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Liver function levels chart: Normal, High, and Low Ranges, Chart & Results

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Blood Test: Hepatic (Liver) Function Panel (for Parents)

What Is a Blood Test?

A blood test is when a sample of blood is taken from the body to be tested in a lab. Doctors order blood tests to check things such as the levels of glucose, hemoglobin, or white blood cells. This can help them detect problems like a disease or medical condition. Sometimes, blood tests can help them see how well an organ (such as the liver or kidneys) is working.

What Is a Hepatic (Liver) Function Panel?

A liver function panel is a blood test that helps doctors check for liver injury, infection, or disease. Liver function panels also can check for side effects in the liver from some medicines.

Why Are Liver Function Panels Done?

A liver function panel is done to learn information about the levels of:

  • Albumin and total protein, which help build and maintain muscles, bones, blood, and organ tissue. Low levels may be seen with liver or kidney disease, or nutritional problems.
  • Liver enzymes: Alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). These enzymes help the liver convert food into energy. When their levels are high, it can be a sign of that the liver is injured or irritated.
  • Bilirubin. Bilirubin is made when red blood cells break down. The liver changes the bilirubin so that it can be excreted from the body. High bilirubin levels may mean there is a problem with the liver. This can make skin look yellow, a condition called jaundice.

How Should We Prepare for a Liver Function Panel?

Your child may be asked to stop eating and drinking for 8 to 12 hours before the test. Tell your doctor about any medicines your child takes because some drugs might affect the test results.

Wearing a T-shirt or short-sleeved shirt for the test can make things easier for your child, and you also can bring along a toy or book as a distraction.

How Is a Liver Function Panel Done?

Most blood tests take a small amount of blood from a vein. To do that, a health professional will:

  • clean the skin
  • put an elastic band (tourniquet) above the area to get the veins to swell with blood
  • insert a needle into a vein (usually in the arm inside of the elbow or on the back of the hand) 
  • pull the blood sample into a vial or syringe
  • take off the elastic band and remove the needle from the vein

In babies, blood draws are sometimes done as a “heel stick collection.” After cleaning the area, the health professional will prick your baby’s heel with a tiny needle (or lancet) to collect a small sample of blood.

Collecting a sample of blood is only temporarily uncomfortable and can feel like a quick pinprick.

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Can I Stay With My Child During a Liver Function Panel?

Parents usually can stay with their child during a blood test. Encourage your child to relax and stay still because tensing muscles can make it harder to draw blood. Your child might want to look away when the needle is inserted and the blood is collected. Encourage your child to relax by taking slow deep breaths or singing a favorite song.

How Long Does a Liver Function Panel Take?

Most blood tests take just a few minutes. Occasionally, it can be hard to find a vein so the health professional may need to try more than once.

What Happens After a Liver Function Panel?

The health professional will remove the elastic band and the needle and cover the area with cotton or a bandage to stop the bleeding. Afterward, there may be some mild bruising, which should go away in a few days.

When Are Liver Function Panel Results Ready?

Blood samples are processed by a machine, and it may take a few hours to a day for the results to be available. If the test results show signs of a problem, the doctor might order other tests to figure out what the problem is and how to treat it.

Are There Any Risks From Liver Function Panels?

A liver function panel is a safe procedure with minimal risks. Some kids might feel faint or lightheaded from the test. A few kids and teens have a strong fear of needles. If your child is anxious, talk with the doctor before the test about ways to make the procedure easier.

A small bruise or mild soreness around the blood test site is common and can last for a few days. Get medical care for your child if the discomfort gets worse or lasts longer.

If you have questions about the test, speak with your doctor or the health professional doing the blood draw.

A review of liver function tests during treatment with atypical antipsychotic drugs: A chart review study

https://doi.org/10.1016/j.pnpbp.2007.05.005Get rights and content

Abstract

Objective

Atypical antipsychotic drugs commonly cause asymptomatic increase in the liver enzymes and serum bilirubin levels. However they rarely may induce a serious hepatic toxicity. In this article we aimed to evaluate the effect of atypical antipsychotic drugs namely olanzapine, risperidone and quetiapine on the hepatic enzymes and serum bilirubin levels in psychiatric patients.

Method

Chart reviews of 312 patient followed-up at Psychiatry Department of Zonguldak Karaelmas University Hospital were examined in detail. The patients whose baseline and follow-up liver function tests including alanine aminotransfeaminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), alkaline phosphotase (ALP) and serum bilirubin that were measured before and within the treatment period of first and sixth months were enrolled. Forty eight males and 62 females whose ages ranging from 12 to 65 years were eligible for this study (no pregnant case was present).

Results

The repartition according to treatment is as follows: olanzapine (n = 33), risperidone (n = 29), and quetiapine (n = 48). Two of the 110 patients (1. 8%) presented with increased AST levels of up to 4 fold and ALT of thrice the basal level and needed to stop treatment (AST increase in one female with olanzapine 20 mg/day; ALT increase in one male with olanzapine 30 mg/day). Thirty of the 110 patients (27.2%) showed asymptomatic increases in ALT, AST, GGT and serum bilirubin levels in the first month of the study. After 6 months of the treatment, abnormalities in the liver function tests were observed in 25 patients (22.7%).

