaction remains unclear. Alcohol consumption has previously been shown to increase cytokine production and subsequent peripheral inflammation and damage to organs [38,39], and cannabis may exert anti-inflammatory properties and mitigate inflammation from alcohol consumption [40][41][42], suggesting opposing effects of cannabis and alcohol on inflammatory pathways. Inflammatory marker IL-6 was previously found to be positively associated with alcohol consumption and further analysis identified a statistical interaction between alcohol consumption and marijuana use, where a significant positive association was observed among non-users and a non-significant negative association was observed among users, demonstrating marijuana may modulate inflammatory cytokines induced by alcohol [43]. ...
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Background Marijuana is the third most commonly used drug in the USA and efforts to legalize it for medical and recreational use are growing. Despite the increase in use, marijuana’s effect on aging remains understudied and understanding the effects of marijuana on molecular aging may provide novel insights into the role of marijuana in the aging process. We therefore sought to investigate the association between cumulative and recent use of marijuana with epigenetic age acceleration (EAA) as estimated from blood DNA methylation. Results A random subset of participants from The Coronary Artery Risk Development in Young Adults (CARDIA) Study with available whole blood at examination years (Y) 15 and Y20 underwent epigenomic profiling. Four EAA estimates (intrinsic epigenetic age acceleration, extrinsic epigenetic age acceleration, PhenoAge acceleration, and GrimAge acceleration) were calculated from DNA methylation levels measured at Y15 and Y20. Ever use and cumulative marijuana-years were calculated from the baseline visit to Y15 and Y20, and recent marijuana use (both any and number of days of use in the last 30 days) were calculated at Y15 and Y20. Ever use of marijuana and each additional marijuana-year were associated with a 6-month ( P < 0.001) and a 2.5-month ( P < 0.001) higher average in GrimAge acceleration (GAA) using generalized estimating equations, respectively. Recent use and each additional day of recent use were associated with a 20-month ( P < 0.001) and a 1-month ( P < 0.001) higher GAA, respectively. A statistical interaction between marijuana-years and alcohol consumption on GAA was observed ( P = 0.011), with nondrinkers exhibiting a higher GAA ( β = 0.21 [95% CI 0.05, 0.36], P = 0.008) compared to heavy drinkers ( β = 0.05 [95% CI − 0.09, 0.18], P = 0.500) per each additional marijuana-year. No associations were observed for the remaining EAA estimates. Conclusions These findings suggest cumulative and recent marijuana use are associated with age-related epigenetic changes that are related to lifespan. These observed associations may be modified by alcohol consumption. Given the increase in use and legalization, these findings provide novel insight on the effect of marijuana use on the aging process as captured through blood DNA methylation.
... The membrane interactions with reactive ethanol metabolites or lipopolysaccharide (LPS) may lead to the generation of adducts with proteins and cellular constituents and induce immune responses towards such neoantigens [9][10][11][12][13][14][15][16][17][18][19]. In addition, alcohol intake may affect pathways of leukocyte regulation together with stimulation of systemic inflammation and oxidative stress [5][6][7][20][21][22][23]. The status of inflammation in alcoholic patients is frequently compromised and could be influenced by both the amounts of drinking and the presence or absence of tissue injury [20,[23][24][25][26][27][28][29]. ...
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Aberrations in blood cells are common among heavy alcohol drinkers. In order to shed further light on such responses, we compared blood cell status with markers of hemolysis, mediators of inflammation and immune responses to ethanol metabolites in alcohol-dependent patients at the time of admission for detoxification and after abstinence. Blood cell counts, indices of hemolysis (LDH, haptoglobin, bilirubin), calprotectin (a marker of neutrophil activation), suPAR, CD163, pro- and anti-inflammatory cytokines and autoantibodies against protein adducts with acetaldehyde, the first metabolite of ethanol, were measured from alcohol-dependent patients (73 men, 26 women, mean age 43.8 ± 10.4 years) at baseline and after 8 ± 1 days of abstinence. The assessments also included information on the quantities of alcohol drinking and assays for biomarkers of alcohol consumption (CDT), liver function (AST, ALT, ALP, GGT) and acute phase reactants of inflammation. At baseline, the patients showed elevated values of CDT and biomarkers of liver status, which decreased significantly during abstinence. A significant decrease also occurred in LDH, bilirubin, CD163 and IgA and IgM antibodies against acetaldehyde adducts, whereas a significant increase was noted in blood leukocytes, platelets, MCV and suPAR levels. The changes in blood leukocytes correlated with those in serum calprotectin (p < 0.001), haptoglobin (p < 0.001), IL-6 (p < 0.02) and suPAR (p < 0.02). The changes in MCV correlated with those in LDH (p < 0.02), MCH (p < 0.01), bilirubin (p < 0.001) and anti-adduct IgG (p < 0.01). The data indicates that ethanol-induced changes in blood leukocytes are related with acute phase reactants of inflammation and release of neutrophil calprotectin. The studies also highlight the role of hemolysis and immune responses to ethanol metabolites underlying erythrocyte abnormalities in alcohol abusers.
