Continued Alcohol Consumption Research Articles

Effect of Orally Ingested Water Containing H2-Filled Ultrafine Bubbles (UFBs) on Ethanol-Induced Oxidative Stress in Rats.

Ultrafine bubbles (UFBs), which are bubbles with diameters of less than 1 µm, are widely recognized for their ability to exist stably in liquid as a result of the effects of Brownian motion. In this study, we focused on hydrogen, known for its antioxidant potential, and explored the function of H2-filled UFBs, which encapsulate hydrogen, to determine their potential use as oral carriers for the delivery bioactive gases to living organisms. To this end, rats were orally administered ethanol to induce hepatic oxidative stress, and the effects of drinking H2-filled UFBs (H2 NanoGAS®) water for two weeks were evaluated to assess the reduction of oxidative stress. Continuous alcohol consumption was found to significantly increase the blood lipid peroxidation levels in the control group, confirming the induction of oxidative stress. An increase in blood lipid peroxidation was significantly inhibited by the consumption of concentrated H2 NanoGAS® (C-HN) water. Furthermore, the measurement of mitochondrial activity in the liver revealed that drinking H2 NanoGAS® water helped to maintain at a normal level and/or boosted the functional activity of the electron transport system in mitochondria affected by ethanol intake. To our knowledge, this study is the first to provide evidence for the use of orally ingested UFBs as carriers for the delivery gases to tissues, thereby exerting their physiological activity in the body. Our findings highlight the potential for the application of UFBs to various physiologically active gases and their utilization in the medical field in the future.

Sex differences in neuronal activation in the cortex and midbrain during quinine-adulterated alcohol intake.

Continued alcohol consumption despite negative consequences is a core symptom of alcohol use disorder. This is modeled in mice by pairing negative stimuli with alcohol, such as adulterating alcohol solution with quinine. Mice consuming alcohol under these conditions are considered to be engaging in aversion-resistant intake. Previously, we have observed sex differences in this behavior, with females more readily expressing aversion-resistant consumption. We also identified three brain regions that exhibited sex differences in neuronal activation during quinine-alcohol drinking: ventromedial prefrontal cortex (vmPFC), posterior insular cortex (PIC), and ventral tegmental area (VTA). Specifically, male mice showed increased activation in vmPFC and PIC, while females exhibited increased activation in VTA. In this study, we aimed to identify what specific type of neurons are activated in these regions during quinine-alcohol drinking. We assessed quinine-adulterated alcohol intake using the two-bottle choice procedure. We also utilized RNAscope in situ hybridization in the three brain regions that previously exhibited a sex difference to examine colocalization of Fos, glutamate, GABA, and dopamine. Females showed increased aversion-resistant alcohol consumption compared to males. We also found that males had higher colocalization of glutamate and Fos in vmPFC and PIC, while females had greater dopamine and Fos colocalization in the VTA. Collectively, these experiments suggest that glutamatergic output from the vmPFC and PIC may have a role in suppressing, and dopaminergic activity in the VTA may promote, aversion-resistant alcohol consumption. Future experiments will examine neuronal circuits that contribute to sex differences in aversion resistant consumption.

Continued use of alcohol accelerates cancer cachexia and impairs ability to induce 4E-BP1 but not p70S6K phosphorylation following muscle contraction

