alcoholic liver disease case presentation

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• Volume 14, Issue 5
• How to manage alcohol-related liver disease: A case-based review
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• http://orcid.org/0000-0003-1530-5328 James B Maurice 1 ,
• http://orcid.org/0000-0001-5140-517X Samuel Tribich 2 ,
• Ava Zamani 3 ,
• Jennifer Ryan 4
• 1 Department of Gastroenterology and Hepatology, Southmead Hospital , North Bristol NHS Trust , Bristol , UK
• 2 Department of Hepatology, Royal London Hospital , Barts Health NHS Trust , London , UK
• 3 Hammersmith Hospital , Imperial College Healthcare NHS Trust , London , UK
• 4 Department of Hepatology and Liver Transplantation, Royal Free Hospital , Royal Free London NHS Foundation Trust , London , UK
• Correspondence to Dr James B Maurice, Department of Gastroenterology and Hepatology, Southmead Hospital, North Bristol NHS Trust, Bristol BS10 5NB, UK; james.maurice{at}nbt.nhs.uk

https://doi.org/10.1136/flgastro-2022-102270

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• alcoholic liver disease
• chronic liver disease

What is already known on this topic

Alcohol-related liver disease (ArLD) is a major cause of morbidity and mortality.

What this study adds

We present a typical case to illustrate current evidence-based investigation and management of a patient with ArLD.

This case-based review aims to concisely support the day-to-day decision making of clinicians looking after patients with ArLD, from risk stratification and fibrosis assessment in the community through to managing decompensated disease, escalation care to critical care and assessment for liver transplantation.

How this study might affect research, practice or policy

We summarise the evolving evidence for the benefit of liver transplantation in alcoholic hepatitis, and ongoing controversies shaping future research in this area.

ArLD is fundamentally a public health problem, and further efforts are required to implement effective policies to reduce consumption and prevent disease.

Introduction

Alcohol is the leading risk factor for premature death in young adults, of which alcohol-related liver disease (ArLD) is a major contributor. 1 The management of ArLD often requires complex decision-making, raising challenges for the clinician and wider multidisciplinary team. This case-based review follows the typical journey of a patient through the progressive stages of the disease process, from early diagnosis and risk stratification in the outpatient clinic through to alcoholic hepatitis and referral for liver transplantation. At each stage, we discuss a practical approach to clinical management and summarise the underlying evidence base.

Case part 1

A 47-year-old man is referred to the general hepatology clinic from his General Practitioner with abnormal liver function tests, ordered in the community following several episodes of non-specific abdominal pain which subsequently resolved. He is now asymptomatic. The referral states that he drinks one bottle of wine each weekday night and more at the weekends. He is on no regular medication, has no other significant medical history and works in construction. On clinical examination, there are a few …

Twitter @jamesbmaurice

Contributors JBM conceptualised the original article and the case. JBM, ST and AZ drafted the initial version of the manuscript. JBM and ST contributed further editing of various sections. JR provided senior critical review and edited the manuscript. All authors agreed upon the final version.

Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests None declared.

Provenance and peer review Not commissioned; externally peer reviewed.

Linked Articles

• Highlights from this issue UpFront R Mark Beattie Frontline Gastroenterology 2023; 14 357-358 Published Online First: 07 Aug 2023. doi: 10.1136/flgastro-2023-102519

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Clinical presentation of alcoholic liver disease and non-alcoholic fatty liver disease: spectrum and diagnosis

Affiliation.

• 1 Department of Gastroenterology & Hepatology, Sir Ganga Ram Hospital, New Delhi, India.
• PMID: 32258523
• PMCID: PMC7063523
• DOI: 10.21037/tgh.2019.10.02

Alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) are commonest causes of chronic liver disease in developing as well as developed countries. Their incidence has increased due to widespread easy availability of alcohol and sedentary life style of people. NAFLD is a spectrum which includes fatty liver (NAFL) which is considered benign disease, steatohepatitis (NASH) which indicates ongoing injury to liver and cirrhosis of liver. Similarly, ALD spectrum comprises simple steatosis, alcoholic hepatitis, and cirrhosis and its complications. Most of the time there is significant overlap between these diseases and clinical presentation depends upon the stage of liver disease. Most of the NAFLD patients are asymptomatic and diagnosed to have fatty liver while undergoing routine health check up. ALD requires significant history of alcohol intake which is supportive by radiological and biochemical tests. In both NAFLD and ALD patients, liver enzymes are seldom raised beyond five times the upper limit of normal. Liver biopsy is required for diagnosis of NASH as it is a histological diagnosis and sometimes in alcoholic hepatitis for confirmation if diagnosis is in doubt. Non-invasive markers and prognostic scores have been developed for avoiding liver biopsy in assessment and treatment response of NASH and alcoholic hepatitis patients.