... Increased expression of proinflammatory genes such as Toll-like receptors (TLRs) and cytokines have been found in the brains of postmortem alcoholics [2][3][4] and chronic alcohol consumption is associated with increased levels of cytokines in circulation. 5 In animal models, alcohol has been shown to increase expression of neuroimmune signalling molecules in the brain, [6][7][8][9] which have in turn been shown to increase voluntary alcohol consumption. [10][11][12][13] Thus, neuroimmune signalling may serve as a positive feedback loop in AUD, being both a cause and consequence of excessive alcohol intake. 1 TLRs are a major component of immune signalling that were discovered to mediate responses to pathogens and necrotic cell damage. ...
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There is growing evidence that immune signalling may be involved in both the causes and consequences of alcohol abuse. Toll-like receptor (TLR) expression is increased by alcohol consumption and is implicated in AUD, and specifically TLR7 may play an important role in ethanol consumption. We administered the TLR7-specific agonist imiquimod in male and female Long-Evans rats to determine (1) gene expression changes in brain regions involved in alcohol reinforcement, the nucleus accumbens core and anterior insular cortex, in rats with and without an alcohol history, and (2) whether TLR7 activation could modulate operant alcohol self-administration. Interferon regulatory factor 7 (IRF7) was dramatically increased in both sexes at both 2- and 24-h post-injection regardless of alcohol history and TLR3 and 7 gene expression was increased as well. The proinflammatory cytokine TNFα was increased 24-h post-injection in rats with an alcohol self-administration history, but this effect did not persist after four injections, suggesting molecular tolerance. Ethanol consumption was increased 24 h after imiquimod injections but did not occur until the third injection, suggesting adaptation to repeated TLR7 activation is necessary for increased drinking to occur. Notably, imiquimod reliably induced weight loss, indicating that sickness behaviour persisted across repeated injections. These findings show that TLR7 activation can modulate alcohol drinking in an operant self-administration paradigm and suggest that TLR7 and IRF7 signalling pathways may be a viable druggable target for treatment of AUD.
Article
Background: Inflammation is implicated in alcohol use disorder (AUD). Ibudilast, a neuroimmune modulator, shows promise for the treatment of AUD. Elevated inflammation, indicated by high levels of C-reactive protein (CRP), represents a possible subtype of AUD, which may be associated with treatment response to ibudilast. Objectives: The current study evaluated CRP as a predictor of treatment response to ibudilast; hypothesizing that ibudilast would be more effective at reducing drinking and alcohol cue-reactivity in individuals with higher CRP levels. Methods: This is a secondary analysis of a clinical trial of ibudilast for AUD, which found that ibudilast reduced heavy drinking in individuals with AUD. Fifty-one individuals were randomized to receive ibudilast (n = 24 [16 M/8F]) or placebo (n = 27 [18 M/9F]) for two weeks. Participants provided blood samples at baseline to assess CRP levels, completed daily assessments of alcohol use, and an fMRI alcohol cue-reactivity task at study mid-point. Models tested the effects of medication, CRP levels, and their interaction on drinks per drinking day and alcohol cue-reactivity. Results: There was a significant interaction between medication and CRP (F = 3.80, p = .03), such that the ibudilast high CRP group had fewer drinks per drinking day compared to the ibudilast low CRP group. CRP moderated the effect of medication on brain activation in a cluster extending from the left inferior frontal gyrus to the right-dorsal striatum (Z = 4.55, p < .001). This interaction was driven by attenuated cue-reactivity in the ibudilast high CRP group relative to the ibudilast low CRP and placebo high CRP groups. Conclusions: This study serves as an initial investigation into predictors of clinical response to ibudilast treatment and suggests that a baseline proinflammatory profile may enhance clinical efficacy.
