Chronic Alcohol Abuse Research Articles

Arterial spin labeling perfusion in acute Wernicke encephalopathy: a case series discussion

Wernicke’s encephalopathy (WE) is a life-threatening neurologic disorder resulting from thiamine (vitamin B1) deficiency that can be secondary to chronic alcohol abuse, gastrointestinal surgery, systemic infectious and non-infectious diseases, and chemotherapy. WE is classically characterized on MRI by reduced diffusion and T2 prolongation along the mammillothalamic tracts, periaqueductal gray and tectal plate. We present two patients with acute WE who had baseline arterial spin labeling (ASL) perfusion at the time of presentation, demonstrating increase in cerebral blood flow (CBF) within the classically involved brain regions and concurrent global cerebral cortical hypoperfusion. Both patients were successfully treated with intravenous thiamine infusion. Post-treatment MRI demonstrated improvement of reduced diffusion and normalization of CBF within the involved structures. Prior histopathological studies have documented prominent undulation and luminal dilatation of arteries and arterioles in acute WE lesions, likely explaining the increased perfusion shown by imaging. The root of this pathophysiologic process may trace back to thiamine’s biochemical role in maintaining osmotic gradients and glucose metabolism, that if failed can lead to arterial hyper-perfusion. Our findings show that ASL-CBF can highlight the underlying pathophysiology in patients with acute WE by demonstrating increased CBF in involved central structures. This luxury perfusion may be a compensatory or protective mechanism by which increased metabolic demand is met in the acute setting and which, if treated timely, will show normalization of CBF on ASL imaging.

Long-term outcome of alcohol withdrawal seizures.

Alcohol withdrawal seizures (AWS) are a well-known complication of chronic alcohol abuse, but there is currently little knowledge of their long-term relapse rate and prognosis. The aims of this study were to identify risk factors for AWS recurrence and to study the overall outcome of patients after AWS. In this retrospective single-center study, we included patients who were admitted to the Emergency Department after an AWS between January 1, 2013 and August 10, 2021 and for whom an electroencephalogram (EEG) was requested. AWS relapses up until April 29, 2022 were researched. We compared history, treatment with benzodiazepines or antiseizure medications (ASMs), laboratory, EEG and computed tomography findings between patients with AWS relapse (r-AWS) and patients with no AWS relapse (nr-AWS). A total of 199 patients were enrolled (mean age 53 ± 12 years; 78.9% men). AWS relapses occurred in 11% of patients, after a median time of 470.5 days. Brain computed tomography (n = 182) showed pathological findings in 35.7%. Risk factors for relapses were history of previous AWS (p = 0.013), skull fractures (p = 0.004) at the index AWS, and possibly epileptiform EEG abnormalities (p = 0.07). Benzodiazepines or other ASMs, taken before or after the index event, did not differ between the r-AWS and the nr-AWS group. The mortality rate was 2.9%/year of follow-up, which was 13 times higher compared to the general population. Risk factors for death were history of AWS (p < 0.001) and encephalopathic EEG (p = 0.043). Delayed AWS relapses occur in 11% of patients and are associated with risk factors (previous AWS >24 h apart, skull fractures, and pathological EEG findings) that also increase the epilepsy risk, that is, predisposition for seizures, if not treated. Future prospective studies are mandatory to determine appropriate long-term diagnostic and therapeutic strategies, in order to reduce the risk of relapse and mortality associated with AWS.

A Case Report on Alcohol Dependence Syndrome with Relation to Insomnia

Alcohol dependence is a pattern of substance use, leading to clinically significant impairment or distress; chronic alcohol abuse has been known to disrupt the normal sleep cycle and lead to sleep disorders, including sleep terror disorder. A male patient of age 42 years was a known alcoholic for 24 years, and the patient does not have any previous psychiatric history. Then, he stopped drinking for four days and developed insomnia. The patient gave an account of emotional outbreaks from 2 days; vital signs included blood pressure 140\90 , pulse rate 81 bpm, respiratory rate 20 , and oxygen saturation 97%@RA and the patient's GRBS level was 210 mg\, and the patient was immediately given with medication in. 4mg (IV), . (2 amp in 100 ml NS, BD), . Panto 40mg (IV), the same drug, was continued for three days, and there was no complaint of visual hallucinations. The patient felt symptomatically better and was discharged on the 4th day with no fresh complaints. The patient was advised to continue Tab. 2mg for three days. The preliminary case investigation evaluated the link between insomnia and alcohol dependence syndrome (ADS).