Conclusion

These results were in accordance with previous studies that asymptomatic increase of liver enzymes are common but significant liver enzyme elevations are rare during atypical antipsychotic treatment. We suggest that obtaining baseline liver enzyme tests before atypical antipsychotic therapy and monitoring regularly specifically in patients with risk factors for liver damage during therapy.

Keywords

Atypical antipsychotic

Hepatotoxicity

Liver enzymes

Olanzapine

Quetiapine

Risperidone

Abbreviations:

ALT,

alanine aminotransferase;

AST,

aspartate aminotransferase;

ALP,

alkaline phosphatase;

GGT,

gamma glutamyl transpeptidase;

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Copyright © 2007 Elsevier Inc. All rights reserved.

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Understanding Your Hepatitis B Test Results

Understanding your hepatitis B blood tests can be confusing. It is important to talk to your health care provider so you understand your test results and your hepatitis B status. Are you infected? Protected? Or at risk? The Hepatitis B Panel of blood tests includes 3 tests and all three results must be known in order to confirm your status.

Below is a chart with the most common explanation of the test results, but unusual test results can occur. Please note that this chart is not intended as medical advice, so be sure to talk to your health care provider for a full explanation and obtain a printed copy of your test results. In some cases, a person could be referred to a liver specialist for further evaluation.

More Detailed Information About Hepatitis B Blood Tests

An acute hepatitis B infection follows a relatively long incubation period – from 60 to 150 days with an average of 90 days. It can take up to six months, however, for a person to get rid of the hepatitis B virus. And it can take up to six months for a hepatitis B blood test to show whether as person has recovered from an acute infection or has become chronically infected .

The following graphic from the U.S. Centers for Disease Control and Prevention (CDC) represents the typical course of an acute hepatitis B infection from first exposure to recovery.

Source: Centers for Disease Control and Prevention Video

According to the CDC, a hepatitis B blood test result (or serologic marker) varies depending on whether the infection is a new acute infection or a chronic infection.

  • HBsAg (hepatitis B surface antigen) is the first serologic marker to appear in a new acute infection, which can be detected as early as 1 week and as late as 9 weeks, with an average of one month after exposure to the hepatitis B virus (HBV). 

– HBsAg is detectable for a variable amount of time, along with the HBV DNA, though about 50% of persons will test HBsAg and HBV DNA negative 7 weeks after symptoms.

– All persons who spontaneously recover from an infection will test negative for HBsAg and negative for HBV DNA about 15 weeks after the appearance of symptoms.

  • Anti-HBs or HBsAb (hepatitis B surface antibody) – this becomes detectable on a blood test after the disappearance of HBsAg in persons who are able to get rid of the virus and avoid a chronic infection. The presence of anti-HBs following a new acute infection generally indicates recovery and a person is then protected (or “immune”) from re-infection with hepatitis B.
  • Anti-HBc or HBcAb (hepatitis B core antibody) this blood test remains positive indefinitely as a marker of past HBV infection.
  • HBeAg (hepatitis B e-antigen) is generally detectable in patients with a new acute infection; the presence of HBeAg is associated with higher HBV DNA levels, thus, increased infectiousness.
  • IgM anti-HBc – a positive blood test result indicates a person has a new acute hepatitis B infection. IgM anti-HBc is generally detectable at the time symptoms appear and declines to sub-detectable levels within 6 – 9 months. Note: An acute exacerbation (or liver flare) in a chronic HBV infection can also result in a positive anti-HBc IgM test result. So follow-up testing after 6 months is required.
  • IgG anti-HBcthis blood test remains positive indefinitely as a marker of past HBV infection.

Abnormal Liver Chemistry – Evaluation and Interpretation

Effective Date: August 1, 2011

Recommendations and Topics

Scope

This guideline provides recommendations for the evaluation and interpretation of abnormal liver test results in adults (≥19 years). Use in conjunction with other guidelines (e.g., Viral Hepatitis Testing).

Diagnosis/Investigation

Abnormal liver tests may indicate an abnormality of the liver and provide clues as to the nature of the problem. However, in an asymptomatic patient, mild abnormalities may not be clinically significant. A systematic approach to evaluating the patient and ordering further tests will help to identify underlying disease. Further testing and referrals may not be necessary in many circumstances.

The term ‘liver function test’ should not be used when referring to serum enzyme levels because they correlate poorly with metabolic activities of the liver.

There are two broad categories of liver enzyme abnormalities: hepatocellular and cholestatic.

Usually the most marked abnormality points to the underlying category of disorder.

  1. Hepatocellular injury (e.g., hepatitis)
    The membranes of liver cells can become permeable when damaged, allowing for escape of intracellular enzymes into the bloodstream. The major intracellular enzymes are alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
     
  2. Cholestasis (e.g., biliary obstruction or hepatic infiltration)
    Obstructed/damaged intra- or extra-hepatic bile ducts cause the induction of synthesis of alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT). In acute biliary obstruction, elevation of these enzyme levels often lags obstruction by approximately 24 hours. An isolated minor elevation of GGT is a relatively common finding and does not necessarily indicate significant liver disease.\

Note: Serum bilirubin is not a useful test for distinguishing between cholestasis and hepatocellular injury because it may be elevated in both situations.