A primary co-morbidity of cancer is cancer cachexia characterized by the wasting of adipose tissue and skeletal muscle. Up to 80% of cancer patients may suffer from this wasting condition leading to reduced quality of life, poor treatment effectiveness and increased morbidity and mortality. The risk of cancer cachexia is enhanced in those with poor lifestyle habits including the habitual consumption of alcohol both prior to a cancer diagnosis and when consumption is continued during disease progression. The use of muscle contraction to improve outcomes in cachexia has been explored in alcohol naïve models with some success, however alcohol at high doses induces anabolic resistance preventing protein synthesis in response to an anabolic stimuli like muscle contraction. Therefore, muscle contraction may not be a suffcient stimuli to overcome cachexia induced catabolism when alcohol has been or is currently being consumed. The purpose of this work was to determine if alcohol induces anabolic resistance in tumor bearing mice or whether it can be used as a therapeutic intervention. It was hypothesized that alcohol would inhibit the stimulation of markers of the anabolic mTORC1 pathway in tumor bearing mice. METHODS: Female BALB/c mice, 12 weeks of age, were randomized into 4 groups (n = 12-14/group): control diet (CON), control diet-cancer (Cancer), Prior EtOH diet-cancer (PE-Cancer), and EtOH diet-cancer (E-cancer). All mice received the isocaloric Lieber DeCarli liquid diet with EtOH mice consuming 20% kcal/daily EtOH for 6 weeks. After 6 weeks, PE-cancer switched to the non-alcohol diet and all cancer groups had C26 carcinoma cells implanted. A single bout of maximal stimulated muscle contraction (10sets of 6 repetitions at 100Hz) was performed ~2 weeks later and muscles were collected 4 hours post contraction. RESULTS: E-cancer lost ~10% body mass, while no other cancer groups exhibited a significant loss in body mass indicating early-stage cachexia. Spleen mass was elevated in all cancer groups relative to control, while quadricep and gastrocnemius muscle weights were reduced in PE-cancer and E-cancer compared to CON. Muscle contraction significantly increased the phosphorylation of S6K1 Thr389 in all of groups except for PE-cancer where a strong trend was still detected (p=0.06). In contrast, phosphorylation of 4EBP1 Ser65 was only increased by muscle contraction in CON, as cancer prevented its stimulation. Therefore, despite accelerating body weight loss, continued alcohol consumption or prior alcohol consumption did not completely impair the anabolic response to maximally stimulated muscle contraction during the early stages of cancer cachexia. However, measurement of rates of degradation and synthesis over time are required to make further conclusions as to its therapeutic potential. Florida Department of Health Grant # 9BC03. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Efficacy evaluation of upper gastrointestinal endoscopy screening for secondary prevention of gastric cancer using the standardized detection ratio during a medical check-up in Japan.

We used standardized detection ratio to evaluate the quality of nasal upper gastrointestinal endoscopy screening for the secondary prevention of gastric cancer, and examined the gastric cancer risk in the era of total Helicobacter pylori (H. pylori) eradication. We performed 21,931 upper gastrointestinal endoscopies, 77 subjects were diagnosed with gastric cancer. Of these, 28 had gastric cancer after H. pylori eradication, 47 had gastric cancer with H. pylori-positive or others, and 2 had H. pylori-negative gastric cancer. The Standardized detection ratios for men and women were 5.33 and 4.82, respectively. Multivariable logistic regression analyses performed exclusively on first endoscopy subjects, excluding H. pylori-negative gastric cancer, revealed that smoking was a risk factor for developing gastric cancer (adjusted odds ratio, 3.31; 95% confidence interval, 1.65-6.64; p = 0.001). A statistically significant interaction was found between daily alcohol consumpption and H. pylori eradication on gastric cancer development (p = 0.005). In conclusion, relatively high standardized detection ratio values suggest that an appropriate endoscopic diagnosis of gastric cancer should be performed during a medical check-up. Smoking is a risk factor for developing gastric cancer, and continued alcohol consumption suggests a possible risk for developing gastric cancer after H. pylori eradication.

Lysine β-hydroxybutyrylation promotes lipid accumulation in alcoholic liver disease

Continuous (chronic or sub-chronic) alcohol consumption induces a metabolic byproduct known as ketone bodies, and the accumulation of ketones leads to a life-threatening syndrome called alcoholic ketoacidosis. However, the mechanism underlining the physiological effects of ketone accumulation in alcoholic liver disease (ALD) is still in its infancy. Here, we discovered that mitochondrial acetyl-CoA accumulation was diverted into the ketogenesis pathway in ethanol-fed mice and ethanol-exposed hepatocytes. Unexpectedly, global protein lysine β-hydroxybutyrylation (Kbhb) was induced in response to increased ketogenesis-derived β-hydroxybutyrate (BHB) levels both in hepatocytes and in livers of mice. Focusing on the solute carrier family (SLCs), we found that SLC25A5 presented obvious Kbhb at lysine residues 147 and 166. Kbhb modifications at these two lysine residues stabilized SLC25A5 expression by blocking ubiquitin–proteasome pathway. Subsequent mutation analysis revealed that Kbhb of SLC25A5 at K147 and K166 had site-specific regulatory roles by increasing peroxisome proliferator activated receptor gamma (PPARγ) expression, which further promoting lipogenesis. Additionally, 3-hydroxy-3-methylglutaryl-coenzyme A synthase 2 (HMGCS2), a rate-limiting enzyme for BHB production, was profoundly induced by ethanol exposure, and knockout of Hmgcs2 with CRISPR/Cas9 attenuated SLC25A5 Kbhb. Together, our study demonstrated a widespread Kbhb landscape under ethanol exposure and clarified a physiological effect of Kbhb modification on liver lipid accumulation.