Human Alcohol-Microbiota Mice have Increased Susceptibility to Bacterial Pneumonia.

Preclinical studies have shown that chronic alcohol abuse leads to alterations in the gastrointestinal microbiota that are associated with behavior changes, physiological alterations, and immunological effects. However, such studies have been limited in their ability to evaluate the direct effects of alcohol-associated dysbiosis. To address this, we developed a humanized alcohol-microbiota mouse model to systematically evaluate the immunological effects of chronic alcohol abuse mediated by intestinal dysbiosis. Germ-free mice were colonized with human fecal microbiota from individuals with high and low Alcohol Use Disorders Identification Test (AUDIT) scores and bred to produce human alcohol-associated microbiota or human control-microbiota F1 progenies. F1 offspring colonized with fecal microbiota from individuals with high AUDIT scores had increased susceptibility to Klebsiella pneumoniae and Streptococcus pneumoniae pneumonia, as determined by increased mortality rates, pulmonary bacterial burden, and post-infection lung damage. These findings highlight the importance of considering both the direct effects of alcohol and alcohol-induced dysbiosis when investigating the mechanisms behind alcohol-related disorders and treatment strategies.

Immune microenvironment changes of liver cirrhosis: emerging role of mesenchymal stromal cells.

Cirrhosis is a progressive and diffuse liver disease characterized by liver tissue fibrosis and impaired liver function. This condition is brought about by several factors, including chronic hepatitis, hepatic steatosis, alcohol abuse, and other immunological injuries. The pathogenesis of liver cirrhosis is a complex process that involves the interaction of various immune cells and cytokines, which work together to create the hepatic homeostasis imbalance in the liver. Some studies have indicated that alterations in the immune microenvironment of liver cirrhosis are closely linked to the development and prognosis of the disease. The noteworthy function of mesenchymal stem cells and their paracrine secretion lies in their ability to promote the production of cytokines, which in turn enhance the self-repairing capabilities of tissues. The objective of this review is to provide a summary of the alterations in liver homeostasis and to discuss intercellular communication within the organ. Recent research on MSCs is yielding a blueprint for cell typing and biomarker immunoregulation. Hopefully, as MSCs researches continue to progress, novel therapeutic approaches will emerge to address cirrhosis.

Diagnosis and Management of Marchiafava-Bignami Disease, a Rare Neurological Complication of Long-term Alcohol Abuse.

Marchiafava Bignami disease (MBD) is a neurological disorder characterized by myelin degeneration and tissue necrosis within the central nervous system. This condition predominantly afflicts individuals with chronic alcohol abuse and malnutrition. The most distinctive pathological feature of MBD is the necrotic degeneration specifically observed in the corpus callosum; however, emerging evidence also indicates the potential involvement of other brain regions. The main pathophysiological mechanisms involve alcohol consumption, which leads to thiamine depletion and disrupts various metabolic pathways. This, in turn, hinders myelin synthesis and impairs signal transmission, resulting in a wide range of symptoms and signs. MBD can manifest in different stages, including acute, subacute, and chronic, each with varying severity. Diagnosing MBD can be challenging due to its presenting symptoms being nonspecific. In the era preceding the development of sophisticated imaging methodologies, the diagnosis of MBD was primarily established through postmortem examination conducted during autopsies. However, with a detailed medical history and imaging modalities such as magnetic resonance imaging (MRI) and computed tomography (CT), it is now possible to diagnose MBD and differentiate it from other diseases with similar clinical presentations. MRI is considered the gold standard for visualizing lesions in the corpus callosum and other affected areas. Also, positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance spectroscopy (MRS) could show brain damage in the corpus callosum associated with MBD. MRI-diffusion-weighted imaging (DWI) detects early lesions, while diffusion tensor imaging (DTI) investigates clinical manifestations and recovery. Poor prognostic indicators for MBD include extensive cerebral cortex involvement and severe disturbances in consciousness. Differential diagnosis involves ruling out other alcohol-related disorders, such as neoplastic conditions, Wernicke's encephalopathy, and multiple sclerosis, among others, through careful evaluation. The therapeutic strategies for the management of MBD are currently lacking definitive establishment; however, available evidence indicates that targeted interventions have the potential to induce amelioration. Corticosteroids offer prospective advantages in addressing brain edema, demyelination, and inflammation; research findings present a heterogeneous outcome pattern. Notably, thiamine treatment reduces the likelihood of unfavorable consequences, particularly when administered promptly, and thus is endorsed as the primary therapeutic approach for MBD. This review will highlight this rare disease that many healthcare providers might not be familiar with. By understanding its clinical presentation, differential diagnosis, imaging, and management, medical providers might better identify and diagnose MBD. Raising awareness about this condition can lead to better prevention, early detection, and timely intervention.