History and Physical Exam

Obtain a history to determine risk factors for liver disease (see Table 1).
Perform a physical examination to look for evidence of liver disease (see Table 2).

Table 1. Risk Factors for Liver Disease

High Risk Behaviour

  • IV drug use (past & present)
  • Multiple sexual partners
  • High-risk sexual activity
  • Tattoos
  • Nonsterile body piercing
  • Alcohol abuse
     

Commonly Implicated Medications

  • Acetaminophen, NSAIDs
  • Antibiotics (e. g., clavulinic acid-amoxicillin, nitrofurantoin, sulfonamides)
  • HMG-CoA reductase inhibitors (statins)
  • Anticonvulsant drugs (e.g., phenytoin, carbamazepine, valproic acid)
  • Isotretinoin (Accutane®)
  • Immunomodulators (e.g., methotrexate, azathioprine)
  • Antituberculous drugs (e.g., isoniazid)
  • Some herbal medications

Systemic Illness

  • Diabetes
  • Obesity
  • Hyperlipidemia
  • Iron overload
  • Autoimmune diseases
  • Metastatic cancer
  • Inflammatory bowel disease

Other

  • Travel to or residence in less developed regions or countries
  • Needlestick injury or other occupational exposure (e.g., razors)
  • Receipt of unscreened blood products, especially prior to 1990*
  • Hemodialysis
  • Contaminated food or water (hepatitis A)

*screening of donated blood products for hepatitis C (anti-HCV) began in 1990 in Canada.

Table 2. Common Clues to Diagnose Liver Disease
Symptoms/Signs Level or Stage of Liver Disease
Jaundice Acute hepatitis, biliary obstruction, or advanced chronic liver disease
Abdominal pain, fever Acute cholangitis, cholecystitis or liver abscess
Chronic stigmata: spider angiomata, palmar erythema, gynecomastia, testicular atrophy, asterixi Cirrhosis
Complications: encephalopathy, ascites, acute gastrointestinal bleeding, coagulopathy, muscle wasting Advanced liver disease (decompensated)
Chronic generalized pruritus Cholestasis (eg., primary biliary cirrhosis)

Initial Investigations

If liver disease is suspected, but the cause is not apparent from the initial history and physical examination, direct further investigations towards determining whether the condition is predominantly hepatocellular or cholestatic. Order ALT and ALP at this time.

In patients with clinically overt hepatobiliary disease, it may be expeditious to include an AST and GGT with the initial blood work. Do not order GGT and lactate dehydrogenase (LDH) in isolation for initial investigation of possible liver disease. Isolated elevation of GGT is nonspecific but may indicate overuse of alcohol and become a useful tool for counselling a patient where alcohol abuse or dependence is a concern.

Cholestasis

If ALP elevation is the predominant abnormality, obtain GGT to confirm hepatobiliary origin. If cholestasis is confirmed, then perform abdominal ultrasound to assess the biliary tree. If ALP and GGT are elevated in the setting of a non-dilated biliary tree, then intra-hepatic cholestasis or hepatic infiltration is suggested. If the biliary tree is dilated, then determine the cause of obstruction.

If GGT is not elevated, then an elevated ALP may be of bone or placental origin.

Hepatocellular Injury

Predominant ALT elevation points to hepatocellular damage. A detailed patient history will help delineate risk factors and potential causes.

Presentation with an ALT exceeding 1000 U/L usually represents one of the following conditions: acute viral hepatitis, acute choledocholithiasis, acute vascular injury of the liver (ischemia or congestion) or ingestion of hepatotoxin (e.g., acetaminophen, poisonous mushrooms).

Test for viral causes in accordance with the Viral Hepatitis Testing guideline available at www.BCGuidelines.ca. Consider other causes of liver disease (see Table 3). If iron overload is being considered, refer to Iron Overload – Investigation and Management available at www.BCGuidelines.ca.

Table 3. Enzyme Elevations in Liver Disease
 

Abbreviation

Full name

When is it likely to be abnormal Specificity for liver disease Other causes
Hepato-cellular injury (Hepatitis – all types)

ALT

Alanine amino-transferase

Hepatitis (particularly viral, auto-
immune, drug induced, non-
alcoholic fatty liver disease (NAFLD), iron overload)
Sensitive and specific Acute obstructive jaundice (within first 24h)

AST

Aspartate
amino-transferase

Hepatitis (particularly alcoholic), hepatic fibrosis/
cirrhosis
Less sensitive and specific than ALT Cardiac or skeletal muscle injury or hemolysis
Cholestasis (Biliary obstruction, hepatic infiltration)

ALP

Alkaline phosphatase

Cholestasis More indicative of liver disease than GGT Bone disease, pregnancy

GGT

Gamma-
glutamyl transpep-tidase

Cholestasis, alcohol More sensitive than ALP May not indicate significant liver disease Medic-ations, hepatic congestion (CHF)

 

Monitoring of liver chemistry with medication use

A thorough medication history is paramount. History should include all prescribed drugs, over-the-counter drugs, as well as natural health products. Almost any medication can cause elevations of liver enzymes and possible liver injury. While the majority of these reactions are idiosyncratic in nature, some are dose-related. Acetaminophen toxicity is dose-related and is the most common cause of medication-induced liver damage and liver failure. For all medications, consult the product monograph for specific information.