Keywords: Alcoholic liver disease (ALD); clinical presentation; diagnosis; non-alcoholic fatty liver disease (NAFLD); spectrum.

2020 Translational Gastroenterology and Hepatology. All rights reserved.

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Chart to follow for diagnosis…

Chart to follow for diagnosis of NAFLD. DM, diabetes mellitus; NAFLD, non-alcoholic fatty…

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Introduction

Case presentation, statement of ethics, conflict of interest statement, funding sources, author contributions, alcoholic hepatitis: a common disease with uncommon presentation.

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Pratik Khatiwada , Jose A. Rodriguez , Andres Reyes-Corcho; Alcoholic Hepatitis: A Common Disease with Uncommon Presentation. Case Rep Gastroenterol 22 September 2020; 14 (2): 448–452. https://doi.org/10.1159/000508426

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Alcoholic liver disease is one of the leading causes of hepatitis, cirrhosis, liver failure, and hepatic carcinoma. Alcoholic hepatitis refers to the acute onset of symptomatic hepatitis. We describe a patient who presented with alcoholic hepatitis with direct hyperbilirubinemia, elevated alkaline phosphatase (ALP), and hypertriglyceridemia. All the imaging and laboratory work excluded obstructive causes, and liver biopsy confirmed the diagnosis. Alcoholic hepatitis is a common condition, but some unusual presentations can lead one to think of uncommon pathologies. This case reflects that alcoholic hepatitis can present with high levels of triglycerides as well as a cholestatic pattern with direct hyperbilirubinemia and ALP without an obvious obstruction cause.

Alcoholic liver disease (ALD) refers to a spectrum of dysplastic and inflammatory changes to hepatic tissues including steatosis, inflammation, fibrosis, and cirrhosis, which are typically co-occurring phenomena resulting from chronic excessive alcohol consumption [ 1 ]. Alcoholic hepatitis refers to the acute onset of symptomatic hepatitis with symptoms such as right upper quadrant pain, jaundice, anorexia, fever, fatigue, and tender hepatomegaly. The diagnosis of ALD is made clinically based on a history of significant alcohol intake and supportive laboratory findings such as elevated liver enzymes AST, ALT( with AST/ALT ratio >2), GGT, and alkaline phosphatase (ALP) along with elevated bilirubin coupled with peripheral stigmata of liver disease and rarely requires a liver biopsy [ 2, 3 ]. Usually, ALD presents with indirect hyperbilirubinemia, but we present a rare case of ALD with direct hyperbilirubinemia, elevated ALP, and hypertriglyceridemia. The patient underwent extensive laboratory and imaging tests that excluded extrahepatic cholestasis and viral, autoimmune, toxic, and ischemic hepatitis. Liver biopsy ruled out nonalcoholic etiologies of such a rare pattern.

A 27-year-old Hispanic male was admitted from the emergency department with a history of progressive worsening yellowish discoloration of the skin and eyes, nausea, and fatigue for the last 7 days. It was associated with generalized pruritus. He denied abdominal pain, fever, chills, diarrhea, abdominal distention, melena, hematemesis, myalgia, joint pain, and other symptoms at the time of presentation. The patient recollected a similar episode of yellowish discoloration about a year ago, but it resolved without medical attention. He was not taking any medications. He denied a family history of jaundice and liver disorders on his mother’s side. The patient lived with his mother and worked at a veterinary hospital as an animal handler. He had a history of EtOH consumption since the age of 14 and mentioned that until last year he was consuming 1/2 L of Vodka daily, but due to gastric reflux issues he switched to beer. He admitted drinking about 4 beers per day, reporting multiple failed attempts at quitting. He denied intravenous drug use, blood transfusion, and multiple sexual partners. Physical examination was notable for icteric sclera and jaundice of his whole body including the palms and soles. Abdominal examination revealed marked hepatomegaly with liver edge palpable up to 5 cm below the right costal margin. There were no signs of peripheral stigmata of liver disease, and his BMI was 24.

