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Cirrhosis

Management Team

Cirrhosis

Overview

Liver cirrhosis is a chronic condition in which healthy liver tissue is replaced by scar tissue (i.e., progression of fibrosis), leading to impaired liver function, which can have serious health implications. 

As with all other manifestations of ALD, chronic alcohol abuse is one of the most common causes of liver cirrhosis. Other causes include:

  • Fatty liver disease (N/AFLD): This condition—linked to obesity, diabetes, and metabolic syndrome—can promote cirrhosis.
  • Chronic viral hepatitis: Hepatitis B and C can promote cirrhosis.
  • Autoimmune hepatitis: In this condition, the immune system attacks the liver cells.
  • Biliary diseases: Diseases that affect the gall bladder and bile ducts, such as primary biliary cholangitis or primary sclerosing cholangitis, can lead to cirrhosis.
  • Genetic conditions: Hemochromatosis (iron overload) and Wilson’s disease (copper buildup) can also cause cirrhosis.
  • Medications and toxins: Long-term use of certain drugs or toxins can also cause cirrhosis; they can also serve as risk factors.
  • Infections: Schistosomiasis or other parasitic infections can also cause cirrhosis.
  • Obesity: Increases risk of N/AFLD, and by extension cirrhosis.
  • Diabetes and insulin resistance: These factors can serve as risk factors for liver cirrhosis.
  • Family history: A family history of liver diseases (genetic predisposition) can also serve as a risk factor.

Cirrhosis shares many symptoms with N/AFLD, N/ASH, and liver fibrosis. The same has been enumerated below.

  • Fatigue
  • Loss of appetite
  • Nausea (urge to vomit)
  • Weight loss
  • Jaundice
  • Ascites (fluid accumulation in the abdomen)
  • Oedema (swelling in the legs)
  • Oesophageal varices (enlarged veins prone to bleeding)
  • Hepatic encephalopathy (confusion, memory problems, drowsiness)
  • Spider angiomas (spider-like blood vessels on the skin)

As cirrhosis shares many symptoms with N/AFLD, N/ASH, and liver fibrosis, it also shares the diagnostic modalities; the same have been enumerated below.

  • Blood tests:
    • Liver function tests (ALT, AST, bilirubin, albumin)
    • Coagulation profile (INR, PT)
    • Platelet count
  • Imaging studies:
    • Ultrasound (detects liver size, texture, ascites)
    • CT or MRI (detailed liver structure)
    • Elastography (evaluates the extent of fibrosis by measuring liver stiffness)
  • Liver biopsy: To confirm the diagnosis in uncertain cases.
  • Endoscopy: To check for oesophageal varices.
  • Serology and genetic tests: To identify underlying causes.

Cirrhosis treatment generally focuses on managing the underlying cause, slowing down disease progression, and preventing complications. The strategies used have been enumerated below.

  • Lifestyle changes:
    • Alcohol cessation
    • Weight loss and dietary management (low sodium, balanced diet)
  • Medications:
    • Antivirals for hepatitis B or C
    • Diuretics for ascites (spironolactone, furosemide)
    • Lactulose or rifaximin for hepatic encephalopathy
    • Beta-blockers for oesophageal varices (e.g., propranolol)
  • Management of complications:
    • Paracentesis for ascites
    • Endoscopic treatment for variceal bleeding
  • Advanced therapies:
    • Liver transplantation: For end-stage liver disease. (advanced cirrhosis and liver cancer).
    • TIPS (transjugular intrahepatic portosystemic shunt): For refractory ascites or variceal bleeding.
  • Nutritional support: Adequate protein intake and vitamin supplementation to manage cirrhosis-associated liver damage.

Strategies for cirrhosis prevention have been enumerated below.

  • Vaccination against hepatitis A and B.
  • Avoidance of excessive alcohol consumption.
  • Regular screening and early management of viral hepatitis.
  • Healthy lifestyle with balanced diet and exercise.
  • Avoiding hepatotoxic drugs and chemicals.
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Charcot-Marie-Tooth Disease (CMTD)

Management Team

Charcot-Marie-Tooth Disease (CMTD)

Overview

CMTD is a hereditary neuropathy that affects the peripheral nerves, and has a prevalence of 1:2500 in general population. The inheritance pattern may be autosomal dominant, autosomal recessive, or X linked.