Smoking cessation pharmacotherapy use during index hospital admission following cystectomy for bladder cancer: A retrospective cohort study.

To identify gaps in urologic oncology quality and evidence-based smoking cessation care by assessing how often smoking cessation pharmacotherapy (SCP) is given in the inpatient setting following cystectomy. The Premier Healthcare Database (PHD), a deidentified all-payer dataset, was used to generate nationally representative estimates of SCP receipt during hospitalization following cystectomy for patients with bladder cancer who smoke. Regressions were used to model associations between SCP receipt and patient- and hospital-level factors. Of the 21,624 patients who underwent cystectomy for bladder cancer, 3,676 patients (17.0%) were identified as current smokers, representing a weighted estimate of 16,063 admissions. Among these admissions, 27.9% of patients received SCP, the vast majority of which (91.5%) received exclusively nicotine replacement therapy. Rates of SCP receipt varied substantially across hospitals (median: 25.0%, IQR: 20.0-33.3, range: 0.0-60.0). Older age and black race (aOR = 0.59, 95% CI: 0.42-0.82) were associated with lower odds of SCP receipt. Increased patient comorbidity score was associated with higher odds of SCP receipt (aOR = 1.02, 95% CI: 1.01-1.03); specifically, chronic pulmonary disease, alcohol abuse, and depression were independently associated with SCP receipt. Hospital teaching status, bed capacity, and mean annual cystectomy volume were not associated with SCP receipt. SCP receipt was not associated with hospital length of stay nor 90-day readmission or mortality following cystectomy. SCP is infrequently given to patients who smoke during their hospitalization following cystectomy for bladder cancer, representing a gap in quality urologic oncology care and a missed opportunity to effectively intervene with evidence-based treatment.

Burden and predictors of subsequent/recurrent stroke, associated sex/racial disparities and in-hospital outcomes in elderly patients with obstructive sleep apnea and prior stroke/TIA

Abstract Funding Acknowledgements Type of funding sources: None. Background Obstructive Sleep Apnea (OSA) increases the risk of cardiovascular events and stroke. However, limited data on burden and impact of OSA on recurrent/subsequent stroke and associated hospitalization outcomes in geriatric patients (G-OSA) with prior stroke/TIA prompted us to perform this analysis. Methods The National Inpatient Sample (2019) was used to identify patients with G-OSA and prior stroke/TIA. We compared the rate of SS by sex and racial subgroups. We subdivided the G-OSA with and without subsequent stroke (SS+ vs SS-) and compared demographics and comorbidities. Primary outcomes included prevalence of SS, subsequentin-hospital all-cause mortality and multivariate predictors of SS in G-OSA patients with prior stroke/TIA. Secondary outcomes included healthcare resource utilization between SS+ vs SS- cohorts. Results Of 133,545 patients admitted with G-OSA and prior history of stroke/TIA, 4.9% (6520) had subsequent strokes including 3.7% of acute ischemic stroke (AIS). SS+ cohort comprised mainly of Males, Asian-Pacific Islander cvs. SS- cohort. On subgroup analysis based on Racial and gender distribution, the rate of SS was highest in Asian/Pacific islander (6%), and Native Americans (5.6%) followed by white, blacks and Hispanics, (4.9%, 4.6% &amp; 4.1%), and Males had higher prevalence vs females (5.2% vs 4.4%; p&amp;lt;0.001). In addition, despite similar median age of admission, SS+ cohort had higher burden of uncomplicated hypertension (42.7% vs 29.7%), diabetes without chronic complications (17.9% vs 12.8%), hyperlipidemia (76.5% vs 71.7%) and alcohol abuse (2.8% vs 1.6%) (all p&amp;lt;0.001). Furthermore, a higher all-cause in-hospital mortality was noticed in in SS+ cohort (5.1% vs 1.6%; p&amp;lt;0.001), which was prominently highger in Hispanics compared to whites and blacks (10.6% vs 4.9% vs 4.4%; p&amp;lt;0.001) respectively with no gender disparity noticed. Significant clinical predictors of SS in G-OSA patients on multivariable regression analysis were found to be complicated and uncomplicated hypertension (aOR 2.17 [95CI 1.78-2.64; 3.18 [2.58-3.92]), diabetes with chronic complications (aOR 1.28 [95CI 1.08-1.51]), hyperlipidemia (aOR 1.24 [95CI 1.08-1.43]) and thyroid disorders (aOR 1.69 [95CI 1.14-2.49]). However, we noticed lower odds of SS in patient with obesity (0.86 [0.76-0.98]), prior MI (aOR 1.27 [95CI 1.22-1.33]) and chronic pulmonary disease (aOR 0.54[95CI 0.47-0.62]) [Table 1]. The SS+ cohort had fewer routine discharges and higher healthcare cost. Conclusion Nearly 5% of G-OSA patients with prior stroke/TIA history were hospitalized with a subsequent stroke which showed significantly higher mortality rate compared to patients with no subsequent stroke and had considerably higher healthcare resource utilization. Comorbidities including hypertension, diabetes, dyslipidemia and admissions in rural hospitals were independent predictors of having SS and warrant preventive strides for secondary prevention of stroke.

