History Of Excessive Alcohol Intake Research Articles

Enhanced liver fibrosis score is stable after withdrawal in patients with heavy alcohol consumption: A pilot study.

Enhanced liver fibrosis (ELF) score is an accurate, noninvasive test for assessing the severity of liver fibrosis in chronic liver disease, including alcohol-related liver disease. However, whether the ELF score changes during alcohol withdrawal is unknown. This pilot study assessed changes in the ELF score during withdrawal in patients with a history of excessive alcohol intake. In this prospective study, ELF was performed on day 0 (D0, at the beginning of hospitalization), at day 7 (D7, on discharge from hospital), and at follow-up visits on days 30 (D30) and 90 (D90). Transient elastography (TE) was also assessed on days 4 (D4) and D30. The study included 35 patients (71% male) with a mean alcohol intake of 139 g/day. On D30 and D90, 8 and 13 patients had resumed alcohol consumption (mean intake of 90 and 80 g/day, respectively). In patients who remained abstinent, the mean ELF score was 8.93 on D0, 9.14 on D30 (p = 0.32), and 9.27 on D90 (p = 0.14). In patients who resumed alcohol, mean ELF score was 9.7 on D0, 10.05 on D30 (p = 0.09), and 9.71 on D90 (p = 0.12). ELF score was comparable over the first months after withdrawal, although there was a slight increase in the first week (mean ELF score increased from 9.24 on D0 to 9.74 on D7, p < 0.001). Mean TE value was 7.9 kPa on D4 and 8.1 kPa on D30 (p = 0.84) in patients who resumed alcohol consumption, and 8.3 and 7.5 kPa (p = 0.03) on D4 and D30, respectively, in abstinent patients. The ELF score is stable during the first months after withdrawal and thus appears to be a useful tool to assess liver fibrosis or cirrhosis in this setting. Nevertheless, because in the first week there is a transient increase in ELF score, caution in interpretation is warranted.

Infections increase the risk of decompensation and death in patients with early alcohol-related liver disease

Background & AimsInfections are frequent in patients with cirrhosis and worsen prognosis. We evaluated the incidence of infections and their impact on decompensation and death in patients with early alcohol-related liver disease (ALD) during long-term follow-up. MethodsWe performed a prospective cohort study of patients in secondary care with a history of excess alcohol intake, no prior decompensation, and with liver biopsies along with clinical investigations conducted at baseline. During follow-up, we reviewed the patients’ electronic healthcare records for cases of infections, hospitalizations, transient elastography measurements, decompensations, all-cause mortality, and alcohol intake. ResultsWe included 461 patients with a mean age of 56±10 years (76% males; fibrosis stage F0-1/F2/F3-4 = 259/107/93 [56%/23%/20%]). During a median follow-up of 4.5 years (IQR 2.9-6.3), 134 patients (29%) developed a total of 312 infections, most frequently pneumonia (106/312, 34%) and urinary tract infections (57/312, 18%). Excessive alcohol intake during follow-up, smoking ≥30 pack years, MELD score and elevated liver stiffness during follow-up were independent predictors of infections. Patients who developed at least one infection had a significantly increased risk of subsequent decompensation (hazard ratio 4.98, 95% CI 2.47-10.03) and death (hazard ratio 8.24, 95% CI 4.65-14.59). Infections increased the risk of decompensation and death independently of baseline fibrosis stage, age, gender, and MELD score. ConclusionsAlmost one-third of patients with early ALD develop an infection, which worsens their prognosis by increasing the risk of decompensation and death. The risk of infections increases with liver disease severity and ongoing harmful use of alcohol. Impact and implicationsThis study reveals that infections significantly worsen the prognosis of patients with early alcohol-related liver disease (ALD), increasing the likelihood of decompensation and death by up to eight times. These findings, pertinent to healthcare providers, researchers, and policymakers, emphasize the importance of early prevention and management of infections in patients with ALD, even those in early stages who may be asymptomatic. It was observed that nearly one-third of patients with early-stage ALD developed infections over 4.5 years, with risk factors including alcohol overuse, smoking, and higher MELD scores. The research underscores the critical need to incorporate these insights into clinical practice and public health policies to improve patient outcomes and mitigate the impact of infections in patients with ALD.