H - 40 The Role of Neuropsychology in Solid Organ Transplantation Candidacy in a Patient with a Diverse Linguistic and Sociocultural Background.

Candidates for transplantation with end stage organ failure (ESOF) undergo extensive pre-surgical medical and psychosocial evaluations, however neuropsychology is rarely required. This is concerning, as patients with ESOF often have cognitive deficits that may impact their ability to safely manage post-transplant care and are at increased risk for morbidity/mortality. This case highlights the novel perspective a comprehensive neuropsychological evaluation provides, especially in patients of diverse sociocultural backgrounds. The patient is a 37-year-old monolingual Spanish-speaking woman referred for evaluation in the context of liver transplant candidacy due to apparent inability to follow medical guidance, medication adherence, and continued alcohol consumption. Medical history includes autoimmune hepatitis, multifocal hepatocellular carcinoma, and diabetes. The patient reported problems with remembering information from providers even with compensatory strategies. Her family assists heavily with scheduling and transportation. When asked about alcohol use, she reported recent use of a few beers due to very hot weather, limited access to clean water, and the death of a family member despite providers urging her to remain abstinent. She was not aware of the hazard that even minimal alcohol use presented to her candidacy. She did not meet criteria for a neurocognitive disorder. The etiology of her noncompliance was secondary to poor social support, limited coping skills, and feeling overwhelmed by team instructions. Conducting a culturally informed evaluation in the patient's native language provided clear evidence of intact cognition and a nuanced understanding of her limitations that would not be appreciated in a more limited evaluation.

Amelioration of ethanol-induced oxidative stress and alcoholic liver disease by invivo RNAi targeting Cyp2e1.

Alcoholic liver disease (ALD) results from continuous and heavy alcohol consumption. The current treatment strategy for ALD is based on alcohol withdrawal coupled with antioxidant drug intervention, which is a long process with poor efficacy and low patient compliance. Alcohol-induced CYP2E1 upregulation has been demonstrated as a key regulator of ALD, but CYP2E1 knockdown in humans was impractical, and pharmacological inhibition of CYP2E1 by a clinically relevant approach for treating ALD was not shown. In this study, we developed a RNAi therapeutics delivered by lipid nanoparticle, and treated mice fed on Lieber-DeCarli ethanol liquid diet weekly for up to 12 weeks. This RNAi-based inhibition of Cyp2e1 expression reduced reactive oxygen species and oxidative stress in mouse livers, and contributed to improved ALD symptoms in mice. The liver fat accumulation, hepatocyte inflammation, and fibrosis were reduced in ALD models. Therefore, this study suggested the feasibility of RNAi targeting to CYP2E1 as a potential therapeutic tool to the development of ALD.

Serotonin regulation of intermittent and continuous alcohol drinking in male and female C57BL/6J mice with systemic SB242084 and buspirone.

This study aims to assess the therapeutic potentials of novel serotonergic compounds in treating alcohol use disorders by investigating the effects of SB242084 and buspirone on intermittent and continuous alcohol consumption in male and female mice. Adult male and female C57BL/6J mice were given two-bottle choice to 20% ethanol and water on an intermittent or continuous availability schedule. Drug testing consisted of intraperitoneal injections of 0.3, 1, 3mg/kg SB242084 or 1, 3, 10mg/kg buspirone, and subsequent alcohol and water consumption were measured. To monitor the drug effects on anxiety-like and locomotor behavior, the highest dose of each compound was administered before free activity in an open field. SB242084 dose-dependently attenuated alcohol drinking for intermittent alcohol drinking in male mice but did not significantly alter alcohol drinking in mice given continuous access. Two-hour and four-hour female drinking behavior was unaffected by SB242084. In comparison, buspirone not only suppressed intermittent and continuous alcohol drinking in both males and females but also reduced distance traveled in the open field test. Observed differences in responses to SB242084 between drinking groups may imply differing neural mechanisms between episodic and continuous drinking driven by serotonin. Reductions in drinking after buspirone treatment may be related to non-specific properties. These findings suggest the therapeutic potential of compounds blocking the 5-HT2C receptor for alcohol use disorders.