  • It is caused due to mutations in various genes

  • Family history is the only known factor.

  • Muscle weakness and atrophy of legs, ankle, and feet
  • Foot deformities (high arches, hammertoes)
  • Imbalance and difficulty in walking
  • Numbness in feet and legs

  • CMT-1 : Mutation in peripheral myelin protein 22 gene (PMP22) on chromosome 17p11.2.
  • CMT-2: Mitofusin 2, connexin 32
  • CMT 3: Also known as Dejerine Sotas disease
  • CMT 4
  • Other variants of CMT are rare

Neurologist

Clinical examination and through nerve conduction studies to determine demyelinating or axonal type of neuropathy, depending on the variant of CMTD; CMT 1 and 3 are demyelinating, whereas CMT 2 is axonal neuropathy.

  • Physical therapy with exercise for maintaining muscle strength
  • Assistive devices
  • Pain management and neurorehabilitation
  • No cure
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Central Nervous System Infections

Management Team

Central Nervous System Infections

Overview

CNS infections are the infections affecting the brain, spinal cord, or their covering (meninges). These can be caused by bacteria, fungi, viruses, and parasites. They are more commonly seen in immunocompromised individuals and also in immunocompetent persons.

  • Bacteria- streptococcus pneumoniae, H. influenzae, mycobacterium tuberculosis
  • Viruses- enterovirus, herpesvirus
  • Fungi- candida, aspergillus, cryptococcus
  • Parasites- plasmodium, toxoplasma and others

  • Preexisting conditions like diabetes, liver cirrhosis, stroke, and chronic alcohol abuse
  • Head trauma and injuries to the spinal cord
  • Extrinsic contamination during neurosurgical procedures, cerebrospinal fluid leakage, and drainage tube placement
  • Immunocompromised states including end-stage HIV, systemic chemotherapy, and hereditary immunologic disorders
  • Other factors including congenital malformations, implanted medical devices, and breaches of the blood-brain barrier

  • Fever
  • Headache
  • Stiff neck
  • Altered sensorium
  • Seizures
  • Paralysis

Neurologist

  • Blood tests- abnormal WBC count, blood cultures
  • CSF examination- altered cell count, protein and sugar ratio.
  • MRI/ CT scan

  • Antimicrobial therapy (antibacterial/ antiviral/ antifungal)
  • Supportive care (fluid and pain management)
  • Surgery is sometimes warranted in case of mass effect caused due to abscess
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Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)

Management Team

CADASIL

Overview

CADASIL is a rare condition that affects blood flow to the brain, potentially leading to stroke, headache, gait disturbances, and dementia.

It occurs due to mutation in the NOTCH 3 gene and affects the small vessels of the brain.

  • Hypertension
  • Smoking habits
  • Family history
  • Migraine with aura
  • Higher homocysteine levels
  • Ovarian hormones may play a role in sex-related differences in CADASIL

  • Migrainous headaches
  • Multiple strokes in various parts of the brain
  • Memory decline
  • Seizures
  • Vision problems
  • Slowness of movements and imbalance while walking

Neurologist

  • MRI
  • Genetic testing for- notch 3 mutation on chromosome 19.

  • Symptomatic treatment for headache, seizures, gait training, and cognitive therapy
  • No specific therapy available
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C

Brain Death

Management Team

Brain Death

Overview

Brain death is the permanent and irreversible cessation of arousal, wakefulness, accompanied by total and irreversible loss of brain stem reflexes, including breathing, coughing, eye movement, and swallowing.