  • Monitoring patients on a potentially hepatotoxic drug Certain drug may require specific monitoring. Please see product monographs.
  • Investigation of abnormal liver tests with medication use. Many hepatotoxic drugs have a “signature” toxicity. In general, any recently started medication or an increased dosage of medication should be considered the primary cause of newly elevated enzymes until proven otherwise. Consider withdrawing or replacing the drug if the liver chemistry abnormality is severe and it is clinically safe to do so. Repeat test in 1 to 3 months to document normalization.

Isolated test abnormality

An isolated minor abnormality (<1.5 times upper limit of normal) in an asymptomatic individual should prompt retesting in 1 to 3 months, particularly after addressing potential causes or modifiable risk factors.

GGT elevation is easily induced by alcohol and medications, so an isolated elevation of this enzyme does not always imply significant liver disease.

Isolated indirect (unconjugated) hyperbilirubinemia is commonly due to Gilbert’s syndrome, a benign condition that occurs in approximately 2-7% of the population, and which is often unrecognised without the provocation of stress or starvation. Less commonly, unconjugated hyperbilirubinemia may be due to hemolysis.

Persistent minor elevations of liver test (≥ 6 months)

Review history for possible exposure to infectious liver disease and other risk factors such as medications or alcohol. If no obvious cause is found, further investigation is indicated (see Table 2). Refer to Viral Hepatitis Testing and Iron Overload – Investigation and Management guidelines and/or consider referral.

Liver biopsy and other special tests

Disease specific tests including auto-antibodies, copper and iron studies, alpha-feto protein (AFP), and specific viral markers should only be obtained in appropriate circumstances and usually in consultation with a specialist.

A liver biopsy may provide important diagnostic and prognostic information regarding the cause of liver disease. Consultation with a specialist is advisable prior to obtaining a liver biopsy.

In the setting of biliary dilatation, consultation with a specialist is recommended to consider visualization of the biliary tract by computed tomography (CT), endoscopic retrograde cholangiopancreatography (ERCP), endoscopic ultrasound (EUS) or magnetic resonance cholangiopancreatography (MRCP).

Serum ammonia levels are seldom useful and should not be obtained.

Evaluation of hepatic function

Standard measurements of liver enzymes do not reflect overall liver function. Synthetic function of the liver may be estimated by measuring serum albumin and international normalized ratio (INR).

Bilirubin may be elevated in hepatitis or cholestasis. In chronic liver disease a rising bilirubin may indicate deteriorating liver function.

Acute presentation with right upper quadrant pain

In a patient presenting with acute right upper quadrant pain, testing is used to identify potential biliary tract disease. Perform AST, ALT, ALP and GGT testing expeditiously to differentiate between cholestasis and hepatitis. In acute biliary obstruction, levels of ALP and GGT may not be increased for approximately 24 hours.

Urgent referral for an abdominal ultrasound is recommended to identify biliary tract disease.

A patient presenting with fever and right upper quadrant pain may require urgent evaluation for possible biliary tract intervention.

Rationale

Liver disease is a common problem in primary care. Its presence and etiology may be appreciated only after blood tests are performed. Order liver enzyme tests in a directed fashion based on a suspicion of liver disease. Non-directed or routine ordering of screening panels is discouraged. Most laboratories maintain serum samples for several days allowing for further testing if required.

The approach to patients with suspected liver disease includes reviewing the history (including risk factors), performing a physical examination, and ordering selected blood tests. An asymptomatic patient with minor abnormalities of liver chemistry may be monitored by the primary care physician, with follow up. Elevated liver enzyme levels are reported in 1-4% of asymptomatic persons, most of whom will not develop clinically significant liver disease.

The differentiation between hepatocellular injury and cholestasis is an important first step leading to a more efficient use of subsequent tests. The importance of alcohol, medications and obesity as causes of abnormal liver enzyme levels cannot be overstated. Normalization of the test abnormality after withdrawal of alcohol or a medication for 1 to 3 months implicates that substance as the cause of the abnormal test.

An isolated non-progressive elevation of GGT seldom reflects significant liver disease and usually does not require specialist referral. In addition, modest ALT and/or AST elevations in obese or diabetic patients may represent non-alcoholic fatty liver disease (NAFLD), which is now a common cause of chronic liver disease. Non-alcoholic steatohepatitis (NASH) is a potentially severe form of NAFLD and may lead to cirrhosis.

For investigations of viral hepatitis and iron overload refer to www.BCGuidelines.ca