Validation of the new nomenclature of steatotic liver disease in patients with a history of excessive alcohol intake: an analysis of data from a prospective cohort study

Steatotic liver disease is a new overarching term that includes metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related steatotic liver disease (MetALD), and alcohol-related liver disease (ALD). We aimed to validate the prognostic importance of MASLD, MetALD, and ALD as steatotic liver disease subclasses. Between April 18, 2013, and Sept 17, 2018, we prospectively recruited patients aged 18-75 years with current or previous excessive alcohol intake (>24 g/day for women and >36 g/day for men) for at least a year and no previous hepatic decompensation from the Department of Gastroenterology and Hepatology at Odense University Hospital (Odense, Denmark). Participants were followed up until Sept 15, 2022. Here, we characterise these patients according to steatotic liver disease subclasses. We classified patients as having MASLD, MetALD, or ALD in accordance with the nomenclature definitions, on the basis of metabolic comorbidity and self-reported average alcohol intake in the 3 months leading up to inclusion. Histological scoring was done by a pathologist who was masked to the clinical data. We compared prognoses between classes using Cox regression analyses on hepatic decompensation and overall mortality as the two outcome measures. Patients not meeting the criteria for steatotic liver disease were classified as no steatotic liver disease and served as a reference group. We enrolled 446 patients with a history of excessive alcohol intake were included in this analysis (334 [75%] were male and 112 [25%] were female; median age 56 years [SD 10]). Cirrhosis was present in 58 (13%), and 435 (98%) had at least one cardiometabolic risk factor. 321 (72%) met steatotic liver disease criteria and 125 (28%) did not have steatotic liver disease, meaning no evident liver steatosis and no significant fibrosis (≥F2). Of the 321 patients with steatotic liver disease, six (2%) were identified as having ALD due to the absence of cardiometabolic risk factors. The remaining 315 (98%) patients presented with at least one cardiometabolic risk factor. Of these patients, 153 (49%) had MASLD, 76 (24%) had MetALD, and 86 (27%) had ALD. During follow-up, 67 (15%) of 446 patients decompensated and 97 (22%) died (median follow-up 70 months [IQR 53-94]). Patients with steatotic liver disease had a significantly higher risk of hepatic decompensation and overall mortality than those without steatotic liver disease, independent of age, sex, and liver stiffness. The risk of decompensation increased in a stepwise manner from MASLD (hazard ratio 4·73 [95% CI 1·03-21·6]), through MetALD (7·69 [1·66-35·6]), to ALD (10·2 [2·24-46·4]). Similarly, overall mortality increased from MASLD (HR 2·30 [95% CI 1·08-4·90]), through MetALD (2·94 [1·31-6·58]), to ALD (3·57 [1·64-7·80]), independent of age, sex, and liver stiffness. Steatotic liver disease and its subclasses portend distinct prognoses. There is a need to specify how historical alcohol intake should be integrated into the nomenclature and risk stratification of steatotic liver disease. EU Horizon 2020 Research and Innovation Program.

Just supplement Thiamine! A simple yet dramatic solution! (P9-4.004)