Initial laboratory studies were significant for elevated liver enzymes (AST 170 IU/L, ALT 64 IU/L, ALP 649 IU/L, GGT 3,792 U/L), elevated total bilirubin of 15.7 mg/dL with direct bilirubin of 11.75 mg/dL, albumin 2.2 mg/dL, and a blood EtOH level of 399. Maddrey’s discriminant function was calculated to be 14.8. The rest of the laboratory findings were within normal limits including BMP, ammonia, PT, INR, and platelet counts. Urine toxicology screen was negative for drugs and toxins. The patient was started on intravenous fluids with normal saline, intravenous thiamine, and folic acid.

Upon admission, the presumptive diagnosis was choledocholithiasis presenting with an extrahepatic cholestatic pattern of liver enzymes and hyperbilirubinemia versus intrahepatic cholestasis (viral hepatitis, ALD). Abdominal sonogram showed hepatomegaly, diffused fatty infiltration of liver, nonspecific gallbladder distention, and gallbladder wall thickening/edema. Abdominal imaging including MRI/MRCP ruled out CBD stones and biliary duct dilatation but revealed hepatic steatosis, pancreatitis, and distended gallbladder wall with mild edematous wall. Acute and chronic viral hepatitis serologies (HAV, HBV, HCV) were negative. ERCP was not performed after MRCP ruled out CBD obstruction.

Due to elevated direct bilirubin, alternative etiologies such as primary biliary cirrhosis, primary sclerosing cholangitis, Wilson’s disease, and hemochromatosis were also considered as co-existing pathologies, and further workup was continued while the patient was being managed with intravenous fluids, benzodiazepines, and alcohol cessation. Other laboratory results included borderline elevated lipase and ceruloplasmin, anemia with markedly increased RDW, increased circulating nucleated RBCs, and macrocytic target cells. ANA screen and antimitochondrial antibody were negative. HIV-1/2 Ag/Ab was negative. Cholesterol (483 mg/dL), LDL (362 mg/dL), and triglycerides (1,040 mg/dL) were markedly increased with decreased HDL (12 mg/dL). Electrophoretic HbA1c was normal, and abnormal hemoglobin was not identified. He had an elevated ferritin level of 1,693.6 ng/mL. Hereditary hemochromatosis DNA mutational analysis was negative for C282Y and H63D mutations in the HFE gene. Antinuclear antibody, anti-mitochondrial antibody, ANCA screen, PR-3 antibody, and MPO antibody tests were negative.

Ultrasound-guided core needle liver biopsy was performed 5 days after presentation which showed diffuse steatosis (>70%), primarily macrovesicular, with scattered lobular and portal inflammation, and hepatocyte ballooning degeneration – findings consistent with alcohol-related etiology (Fig.  1 a–d).

a–d Liver core biopsy. H&E stain, CK19, CK7, and Retic at both 10× and 20× magnifications. a–d Diffuse steatosis (>70%), primarily macrovesicular, with scattered lobular and portal inflammation, and hepatocyte ballooning degeneration. c Mallory hyaline and rare acidophilic bodies, and mild pericellular and periportal fibrosis (trichome stain). d No parenchymal iron deposition (iron stain); hepatocyte intracytoplasmic hyaline globules suggestive of alpha-1 antitrypsin deficiency are absent (PAS stain with diastase).

Clinically, his symptoms were better during the hospital stay; liver enzymes and bilirubin trended up for 2 days before trending down. He was discharged after 6 days of conservative treatment with alcohol cessation counseling and recommendations to follow up in the gastroenterology office.

ALD is clinically silent with little or no symptoms, especially in the patients with early ALD and compensated cirrhosis. On top of that, most patients are reluctant to openly admit their drinking behavior, so diagnosis depends highly on clinical suspicion, various laboratory tests, and sometimes even invasive tests.

In most cases, ALD can be diagnosed easily with reliable history, hepatic function panel, and imaging to support the diagnosis [ 4 ]. Patients with ALD typically have elevated red blood cell MCV, moderate elevations of AST and ALT (typically less than 400 IU/L with AST/ALT ratio of >2), elevated serum bilirubin, GGT, and INR, and low albumin and platelet count [ 5 ]. Acute-phase reactants such as serum ceruloplasmin, ferritin, and alpha-1 antitrypsin may be elevated in patients with severe alcoholic hepatitis.