A patient with dyskeratosis congenita and portal hypertension

AbstractPortal hypertension (PH) refers to a collection of syndromes characterized by an increase in pressure within the portal venous system and/or elevated portal venous blood flow, most commonly caused by cirrhosis. This condition is frequently associated with viral hepatitis and chronic alcohol abuse, and its complications, such as ascites, hepatic encephalopathy, and esophageal varices, have a considerable impact on mortality. Dyskeratosis congenita (DC) is a rare genetic disorder that affects multiple systems, most notably manifesting as dystrophy of the fingernails and toenails, skin pigmentation, and mucosal leukoplakia. While cirrhotic PH is an uncommon complication of DC, we present a case of a young patient who presented with PH and had no history of hepatitis or heavy alcohol use. The patient underwent splenectomy and devascularization to treat hypersplenism and esophagogastric varices caused by PH but developed portal vein thrombosis following the surgery. Given the patient's cutaneous manifestations and cirrhosis that could not be attributed to common causes, we continued to search for the underlying cause of PH until the diagnosis of DC was finally made. The patient was subsequently treated with carvedilol to prevent variceal rebleeding and showed no significant complications or bleeding during follow‐up.

Ruptured arteriovenous malformation mortality: Incidence, risk factors, and inpatient outcome score.

Limited literature exists on the morbidity and mortality of AVM associated intracerebral hemorrhage (ICH) compared with non-AVM ICH. We examine morbidity and mortality in cAVM in a large nationwide inpatient sample to create a prognostic inpatient ruptured AVM mortality score. This retrospective cohort study from 2008 to 2014 compares outcomes in cAVM related hemorrhages and ICH utilizing the National Inpatient Sample database. Diagnostic codes for ICH and AVM underlying ICH were identified. We compared case fatality according to medical complications. Multivariate analysis was used to derive hazard ratios and 95% confidence intervals to assess odds of mortality. We identified 6496 patients with ruptured AVMs comparing them to 627,185 admitted with ICH. Mortality was lower for ruptured AVMs (11%) compared to ICH (22%) [p < 0.01]. Mortality associated factors were liver disease (OR 2.64, CI 1.81-3.85, p < .001), diabetes mellitus (OR 2.42, CI 1.38-4.22, p = 0.002), alcohol abuse (OR 1.81, CI 1.31-2.49, p = 0.001), hydrocephalus (OR 3.35 CI 2.81-4.00, p < 0.001), cerebral edema (OR 1.5, 1.25-1.85, p < 0.001), cardiac arrest (OR 15, CI 7.9-30, p < 0.001), and pneumonia (OR 1.93, CI 1.51-2.47, p < 0.001). A 0-5 ruptured AVM mortality score was developed: Cardiac arrest (=3), age >60 (=1), Black race (=1), chronic liver failure (=1) diabetes mellitus (=1), pneumonia (=1), alcohol abuse (=1) and cerebral edema (=1). Mortality increased with score. No patient with 5 or more points survived. The Ruptured AVM Mortality Score allows for risk stratification on patients with ICH due to ruptured AVM. This scale could prove useful in prognostication and patient education.