<h3>Objective:</h3> We present a case showing how while the diagnostic process in neuropathy may be long and cumbersome, the solution is usually simple, dramatic and life changing. <h3>Background:</h3> 55-year-old female with acute-on-chronic, rapidly progressive numbness and weakness. She first noted numbness and tingling in her feet over 8 years ago, but with rapid progression over the past year up to her trunk and hands. She presented to the ER after falling in the house, laying on the floor for hours, unable to be lifted by her husband. Examination revealed several bruises, symmetric wasting of upper and lower extremity muscles, proximal greater than distal weakness, loss of pinprick, vibration and temperature sensation from toes up to the thighs. She was areflexic with bowel and bladder incontinence and urine retention of 1L on arrival. She gave a history of excessive alcohol intake since her teenage years, with a heavy increase in intake over the COVID pandemic due to loss of employment and depression. Low folic acid, ESR 72, CT abdomen notable for steatohepatitis, fecal loading and urine retention. CSF analysis showed no albumino-cytological dissociation. Autoimmune workup, RPR, B12, serum copper, CSF paraneoplastic panel, CT chest, MRI brain and complete spine were unremarkable. EMG/NCV showed moderate, length dependent, sensory-motor axonal polyneuropathy. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> She was started on high dose thiamine and folic acid supplementation in hospital. Initially, she was unable to feed herself, turn in bed or sit without support. She slowly recovered, regained continence and can ambulate independently with a walker now. She can play the piano. <h3>Conclusions:</h3> Thiamine associated neuropathy or Dry Beri-Beri can present with axonal predominant sensorimotor polyneuropathy that can mimic Guillain Barre Syndrome. While workup for other etiologies of neuropathy should be simultaneously pursued in alcoholics, thiamine supplementation is a simple treatment that can lead to satisfying and dramatic results. <b>Disclosure:</b> Dr. Bhende has nothing to disclose. Dr. Zafar has nothing to disclose. Dr. Prabhu has nothing to disclose. Dr. Undavia has nothing to disclose.

The Protection Conferred by HSD17B13 rs72613567 on Hepatic Fibrosis Is Likely Mediated by Lowering Ballooning and Portal Inflammation

The Protection Conferred by HSD17B13 rs72613567 on Hepatic Fibrosis Is Likely Mediated by Lowering Ballooning and Portal Inflammation

Alcohol Intake in Patients With Cardiomyopathy and Heart Failure: Consensus and Controversy.

Alcohol is often cited to be a common cause of cardiomyopathy and heart failure. However, in most available population-based studies, a modest-to-moderate alcohol consumption has been associated with favorable effects on the cardiovascular system, including a lowered risk of heart failure, compared with no alcohol consumption. Available genetic epidemiological data have not supported a causal association between alcohol consumption and heart failure risk, suggesting that alcohol may not be a common cause of heart failure in the community. Data linking alcohol intake with cardiomyopathy risk are sparse, and the concept of alcoholic cardiomyopathy stems mainly from case series of selected patients with dilated cardiomyopathy, where a large proportion reported a history of excessive alcohol intake. This state-of-the-art paper addresses the current knowledge of the epidemiology of alcoholic cardiomyopathy and the role of alcohol intake in patients with non-alcohol-related heart failure. It also offers directions to future research in the area. The review questions the validity of current clinical teaching in the area. It is not well known how much alcohol is needed to cause disease, and the epidemiological pathways linking alcohol consumption to cardiomyopathy and heart failure are not well understood. Until more evidence becomes available, caution is warranted before labeling patients as having alcoholic cardiomyopathy due to a risk of neglecting other contributors, such as genetic causes of cardiomyopathy. In non-alcohol-related heart failure, it is unknown whether total abstinence is improving outcomes (compared with moderate drinking). Ideally, randomized clinical trials are needed to answer this question.

Complete regression of multiple biventricular thrombi in dilated cardiomyopathy: the role of cardiovascular magnetic resonance imaging for diagnosis and assessing treatment response

A 40-year-old man presented with a 7-day history of progressive breathlessness, orthopnoea and peripheral oedema. He had a history of excess alcohol intake, cannabis use and learning difficulties. The electrocardiogram...