Generally, clinical and laboratory features are often adequate to establish the diagnosis of ALD in a patient with long-standing history of heavy alcohol use. In our patient with his AST/ALT ratio of 170/64 (= 2.65), elevated serum bilirubin, low albumin (2.2 mg/dL), and ruling out other common causes of acute hepatitis, alcoholic hepatitis was the most likely diagnosis. However, the unusual cholestatic pattern of elevated direct bilirubin and markedly elevated ALP (649 IU/L) and high ferritin level (1,693.6 ng/mL) added more to the diagnostic dilemma in our case.

While many patients with suspected alcoholic hepatitis will not require a liver biopsy, we ended up ordering an ultrasound-guided liver biopsy in our patient because of the questionable differential diagnosis and unknown family history of liver disease on the father’s side. The biopsy demonstrated toxic hepatocellular injury most supportive of alcohol etiology and ruled out any evidence of iron overload to suggest primary (hemochromatosis) or secondary hemosiderosis or alpha-1 antitrypsin deficiency. Biopsy also ruled out significant biliary duct obstruction.

Painless jaundice with elevated direct bilirubin and elevated ALP is commonly attributed to choledocholithiasis or hepatobiliary, pancreatic carcinoma. ALD can also manifest with clinical and histological evidence of cholestasis with elevated ALP but generally up to 2–3 times the upper limit of normal [ 6 ]. This case represents a rare manifestation of ALD with marked elevation of direct bilirubin and ALP.

Alcoholic hepatitis is a common condition, but some presentations can lead one to think of unusual pathologies. This case reflects that alcoholic hepatitis can present with high levels of triglycerides as well as a cholestatic pattern with direct hyperbilirubinemia and ALP without an obvious obstruction cause.

The patient gave written informed consent to write this case, and the protocol was approved by the institute’s committee on human research.

All authors have no financial disclosure or conflicts of interest.

This research was performed under the guidance of the Memorial Healthcare System Internal Medicine Residency, without specific funding support.

Pratik Khatiwada and Jose A. Rodriguez: data collection, manuscript preparation, and literature search. Andres Reyes-Corcho: data interpretation and manuscript preparation.

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• Nutrition counsellor
• Food Allergy
• gastroenterology
• Heptologist In Delhi
• Liver transplant
• Alcoholic Liver Cirrhosis

Alcoholic liver cirrhosis is a late stage of fibrosis of the liver caused by many forms of liver diseases and conditions, such as chronic alcoholism. A person diagnosed with an alcoholic liver case may start from having fatty liver disease, then alcoholic hepatitis, and ultimately develop alcoholic cirrhosis. Hence, alcoholic liver cirrhosis stages in three levels. The diagnosed liver cirrhosis can be of two types :

• Compensated cirrhosis – when symptoms are not noticeable
• Uncompensated cirrhosis- when the symptoms can be noticed

The most common alcoholic liver causes are:

• Chronic alcohol consumption
• Chronic hepatitis
• Fatty liver disease
• Iron buildup in the body or hemochromatosis
• Copper accumulated in the liver (Wilson’s disease)
• Cystic fibrosis
• Biliary Atresia
• Inherited sugar metabolism or digestive disorders
• Infection like syphilis

Many other factors like the destruction of bile ducts(Primary Biliary Cirrhosis) or leaky gut also called, increased intestinal permeability are cofactors for the development of alcoholic liver cirrhosis.

Now, let us have a look at alcoholic liver cirrhosis symptoms:

• Food pipe problems
• Portal hypertension
• Swelling in legs (oedema) and abdomen (ascites)
• Bleeding in mouth
• Confusion, poor memory, loss of appetite
• Patchy red skin on palms (erythema)

Food pipe problem is also known as esophageal varices. Kidney failure and hypersplenism are other complications that happen due to this medical condition. If the symptoms are not taken seriously, then this deficient liver may arise a life-threatening situation. Hence, a person needs to keep a track of these indicators as if these signs are caught early and treated, it may slow down the progression of the disease.