Article
As the percentage of the global population over age 65 grows, and with it a subpopulation of individuals with alcohol use disorder (AUD), understanding the effect of alcohol on the aged brain is of utmost importance. Neuroinflammation is implicated in both natural aging as well as alcohol use, and its role in alterations to brain morphology and function may be exacerbated in aging individuals who drink alcohol to excess. The neuroimmune response to alcohol in aging is complex. The few studies investigating this issue have reported heightened basal activity and either hypo- or hyper-reactivity to an alcohol challenge. This review of preclinical research will first introduce key players of the immune system, then explore changes in neuroimmune function with aging or alcohol alone, with discussion of vulnerable brain regions, changes in cytokines, and varied reactions of microglia and astrocytes. We will then consider different levels of alcohol exposure, relevant animal models of AUD, and neuroimmune activation by alcohol across the lifespan. By identifying key findings, challenges, and targets for future research, we hope to bring more attention and resources to this underexplored area of research.
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Background High levels of sleep disturbances reported among individuals with alcohol use disorder (AUD) can stimulate inflammatory gene expression, and in turn, may alter pro-inflammatory cytokines levels. We aimed to investigate associations between pro-inflammatory cytokine markers with subjective measures of sleep quality, psychological variables and alcohol consumption among individuals with AUD. Methods This exploratory study is comprised of individuals with AUD ( n = 50) and healthy volunteers ( n = 14). Spearman correlation was used to investigate correlations between plasma cytokine levels and clinical variables of interest (liver and inflammatory markers, sleep quality, patient reported anxiety/depression scores, and presence of mood and/or anxiety disorders (DSM IV/5); and history of alcohol use variables. Results The AUD group was significantly older, with poorer sleep quality, higher anxiety/depression scores, and higher average drinks per day as compared to controls. Within the AUD group, IL-8 and MCP-1 had positive significant correlations with sleep, anxiety, depression and drinking variables. Specifically, higher levels of MCP-1 were associated with poorer sleep ( p = 0.004), higher scores of anxiety ( p = 0.006) and depression ( p < 0.001), and higher number of drinking days ( p = 0.002), average drinks per day ( p < 0.001), heavy drinking days ( p < 0.001) and total number of drinks ( p < 0.001). The multiple linear regression model for MCP-1 showed that after controlling for sleep status and heavy drinking days, older participants ( p = 0.003) with more drinks per day ( p = 0.016), and higher alkaline phosphatase level ( p = 0.001) had higher MCP-1 level. Conclusion This exploratory analysis revealed associations with cytokines MCP-1 and IL-8 and drinking consumption, sleep quality, and anxiety and depression in the AUD group. Furthermore, inflammatory and liver markers were highly correlated with certain pro-inflammatory cytokines in the AUD group suggesting a possible relationship between chronic alcohol use and inflammation. These associations may contribute to prolonged inflammatory responses and potentially higher risk of co-morbid chronic diseases.
Thesis
Multiple Sclerosis (MS) is an auto-immune mediated inflammatory and degenerative disease of the central nervous system characterized by loss of myelin and axonal integrity. MS often leads to an accrual of walking disability and worsening of fatigue. Exercise-dependent plasticity in the central nervous system, which involves upregulation of growth-promoting neurotrophins and suppression of inflammatory cytokines, may help restore lost ability to walk. Although aerobic training is an intervention that can potentially improve walking disability and reduce fatigue, these factors are also significant barriers to participating in exercise. Furthermore, because of thermal dysregulation, exercise-induced increases in body temperature leads to temporary worsening of symptoms in some MS patients. The purpose of my doctoral work was to develop and determine the feasibility of implementing a progressively intense aerobic treadmill training, in a room cooled to 16°C, for people with MS having walking disability, fatigue, and heat sensitivity. In the first study, I critically appraised and consolidated the research in animal models and clinical trials in order to determine the optimal training dosage and outcomes for a future exercise trial. The second study showed that people with MS-related disability consumed about three times more oxygen to complete relatively simple mobility activities such as rolling in bed, when compared to age and sex-matched healthy controls. The results of this study supported the importance of testing therapeutic aerobic training for this cohort of patients with barriers to exercise, such as fatigue. The third study outlined the effects of maximal aerobic exercise on neurotrophins and inflammatory cytokines iii among people with MS and controls. The final study established preliminary evidence for the feasibility of conducting progressively intense aerobic training on a bodyweight supported treadmill in a room cooled to 16°C. The benefits included significant improvements in walking speed, fatigue, aerobic fitness, and quality of life, while simultaneously altering serum levels of blood biomarkers of recovery such as brain-derived neurotrophic factor and interleukin-6, shifting the balance between repair and inflammation. Randomized controlled trials are needed to substantiate these preliminary findings, which in turn could lead to effective training options for people living with MS-related barriers to exercise participation.