Pancreatoduodenectomy and non-alcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome with similar hepatic histological changes to alcoholic liver disease, but without a history of excessive alcohol intake. Obesity, hyperlipidemia, diabetes, hypertension and other metabolic disorders are closely related to its occurrence and development, and its core mechanism is insulin resistance. In addition, there are also non-metabolic-related factors for the occurrence of non-alcoholic fatty liver disease, such as pancreatoduodenectomy. Pancreatoduodenectomy is the standard procedure for the treatment of tumor around the head of pancreas and ampulla. Postoperative pancreatic malfunction induced by pancreatic exocrine function after pancreatoduodenectomy is associated with the occurrence and development of secondary non-alcoholic fatty liver disease.

Imaging of genetically-mediated pancreatitis

ObjectivesTo review the imaging of patients with Genetically-Mediated Pancreatitis (GMP), identify common imaging findings in this cohort and assess phenotypical characteristics of specific genotypes. Materials and methodsRetrospective review of the databases of the Irish National Surgical Centre for Pancreatic Cancer (NSCPC) and Cystic Fibrosis (CF) from November 2010 to January 2018. Retrospective imaging and chart review for the patients with positive genetics for GMP. ResultsThe NSCPC database contained 699 patients; the CF database included 352 patients. Of these 1051, 14 were identified as having GMP (age range: 20–65, M:F ratio of 1:1). 14 of 1051 patients from the database had positive genetics for GMP. 10 had imaging to support a diagnosis of hereditary pancreatitis or familial recurrent pancreatitis (1.3%) and 4 had imaging to support a diagnosis of CF-related pancreatitis. Imaging findings were considered in 3 categories, determined by genotype - PRSS1 hereditary pancreatitis, SPINK 1 autosomal recessive pancreatitis and those for CFTR - cystic fibrosis related pancreatitis. Imaging findings in PRSS1 hereditary pancreatitis patients included: pancreatic atrophy, calcification and main pancreatic duct (MPD) dilatation, referred to as the PRSS1 imaging triad. Patients with the SPINK1 gene mutation had less severe imaging manifestations (pancreatic atrophy 33%, MPD dilatation 33%, pancreatic calcification 33%). CFTR patients with imaging findings had pancreatic atrophy (100%). ConclusionGMP should be suspected when the features of ‘chronic pancreatitis’ are seen in young adults with no history of excess alcohol intake. Genetic testing, endocrinology review and long-term imaging follow-up for pancreatic carcinoma are indicated.

A study of psychiatric referrals from other specialties at a tertiary care center

Objective: The objective was to study the reasons for referral, to study diagnostic categories of psychiatric referrals, and to study the associations if any between reasons for referral and diagnostic categories of psychiatric referrals. Materials and Methods: The present study was conducted at the Department of Psychiatry, Mamata General Hospital, Khammam. The present study consists of 112 psychiatric referrals; 12 referrals were excluded from the study as they are not willing to give consent, so the study was conducted on 100 psychiatric referrals. The study protocol was approved by the Institutional Ethics Committee. Results: In the present study, based on the sources of referrals, it was found that majority of the patients were from the Department of General Medicine (38%). In the present study, the most common reason stated for referral was suicidal/self-harm act by 29% of the sample. The most common psychiatric disorder diagnosed in the present study was found to be substance use disorder which is seen in 33% of the sample. On evaluation of diagnostic categories with reference to reasons for referral, it is found that most of the referrals with a history of excessive alcohol intake were diagnosed as substance use disorders (91.6%). Majority of referrals with a history of suicidal attempts were diagnosed as intentional self-harm (58.6%). Referrals with a history of altered sensorium were diagnosed with organic mental disorders (50%), substance use disorder (37.5%), and 12.5% had no psychopathology. Conclusion: Suicidal attempts are most commonly diagnosed to have intentional self-harm. Substance use disorder came to be high in referrals which are referred for excessive alcohol intake. Regarding referrals to psychiatry department, majority of the patients were from the Department of General Medicine. The most common reason stated for referral to psychiatry was suicidal/self-harm.

Severe liver disease related to chronic hepatitis C virus infection in treatment-naive patients: epidemiological characteristics and associated factors at first expert centre visit, France, 2000 to 2007 and 2010 to 2014.