How to treat alcoholic liver cirrhosis:

The first and foremost step in treatments is to help the patient to cease alcohol consumption. Medications like corticosteroids, calcium channel blockers, insulin can also be prescribed by the doctor as per the alcoholic liver care plan. Hepatologists may advise the patient to follow an alcoholic liver disease diet inclusive of fiber and protein. If the condition of the patient gets worsened, then the hepatologist may have to suggest a liver transplant surgery.

Dr. Nivedita Pandey is one of the best liver specialist doctors in Patna, Bihar. She is a well-renowned liver specialist doctor in Delhi, the best stomach doctor in Patna, the best gastroenterologist in Jammu, and a notable stomach doctor in Faridabad. Now, you can sway off all your gastroenterological worries online by booking an online gastroenterologist consultation with one of the best hepatologists in India. She is a liver specialist in Delhi NCR, one of the finest gastroenterologists in Jhansi and Jammu, and an acidity specialist doctor in Patna. Dr. Pandey’s gastroenterologist live chat has also helped people in several ways.

Case Review

This alcoholic liver case study presents a patient with liver cirrhosis. A 43-year-old man was brought into the hospital with a complaints of loss of appetite, abdominal distention, and arrhythmia. He also experienced itchy skin and blood in the stool. The patient’s family rushed him into the hospital, and he was in a half-conscious state. The patient was taken to the emergency room for evaluation. As told by the family, he had a past medical history and was a heavy alcohol consumer. This alcoholic liver case history consisted of various medical ailments like fatty liver, asthma, tuberculosis, malnutrition, hypertension, and hepatitis C. The patient had a heart attack three years back and stented for the same. Due to his health conditions, he was on several medications. In the emergency room, when the patient was under observation by a stomach specialist doctor in Patna and her team, they were able to diagnose from his symptoms that it was alcoholic liver cirrhosis. The patient went for a few scans including, a liver function test, liver ultrasound, and endoscopy along with CT, blood test, and urine tests.

Case Discussion

Though most of the liver cirrhosis causes remain unknown, with the help of her team, the best liver doctor and specialist in Patna was able to find out the reason for this one. The liver cirrhosis caused in this case was due to the medical history of the patient. His scans came out to be reasonably sound, and a liver biopsy was conducted to confirm the severity and type of liver disease. There were problems in his blood and urine culture, and they were taken care of by the team. His liver appeared swollen in the reports. There were certain other problems seen in his ultrasound and endoscopy. The crew decided to start with the treatment while keeping him under observation for the next 72 hours.

Clinical Symptoms

He was initially confused and was not able to respond or hear properly. According to the condition reported by his family i.e.- appetite loss, memory loss, and confusion were some other clinical symptoms of alcoholic liver cirrhosis. When the doctor talked to the family of the patient, she was able to get a clearer picture. The patient complained about acute abdominal pain. When Dr. Pandey, one of the best doctors in Patna for the stomach, observed the patient and talked to him, she noticed bleeding in his mouth. This further helped doctors to eliminate all doubts, and after looking at the lab results, they made out it was alcoholic liver cirrhosis.

The first and foremost management required when treating the alcoholic liver cirrhosis case is calming the patient down. The liver specialist with the help of her fellow doctors was able to counsel the patient and explain his medical condition to the family. After a complete diagnosis, the patient was taken to the ICU as he was under observation. The doctor prescribed him antioxidant drugs and insulin to control any future problems while treating the present one. The doctor is the best gastroenterologist in Faridabad, Delhi, and Patna, and she handled the situation well before any further complications. The patient got his discharge in due time and was sent back home in a healthy and sound condition.

1.   Which Group of People are More Likely to get diagnosed with alcoholic liver cirrhosis?

A person who has drunk heavily for a long time is more prone to acquire this disease. Women are also at risk for this medical disease due to the absence of many enzymes which break down alcohol particles.

Consider consulting the best gastroenterologist in India , Dr. Nivedita Pandey who is also well known for her nutritional counselling services and teleconsultation services. She is also famous for her care from afar service. You can also find her as the best liver specialist doctor in Patna, Bihar or hepatologist in Patna or the best doctor for hepatitis b in Patna , a gastroenterologist in Faridabad , the best gastro doctor in Delhi, NCR , a gastroenterologist In Uttarakhand , a liver specialist in Jhansi , best gastroenterologist in Jammu take advantage of the online gastroenterology consultation to gastroenterologist live chat and receive the best treatment that your body deserves!