Alcoholic cardiomyopathy- characterization and outcomes

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Alcoholic cardiomyopathy is a severe consequence of chronic alcohol abuse and causes gradual changes in the structure and function of the heart, being a form of dilated cardiomyopathy. Purpose To characterize the population of patients (pts) with alcoholic cardiomyopathy (AC) in terms of baseline characteristics, echocardiographic parameters, alcohol consumption, medication and outcomes. We also intended to evaluate the impact of alcohol reduction/cessation. Methods We performed a retrospective study of the group of pts with the diagnosis of AC, established after exclusion of other aetiologies, followed in the heart failure consultation between 2018 and 2022. We divided the population into patients who maintained (2), reduced (1) (to an average of 2 drinks in men and 1 in women) or discontinued consumption (0). Results A total of 39 pts with a mean age of 68.13 ± 11 years were included. Of these, 35 were males (89.7%). In terms of cardiovascular risk factors, 64.1% had hypertension, 33.3% had diabetes, 53.5% dyslipidaemia, 10.3% had chronic hepatic disease, 30.8% were smokers and 10.3% ex-smokers. The prevalence of atrial fibrillation (AF) was 46.2%, with a median heart rate of 72.50 ± 20.99 bpm. At the beginning of follow-up, this population had a mean left ventricular ejection fraction (LVEF) of 30.46% ± 9.99, a mean indexed LA volume of 58.5 ml/m2 ± 32.63 and a mean indexed LV volume 87.44% ± 27.73. Concerning the alcohol consumption, during the follow-up, 43.6% of the patients stopped drinking alcohol, 10.3% reduced the habits and 20.5% maintained the consumption. Regarding the medication, at the end of follow-up 24.4% were medicated with sacubitril/valsartan, 51.1% with angiotensin-converting enzyme inhibitors, 71.1% with beta blockers, 51.1% with mineralocorticoid receptor antagonists and 35.6% with SGLT2 inhibitors. In a mean follow-up of 26.62± 11.11 months, there was a significant improvement of the ejection fraction (mean of 9.59% ± 12.97, p&amp;lt; 0.001), with a mean LVEF of 40.59% ± 12.78 at the end of follow-up. In fact, in 17.8% of the patients the final LVEF was more than 50%. Regarding indexed LV volume, there was a significant reduction during follow-up (102.250 ± 43.46 ml/m2, p= 0.018). Concerning alcohol consumption, pts who quit drinking had a mean improvement of LVEF of 13,73% ± 15.83 (p= 0.003), pts who reduced alcohol consumption 8.6% ± 5.81 (p=0.03) and pts that kept the consumption 2.67% ± 3.01 (p= 0.82). The variation of LVEF was statistically significant between the groups (p=0.03). These three groups had no statistically significant differences in medical history of hypertension (p=0.37), diabetes (p=0.22), dyslipidaemia (p=0.17), AF (p=0.70) and medication. Conclusion Pts with alcoholic cardiomyopathy had a high prevalence of atrial fibrillation and cardiovascular risk factors. Improvement and even recovery of cardiac function depends on reduction/extinction of alcohol consumption.

PO-05-134 BURDEN OF ARRHYTHMIAS IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND SLEEP APNEA

The prevalence of sleep apnea in patients with chronic kidney disease (CKD) is much more than in the general population. There is evidence of a bidirectional relationship between sleep apnea and CKD. Cardiovascular manifestations leading to worse outcomes in both conditions are well known. We studied the burden of arrhythmias and its impact on patients with CKD and sleep apnea. To study the burden of arrhythmias and its impact on patients with CKD and sleep apnea National Inpatient sample 2018-2020 was queried for adult patients with CKD stage 3-5. These patients were stratified based on the prevalence of sleep apnea. Demographics and association with different arrhythmias were analysed in both groups. Multivariate regression analysis was performed to study the impact of arrhythmias on mortality and total hospital cost in patients with CKD stage 3-5 and sleep apnea. A total of 13216345 adults with CKD stage 3-5 were hospitalised from 2018-2020 with a mean age of 73 years. 14.92% (n=1971955) of these patients had underlying sleep apnea out of which 40.03% were females. In the cohort of CKD, patients with sleep apnea had a higher prevalence of obesity (48.13% vs 16.49%; P<0.0001), hypertension (93.24% vs 88.78%; P<0.0001), chronic heart failure (21.98% vs 15.87%; P<0.0001), alcohol abuse (1.20 vs 0.92; P<0.0001) and hypothyroidism (21.16% vs 19.66%; P<0.0001). Arrhythmias including atrioventricular blocks, atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation were also more prevalent in patients with sleep apnea (Table 1). The prevalence of all these arrhythmias in patients with sleep apnea was 42.87% compared to 34.77% in patients without sleep apnea in a subgroup of CKD (P<0.0001). Multivariate regression analysis revealed 1.58 times higher odds of developing arrhythmias due to sleep apnea in patients with CKD (OR-1.58; C.I: 1.57- 1.59; P<0.0001). In a subgroup of patients with CKD and sleep apnea, the adjusted odds of mortality due to arrhythmia was 1.74 and total hospital cost was $13023 higher than those without arrhythmias (Table 2). Sleep apnea is an independent predictor for developing arrhythmias in patients with CKD. Arrhythmias tend to portend a worse prognosis and levy a higher burden on healthcare in patients with CKD and sleep apnea. Further studies are needed to better manage these cardiac complications to improve outcomes in patients with CKD.