Article
Alcohol-associated hepatitis (AH) is a clinical syndrome of jaundice, abdominal pain and anorexia due to prolonged heavy alcohol intake. AH is associated with changes in gene expression, cytokines, immune response, and the gut microbiome. There are limited biomarkers to diagnose and prognosticate in AH, but several non-invasive biomarkers are emerging. In this review, clinical risk-stratifying algorithms, promising AH biomarkers like cytokeratin-18 fragments, genetic polymorphisms and microRNAs will be reviewed.
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A molecular test for Alzheimer's disease could lead to better treatment and therapies. We found 18 signaling proteins in blood plasma that can be used to classify blinded samples from Alzheimer's and control subjects with close to 90% accuracy and to identify patients who had mild cognitive impairment that progressed to Alzheimer's disease 2–6 years later. Biological analysis of the 18 proteins points to systemic dysregulation of hematopoiesis, immune responses, apoptosis and neuronal support in presymptomatic Alzheimer's disease.
Article
Recent studies in alcoholic hepatitis have proposed a role for the cytokine tumour necrosis factor-alpha (TNF-alpha) a mediator of endotoxic shock in sepsis. In this study plasma levels of the closely related cytokine interleukin-6 (IL-6) were assayed in 96 samples from 58 patients with severe alcoholic hepatitis, and 69 patients in control groups (21 normal, 10 alcoholic without liver disease, 10 inactive alcoholic cirrhosis, 18 chronic liver disease, 10 chronic renal failure). Plasma IL-6 levels were markedly elevated in patients with alcoholic hepatitis when compared with all control groups (P less than 0.001). IL-6 levels were higher in patients who died (P = 0.04) and correlated with the features of severe disease including: increased grade of encephalopathy, increased neutrophil count, increased prothrombin ratio, hypotension, increased serum creatinine and increased serum bilirubin. Surprisingly, no correlation was found between levels of plasma IL-6 and plasma TNF-alpha or endotoxin, or the presence of infection; an inverse correlation was found between plasma IL-6 and serum globulins. These findings provide further evidence that the IL-6/TNF cytokine system is activated in severe alcoholic hepatitis and may mediate hepatic or extra-hepatic tissue damage.
Article
The aim of this review is to present and discuss the effect of different levels of alcohol consumption on the immune system. Not only the amount consumed but also the type of alcoholic beverage have to be taken into account in order to determine the consequences on activity, number, distribution, balance, interaction and response of immunocompetent cells. The association between alcohol exposure and the risk of developing an alcohol-related disease is multifactorial. In fact, age, gender, smoking habits, dietary intake and exercise are involved among other factors. The evaluation of the host cellular and humoral immune responses has shown that alcohol may induce some benefits when consumption is moderate. Moreover, those alcoholic beverages that contain antioxidants, such as red wine, could be protectors against immune cell damage. According to the literature consulted, the daily consumption of 10-12 g and 20-24 g of alcohol for women and men, respectively, is considered to be a moderate intake; the type of beverage has been established not to be important when defining moderation. Particular attention is often focused on the U- or J-shaped curve which also suggests that light to moderate drinking produces a protective effect. Such an inverse relationship indicates a reduction of risk for both light and moderate consumers and a higher risk not only for hard drinkers, but also for non-consumers.