References

  1. Green RM, Flamm S. AGA Technical review on the evaluation of liver chemistry tests. Gastroent. 2002;123:1367-1384.
  2. Minuk GY. Canadian Association of Gastroenterology Practice Guidelines: Evaluation of abnormal liver enzyme tests. Can J Gastroenterol. 1998;12:417-21.
  3. Pratt DS, Kaplan MM. Evaluation of abnormal liver-enzyme results in asyptomatic patients. New Engl J Med. 2000;342:1266-71.
  4. Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guide for clinicians. Can Med Assoc J. 2005;172:367-79.
  5. Storr JG. The Interpretation of abnormal liver tests. Nutrition. 2008;24:503.
  6. Canadian Blood Services. www.bloodservices.ca c1998-2011 cited 2011;May 30. Available from http://www.bloodservices.ca/CentreApps/Internet/UW_V502_MainEngine.nsf/page/E_Hepatitis?OpenDocument
  7. Goessling W, Friedman LS. Increased liver chemistry in an asymptomatic patient. Clin Gastroent and Hepatol. 2005;2:852-585.
  8. Lewis JH, Ahmed M, Shobassy A, et. al. Drug-induced liver disease. Current Opin Gastroen. 2006;22:223-233.
  9. Bjornsson E. Review article: drug-induced liver injury in clinical practice. Aliment Pharmacol Ther. 2010;32:3-13.
  10. Kaplowitz N. Drug-induced liver injury. Clin Infect Dis. 2004;38 Suppl 2:S44-8.
  11. Reuben A, Koch DG, Lee WM. Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatol. 2010;52:2065-76.
  12. Giboney PT. Mildly elevated liver transaminase levels in the asymptomatic patient. Am Fam Physician. 2005;71(6):1105-1110.
  13. Hirshfeild GM. & Alexander GJ. Gilberst syndrome: an overview for clinical biochemists. Ann Clin Biochem. 2006;43:340-343.
  14. Pascale A, Pais R, Ratziu V. An overview of nonalcoholic steatohepatitis: past, present and future directions. J Gastrointestin Liver Dis. December 2010;19 (4) 415-423.

This guideline is based on scientific evidence current as of the Effective Date.

This guideline was developed by the Guidelines and Protocols Advisory Committee, approved by the British Columbia Medical Association and adopted by the Medical Services Commission.

Guidelines and Protocols Advisory Committee Principles

The principles of the Guidelines and Protocols Advisory Committee are to:

  • encourage appropriate responses to common medical situations
  • recommend actions that are sufficient and efficient, neither excessive nor deficient
  • permit exceptions when justified by clinical circumstances.

Disclaimer

The Clinical Practice Guidelines (the “Guidelines”) have been developed by the Guidelines and Protocols Advisory Committee on behalf of the Medical Services Commission. The Guidelines are intended to give an understanding of a clinical problem and outline one or more preferred approaches to the investigation and management of the problem. The Guidelines are not intended as a substitute for the advice or professional judgment of a health care professional, nor are they intended to be the only approach to the management of clinical problems. We cannot respond to patients or patient advocates requesting advice on issues related to medical conditions. If you need medical advice, please contact a health care professional.

Alcoholic Liver Disease Sharply Rising Among Young Women, U.S. Doctors Say : Shots

For many years, Jessica Duenas led what she calls a double life. She was the first in her immigrant family to go to college. In 2019, she won Kentucky’s Teacher of the Year award. That same year, Duenas typically downed nearly a liter of liquor every night.

By the time she was 34, she was diagnosed with alcoholic hepatitis, a serious inflammation of her liver that doctors warned could could soon lead to irreversible scarring and even death if she didn’t didn’t stop drinking, and quickly.

“I couldn’t keep down any food,” Duenas says. “My belly was supersensitive, like if I pressed on certain parts of it, it would hurt a lot. My eyes were starting to get yellowish.”

Cases of alcoholic liver disease — which includes milder fatty liver and the permanent scarring of cirrhosis, as well as alcoholic hepatitis — are up 30% over the last year at the University of Michigan’s health system, says Dr. Jessica Mellinger, a liver specialist there.

The pathway to that sort of liver disease, especially severe versions, varies from person to person, liver specialists say, and can be exacerbated by obesity, certain genetic factors, and underlying health problems. Drinking a glass or two of wine — even every day — is unlikely to cause this sort of liver damage in many people, the experts say, though it’s possible.

But Mellinger says she and other doctors are seeing patients who have edged up to higher amounts of drinking in the last year — to a bottle of wine, or 5-6 drinks, a day — which increases the chances of liver disease severe enough to require hospitalization. And binge drinking, even if less frequent, can also be damaging.

The Centers for Disease Control and Prevention has not yet compiled data on any overall increase in hospitalizations from alcoholic liver disease since the pandemic began. But, Mellinger says, “in my conversations with my colleagues at other institutions, everybody is saying the same thing: ‘Yep, it’s astronomical. It’s just gone off the charts.’ “

The damage can be lethal. Survival rates for alcoholic hepatitis and cirrhosis vary but can be as low as 10% in the most severe cases, research suggests.

In the U.S., more than 44,000 people died of alcoholic liver disease in 2019. And although liver diseases still affect more men, younger women are driving the increase in deaths, a trend that began several years ago and is now supercharged by the pandemic, says Mellinger. “We’re seeing kids in their late 20s and early 30s with a disease that we previously thought was kind of exclusive to middle age,” she says.

Alcoholic liver disease often takes years to manifest. But it can become a threat for women more quickly because their bodies process alcohol somewhat differently than men’s.

Women have also borne the brunt of many new pressures of pandemic life, from virtual school and increased responsibilities at home, even as ads and pop culture have continued to validate the idea of drinking to cope: Mommy Juice, Rosé All Day, Wine Down Wednesdays. On top of that, eating disorders and underlying trauma from physical or sexual violence often add fuel to the fire, fanned by social isolation.