2.   Is liver cirrhosis cancer?

No, liver cirrhosis is not a type of cancer. If a person has alcoholic liver cirrhosis, he/she has an increased risk of liver cancer.

3.   Is liver cirrhosis a hereditary disease?

Negative, alcoholic liver cirrhosis is not a hereditary disease, rather it is a type of an acquired disease.

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Clinical Case Presentation: Alcoholic Liver Disease

Sep 29, 2014

1.03k likes | 5.42k Views

Clinical Case Presentation: Alcoholic Liver Disease. Gaurav Jain Roll No: 174/11. Clinical Case Presentation: Ascites with ARF. Lakshmi Narayan, 42 years old patient , who is a chronic alcoholic , farmer by occupation presented with: Abdominal distension from 15 days

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Presentation Transcript

Clinical Case Presentation: AlcoholicLiver Disease Gaurav Jain Roll No: 174/11

Clinical Case Presentation:Ascites with ARF • Lakshmi Narayan, 42 years old patient , who is a chronic alcoholic, farmer by occupation presented with: • Abdominal distension from 15 days • Abdominal pain from 15 days • Fever from 15 days • Decreased urine output from 10 days • Decreased passage of stools from 10 days

HISTORY • H/O Present illness: • HDBT 15 days when patient developed: • insidious, gradually progressive Abdominal distension a/w pin-pricking pain in the epigastrium & right hypochondrium region , relieved by medication. • Intermittent, mild to moderate grade fever, insidious onset & subsides on medication a/w nausea ,retching, cachexia, altered sleep patterns with day-time sleepiness. • Pt. developed decrease in urine output without burning or other discomfort from past 10 days. • Pt. developed decreases stool passage ,insidious onset and gradually progressive, not a/w flatulence, dyspepsia, heart burn from 10 days. • A single episode of haemetemesis containing 30 ml of fresh blood.

Negative History: No H/Ochills, rigor, sweating,headache,rashes retrobulbar pain, cough, joint pain, steatorrhea, malena, facial puffiness, xanthelasma, xanthomata, flapping tremors, blood transfusion. • Past History: No H/O TB, Diabetes, Asthma, Hypertension. No such complaint in the past. • Personal History: Married with two children • Non vegeterian diet. • Smoking-15 pack years but one bundle daily from past 2 months. • Chronic alcoholic from past 30 years consuming 4.5-5.6 units of alcohol daily. Tobacco chewing from past 12 years. • Lost 15 kgs of weight in past 2 months. • Family History: No such family history. • Drug History: No significant history.

EXAMINATION • General Physical Examination • Patient is conscious, oriented to time,place and person and cooperative. • No pallor, icterus, cyanosis, clubbing, JVP and lymphadenopathy. Pedal edema present. • No gynaecomasatia, skin pigmentation , palmar erythema, spider nevi, leuconychia, koilonychia, angular stomatitis present. • Axillary ,pubic hair decreased. Mild Glossitis present • PR- 86/min RR-20/min BP-96/60mmHg • Abdominal Girth: 114.3 cm • Umblico-ischial spine distance: 19.05 cm • Umblico-Symphysis distance: 21.59 cm

Abdominal Examination • Inspection: globular shape stomach with full flanks and everted umblicus. There is a single scar present on the right lateral side. Engorged veins seen.(downward to upward blood • flow). • Palpation: afebrile .Liver not palpable. Spleen palpable by Dipping method but size cant be established. Fluid thrill present. . Tense and tendor • Percussion: Shifting Dullness present. • Auscultation:Bowel sounds heard and Bruits not heard. • Other systemic findings were normal.

INVESTIGATIONS HIV, Hep B, Hep C-negative

Complete Urine Examination: Within normal limits. Ultrasonography

Differential Diagnosis: • Based on clinical, lab & USG findings, patient is suffering from Chronic Liver Disease showing complications of Ascites and Portal Hypertension with derangement of KFT, cause of which can be 1) Hepato-Renal Syndrome 2) Pre –Renal Azotemia • High SAAG in the case indicates presence of Portal Hypertension. • Low Ascitic Protein (1.5g/dl) indicates Transudative Ascites. • Based on patients alcoholic history & lab findings,Cirrhosis is the cause of Ascitis and Portal Hypertension. • Complete Urine Analysis within normal limit shows that Chronic Kidney Disease is not the cause of acute renal failure. • Hereditary causes of Cirrhosis are ruled out based on family history while patient gives no history of skin pigmentation,xanthoma and jaundice which rules out Biliary Cirrhosis.