The Effect of Alcohol Consumption in Unresectable Hepatocellular Carcinoma with Transarterial Chemoembolization.

Alcohol consumption can increase the risk of developing hepatocellular carcinoma (HCC). However, whether continuous alcohol consumption can influence outcomes in patients with HCC who undergo transarterial chemoembolization (TACE) remains unclear. This study aimed to explore the effect of alcohol consumption in patients with unresectable HCC who underwent TACE. The data used in the study were obtained from two centers and were retrospectively reviewed between January, 2014, and December, 2021. 254 patients with TACE were included in this study. Among them, 101 patients were continuous alcohol consumers and 153 patients had alcohol abstinence. Propensity score matching (PSM) and competing risk analysis were used to reduce the selection bias. The median overall survival (mOS) and median progression-free survival (mPFS) in the alcohol consumers' group were longer than those in the alcohol abstinence group, before and after PSM. Multivariate regression analysis showed that alcohol consumption increased all-cause mortality risk (HR: 1.486, 95% CI: 1.074-2.055; P=0.016) and tumor progression risk (HR: 1.434, 95% CI: 1.091-1.886; P=0.01) more than that with alcohol abstinence. In the competing risk analysis, after excluding deaths caused by other reasons, alcohol consumption increased cancer-specific mortality risk more than alcohol abstinence did before and after PSM. Adverse event analysis showed that alcohol consumption increased the risk of all grades of nausea and vomiting and grade III or IV nausea more than alcohol abstinence did after patients underwent TACE. Alcohol consumption may lead to a poor prognosis and increase adverse events in patients receiving TACE compared to those with alcohol abstinence.

Expert consensus on the diagnosis and management of alcoholic liver disease

<p>Alcoholic liver disease (ALD) is a spectrum of liver injuries caused due to harmful use of alcohol. It is the primary cause of liver disease and is responsible for around 4% of mortality worldwide. ALD progresses from fatty liver to alcoholic hepatitis depending upon risk factors, such as continued alcohol consumption or comorbid liver diseases. Screening and diagnosis are suggested for patients with histological symptoms and in high-risk populations. Management of ALD includes strategies such as abstinence from alcohol consumption, nutrition therapy, pharmacological therapy, and liver transplantation, with alcohol abstinence being the most beneficial to reverse fatty liver conditions. Various novel treatment approaches having distinct mechanisms of action are also developed besides conventional corticosteroid therapy, which include microbiota-based precision medicine, monoclonal antibody therapy, hepatocyte regeneration therapy, epigenetic modulators, liver degeneration boosters, and targeting the gut-liver axis. Ursodeoxycholic acid (UDCA) has shown to benefit ALD patients with cholestasis by exerting biochemical improvements; hence, it can be considered as an adjunct therapy. National and regional advisory board meetings were conducted to discuss the current diagnostic and management techniques, including existing and novel pharmacological treatments available for ALD along with current clinical practices in India.</p>

Chronic Ethanol Consumption Alters Presynaptic Regulation of Dorsal Striatal Dopamine Release in C57BL/6J Mice.

Alcohol use disorder (AUD) is characterized by escalating alcohol consumption, preoccupation with alcohol, and continued alcohol consumption despite adverse consequences. Dopamine has been implicated in neural and behavioral processes involved in reward and reinforcement and is a critical neurotransmitter in AUD. Clinical and preclinical research has shown that long-term ethanol exposure can alter dopamine release, though most of this work has focused on nucleus accumbens (NAc). Like the NAc, the dorsal striatum (DS) is implicated in neural and behavioral processes in AUD. However, little work has examined chronic ethanol effects on DS dopamine dynamics. Therefore, we examined the effect of ethanol consumption and withdrawal on dopamine release and its presynaptic regulation with fast-scan cyclic voltammetry in C57BL/6J mice. We found that one month of ethanol consumption did not alter maximal dopamine release or dopamine tissue content. However, we did find that D2 dopamine autoreceptors were sensitized. We also found a decrease in cholinergic control of dopamine release via β2-containing nAChRs on dopamine axons. Interestingly, both effects were reversed following withdrawal, raising the possibility that some of the neuroadaptations in AUD might be reversible in abstinence. Altogether, this work elucidates some of the chronic alcohol-induced neurobiological dysfunctions in the dopamine system.