  • Hypoxic brain damage
  • Trauma
  • Vascular- ischemic / haemorrhagic stroke
  • Fulminant systemic/ brain infections
  • Inflammatory conditions- vasculitis
  • Autoimmune conditions- neurosarcoidosis

  • Cardiopulmonary arrest
  • Traumatic brain injury
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
  • Other causes of brain death include heart attack, stroke, blood clot, infections like encephalitis or meningitis, and brain tumour

  • Fixed pupils with no response to light
  • Absence of corneal or conjunctival reflex
  • No response on caloric testing
  • Absence of spontaneous breathing
  • Absence of gag reflex
  • No motor response to painful stimulus
  • No respiratory movements on disconnection from ventilator, even after increase in CO2 in blood

  • The aetiology for irreversible brain damage should be confirmed.
  • The causes of coma such as sedative medications, hypothermia, metabolic and endocrine causes should be excluded
  • The Patient should be hemodynamically stable on ventilator
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B

Botulism

Management Team

Botulism

Overview

Botulism is a a severe and potentially life-threatening disease caused by the botulinum toxin, which is produced by the bacterium Clostridium botulinum.

  • Ingestion of contaminated food or water
  • Infected wounds
  • Inhalation of toxin used in biological warfare

  • Injecting illicit drugs such as black tar heroin
  • Drinking certain kinds of homemade alcohol, such as “pruno” or “hooch”
  • Eating improperly canned, preserved, or fermented foods, Foods commonly linked to botulism include home-canned foods and Alaska Native foods.
  • Being injected with too much botulinum toxin for medical or cosmetic reasons

  • Drooping of eyelids
  • Muscle weakness or paralysis
  • Slurring of speech
  • Difficulty in swallowing
  • Diarrhoea or vomiting
  • Difficulty in breathing

Neurologist

  • Antitoxin (if given early)
  • Supportive care (mechanical ventilation)
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B

Alcohol-associated Hepatitis (AAH)

Management Team

Alcohol-associated Hepatitis (AAH)

Overview

Alcohol-associated hepatitis (AAH) is a serious form of ALD whose key features include liver cell injury, inflammation, and liver dysfunction. AAH can range from mild (acute) to severe (chronic). Importantly, it can sometimes lead to liver failure.

The most significant risk factor for AAH is long-term excessive alcohol consumption. Other factors affecting AAH development include:

  • Family history: An individual’s genetic background influences how the liver metabolises alcohol, thereby affecting the likelihood of developing AAH. Certain genetic variations in liver enzymes can make some individuals more susceptible to developing AAH.
  • Gender: Women are more susceptible to alcohol-associated liver damage, developing AAH even in response to lower alcohol intake (compared to men).
  • Obesity: Obesity, especially when associated with fatty liver disease (N/AFLD), can worsen liver injury in individuals who drink excessively.
  • Hepatitis C and B infection: Co-existing chronic viral hepatitis (hepatitis C or B) increases the risk of developing AAH and worsens its outcomes.
  • Other liver diseases: Individuals with preexisting liver diseases like cirrhosis or non-alcoholic fatty liver disease (NAFLD) may be more likely to develop AAH after heavy alcohol consumption.
  • Nutritional deficiencies: Chronic alcohol consumption can lead to poor nutrition, which may further exacerbate liver injury.

The symptoms of alcohol-associated hepatitis can vary, ranging from mild to severe. They include: 

  • Jaundice: This is a hallmark symptom, indicating liver dysfunction.
  • Abdominal pain: This is more prominently felt in the upper right side of the abdomen.
  • Fatigue: Owing to compromised liver function, the affected individuals feel excessively tired or weak.
  • Loss of appetite: This is often associated with nausea (urge to vomit) or vomiting.
  • Fever: Mild to moderate fever can occur in the case of AAH.
  • Ascites: Fluid buildup in the abdomen is often seen in advanced cases of AAH.
  • Hepatomegaly: AAH causes enlargement of the liver, which can result in discomfort or a sensation of fullness.
  • Confusion or mental changes: In severe cases, particularly in case of liver failure, confusion or disorientation can occur (hepatic encephalopathy); the person might even slip into a coma.
  • Easy bruising or bleeding: Affected individuals become susceptible to easy bruising or bleeding owing to impaired clotting function of the liver.
  • Liver failure: In severe cases, AAH can rapidly progress to liver failure, which is a medical emergency.

AAH is diagnosed using several strategies (clinical evaluation, laboratory tests, and imaging). These include:

  • Clinical history: Information regarding the quantity, frequency, and duration of alcohol use—along with other risk factors—is collected.
  • Physical examination: Patients are evaluated for signs of liver damage (jaundice, hepatomegaly (enlarged liver), ascites, or mental status changes) are observed.
  • Laboratory tests:
    • Liver function tests: In AAH, AST levels are often more elevated than ALT levels, and the AST to ALT ratio is typically greater than 2.
    • Complete blood count (CBC) test: Reduced counts of white blood cells (leukopenia) and platelets (thrombocytopenia) may be observed in AAH.
    • Coagulation tests: Prolonged prothrombin time (PT) or increased international normalised ratio (INR) can indicate impaired liver function.
    • Serum bilirubin: Elevated bilirubin levels indicate AAH with jaundice.
    • Albumin levels: Extremely low albumin levels are a sign of liver failure.
  • Imaging:
    • Ultrasound: This modality helps assess the liver size, texture, and any evidence of cirrhosis or fatty liver; however, it cannot definitively diagnose AAH.
    • CT or MRI: These modalities may be used to rule out other liver diseases or complications.
  • Liver biopsy: A liver biopsy may be performed to confirm the diagnosis, particularly in uncertain cases, and to assess the extent of liver damage (inflammation, fibrosis, or cirrhosis).
  • Rule out other causes: As hepatitis can have multiple causes, tests need to be performed to rule out other types of hepatitis (e.g., hepatitis B, C, A, E).

The treatment for AAH aims to manage symptoms, prevent complications, and address the underlying alcohol use disorder.

  • Support groups, counselling, or alcohol rehabilitation programs: These may be necessary to help individuals stop drinking.
  • Medications:
    • Corticosteroids (e.g., prednisolone): These are often used to manage moderate to severe cases of AAH. However, they are not effective in all cases and may have side effects, particularly in patients with underlying infections or liver failure.
    • Pentoxifylline: This medication may help reduce the risk of renal failure in patients with severe AAH.
  • Liver transplantation: In patients with severe, life-threatening AAH for whom management using medications might not work or who have progressed to liver failure, a liver transplant may be necessary.
  • Nutritional support: Malnutrition is common in AAH, so providing adequate nutrition (vitamin B supplementation) is essential to prevent complications such as Wernicke-Korsakoff syndrome (which is due to vitamin B deficiency). Patients may require enteral nutrition (feeding through a tube) or parenteral nutrition (intravenous (IV) feeding) in severe cases.
  • Management of complications:
    • Diuretics (e.g., spironolactone): These may be used to reduce fluid buildup in the abdomen (ascites).
    • Therapeutic paracentesis (removal of fluid): This might need to be performed in severe cases of ascites.
    • Lactulose: This can be used to lower blood ammonia levels and reduce confusion in case of hepatic encephalopathy.
  • Supportive care: In severe cases, particularly when liver failure is imminent, hospitalisation and intensive care may be required to monitor vital signs, kidney function, and prevent infections.
  • Liver transplantation: Liver transplantation is considered for individuals with acute AAH and severe liver failure who do not improve with medical treatment.

Limiting alcohol consumption is the key to preventing the occurrence of AAH. For individuals with existing liver disease, it is critical that alcohol consumption be avoided completely to prevent further liver damage.

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Advanced Liver Fibrosis

Management Team

Advanced Liver Fibrosis

Overview

Advanced liver fibrosis is the later stage of liver fibrosis, where significant scarring and damage to the liver tissue have occurred. This type of liver fibrosis can progress to cirrhosis, ultimately culminating in severe life-threatening conditions like portal hypertension, hepatocellular carcinoma (a type of liver cancer), or liver failure.

The causes of advanced liver fibrosis are typically the same as those for early fibrosis, but the only difference is that they have persisted over a long period, leading to more severe liver damage. The causes and risk factors that differ to some extent from those of early liver fibrosis have been enumerated below (for others, please check early liver fibrosis).

  • Chronic hepatitis C: Hepatitis C is associated with a higher risk of progressing to advanced fibrosis as compared to hepatitis B.
  • Viral infections (other than hepatitis): HIV and other viral infections can exacerbate liver damage, particularly in individuals with hepatitis C.
  • Chronic inflammation: Persistent liver inflammation due to autoimmune diseases, cholestasis (condition when the flow of bile from the liver is reduced or blocked), or chronic infections contribute to advanced fibrosis.

The symptoms of advanced liver fibrosis overlap to a large extent with those of early liver fibrosis and, therefore, can be checked by referencing the “early liver fibrosis” section. Other symptoms have been detailed below.

  • Spider angiomas: In advanced stages of liver fibrosis, small, spider-like blood vessels appear on the skin (often on the chest, face, or hands).
  • Palmar erythema: Redness in the palms of the hands—caused by blood flow changes in the liver—is also observed in some cases.
  • Bruising and bleeding: Liver dysfunction can impair the production of clotting factors, leading to easy bruising and bleeding, such as nosebleeds or gum bleeding.
  • Swelling in the legs or abdomen (oedema and ascites): Fluid retention can occur with declining liver function.
  • Confusion or mental changes (hepatic encephalopathy): In severe cases, toxins that the liver can no longer filter out can affect the brain, leading to confusion, forgetfulness, or changes in behaviour.

Most of the diagnostic techniques for advanced liver fibrosis overlap with those of early liver fibrosis, and the ones that differ (even slightly) have been enumerated below.

  • Blood tests:
    • Liver function tests: In advanced fibrosis, ALT, AST, ALP, and bilirubin levels may be persistently elevated, and albumin levels can be low.
    • Prothrombin time (PT) test: PT is an indicator of the liver's ability to produce clotting factors. Though PT may be normal in early fibrosis, it is prolonged in advanced liver fibrosis.
    • Analysis of fibrosis markers: The AST-to-platelet ratio index (APRI) is considered to be the best index for predicting significant liver fibrosis, and the combination of APRI and Fibrosis-4 (FIB-4) is the best for predicting patients with advanced fibrosis or cirrhosis. 

Most of the treatment strategies for advanced liver fibrosis overlap with those of early liver fibrosis, and the ones that differ (even slightly) have been enumerated below.

  • Treating complications:
    • Salt restriction, diuretics, and paracentesis (removal of fluid): These may be used to manage fluid retention or ascites.
    • Lactulose: This can be used to reduce ammonia accumulation in the blood, thereby countering hepatic encephalopathy.
    • Beta-blockers: These medications can be used to manage portal hypertension.
    • Transjugular intrahepatic portosystemic shunt (TIPS): This procedure is used to reduce pressure in the liver’s blood vessels (portal hypertension).
    • Liver cancer surveillance: Individuals with advanced liver fibrosis—especially cirrhosis—are at an increased risk of developing hepatocellular carcinoma (type of liver cancer). Regular screening via imaging and blood tests (e.g., AFP) is recommended.

Vaccination: Individuals at risk should get vaccinated for hepatitis B and hepatitis A.

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A

Early Liver Fibrosis

Management Team

Early Liver Fibrosis

Overview

Liver fibrosis refers to the excessive accumulation of a fibrous mesh (scar tissue) in the liver as a response to chronic injury or inflammation. Early liver fibrosis refers to the initial stage of this condition and may not produce noticeable symptoms. However, if untreated, it can progress to advanced fibrosis, which can further progress to severe forms, such as cirrhosis, which can result in liver failure.

The primary cause of liver fibrosis is ongoing liver injury. Some common causes include:

  • Chronic alcohol consumption: Heavy, long-term alcohol abuse is one of the major causes of liver fibrosis. Alcohol consumption leads to liver damage and inflammation, which triggers the formation of scar tissue.
  • Chronic viral hepatitis: Persistent inflammation from Hepatitis B and Hepatitis C promotes fibrosis.
  • Fatty liver disease: Both alcoholic and non-alcoholic fatty liver disease (AFLD and NAFLD) can progress to steatohepatitis (alcoholic and non-alcoholic; ASH and NASH), which leads to fibrosis.
  • Steatohepatitis: Both alcoholic and non-alcoholic steatohepatitis (ASH and NASH) induce liver inflammation, which promotes fibrosis.
  • Chronic liver disease (other causes): Conditions such as autoimmune hepatitis (the body's immune system mistakenly attacks its own liver cells), Wilson’s disease (copper buildup in the liver), and hemochromatosis (iron accumulation) can lead to liver fibrosis.
  • Medications and toxins: Certain medications—methotrexate, isoniazid, amiodarone—and long-term exposure to toxic substances can damage the liver and promote fibrosis.
  • Obesity and insulin resistance: Being overweight or obese, especially with insulin resistance (a precursor to diabetes), increases the risk of developing liver fibrosis.
  • Genetic conditions: Genetic disorders such as alpha-1 antitrypsin deficiency or cystic fibrosis can also cause chronic liver injury, resulting in fibrosis.
  • Cholestatic liver diseases: Conditions that obstruct bile flow, like primary biliary cholangitis or primary sclerosing cholangitis, can lead to fibrosis.

Several factors increase the likelihood of developing early liver fibrosis; these include:

  • Chronic alcohol use: Excessive drinking over many years increases the risk of fibrosis, especially in genetically predisposed individuals.
  • Obesity and overweight: Being overweight or obese is a major risk factor, especially in the context of metabolic disorders like type 2 diabetes or insulin resistance.
  • Viral hepatitis: Chronic hepatitis B or hepatitis C infections are a major risk factor for developing fibrosis and cirrhosis.
  • Metabolic syndrome: A combination of high blood pressure, high cholesterol levels, elevated blood sugar levels, and abdominal obesity increases the likelihood of developing fibrosis.
  • Diabetes: Diabetes, especially when poorly controlled, increases the risk of liver fibrosis due to associated fatty liver.
  • Age: As people age, the liver’s ability to regenerate decreases, which can lead to a higher risk of fibrosis in individuals with ongoing liver injury.
  • Gender: Men are generally at a higher risk of developing liver fibrosis due to alcohol use, but women are more susceptible to fibrosis associated with NAFLD/NASH.
  • Genetics: Individuals with specific genetic mutations, such as those associated with hemochromatosis (iron overload), Wilson’s disease, or alpha-1 antitrypsin deficiency, are at higher risk of liver fibrosis.

n the early stages of liver fibrosis, symptoms are often absent (asymptomatic) or very mild, which is why early fibrosis may not be detected until the liver has sustained significant damage. However, as the condition progresses, individuals may experience:

  • Fatigue: Persistent tiredness or low energy levels are associated with declining liver function.
  • Discomfort or pain in the upper right abdomen: As the liver is located in the upper right abdomen, enlargement or swelling can cause discomfort.
  • Itchy skin: This is caused as a result of bile salt accumulation.
  • Loss of appetite and weight loss: These may occur as a result of impaired liver function.
  • Nausea (urge to vomit) and vomiting: These are common symptoms associated with declining liver function.
  • Jaundice and dark urine: These conditions may develop as a result of worsening liver function, i.e., inability to process bilirubin.

The diagnosis of early liver fibrosis often involves a combination of medical history, physical exams, and diagnostic tests.

  • Medical history and physical examination: Information is collected about alcohol use, risk factors for liver disease (e.g., viral hepatitis, obesity, diabetes), and any symptoms. Physical examination may reveal signs of liver enlargement or tenderness.
  • Blood tests:
    • Liver function tests: Elevated AST, ALT, ALP, and bilirubin levels can indicate liver injury.
  • Imaging tests:
    • Elastography (FibroScan): This specialised ultrasound technique measures liver stiffness, which correlates with the degree of fibrosis.
    • Magnetic resonance elastography (MRE): This is an advanced form of elastography that assesses liver stiffness more accurately.
  • Liver biopsy: In some cases, a liver biopsy may be necessary to definitively diagnose and grade the extent of liver fibrosis.

The treatment of early liver fibrosis focuses on addressing the underlying causes of liver fibrosis and preventing further liver damage. The earlier the diagnosis of fibrosis, the more likely it is to be reversible.

  • Stop alcohol consumption: Abstinence from alcohol is critical for preventing further liver damage. Support programs, therapy, or medications may help individuals quit alcohol use.
  • Manage underlying conditions:
    • Viral hepatitis: Antiviral treatment for hepatitis B and hepatitis C (e.g., direct-acting antivirals (DAAs)) can help reduce inflammation and fibrosis progression and prevent further liver damage.
    • Steatohepatitis (N/ASH): Managing obesity, type 2 diabetes, and insulin resistance through weight loss, exercise, and medications can help reduce liver fat and inflammation, i.e., steatohepatitis, which induces fibrosis.
  • Medications: There are currently no approved drugs specifically for treating fibrosis, but anti-inflammatory drugs (such as steroids) may be used in specific cases of liver inflammation (like autoimmune hepatitis). Further, vitamin E has shown benefits in individuals with N/ASH, particularly in those who do not have diabetes.
  • Weight loss: For individuals with obesity, N/AFLD, or N/ASH, gradual weight loss (5‒10% of the body weight) can significantly reduce liver fat and inflammation, thereby improving liver health and potentially reversing early fibrosis.
  • Stringent control of diabetes and cholesterol: Tight control of blood glucose—in diabetes—and cholesterol levels can reduce the risk of fibrosis progression.
  • Monitoring liver function: Regular monitoring of liver function through blood tests and imaging is essential to assess the progression of liver fibrosis and adjust treatment as needed.

The best strategy for preventing liver fibrosis involves avoiding heavy alcohol consumption; individuals at risk of developing liver fibrosis should stick to the recommended drinking limits or avoid alcohol entirely. Other strategies include: 

  • Maintaining a healthy weight: Regular exercise and a balanced diet can help prevent obesity and reduce liver fat, which can prevent fibrosis.
  • Managing metabolic risk factors: Controlling blood glucose levels, high blood pressure, and cholesterol levels can help prevent liver fibrosis.
  • Vaccination: Individuals who are at risk of developing liver fibrosis should get themselves vaccinated against hepatitis B and C.
  • Undergoing regular check-ups: Individuals with risk factors like viral hepatitis, obesity, or heavy alcohol use should undergo regular health check-ups to monitor their liver health.
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E

Alcoholic Steatohepatitis (ASH)

Management Team

Alcoholic Steatohepatitis (ASH)

Overview

Alcoholic steatohepatitis (ASH) is an advanced form of AFLD characterised by inflammation of the liver and fat accumulation in response to excessive alcohol consumption. It represents a progression from AFLD to more severe liver damage. If left untreated, it can lead to liver fibrosis, cirrhosis, and even liver failure.

The primary cause of ASH is excessive alcohol consumption. I have enumerated the causes and risk factors of ASH below.

  • Oxidative stress: Alcohol metabolism increases the production of reactive oxygen species (ROS), which contribute to oxidative stress and damage liver cells, leading to inflammation (hepatitis).
  • Toxic effects of alcohol: Acetaldehyde—a byproduct of alcohol metabolism—is toxic to liver cells and induces oxidative stress, leading to inflammation (hepatitis) and liver cell injury.
  • Fatty liver: AFLD coupled with inflammation can result in ASH.
  • Inflammation and immune response: Chronic alcohol consumption (prolonged and excessive consumption of alcohol) triggers an immune response, resulting in liver inflammation (hepatitis).

Several factors increase the risk of developing ASH, including:

  • Heavy and chronic alcohol consumption: Long-term alcohol abuse is the primary risk factor for ASH.
  • Malnutrition: Chronic alcohol use often leads to poor nutrition, which can enhance liver damage and increase the risk of developing ASH.
  • Genetics: Genetic predisposition plays a role in determining how individuals metabolise alcohol and how their liver responds to alcohol-induced damage. Specific genetic variations can make some individuals more prone to developing ASH.
  • Gender: Women are at higher risk of developing ASH than men due to differences in alcohol metabolism and liver function.
  • Age: With age, the liver becomes less efficient at metabolising alcohol, increasing the likelihood of liver damage.
  • Obesity and overweight: Individuals who are overweight or obese and are chronic alcohol consumers are at high risk of developing ASH.
  • Diabetes and insulin resistance: Type 2 diabetes and insulin resistance increase the risk of developing ASH, as high blood sugar levels and insulin resistance promote fat accumulation in the liver.
  • Other liver diseases: Individuals with a history of viral hepatitis (e.g., hepatitis C) or other pre-existing liver conditions are more likely to develop ASH if they consume alcohol.

In the early stages, ASH may not cause any noticeable symptoms. However, as the disease progresses, symptoms can become more apparent and include:

  • Fatigue: Affected individuals feel unusually tired or weak.
  • Abdominal pain or discomfort: Affected individuals feel discomfort, especially in the upper right part of the abdomen (where the liver is located).
  • Nausea (urge to vomit) and vomiting: These symptoms often accompany liver dysfunction.
  • Loss of appetite: Affected individuals feel a decreased desire to eat, leading to weight loss.
  • Enlarged liver (hepatomegaly): The liver becomes enlarged due to inflammation.

The first step in ASH diagnosis involves reviewing the complete medical history of the patient (alcohol consumption patterns, duration of drinking, and any history of liver disease or other related conditions). Other diagnostic strategies include:

  • Physical examination: A physical exam may reveal signs of liver enlargement, jaundice, or abdominal tenderness.
  • Blood tests:
    • Liver function tests: In ASH, the AST to ALT ratio tends to be higher (AST > ALT).
    • Complete blood count (CBC): This test can help detect abnormalities, such as low platelet counts, which are often seen in cirrhosis or advanced liver disease.
    • Bilirubin levels: Elevated bilirubin levels can indicate impaired liver function.
    • Albumin and prothrombin time: These tests assess the liver’s ability to produce clotting factors, a phenomenon that may be impaired in liver disease.
  • Imaging tests:
    • Ultrasound: This non-invasive technique can be used to check for liver enlargement and fat accumulation.
    • CT or MRI: These imaging modalities can provide more detailed images of the liver and may help identify fibrosis or cirrhosis.
    • Elastography: This specialised ultrasound technique is used to measure liver stiffness, which is an indicator of liver fibrosis or cirrhosis.
  • Liver biopsy: A liver biopsy may be performed to confirm the diagnosis of ASH, assess the degree of inflammation, and evaluate liver damage. It is often used when other tests do not provide definitive answers or if the disease progression needs to be assessed.

Stopping alcohol consumption is the most important step in treating ASH as continuing to drink alcohol can worsen liver inflammation and damage, leading to cirrhosis and liver failure. The treatment and management modalities of ASH include:

  • Support for alcohol cessation: Modalities, such as counselling, rehabilitation programs, or medications (e.g., disulfiram, naltrexone, or acamprosate) may be needed to help patients stop drinking.
  • Nutritional support: Individuals with ASH often suffer from malnutrition; therefore, proper dietary management is essential. A balanced diet rich in vitamins, minerals, and protein can help support liver regeneration. In some cases, nutritional supplements or enteral feeding may be necessary.
  • Medications: While there are no specific drugs approved for treating ASH, certain medications may be used to reduce liver inflammation and manage associated conditions:
    • Corticosteroids: In severe cases of ASH, corticosteroids (e.g., prednisolone) may be used to reduce inflammation, though their use is controversial and depends on the severity of the disease.
    • Antioxidants: Some studies suggest that vitamin E may help reduce liver inflammation, especially in non-diabetic patients.
  • Managing complications: Treating associated conditions, like diabetes, high cholesterol levels, or high blood pressure can help reduce the strain on the liver.
  • Regular monitoring: Individuals diagnosed with ASH require continuous monitoring to assess liver function, detect complications early, and adjust treatment as needed.

The best way to prevent ASH is to avoid heavy alcohol use. Other strategies include:

  • Maintaining a healthy weight: Obesity can enhance liver damage, so maintaining a healthy weight can help protect liver health.
  • Eating a balanced diet: A healthy diet supports liver function and reduces the risk of liver disease.
  • Avoiding excessive use of medications: Some drugs can accelerate liver damage, so it is important to avoid unnecessary medications or use them under the guidance of a healthcare provider.
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