Given recent profound improvements in the effectiveness of antiviral treatment for chronic Hepatitis C virus (HCV) infection, we aimed to describe the characteristics of patients referred to hepatology expert centres in France from 2000 to 2007 and from 2010 to 2014, and to identify factors associated with severe liver disease at their first visit for evaluation. We analysed data from two sources covering all of France: the former hepatitis C surveillance network, which included patients between 2000 and 2007, and the ANRS CO22 HEPATHER multi-centre cohort, which included patients between 2012 and 2014. Severe liver disease (SLD) was defined as the presence of either cirrhosis (histological, biochemical or clinical) or hepatocellular carcinoma. Multivariable Poisson regression models were used to identify the factors associated with SLD in complete-case analysis and after multiple imputation. Overall, 16,851 patients were included in the analysis and SLD was diagnosed in 11.6%. SLD at first visit was significantly associated with known risk factors (male sex, history of excessive alcohol intake, HCV genotype 3), late referral to hepatologists after diagnosis and HCV diagnosis at an older age. Providing earlier specialised care and treatment may be an important target for public health action.

The Neurotrophic Factor Receptor p75 in the Rat Dorsolateral Striatum Drives Excessive Alcohol Drinking.

Brain-derived neurotrophic factor (BDNF) signaling in the dorsolateral striatum (DLS) keeps alcohol intake in moderation. For example, activation of the BDNF receptor tropomyosin receptor kinase B (TrkB) in the DLS reduces intake in rats that consume moderate amounts of alcohol. Here, we tested whether long-term excessive consumption of alcohol produces neuroadaptations in BDNF signaling in the rat DLS. We found that BDNF was no longer able to gate alcohol self-administration after a history of repeated cycles of binge alcohol drinking and withdrawal. We then elucidated the possible neuroadaptations that could block the ability of BDNF to keep consumption of alcohol in moderation. We report that intermittent access to 20% alcohol in a two-bottle choice paradigm that models excessive alcohol drinking produces a mobilization of DLS p75 neurotrophin receptor (p75NTR), whose activities oppose those of the Trk receptors, including TrkB. These neuroadaptations were not observed in the DLS of rats exposed to continuous access to 10% alcohol or in rats consuming sucrose. Furthermore, short hairpin RNA (shRNA)-mediated knockdown of the p75NTR gene in the DLS, as well as intra-DLS infusion or systemic administration of the p75NTR modulator, LM11A-31, significantly reduced binge drinking of alcohol. Together, our results suggest that excessive alcohol consumption produces a change in BDNF signaling in the DLS, which is mediated by the recruitment of p75NTR. Our data also imply that modulators of p75NTR signaling could be developed as medications for alcohol abuse disorders. Neuroadaptations gate or drive excessive, compulsive alcohol drinking. We previously showed that brain-derived neurotrophic factor and its receptor, TrkB, in the dorsolateral striatum (DLS), are part of an endogenous system that keeps alcohol drinking in moderation. Here, we show that a history of excessive alcohol intake produces neuroadaptations in the DLS that preclude BDNF's ability to gate alcohol self-administration in rats by the recruitment of the low-affinity neurotrophin receptor, p75NTR, whose activities opposes those of the Trk receptors. Finally, we show that the administration of the p75NTR modulator, LM11A-31, significantly reduces excessive alcohol intake suggesting that the drug may be developed as a new treatment for alcohol abuse disorders.

A Case of a Chronic Pancreatic Pseudocyst Causing Atraumatic Splenic Rupture without Evidence of Acute Pancreatitis.