Alcohol Liver Disease • Chronic alcohol ingestion is one of the major causes of liver disease. • It causes 3 major lesions: a)fatty liver b)alcoholic hepatitis c)cirrhosis • Quantity and Duration of alcohol intake are the major risk factors.160g/d for 10-20 years in man produces cirrhosis. • Hepatic metabolism of alcohol initiates a process that promotes lipogenesis& the inhibition of fatty-acid oxidation. Endotoxins, oxidative stress, immunologic activity, and pro-inflammatory cytokine release contribute to the resulting liver injury. • Alcoholic fatty liver and hepatitis is reversible with alcohol abstention but cirrhosis is not. • Diagnosis is based on AST, ALT, GGTP, Bilirubin and USG findings.

A discriminant function can determine patients with poor prognosis.(>32) • The presence of ascites, variceal hemorrhage, deep encephalopathy, or hepatorenal syndrome predicts a dismal prognosis. • Management • Lifestyle modifications: decreased alcohol intake, smoking obesity • Appropriate nutrition/nutritional support • Use of pentoxifylline or prednisone for alcohol hepatitis • Advice on complementary & alternative medicine for cirrhosis(eg silymarin) • Transplantation in selected abstinent patients with severe disease.

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Interactive case report

An alcoholic patient who continues to drink: case presentation, stuart mcpherson.

1 Department of Gastroenterology, South Tyneside Healthcare NHS Foundation Trust, South Shields NE34 0PL

Colin John Rees

Mr Bond is a 42 year old man with alcoholic cirrhosis who was admitted to our unit with haematemesis. He had had three previous admissions with alcohol related problems and had twice bled from oesophageal varices. The varices had been treated by sclerotherapy and banding, and he was taking propranolol 40 mg twice daily as secondary prophylaxis. His most recent endoscopy had shown three, barely noticeable oesophageal varices.

Mr Bond has a history of excessive alcohol intake over five years, with no periods of abstinence. He was drinking 3-4 litres of strong cider a day up until the day of admission. A consultant psychiatrist had previously diagnosed depression and alcohol dependence syndrome. Although Mr Bond had been treated with paroxetine, he discontinued it as he thought it was unhelpful. He had also seen the drug and alcohol team several times. His attendance at appointments with the psychiatrist and drug and alcohol team was sporadic as he felt that these were of little benefit to him. He complied with medical drug treatment.

• What are the likely causes of Mr Bond's bleeding?
• How would you rate the severity of this bleed?
• What initial steps should be taken in his management?
• Given Mr Bond's continued alcohol consumption, how far should we go with treatment?

Please respond through bmj.com , remembering that Mr Bond is a real patient and that he and his carers will read your response

Mr Bond lives with a partner and has three children from a previous marriage, whom he rarely sees. He worked for the local council for 22 years but stopped working several years ago because of his alcohol dependence and depression. His marriage breakup a few years earlier had precipitated particularly heavy drinking. Mr Bond describes himself as a worrier and turns to alcohol when things go wrong. His mother died at the age of 60 from alcoholic liver disease.

On presentation with gastrointestinal bleeding he was jaundiced and showed signs of chronic liver disease ( table ). He was not encephalopathic. His pulse was 140/min and blood pressure 118/67 mm Hg with no appreciable postural drop. He had mild ascites but no hepatosplenomegaly. Per rectal examination showed melaena.

Results of investigations at presentation

Competing interests: None declared.

This is the first of a three part case report where we invite readers to take part in considering the diagnosis and ethical issues surrounding the management of a case using the rapid response feature on bmj.com . Next week we will report the case progression, and in four weeks' time we will report the outcome and summarise the responses

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Experts call for more clinical trials on alcohol use, liver disease

by UT Southwestern Medical Center

More clinical research is needed to investigate how reducing alcohol consumption in patients with alcohol-related liver disease (ALD) may slow disease progression and improve outcomes, according to an international task force of experts from more than two dozen institutions including UT Southwestern Medical Center.

In a consensus statement published in Nature Reviews Gastroenterology & Hepatology , the group, commissioned by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), issued a set of 28 recommendations to guide the design of future clinical trials addressing alcohol use disorder (AUD) and ALD. The recommendations call for multidisciplinary teams, including experts from hepatology and addiction medicine, and the need to address the stigma of alcoholism.