Urolithin A attenuates severity of chronic pancreatitis associated with continued alcohol intake by inhibiting PI3K/AKT/mTOR signaling.

Heavy alcohol consumption is the dominant risk factor for chronic pancreatitis (CP); however, treatment and prevention strategies for alcoholic chronic pancreatitis (ACP) remains limited. The present study demonstrates that ACP induction in C57BL/6 mice causes significant acinar cell injury, pancreatic stellate cell (PSC) activation, exocrine function insufficiency, and an increased fibroinflammatory response when compared with alcohol or CP alone. Although the withdrawal of alcohol during ACP recovery led to reversion of pancreatic damage, continued alcohol consumption with established ACP perpetuated pancreatic injury. In addition, phosphokinase array and Western blot analysis of ACP-induced mice pancreata revealed activation of the phosphatidylinositol 3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) and cyclic AMP response element binding protein (CREB) signaling pathways possibly orchestrating the fibroinflammatory program of ACP pathogenesis. Mice treated with urolithin A (Uro A, a gut-derived microbial metabolite) in the setting of ACP with continued alcohol intake (during the recovery period) showed suppression of AKT and P70S6K activation, and acinar damage was significantly reduced with a parallel reduction in pancreas-infiltrating macrophages and proinflammatory cytokine accumulation. These results collectively provide mechanistic insight into the impact of Uro A on attenuation of ACP severity through suppression of PI3K/AKT/mTOR signaling pathways and can be a useful therapeutic approach in patients with ACP with continuous alcohol intake.NEW & NOTEWORTHY Our novel findings presented here demonstrate the utility of Uro A as an effective therapeutic agent in attenuating alcoholic chronic pancreatitis (ACP) severity with alcohol continuation after established disease, through suppression of the PI3K/AKT/mTOR signaling pathway.

Association Between Alcohol Consumption and Risk of Pancreatic Cancer: The Japan Public Health Center-Based Prospective Study.

Several studies have investigated the association between alcohol consumption and pancreatic cancer risk. However, these studies reported inconsistent results. This study included 95,812 participants from the Japan Public Health Center-Based Prospective Study, whose alcohol drinking habit was collected through the questionnaire of the baseline survey in 1990 to 1994 for Cohort I and in 1993 to 1995 for Cohort II, and followed-up until December 2013. The hazard ratios (HR) and 95% confidence intervals (CI) were calculated using multivariable-adjusted Cox proportional hazard regression models. During 1,969,101 person-years of follow-up, 598 patients (315 men and 283 women) were newly diagnosed with pancreatic cancer. No association was observed between alcohol consumption at baseline and pancreatic cancer risk in either men or women, even in the analyses conducted among men stratified by facial flushing responses or smoking status. When the population was limited to men whose alcohol drinking habit remained unchanged from the baseline survey to the 5-year follow-up survey, a significant association was observed in drinkers with alcohol consumption of 1 to 299 g/week compared with non/occasional drinkers (multivariable-adjusted HR, 1.73; 95% CI, 1.15-2.60). A significant association between alcohol consumption and pancreatic cancer risk was observed when the population was limited to men with a 5-year unchanged alcohol drinking habit and was particularly strong in never smokers. This study suggested an association between continuous alcohol consumption and pancreatic cancer risk in the Japanese population. However, further investigations using other cohort studies are required.

Novel Insights into Alcoholic Liver Disease: Iron Overload, Iron Sensing and Hemolysis.