“Whether this is early life sexual trauma or they are in a recent or ongoing abusive relationship, we see this link very, very closely,” says psychiatrist Dr. Scott Winder, a clinical associate professor at the University of Michigan who treats patients with alcoholic liver disease. “Just the sheer amount of trauma is really, really tragic.”

Alcoholic liver disease is complex because it isn’t just one thing; it’s the physical manifestation with roots in emotional and psychological distress. Successful treatment needs to address both, Winder says, but usually doesn’t.

He calls that a “tragic gap” in care. A patient discharged from the hospital with alcoholic liver disease is often motivated to get psychological help but frequently can’t find outpatient care until weeks or months later, he says.
“The cultures of hepatology and the cultures of psychology and psychiatry are very disparate; we see patients very differently,” so physicians aren’t coordinating care, even when they should, he says.

For patients with advanced liver disease, that often leaves no options for curative treatment. Some need a liver transplant to survive, but they won’t qualify if they’re still drinking.

“Unfortunately, transplantation is finite,” says Dr. Haripriya Maddur, a hepatologist at Northwestern University. “There aren’t enough organs to go around. What it unfortunately means is that many of these young people may not survive, and die very young — in their 20s and 30s. It’s horrific.”

Facing death frightened Duenas, who is now 36. She says after her doctor told her she had alcoholic hepatitis, she thought: “My secret’s out.”

She made multiple attempts to curb her drinking but ended up consuming ever more and became despondent.

“I felt so terrible about who I was as a person because of my addiction that I just threw myself into everything else to make everything else look good,” she says.

Duenas checked herself into rehab on New Year’s Day in 2020 for four days. Her liver began to heal. And when the world went to pandemic lockdown last March, she attended recovery meetings on Zoom.

Then, on April 11, she discovered her boyfriend — who had also been in recovery — was relapsing on heroin. Two weeks later, she and the police found him dead in his apartment. Though he and Duenas had talked about marriage, he’d died from an overdose just after his 42nd birthday.

Duenas relapsed, hard.

Jessica Duenas on her 36th birthday in February of this year.

Jessica Duenas


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Jessica Duenas

Jessica Duenas on her 36th birthday in February of this year.

Jessica Duenas

“The next eight months are such a blur,” she says — eight hospitalizations, a major car wreck, and repeat stints in rehab. Duenas describes herself as normally politically active. But the last year passed by in a fog. She only vaguely recalls hearing about news in rehab: protests over Breonna Taylor’s shooting; Election Day.

Last November, she says, she completely surrendered to the changes she knew she had to make. She quit her beloved job to focus on recovery, and her last drink was on Thanksgiving Day, she says. Days later, she wrote about her long-held secret in the Louisville Courier-Journal: “I’m Jessica, I’m the 2019 Kentucky State Teacher of the Year, I’m an alcoholic and I’ve been suffering in silence for years.”

Hundreds of people wrote back — mostly women describing experiences like hers.

“What I’ve noticed is quite a few of the women, typically, they were either educators, they were moms or they happened to be nurses or attorneys,” Duenas says. They poured their hearts out about the crushing and constant stress of kids, work and home life.

They also vented about pressures from beyond the home. “Imagine being a teacher who gets evaluated on how your students do, given the situation today,” Duenas says. “I mean, that makes me want to drink for them, you know — like that’s a terrible pressure to be under.”

Duenas says she’s since heard many, many other stories like her own. She has started interviewing them and relaying their stories on her website about recovery, www.bottomlesstosober.com.

11 Ways to Lower Elevated GGT + Function, Diseases

Tests for gamma-glutamyl transferase (GGT) are important in the diagnosis of liver/biliary tract disease and useful in identifying alcohol abuse. Read on to learn more about the function of GGT, its health effects, and ways to lower GGT levels.

What is GGT?

Gamma-glutamyl transferase (GGT) is a cell surface enzyme. It is located throughout the human body with the highest levels being in the kidneys, intestines, liver, prostate gland, and gallbladder. Smaller amounts are found in the pancreas, lungs, testis, and thyroid gland. The liver produces most of the GGT in the blood [1, 2, 3].

GGT is elevated in liver/biliary tract disease or as a result of moderate to excessive alcohol consumption.

Higher GGT levels also increase the risk of several diseases and may point to health problems. This article will cover the functions of GGT, its role in diagnosing or predicting disease, and ways to lower GGT levels in the body.

Function

The primary function of GGT is the breakdown and recycling of glutathione, the most important antioxidant in the human body [4, 5].

It increases the number of available amino acids (especially cysteine), that are used to make glutathione inside the cell [6].

GGT is also involved in:

  • Breaking down drugs and toxins
  • Forming amino acids important for the brain and heart (gamma-glutamyl-taurine to taurine)
  • Transforming inflammatory molecules (leukotriene C4 to leukotriene D4) [4, 7]

Normal GGT Levels

Tests for GGT measure the level of the enzyme in the blood. Age, gender, exercise, weight, pregnancy, diet, and medications can all influence GGT levels in the body [8, 9, 10].

The reference ranges for GGT levels vary between sources and laboratories. Normal levels are dependent on age and sex. Generally, they are higher in adult males than in adult females. The reference ranges based on 1,160 alcohol abstainers are organized below (one retrospective meta-analysis and one clinical study) [11, 12]:

The risk for heart disease increases around the middle of what is considered a “normal” range for both males and females (prospective clinical studies). Therefore, optimal levels of GGT are below the reference range midpoint (based on age and gender).