NEUROGENIC BLADDER INDUCED BY CHRONIC ALCOHOL ABUSE: A CASE REPORT

Long-term alcohol consumption may produce wide-ranging effects on the autonomic and peripheral nervous systems like almost all body tissues, but the pathogenesis is still under debate. We presented an extremely rare case of autonomic neurogenic bladder with bilateral hydroureteronephrosis in a male patient describing progressive abdominal distension over a year that is most significant in the last 4 months following alcohol withdrawal after a long duration of alcohol abuse. Chronic alcoholism should be considered in the differential diagnosis of a neurogenic bladder, which may be caused by autonomic dysfunction due to chronic alcohol abuse and may be precipitated by alcohol withdrawal.

Autophagy and exosomes coordinately mediate quercetin's protective effects on alcoholic liver disease

Alcoholic liver disease (ALD), a spectrum of liver abnormalities induced by chronic alcohol abuse, continues to be the major cause of life-threatening liver disease in developed countries. Autophagy and exosomes were individually confirmed to be involved in the pathogenesis of ALD. Here, we sought to identify the role of autophagy and exosomes in the liver protective effects of quercetin. We observed decreased hepatic LC3II/LC3I and increased p62 level in ethanol-fed mice, and these changes were alleviated by quercetin. Meanwhile, nanoparticle tracking analysis (NTA) showed elevated serum exosomes numbers in ethanol-fed mice, which was combated by quercetin. Ethanol induced elevated LDH, ALT, and AST in HepG2 supernatant, which was alleviated by cytochalasin D (exosomes uptake inhibitor). Moreover, quercetin reduced ethanol-induced LDH and ALT elevation in vitro, and the effects of quercetin were reversed by Rab27a overexpression (induce exosomes release) or wortmannin treatment (autophagy inhibitor). Transcriptomic analysis supported that quercetin reversed the change of lysosome related genes disturbed by ethanol. Meanwhile, western blot analysis exhibited decreased hepatic expression of LAMP2 and ATPA6V1B2, and active Cathepsin B/Cathepsin B by quercetin treatment, indicating quercetin alleviated lysosome dysfunction in ethanol-fed mice. Baf A treatment or transfection of siTFEB offset quercetin's effects in ethanol-induced LDH and ALT elevation, exosomes release, and autophagy inhibition (LC3II/I and p62 accumulation). Taken together, quercetin coordinately activates autophagy and combats exosomes release by restoring lysosome function, and further mitigates ethanol-induced liver damage.

THE COMPLEXITY OF DUAL PATHOLOGY: REGARDING A CASE REPORT OF SEIZURES

IntroductionWernicke’s encephalopathy (WE) is a potentially reversible neuropsychiatric emergency caused by thiamine deficiency, whose classical triad consists of acute onset of confusion, gait ataxia, and oculomotor dysfunction. The diagnosis is missed in 75-80% of cases and approximately 80% of untreated patients develop Korsakoff Syndrome, which is characterized by memory impairment associated with confabulation. Early recognition of nutritional deficiency or any portion of the triad is critical and should prompt treatment, since WE is readily reversible if treated with adequate doses of parenteral thiamine.ObjectivesStarting from a case report of suspected WE, we pretend to discuss the differential diagnosis of seizures in dual pathology.MethodsNon-systematic review of the literature was performed in PubMed database using the keywords “Wernicke’s Encephalopathy”, “Seizures”, “Alcohol” and “Benzodiazepines”. The articles were selected according to their relevance. A patient´s clinical record was reviewed and presented.ResultsWe present a case of a 44-year-old Ukrainian man with suspected background of chronic alcohol abuse and psychiatric history of schizoaffective disorder, who presented with acute onset of confusion, psychomotor agitation, gait ataxia and nystagmus. Anamnesis was hampered by the language barrier and absence of past medical history and patient’s alcoholic habits remained unclear. After suspicion of WE it was introduced thiamine and diazepam, with significant improvement. After discontinuation of diazepam, the patient presented with several episodes of tonic-clonic seizures. He was medicated for seizures with clinical stabilization. At time of discharge the diagnostic discussion prevailed.Seizures are a common presentation of various conditions associated with alcohol use, whose differential diagnosis is difficult, especially in patients with dubious alcohol consumption. Alcohol abuse is a major precipitant of status epilepticus as seizure threshold is raised by alcohol drinking. Seizures may also occur during alcohol withdrawal, for which treatment with benzodiazepines is recommended, however carefully, since both abrupt cessation and high-dose use are critical for the appearance of seizures. Although very rare, WE may also present with seizures, whereby overdiagnosis and overtreatment are preferred to prevent persistent neurocognitive impairments.ConclusionsThis case illustrates the complexity of neuropsychiatric diagnoses in dual pathology. It requires a longitudinal assessment for a better understanding of clinical conditions and establishment of the best therapeutic approach.Disclosure of InterestNone Declared