The liver is the major target organ of continued alcohol consumption at risk and resulting alcoholic liver disease (ALD) is the most common liver disease worldwide. The underlying molecular mechanisms are still poorly understood despite decades of scientific effort limiting our abilities to identify those individuals who are at risk to develop the disease, to develop appropriate screening strategies and, in addition, to develop targeted therapeutic approaches. ALD is predestined for the newly evolving translational medicine, as conventional clinical and health care structures seem to be constrained to fully appreciate this disease. This concept paper aims at summarizing the 15 years translational experience at the Center of Alcohol Research in Heidelberg, namely based on the long-term prospective and detailed characterization of heavy drinkers with mortality data. In addition, novel experimental findings will be presented. A special focus will be the long-known hepatic iron accumulation, the somewhat overlooked role of the hematopoietic system and novel insights into iron sensing and the role of hepcidin. Our preliminary work indicates that enhanced red blood cell (RBC) turnover is critical for survival in ALD patients. RBC turnover is not primarily due to vitamin deficiency but rather to ethanol toxicity directly targeted to erythrocytes but also to the bone marrow stem cell compartment. These novel insights also help to explain long-known aspects of ALD such as mean corpuscular volume of erythrocytes (MCV) and elevated aspartate transaminase (GOT/AST) levels. This work also aims at identifying future projects, naming unresolved observations, and presenting novel hypothetical concepts still requiring future validation.

Auricular transcutaneous vagus nerve stimulation for alcohol use disorder: A chance to improve treatment?

Alcohol use disorder (AUD) is a relapsing-remitting condition characterized by excessive and/or continued alcohol consumption despite harmful consequences. New adjuvant tools, such as noninvasive brain stimulation techniques, might be helpful additions to conventional treatment approaches or even provide an alternative option for patients who fail to respond adequately to other treatment options. Here, we discuss the potential use of auricular transcutaneous vagus nerve stimulation (atVNS) as an ADD-ON intervention in AUD. Compared with other techniques, atVNS has the advantage of directly stimulating nuclei that synthesize GABA and catecholamines, both of which are functionally altered by alcohol intake in AUD patients. Pharmacological options targeting those neurotransmitters are widely available, but have relatively limited beneficial effects on cognition, even though restoring normal cognitive functioning, especially cognitive control, is key to maintaining abstinence. Against this background, atVNS could be a particularly useful add-on because there is substantial meta-analytic evidence based on studies in healthy individuals that atVNS can enhance cognitive control processes that are crucial to regaining control over drug intake. We discuss essential future research on using atVNS as an ADD-ON intervention in AUD to enhance clinical and cognitive outcomes by providing a translational application. Given that this novel technique can be worn like an earpiece and can be employed without medical supervision/outside the clinical settings, atVNS could be well integratable into the daily life of the patients, where the task of regaining control over drug intake is most challenging.

Alcohol dependence decreases functional activation of the caudate nucleus during model-based decision processes.

Impaired decision making, a key characteristic of alcohol dependence (AD), manifests in continuous alcohol consumption despite severe negative consequences. The neural basis of this impairment in individuals with AD and differences with known neural decision mechanisms among healthy subjects are not fully understood. In particular, it is unclear whether the choice behavior among individuals with AD is based on a general impairment of decision mechanisms or is mainly explained by altered value attribution, with an overly high subjective value attributed to alcohol-related stimuli. Here, we use a functional magnetic resonance imaging (fMRI) monetary reward task to compare the neural processes of model-based decision making and value computation between AD individuals (n=32) and healthy controls (n=32). During fMRI, participants evaluated monetary offers with respect to dynamically changing constraints and different levels of uncertainty. Individuals with AD showed lower activation associated with model-based decision processes in the caudate nucleus than controls, but there were no group differences in value-related neural activity or task performance. Our findings highlight the role of the caudate nucleus in impaired model-based decisions of alcohol-dependent individuals.

Long-term outcomes of hemostatic therapy for variceal bleeding and the challenge pending in the post-direct-acting antivirals era.

This study evaluated the longterm outcomes of mainly endoscopic hemostatic therapy for gastrointestinal variceal bleeding and of the transition of hemostatic therapy. Among 1,163 patients treated for gastrointestinal varices between April 2006 and June 2020, a total of 125 patients who underwent emergency hemostatic therapy were enrolled. Survival rates and secondary evaluation points were analyzed. Additionally, patients were classified into two groups: the previous and latter term. Patients' background, therapeutic method, and treatment results were compared between the groups. 94.4% had cirrhosis. The average Child-Pugh score was 8.90. Successful primary hemostasis rate was 98.4%, and 5.6% died within 2 weeks, all with a Child-Pugh score ≥9. The respective 1- and 5-year survival rates for Child-Pugh grade A/B were 81.3% and 55.4%, while those for Child-Pugh grade C were 58.1% and 17.8%. Child-Pugh grade C or hepatocellular carcinoma was significantly associated with poor prognosis. In total, 21.6% experienced variceal re-bleeding; 62.9% of these cases were triggered by continued alcohol consumption. There was no significant difference in survival between patients with and without variceal re-bleeding and in post-treatment survival between the previous and latter terms. In the latter term, the number of cases caused by continued alcohol consumption significantly increased. Multidisciplinary treatment and continuation of proper management after hemostatic therapy for variceal bleeding are crucial. Continued alcohol consumption leads to variceal bleeding and re-bleeding; its proper management, including alcohol abstinence, is one of the major challenges left in the post-directacting antivirals era.