High GGT Levels

Elevated levels of GGT point to high glutathione use in the body and oxidative stress. Maintaining normal/optimal levels of glutathione in the body has a wide range of health benefits [13, 14, 15].

GGT is useful in 3 ways:

  • Diagnose disease: Used to screen for liver/biliary tract disease, and to identify alcohol abuse [16, 17, 18, 19, 20, 21].
  • Assess disease risk: Elevated levels of GGT are linked to increased risk of disease and disease-related death [22, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34].
  • All-cause mortality: Clinical studies show a relationship between higher levels of GGT and increased the chance of death from any cause [35, 36, 37, 38, 24, 39].

GGT alone does not directly cause a particular disease or disorder. However, high levels of GGT may be a sign of systemic cellular damage.

GGT may increase oxidative stress, starting with the breakdown of glutathione (and production of cysteinylglycine). Other toxic molecules are then formed, leading to tissue, cellular, and DNA damage [13, 15].

GGT is present in plaques because it attaches itself to circulating fats (LDL). Once in the plaque, GGT can become pro-oxidant, injuring blood vessels (via oxidative stress), and contribute to heart disease [40, 29, 41].

Diseases Linked to High Levels

1) Liver Disease

GGT is increased in patients with liver diseases, such as cirrhosis, hepatitis, and fatty liver. These conditions are caused by a number of factors, including drug and alcohol abuse, toxins, or viruses [42, 43, 44, 45, 46, 47].

GGT levels are used with other liver enzyme tests to diagnose liver disease. For example, GGT levels are measured when alkaline phosphatase (ALP) is high. Elevated levels of both enzymes point to a liver or biliary tract disease. Normal levels of GGT in the presence of increased alkaline phosphatase (ALP) point to bone disease [16].

2) Biliary Tract Disease

High levels of GGT are also found in patients with biliary tract disease (cholestasis). This is usually caused by bile duct obstructions from one or more conditions including gallstones, inflammation, injury, infection, cysts, and/or carcinomas (cancer) [16, 48, 49].

Like with liver disease, GGT is used in combination with additional tests, such as alkaline phosphatase (ALP), for diagnosing biliary tract disease [16].

3) Alcohol Consumption and Cigarette Smoking

Prolonged alcohol use raises GGT levels. In some cases, additional tests may be conducted to identify alcohol abuse [17, 18, 19].

Increased levels of GGT in combination with another marker (CDT) were better at predicting alcohol abuse than either test alone [20].

Cigarette smoking has also been linked to elevated GGT levels. One clinical study conducted in 46k men found that regular alcohol consumption and daily cigarette smoking increased levels of GGT greater than each activity alone. Those people who drank and/or smoked more had higher levels of GGT [20, 21].

4) Coronary Heart Disease (CHD)

CHD is a condition caused by the narrowing of the coronary arteries, potentially leading to a heart attack. Elevated GGT levels are associated with an increased risk for coronary heart disease [29, 22].

Further studies also linked high GGT to death from coronary heart disease [23, 24].

5) Stroke

The largest meta-analysis to date (10 studies) found that higher levels of GGT increased the risk of stroke (independent of excessive alcohol consumption), but only in men [50].

6) Arteriosclerosis

Arteriosclerosis is a narrowing and clogging of the arteries, usually due to plaques. GGT is present in human plaques, and levels are higher in patients with plaques, especially in those with more severely clogged arteries [40, 51].

7) Heart Failure

Heart failure is a condition where the heart is unable to supply enough blood to meet bodily demand. Clinical studies found an association between elevated GGT levels and an increased risk of heart failure, even when values fell within the “normal” range [26, 27, 28].

8) High Blood Pressure

In-depth meta-analyses found people with elevated levels of GGT also have an increased risk of high blood pressure. As levels of GGT went up, so did the risk of developing hypertension [52, 53].

9) Cardiac Arrhythmias

Atrial fibrillation causes rapid irregular heart beating. Higher levels of GGT were linked to an increased risk for atrial fibrillation in several studies.

Increased levels of GGT were also correlated with increased risk of sudden cardiac death/ventricular fibrillation [54, 55, 56].

10) Diabetes

Elevated levels of GGT may increase the risk of type 2 diabetes. However, a recent meta-analysis found no link between the two. Further studies looking at this relationship would be beneficial [57, 23, 58, 59].

11) Metabolic Syndrome

Metabolic syndrome is 2 or more of the following conditions including insulin resistance, high blood pressure, blood fat abnormalities (dyslipidemia), and obesity. Independent of other risk factors, a number of clinical studies have found that elevated levels of GGT increased the risk of metabolic syndrome [29, 30, 31].

12) Cancer

GGT may be useful at predicting cancer risk and disease outcome. According to several clinical studies, elevated GGT levels increase overall cancer risk [32, 60].

In a few early studies, elevated GGT levels have been associated with some types of cancer [61, 62]:

  • Breast cancer: Those with higher GGT have a greater risk of developing several subtypes of breast cancer, according to a study in 231k cancer-free women [63].
  • Esophageal cancer: A study of 8.3 million Koreans found an increased risk for esophageal cancer in those with levels of GGT > 18 U/L, a value considered “normal”. As the level of GGT rose, so did the risk of esophageal cancer [64].
  • Liver cancer: Higher GGT levels were associated with a worse prognosis in liver cancer [65, 66].
  • Endometrial cancer: Elevated levels of GGT were associated with decreased survival rates for women with endometrial and cervical cancer [67, 68].