Groove Pancreatitis-Tumor-like Lesion of the Pancreas.

Groove pancreatitis (GP) is an uncommon appearance of pancreatitis represented by fibrous inflammation and a pseudo-tumor in the area over the head of the pancreas. The underlying etiology is unidentified but is firmly associated with alcohol abuse. We report the case of a 45-year-old male patient with chronic alcohol abuse who was admitted to our hospital with upper abdominal pain radiating to the back and weight loss. Laboratory data were within normal limits, except for the level of carbohydrate antigen (CA) 19-9. An abdominal ultrasound and computed tomography (CT) scan revealed swelling of the pancreatic head and duodenal wall thickening with luminal narrowing. We performed an endoscopic ultrasound (EUS) with fine needle aspiration (FNA) from the markedly thickened duodenal wall and the groove area, which revealed only inflammatory changes. The patient improved and was discharged. The principal objective in managing GP is to exclude a diagnosis of malignancy, whilst a conservative approach might be more acceptable for patients instead of extensive surgery.

Protective Role of Herbal Plants in Hepatotoxicity

Purpose: The liver is largest metabolic organ involved in detoxification and synthesis of essential biomolecules in the human body. Liver damage occurs due to chronic alcohol abuse, viral infections (Hepatitis A, B, C) medicines, poor hygiene, smoking, dietary substances, chemicals (Carbon tetra chloride, thioacetamide, acetaminophen, D-Galactosamine) or herb induced hepatotoxicity. The liver filters all the blood from the digestive tract, before passing it to the rest of the body to avoid the entry of toxins in the other body system and prevent severe consequences. Hepatic insufficiency may increase plasma total cholesterol and triacylglycerols with high risk of atheroscelerosis and cardiovascular disease. Free radical formation in the alcohol use result in development of hepatitis leading to cirrhosis. Plants have been used to protect liver injury by various chemicals.&#x0D; Methodology: In this study we reviewed some popular herbal plants having hepatoprotective potential.&#x0D; Findings: Polyphenols, flavonoids, terpenoids are natural antioxidants and the consumption of foods that contain these compounds in large quantities seems to play an important role in prophylaxis against many diseases.&#x0D; Unique Contribution to Theory, Practice and Policy: Herbal drugs are safe and have potential to cure hepatotoxicity. In India many plants have been identified as hepatoprotective drugs and used to treat liver disorders.

Abstract TP66: Trends In Alcohol Abuse In Patients With Intracerebral Hemorrhage: A 20-year Analysis Of The Nationwide Inpatient Sample