Article
Alcohol biomarkers include tests indicative of acute or chronic alcohol consumption (state markers), and markers of a genetic predisposition to develop alcohol dependence after chronic exposure (trait markers). While a comprehensive trait marker for alcohol dependence has not been identified, a number of successful state markers for monitoring drinking status are used clinically. These tests provide direct or indirect ways to estimate the amounts of alcohol consumed and the duration of ingestion, and to detect any harmful effects on body functions resulting from long-term misuse. The most obvious method to prove recent drinking is by demonstrating the presence of ethanol in body fluids or breath, but, because ethanol is cleared fairly rapidly from the body, this method is limited to detect only very recent drinking. Measurement of urinary 5-hydroxytryptophol or ethyl glucuronide provide more sensitive methods to disclose recent drinking, because their washout constants are much longer than for ethanol. The liver functions test (GGT, AST and ALT in serum) and the mean corpuscular volume of erythrocytes (MCV) are among the standard diagnostic tools used to identify chronic alcohol exposure. The main disadvantage with these measures is that they have low sensitivity for recent excessive intake, and that raised levels may result from several causes besides heavy drinking, implying a low specificity for alcohol. Carbohydrate-deficient transferrin (CDT), which refers to changes in the carbohydrate composition of serum transferrin, is a more specific marker for identifying excessive alcohol consumption and monitoring abstinence during Outpatient treatment. The alcohol biomarkers improves knowledge of drinking patterns in both individuals and populations, and they are also valuable tools for the objective evaluation of treatment efforts. Alcohol markers have, for example, found uses in early identification of at-risk and harmful drinking, and they help to monitor abstinence and relapse in response to outpatient treatment.
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Four clinical interview questions, the CAGE questions, have proved useful in helping to make a diagnosis of alcoholism. The questions focus on Cutting down, Annoyance by criticism, Guilty feeling, and Eye-openers. The acronym "CAGE" helps the physician to recall the questions.How these questions were identified and their use in clinical and research studies are described.(JAMA 1984;252:1905-1907)
Article
Plasma tumor necrosis factor α (TNF α), interleukin 1 α (IL-1α), and interleukin 1 β (IL-1β) were measured in plasma samples obtained from 23 patients with severe alcoholic hepatitis on admission and after 30 days of hospitalization. Over a 2-year follow-up period, 14 patients died at a mean time of 8 months following discharge. The presence of elevated plasma TNF α either at admission or discharge from the hospital was associated with death in 82% (14/17) of patients. By contrast absence of elevated plasma TNF α was associated with survival in 100% (6/6). The difference in survival with and without detectable plasma TNF α was significant at p= 0.0022. Plasma TNF α was not elevated in alcoholic patients without clinically apparent liver disease, with alcoholic cirrhosis, or in nonalcoholic healthy controls. Plasma IL-1a was also significantly increased in alcoholic hepatitis whereas IL-1β was not. Neither IL-1α nor β was correlated with outcome in the alcoholic hepatitis group. It is concluded that the presence of elevated plasma TNF α is a significant predictor of decreased long-term survival in patients with severe alcoholic hepatitis.
Article
Alcohol use in response to stress in college students may be affected by the presence of symptoms of depression. However, this is a challenging issue to study due to the various methodologies used as well as the possible effect of depressed mood on the accuracy of self-report. This study focused on methodological issues as possible sources of equivocal findings regarding the relationship between depressed mood and alcohol use in response to stress in a college student population. Findings may differ when these variables are examined cross-sectionally versus longitudinally. Depressed mood and alcohol coping were assessed both cross-sectionally and repeatedly over time in 125 college students. Participants were assessed at baseline using a diagnostic self-report measure of depression as well as a measure of typical coping style. In addition, daily measures of stress, symptoms of depression, and coping were completed for 45 consecutive days. Different relationships between depressed mood and alcohol coping were found when depressed individuals were analyzed separately from those who were not depressed. Although a significant correlation between daily use of alcohol coping and daily depressed mood was found, there were no differences between depressed and nondepressed participants (as assessed at baseline) on daily alcohol coping. These findings have implications for research design as well as clinical assessment regarding the relationships between mood and use of alcohol for coping; the findings suggest that cross-sectional measures of mood and alcohol use may obscure differences as assessed repeatedly over time. In addition, these findings support the utility of frequent assessment of depressive symptoms when implementing or evaluating programs that target coping skills in college students.