Comparison of Pattern of Alcohol Consumption and Related Factors in Patients Referred to Referral Hospitals in Shahrekord, Iran (2016-2017)

Background and aims: The aim of the present study was to investigate the pattern of alcohol consumption and its related factors in the patients referring to hospitals. Methods: A hospital-based case control study was carried out in Shahrekord during 2016-2017. A total of 150 individuals who had self-report of alcohol consumption and history of alcoholism entered into the case group based on the convenience sampling method. Likewise, 300 individuals who did not have self-report of alcohol consumption entered into the control group. Group matching was performed based on the date of admission to the hospital, type of disease, complications, and duration of the disease. This study explored the pattern of alcohol consumption variables, spiritual health, quality of life, and general health. Odds ratios (ORs) with a 95% confidence interval (CI) were calculated as well. Results: The causes of onset of alcohol consumption were curiosity (41.40%), social class and imitation of others (17.40%), and life problems (15.30%). Further, the causes of continued alcohol consumption were attributed to the interest in taste and smelling (23.30%), emotional problems (20%), as well as loneliness feeling and life problems (12.60%). The mean of general health scores in the case and control groups were 29.8± 5 and 29.3± 4, respectively (P=0.296). The mean of the quality of life in the case group and control group were 32.13± 7 and 32.11± 5, respectively (P=0.98). The differences in the scores of spiritual health in two groups were not statistically significant (P=0.96). Conclusion: An attempt should be made to improve the strategies to satisfy the emotional sense and health recreations of society.

Continued alcohol consumption and hepatic encephalopathy determine quality of life and psychosocial burden of caregivers in patients with liver cirrhosis

BackgroundPatients with liver cirrhosis suffer from significantly reduced health-related quality of life and are often dependent on support from caregivers. In this context, caregivers often suffer from impaired quality of life (QoL) as well as psychosocial burden (PB). The aim of the present study was to identify factors influencing QoL and PB of caregivers in order to improve the social care of patients and caregivers.MethodsIn this cross-sectional study, 106 patients with liver cirrhosis and their caregivers were included. (Health-related) QoL was surveyed in patients (CLDQ) and caregivers (SF-36) and PB was determined by Zarit Burden Interview.ResultsAlcohol related liver cirrhosis (55%) was the predominant etiology of liver cirrhosis and the median MELD of the cohort was 14. QoL did not differ between patients with and without alcohol-related liver cirrhosis (p = 0.6). In multivariable analysis, continued alcohol consumption (p = 0.020), a history of hepatic encephalopathy (HE) (p = 0.010), poorer QoL of patients (p = 0.030) and poorer QoL of caregivers (p = 0.005) were associated with a higher PB of caregivers. Factors independently associated with poorer QoL of caregivers were continued alcohol consumption (p = 0.003) and a higher PB of caregivers (p = 0.030).ConclusionCaregivers of patients with liver cirrhosis suffer from impaired QoL and PB, especially in case of continued alcohol consumption or the occurrence of HE.

Las otras dianas del trastorno por uso de alcohol: Afectaciones sistémicas derivadas del consumo excesivo de alcohol

Drinking alcohol is an established and normalised practice in our society, even though it can physically harm us. High-risk alcohol drinking patterns can increase the chance of negative consequences for the drinkers or their environment. The liver is by far the organ most affected by alcohol abuse; however, alcohol use disorder is a systemic disease which affects a wide range of organs and psychological processes. Other systems that can be affected by continued alcohol consumption include the immune, neurological, and cardiovascular systems. In addition, alcohol can lead to epigenetic alterations that may be transmitted from one generation to the next.