Introduction: While chronic alcohol (EtOH) abuse has long been considered a risk factor for several cardiovascular disorders including ischemic stroke, the relationship between intracerebral hemorrhage (ICH) and EtOH abuse is less known. Objective: To characterize ICH patients with EtOH abuse and examine the effects of EtOH abuse on in-hospital outcomes over 20 years. Methods: A query of the 2000-2019 National Inpatient Sample was performed for patients admitted with ICH (ICD9 431, 432.9, ICD-10 I61, I62.9). Demographics, comorbidities, and outcomes were identified. Univariate analysis with t-tests or chi-square performed as appropriate. A 1:1 nearest neighbor propensity score matched cohort was generated. Variables with standardized mean differences &gt;0.1 used in multivariate regression to generate adjusted odds ratios (AOR)/β-coefficients for EtOH abuse on outcomes. Significance set at an alpha level of &lt;0.001. All analysis performed in R version 4.1.3. Results: In total, 2,000,868 patients with ICH were identified; 106,987 (5.3%) abused EtOH. EtOH abuse patients had higher Elixhauser Comorbidity Score (12.95 ± 10.51 vs. 10.28 ± 8.98; p&lt;0.001) and a non-significantly lower NIH Stroke Score (11.0 ± 8.69 vs. 11.34 ± 9.53; p &gt;0.001). Patients with EtOH abuse were more likely to be male, younger, smokers, on Medicaid, be in the 0-25% percentile median income bracket, and have atrial fibrillation, hyperlipidemia, diabetes, and seizures (all p&lt;0.001). Patients with EtOH abuse had less in-hospital mortality, more discharge home or short term hospital, longer hospital stays and more hospital charges (all p&lt;0.001), but after propensity matching and regression analysis these differences were no longer significant. Conclusion: This 20 year nationally representative propensity matched analysis of patients with ICH demonstrates that concomitant EtOH does not significantly worsen in-hospital outcomes despite a higher association of other comorbidities.

Phenobarbital and Alcohol Withdrawal Syndrome: A Systematic Review and Meta-Analysis.

Alcohol withdrawal syndrome (AWS) is a complication frequently encounteredamongpatients who are chronic alcohol abusers. It is considered to have a significant impact on the United States healthcare system. It not only has a toll on the healthcare spending but also contributes to significant morbidity and mortality. Benzodiazepines are considered first line in the treatment of AWS. Since patients with alcohol use disorder have downregulated gamma aminobutyric acid (GABA) receptors, this often leads to benzodiazepine resistance. Phenobarbital is also usedin the management of alcohol withdrawal syndrome. Here we present a systematic review and meta-analysis of the efficacy and safety of the drug. We conducted an electronic database search for relevant studies published between the inception of the project and November 20, 2022, in three databases, including Medline/PubMed, Embase, and Cochrane Library. Our study included all original studies with prime focus on the baseline characteristics of patients admitted to the intensive care unit (ICU) for alcohol withdrawal syndrome and management/monitoring protocol implemented for its treatment.The primary outcomes that were the focus of our study consisted of changes in the length of hospital stay, length of ICU stay, and changes in scoring systems (for alcohol withdrawal assessment and monitoring) following the implementation of phenobarbital. The secondary outcomes included complications such as intubation and mortality. Based on our analysis, the mean difference in hospital stay was statistically significant at -2.6 (95% CI, -4.48, -0.72, P=0.007) for phenobarbital compared to the benzodiazepine group. We were unable to comment on the heterogeneity in our meta-analysis due to the standard deviationnot being reported in one study. There was no statistically significant difference regarding the length of stay in the intensive care unit compared to the control/comparative arm, with a mean difference of -1.17 (95% CI, -1.17, 0.09, P=0.07), with considerable heterogeneity (I2=77%, P=0.002). Our meta-analysis also investigated the risk of intubation between the phenobarbital and the control/comparative group. There was statistically significant difference in the incidence of intubation, relative risk (RR) 0.52 (95% CI, 0.25, 1.08, P=0.08), with considerable heterogeneity (I2=80%, P=0.0001). Our study concludes that phenobarbital is an effective tool in the management of AWS in an ICU setting. However, various studies have reported contradictory results, and vital information appears to be lacking. Moreover, there is a lack of uniformity in terms of phenobarbital dosing. Drug administration should be adapted according to the severity of the symptoms. Further studies need to be conducted discussing the safety profile and adverse effects of the drug when it comes to the management of alcohol withdrawal syndrome.

Groove pancreatitis and how to differentiate it from pancreatic adenocarcinoma.

Groove pancreatitis is an uncommon type of chronic pancreatitis that affects the space between the head of the pancreas, the second portion of the duodenum, and the common bile duct. The main trigger is chronic alcohol abuse, which eventually leads to leakage of pancreatic juices into the pancreaticoduodenal groove, causing inflammation and fibrosis. The main differential diagnosis is with pancreatic adenocarcinoma, which is more common than groove pancreatitis. Different imaging techniques make it possible to identify various findings (e.g., duodenal thickening or duodenal and paraduodenal cysts, which are characteristic of groove pancreatitis) that sometimes enable differentiation between groove pancreatitis and other entities, although there are no specific findings for each of them. Sometimes biopsy or surgery is required to establish the definitive diagnosis. The treatment of groove pancreatitis is usually conservative, but in cases in which the symptoms do not improve, interventional procedures (biliary drainage) or surgery (Whipple technique) can be done.