Atraumatic splenic rupture is a rare complication of a pancreatic pseudocyst (PP), described in the setting of chronic pancreatitis. There is common understanding, within the literature, that an inflammatory process at the tail of the pancreas may disrupt the spleen and result in such splenic complications. The authors present a case report of a 29-year-old male with a PP, associated with chronic pancreatitis. The patient had a history of excessive alcohol intake and presented to the emergency department with a short history of abdominal pain and vomiting. He denied any significant history of trauma and serum amylase levels were normal. An admission computed tomography (CT) scan of the abdomen confirmed the presence of a PP in direct contact with the spleen. The CT also demonstrated a heterogenous hypodense area of the splenic hilum, along with perisplenic fluid. The patient was admitted for observation. His abdominal pain progressed, and he became haemodynamically unstable. An emergency ultrasound scan (USS) at this time revealed intra-abdominal haemorrhage. A subsequent CT confirmed splenic rupture, which was managed surgically with a full recovery. Few such cases are documented within the literature and more understanding of preempting such events is needed.

Glial cell line-derived neurotrophic factor (GDNF) is an endogenous protector in the mesolimbic system against excessive alcohol consumption and relapse.

Moderate social consumption of alcohol is common; however, only a small percentage of individuals transit from social to excessive, uncontrolled alcohol drinking. This suggests the existence of protective mechanisms that prevent the development of alcohol addiction. Here, we tested the hypothesis that the glial cell line-derived neurotrophic factor (GDNF) in the mesolimbic system [e.g. the nucleus accumbens (Acb) and ventral tegmental area (VTA)] is part of such a mechanism. We found that GDNF knockdown, by infecting rat Acb neurons with a small hairpin RNA (shRNA) targeting the GDNF gene, produced a rapid escalation to excessive alcohol consumption and enhanced relapse to alcohol drinking. Conversely, viral-mediated overexpression of the growth factor in the mesolimbic system blocked the escalation from moderate to excessive alcohol drinking. To access the mechanism underlying GDNF's actions, we measured the firing rate of dopaminergic (DAergic) neurons in the VTA after a history of excessive alcohol intake with or without elevating GDNF levels. We found that the spontaneous firing rate of DAergic neurons in the VTA was reduced during alcohol withdrawal and that GDNF reversed this alcohol-induced DA deficiency. Together, our results suggest that endogenous GDNF in the mesolimbic system controls the transition from moderate to excessive alcohol drinking and relapse via reversal of alcohol-dependent neuro-adaptations in DAergic VTA neurons.

Etiologic and epidemiologic study of hepatocellular carcinoma in West Azarbaijan of Iran (2006-2011)

Background:Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Epidemiologic and etiologic studies help in the prevention of disease and improve surveillance of affected patients. The aim of this study was to study the etiology and epidemiology of HCC in West Azarbaijan of Iran.Materials and Methods:In this cross-sectional, retrospective study, medical records of 60 patients with HCC who were diagnosed between 2006 and 2011 in West Azarbaijan of Iran were analyzed for age, sex, location, presence of liver cirrhosis and/or well-known risk factors of HCC. Data were analyzed by SPSS 17 software.Results:From 60 patients with HCC, 75% were male and 25% were female. Mean age of the patients was 63.47 years. 51.66% were from rural areas and 48.33% were from urban areas. 43.33% of HCC patients were cirrhotic while 56.66% patients were non-cirrhotic. Of the 26 cirrhotic patients, 57.69% were seropositive for hepatitis B surface antigen (HBsAg), 15.38% not only had history of excess alcohol intake but were also HBsAg positive, 3.84% had history of alcoholism, 3.84% had history of Wilson disease and the rest (19.24%) had cryptogenic cirrhosis. Of the 34 non-cirrhotic patients, 35.29% were positive for HBsAg. None of the 60 patients with HCC had positive serology for hepatitis C virus (HCV) or history of hepatitis C infection.Conclusion:In our study, most of the patients (>50%) with HCC did not have underlying liver cirrhosis. In the cirrhotic patients, hepatitis B infection was the most common predisposing factor, followed by hepatitis B infection concomitant with alcoholism, alcoholism alone and Wilson disease. In the remaining cirrhotic patients, we could not find any predisposing factor for cirrhosis. Infection with HCV was not found in our studied group. We concluded that etiology of HCC in our province is different from that in the western countries.