13) Kidney Disease

One study in 10k Korean men found that the risk of chronic kidney disease was greater in patients with elevated GGT levels. Another study of 9.5k Americans found no such link [69, 70].

Elevated levels of GGT may be associated with an increased risk of chronic kidney disease in specific populations.

14) Alzheimer’s Disease and Dementia

GGT can be elevated in patients with Alzheimer’s disease. However, a genetic study looking at 26 GGT-related gene variations (single nucleotide polymorphisms (SNPs)) and the risk of Alzheimer’s disease found no correlation between the two [71, 72].

One clinical study in 2.4k men found elevated GGT levels to be associated with an increased risk of dementia [73].

15) Thyroid Disease

Diseases of the thyroid include hyperthyroidism (higher T3/T4, usually with lower TSH levels) and hypothyroidism (lower T3/T4, usually with higher TSH levels).

In a study of 110 people, GGT was elevated in patients with hyperthyroidism. In a larger study of 1.5k subjects with hyperthyroidism, GGT levels were normal [74, 75].

GGT was slightly increased in patients with hypothyroidism in one study and decreased in another study. Additional research is needed to clarify the relationship between GGT and thyroid disease [76, 77].

16) Decreased Bone Mineral Density

Bone mineral density (BMD) represents overall bone health and strength. One clinical study in 462 people found people with high GGT levels have low BMD (independent of alcohol consumption) [78].

Factors That Increase GGT Levels

High levels of GGT usually indicate present disease or a higher risk of disease. Here we give a summary of the factors that increase levels of GGT.

1) Medications/Prescription Drugs and Supplements

Several medications increase GGT levels and must be taken into consideration when interpreting test results. These include older anti-seizure medications (such as phenytoin, phenobarbital, and carbamazepine) [79, 80, 81, 82].

2) Alcohol

GGT levels are elevated following prolonged alcohol use. As drinking increases, the level of GGT in the blood also rises [17, 18, 19].

3) Red Meat

Red meat intake over 10 years increased GGT levels [10].

4) Kava

One pilot study of 62 healthy adults found that GGT levels were increased by about 40% in those who drank kava [83].

5) Thyroid Hormone

Several clinical studies have found that elevated levels of thyroid hormone increased levels of GGT in patients with hyperthyroidism [84, 74].

How to Reduce GGT Levels

1) Treat the Underlying Condition

GGT is ultimately just a biomarker that indicates an underlying problem. Talk to your doctor to identify any underlying health conditions and determine the best strategies for treating those.

2) Decrease Alcohol Consumption

Alcohol abuse increases GGT levels. GGT is only slightly elevated in moderate drinkers, but the increase is relevant. The best way to lower GGT is to simply abstain from alcohol use. Levels should return to “normal” after 2 to 6 weeks [17, 18].

3) Eat More Fruits and Vegetables

Many fruits and vegetables contain moderate to high amounts of natural antioxidants. A study of 3k people found that eating fruits and/or vegetables 10-11 times per week, or drinking fruit juice 6-7 times a week for 10 years lowered GGT levels [10].

4) Drink Coffee

Drinking coffee decreased GGT levels in 1,300 Japanese men (independent of other risk factors) [85].

Two other clinical studies, conducted in a total of 31k participants, found that coffee consumption only lowered GGT levels in alcohol-drinking males [86, 87].

5) Eat Less Red Meat

Red meat contains large amounts of heme iron, the most readily absorbed form of iron. The same study that showed fruits and vegetables reduced GGT found that eating red meat over 10 years increased GGT levels [88, 10].

Note: Vegetarian sources do contain varying levels of iron, but in the form that’s harder to absorb (non-heme iron). Vegetarian iron contributes to overall iron levels in the body much less than meat sources. This is one reason that vegetarians sometimes suffer from iron deficiency or anemia [88, 89].

6) Moderate Exercise

One study of 10k participants found that moderate exercise (walking) was associated with decreased GGT levels in men, but not women [90].

7) Fish Oil

High doses of fish oil (4 grams/day) for 3 months significantly lowered GGT levels in 36 participants who had characteristics of non-alcoholic fatty liver disease [91].

8) Avoid Pollutants

Certain environmental pollutants such as lead, cadmium, dioxin, and organochlorine-containing pesticides increase GGT levels [92].

9) Magnesium

Six weeks of magnesium supplementation decreased levels of GGT in a group of chronic alcoholics. However, this was a small study and further research is needed [93].

Limitations and Caveats

The full range of functions for GGT is not known. It is a topic of continued scientific and clinical study.

There are disease states such as diabetes, chronic kidney disease, and hypothyroidism where clinical studies show conflicting conclusions regarding risk and elevated GGT levels. Further studies need to be done to determine if high GGT levels increase the risk of these diseases.

Clinical studies show elevated GGT levels to be associated with the development of diseases even within what would be considered “normal” ranges. This is mostly the case with GGT and the risk of cardiovascular diseases. