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Ald & Masld

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ALCOHOLIC LIVER DISEASE

Alcohol is one of the most common causes of chronic liver disease


worldwide,
In the UK, a unit of alcohol contains 8 g of ethanol . A threshold of 14
units/week in women and 21 units/week in men is generally
considered safe.
The risk threshold for developing ALD is variable but begins at 30 g/day
of ethanol.
Risk factors for ALD are:
• Drinking pattern. Liver damage is more likely to occur in continuous rather
than intermittent, as this pattern gives the liver a chance to recover. so It is
recommended that people should have at least two alcohol-free days each
week.
• Alcohol type (unit = 8 g).
• Beer , Wine , Vodka/rum/gin , Whisky/brandy
• Gender. The incidence of alcoholic liver disease is increasing in women.
• Genetics..
• Nutrition. Obesity and nutritional deficiencies increases the incidence of
liver-related mortality
Clinical features
Alcohol is metabolized almost exclusively by the Liver,
ALD has a wide clinical spectrum ranging from mild
abnormalities of LFTs on biochemical testing to advanced cirrhosis. The liver
is often enlarged in ALD,
stigmata of chronic liver disease, such as palmar erythema, are more common
in alcoholic cirrhosis than in cirrhosis of other etiologies.
Alcohol misuse may also cause damage of other organs. Three types of ALD
are recognized but these overlap considerably, as do the pathological changes
seen in the liver.
1- Alcoholic fatty liver disease
Alcoholic fatty liver disease (AFLD) usually presents with elevated transaminases in the absence of
Hepatomegaly. It has a good prognosis and steatosis usually disappears after 3 months of abstinence
2- Alcoholic hepatitis
This presents with jaundice and hepatomegaly; complications of
portal hypertension may also be present. It has a significantly worse
Prognosis than AFLD . Cirrhosis often coexists; if not present, it is the
Likely outcome if drinking continues.

3- Alcoholic cirrhosis
Alcoholic cirrhosis often presents with a serious complication, such as
variceal hemorrhage or ascites,
Investigations
Investigations aim to establish
1-alcohol misuse,
2- to exclude alternative or additional coexistent causes of liver disease and
3-assess the severity of liver damage.
The clinical history from patient, relatives and friends is important to establish
alcohol misuse duration and severity.
Biological markers, particularly macrocytosis in the absence of anaemia, may
suggest and support a history of alcohol misuse.
A raised GGT may be elevated , PT and bilirubin are used to assess prognosis
Management
Cessation of alcohol consumption is the single most important
treatment and prognostic factor. Life-long abstinence is the best advice.
Abstinence is even effective at preventing progression, hepatic
decompensation and death once cirrhosis is present.
In the acute presentation of ALD it is important to identify and anticipate
alcohol withdrawal and Wernicke’s encephalopathy, which need treating
in parallel with the liver disease and any complications of cirrhosis.
Nutrition
Good nutrition is very important, and enteral feeding via a fine-bore
nasogastric tube may be needed in severely ill patients.
Corticosteroids
These are of value in patients with severe alcoholic Hepatitis . Sepsis is the
main side-effect of steroids, Discriminant Function Score (DF Score)
Pentoxifylline

Liver transplantation
Metabolic Dysfunction – Associated Steatotic Liver
Disease (MASLD)

Formerly Non-alcoholic fatty liver disease (NAFLD) represents


1- fatty infiltration (steatosis),
2- fat and inflammation (Metabolic Dysfunction- Associated Steatohepatitis,
MASH/ Formerly NASH) and
3- Cirrhosis, in the absence of excessive alcohol consumption ,
NASH is linked with progressive liver fibrosis, cirrhosis and liver cancer, as well
as increased cardiovascular risk.
MASLD is strongly associated with obesity, dyslipidaemia, insulin resistance and
type 2 diabetes mellitus, and so may be considered to be the hepatic
manifestation of the ‘metabolic syndrome’
Increasingly sedentary lifestyles and changing dietary patterns mean that the
prevalence of obesity and insulin resistance has increased, making MASLD the
leading cause of liver dysfunction in the non-alcoholic, viral hepatitis-negative
population in Europe and North America.
Whilst the majority of patients with the metabolic syndrome develop steatosis,
only a minority exhibit NASH or fibrosis.
Clinical features
MASLD is frequently asymptomatic, although it may be associated with fatigue
and mild right upper quadrant discomfort.
It is commonly identified as an incidental biochemical abnormality during
routine blood tests.
Alternatively, patients with progressive NASH may present late in the natural
history of the disease with complications of cirrhosis and portal hypertension,
such as variceal haemorrhage, or HCC.
The average age of MASH is 40–50 years (50–60 years for NASH–
cirrhosis);
Most patients with MASLD have insulin resistance and exhibit features
of the metabolic syndrome .
MASLD is also associated with polycystic ovary syndrome, obstructive
sleep apnoea and small-bowel bacterial overgrowth.
Investigations
Investigation of patients with suspected MASLD should
be directed first towards exclusion of excess alcohol
consumption and other liver diseases (including viral,
autoimmune and other metabolic causes), and then
at confirming the presence of MASLD, discriminating
simple steatosis from NASH and determining the extent of any hepatic fibrosis
that is present.
So mainly we need LFTs and imaging studies
Management
Non-pharmacological treatment
Current treatment comprises lifestyle interventions to promote weight loss and
improve insulin sensitivity through dietary changes and physical exercise.
Sustained weight reduction of 7–10% is associated with significant
improvement in histological and biochemical NASH severity.
Pharmacological treatment
Treatment directed at coexisting metabolic disorders, such as dyslipidaemia
and hypertension, should be given. Although use of HMG-CoA reductase
inhibitors (statins) does not ameliorate MASFLD, there does not appear to be
any increased risk of hepatotoxicity or other side-effects from these agents,
and so they may be used to treat dyslipidaemia. Specific insulin-sensitising
agents, in particular glitazones, may help selected patients, and high-dose
vitamin E.
Artichoke leaf extract (ALE) has shown potential as a hepatoprotective agent.
Obesity treatment pyramid

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