Letter: peptic ulcer bleeding in patients with cirrhosis

SIRS, The study by Rudler et al. on the aetiology and outcomes of peptic ulcer bleeding in cirrhotic and noncirrhotic patients has several limitations. First, the study recruited only 203 patients, the majority (85%) of whom were noncirrhotic. These were compared with only 29 (14%) cirrhotic patients, who were loosely defined using clinical, biochemical and radiological parameters. Based on the very small numbers in the cirrhosis group, and as the patients in the two groups were not matched, the study was not sufficiently powered to address the questions they set out to answer. The gold standard test for diagnosing cirrhosis is a liver biopsy, although hepatic elastography is an acceptable alternative. Reliance on tests such as radiology, blood parameters and endoscopic findings can be misleading and lack specificity. For instance, noncirrhotic idiopathic portal hypertension can mimic cirrhosis both clinically and radiologically. Hence, it is conceivable that some of the patients they considered cirrhotic were not. Second, the authors throughout the manuscript refer to ‘idiopathic’ peptic ulcer disease (PUD), meaning those patients who had no evidence of Helicobacter pylori infection or nonsteroidal anti-inflammatory drug (NSAID)/aspirin use. This gives the erroneous impression that these two factors are the only causes of PUD. Before an ulcer can be labelled as idiopathic, one has to exclude other known but rare causes of peptic ulcers (such as other ulcerogenic drugs and diseases including Crohn’s and Zollinger–Ellison syndrome). The authors made no such attempts in their study; hence, it is impossible to know whether other aetiologies were involved. Moreover, recent alcohol intake in cirrhotic patients has been implicated in the pathogenesis of gastroduodenal ulcers; hence, it is misleading to disregard alcohol as a causative factor for ulcers in these patients. Third, the use of H. pylori serology to diagnose H. pylori infection in this study is questionable. It is well known that serological tests for H. pylori are unreliable in patients with cirrhosis and portal hypertension, with high sensitivity but low specificity (83.6 and 55.9, respectively). 5 Gastric biopsies for H. pylori histology and/or rapid urease test would have been preferable due to their higher accuracy in this setting. Thus, the figures they quote for H. pylori infection rate in the study are likely to be inaccurate. Moreover, the authors’ make no mention of whether the patients had received any prior H. pylori eradication therapy, which makes it impossible to determine whether the patients who were positive had current or prior infection, as H. pylori antibodies can take several months to years to disappear following eradication. In addition, noncirrhotic patients were much older than cirrhotic patients, and the differences seen in H. pylori infection rate between the two groups could have been influenced by the age difference. It is well known that the prevalence of H. pylori infection increases with age. Peptic ulcer disease, particularly gastric ulcer, is found more commonly in patients with portal hypertension. Although the exact pathogenetic mechanisms are unknown, it is generally believed that portal hypertension leads to impairment of gastric mucosal defences, hence rendering the gastric lining more susceptible to injury by aggressors such as NSAIDs alcohol and bile salts, culminating in peptic ulcers. Although a high alcohol intake alone has not been unequivocally identified as a risk factor for PUD in noncirrhotic patients, Aurox et al. found that in cirrhotic patients, recent alcohol intake prior to endoscopy was independently associated with gastroduodenal erosions. Almost all cirrhotic patients in this study had a history of excessive alcohol intake. Thus, the only

A typical feature of groove pancreatitis

A 57-year-old man with a history of excessive alcohol intake presented with painless jaundice. Contrast-enhanced abdominal computed tomography demonstrated a heterogeneous 6-cm mass in the pancreatic head associated with cysts in the duodenal wall and pancreatic parenchyma, suggestive of groove pancreatitis (Fig. 1). However, CA 19-9 (carbohydrate antigen 19-9) was elevated at 97.4 U/ml (normal: <34 U/ml). The patient underwent pancreaticoduodenectomy and groove pancreatitis was confirmed on pathological examination. This rare entity is characterized by the presence of numerous large cysts within the thickened duodenal wall, a pancreaticoduodenal groove, and cavities that extend into the pancreatic parenchyma (Fig. 2). Microscopy (Fig. 3) showed histological architectural disruption of the pancreatic parenchyma, chronic inflammation of the pancreaticoduodenal interface (the groove area), Brunner's gland hyperplasia and extensive fibrosis with dilatation of the pancreatic duct. Knowledge of this entity is crucial as it can mimic a pancreatic head cancer.1 Figure 1 Abdominal computed tomography shows the pancreatic head tumour with numerous cysts within the duodenal wall and pancreatic parenchyma Figure 2 Macroscopic appearance of the resected specimen. Observe the thickened duodenal wall with large cysts and a larger cyst in the pancreatic parenchyma Figure 3 Microscopy shows (a) the pancreaticoduodenal interface with chronic inflammation and Brunner's gland hyperplasia (magnification ×100), and (b) extensive fibrosis and mild pancreatic duct dilatation (magnification ×40)

061 Central pontine myelinolysis: a CNS manifestation of re-feeding syndrome?

A 55-year-old lady with history of excess alcohol intake presented to the acute medical unit following concerns regarding her electrolyte disturbances. During correction of the electrolytes, the patient developed central...

Verrucous Squamous Carcinoma of the Esophagus Successfully Diagnosed by Endoscopic Mucosal Resecion: A Case Report

A 62-year-old male with a history of type 2 diabetes mellitus and alcoholic liver disease presented with dysphagia, heartburn, and appetite loss. He had lost 10 kg weight within 1 month. The patient gave a history of excessive alcohol intake and a smoking habit of 60 cigarettes per day for 40 years. Upper gastroenteroscopy revealed a wartlike, whitish, protruding mass with circumferential stricture at a point 35 cm from the incisor down to the cardia. Although esophageal cancer was suspected, repeated biopsies of the mass revealed no malignant findings. Concurrent esophageal candidiasis was treated with an antifungal drug. Increased esophageal stricture made food intake impossible; therefore, total parenteral nutrition was initiated. Endoscopic mucosal resection revealed highly keratinized, well-differentiated squamous cell carcinoma with invasion into the submucosa. A diagnosis of verrucous squamous carcinoma was confirmed. Subtotal esophageal resection and esophagostomy was performed with video assistance. Postoperative pathological findings were compatible with the diagnosis of verrucous squamous carcinoma, which is known to be a slow-growing tumor that rarely metastasizes to lymph nodes or distant organs. However, verrucous squamous carcinoma is rarely diagnosed by endoscopic biopsy. Moreover, endoscopic mucosal resection or surgery should be considered in cases when endoscopic examination fails to confirm the diagnosis of carcinoma and if the lesion presents some characteristics of verrucous squamous carcinoma.

Double gap metabolic acidosis in a Chinese alcoholic

Alcoholic ketoacidosis is an important cause of double gap metabolic acidosis. The differential diagnosis includes toxic alcohol (such as methanol and ethylene glycol) ingestion. We report a patient with alcoholic ketoacidosis. He had a history of excessive alcohol intake and presented with repeated vomiting, loss of appetite and hypovolemic shock. Laboratory results revealed high anion gap metabolic acidosis, increased serum osmolal gap, ketonemia, lactic acidosis and acute renal failure. He was successfully treated with hemodialysis, and hydration with glucose and thiamine. 酒精性代謝酮酸中毒是雙重間隙代謝性酸中毒的重要成因，其鑑別診斷為有毒酒精(如甲醇、乙二醇)的攝入。以下個案是一位酒精性代謝酮酸中毒患者，具過度攝入酒精的習慣，入院時呈現重複嘔吐、無食慾、及低血容積性休克。化驗結果顯示高陰離子間隙之代謝性酸中毒、高血清滲透間隙、酮血症、乳酸中毒、及急性腎衰竭。在接受血液透析、合併葡萄糖與硫胺素補充療法後，病人反應良好。