"Physicians know anecdotally that reducing or eliminating heavy drinking after diagnosis can extend and improve life for patients with ALD, but research on the subject has been limited," said Mack Mitchell, M.D., Professor of Internal Medicine in the Division of Digestive and Liver Diseases and Vice President for Medical Affairs at UT Southwestern, who co-chaired the task force and is the lead author on the article. "Our hope is that well-designed clinical trials focused on alcohol use and ALD could lead to effective changes in clinical practice."

Deaths linked to excessive alcohol use have increased over the past two decades, including a surge during the COVID-19 pandemic. Alcohol consumption is a primary cause of death from liver-related diseases, accounting for more than half of all cirrhosis-related deaths in the U.S. in 2022 and 46% of all liver disease deaths, according to NIAAA. While abstinence has been associated with improved life expectancy for ALD patients, few clinical trials have been conducted to investigate how interventions to reduce or eliminate heavy drinking will affect disease progression .

The task force included hepatologists, addiction medicine specialists, clinical trialists, and members of regulatory agencies. Among its recommendations are definitions for disease categories, criteria for trial participants, treatment considerations, and safety and regulatory concerns.

The article notes that diseases related to alcohol use are among the most stigmatized, resulting in stereotypes that create barriers to treatment, such as ineligibility for liver transplantation. The group proposed that researchers discuss ways to reduce those negative beliefs among all team members in trials for AUD and ALD and, when possible, involve patient representatives and other stakeholders in trial design.

Thomas Cotter, M.D., M.S.C.P., Assistant Professor of Internal Medicine in the Division of Digestive and Liver Diseases at UT Southwestern, also participated in the consensus statement .

"The field of alcohol-associated liver disease lacks well-designed clinical trials integrating alcohol use disorder treatment, a pivotal component in order to optimize patient outcomes. These recommendations will serve as an important blueprint to help guide the field going forward," Dr. Cotter said.

Nature Reviews Gastroenterology & Hepatology has also published a companion commentary on the subject.

Commentary: Juliana Serrazina et al, Shaping new paths in clinical trial design to address alcohol use disorders and alcohol-associated liver disease, Nature Reviews Gastroenterology & Hepatology (2024). DOI: 10.1038/s41575-024-00948-7

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Male Endometriosis: Extremely Rare Condition with Unusual Presentation as Haematuria—A Case Report

• Case Report
• Published: 26 June 2024

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• Abhishek Mandal   ORCID: orcid.org/0000-0001-8577-0706 1 ,
• Om Tantia   ORCID: orcid.org/0000-0003-0128-8766 1 ,
• Jayati Datta   ORCID: orcid.org/0000-0002-8212-4677 2 &
• Subhendu Roy 2  

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Male endometriosis is a rare condition whose exact cause remains elusive, with only a handful of cases (17 cases) documented in literature. In the instances reported previously, endometriotic lesions were frequently observed affixed to the urinary bladder, in the inguinal region, and within the lower abdomen. Proposed explanations for its origin point to a hyper estrogenic environment, possibly linked to prolonged estrogen treatment, cirrhotic liver disease, or chronic surgical inflammation.

We report here a rare case of male endometriosis in a 52-year-old diabetic man, who exhibited unusual hematuria and was subsequently diagnosed to have a mass related to the urinary bladder on investigation. Surgical removal and histopathological examination validated the diagnosis. Notably, known etiological factors of male endometriosis were not present in this patient. It is conceivable that persistent embryonic remnants or latent non-alcoholic fatty liver disease in the context of Type II diabetes or obesity may have contributed in the development of endometriosis.

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Acknowledgements

I acknowledge the immense contribution of Dr. Anita Borges, Lab Director & Consultant Pathologist, Centre for Oncopathology, Mumbai, for arriving histopathological diagnosis. Special thanks to Dr. Ranjan Kumar Dey (Urologist) for clinical management.

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Mandal, A., Tantia, O., Datta, J. et al. Male Endometriosis: Extremely Rare Condition with Unusual Presentation as Haematuria—A Case Report. Indian J Surg (2024). https://doi.org/10.1007/s12262-024-04105-x

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DOI : https://doi.org/10.1007/s12262-024-04105-x

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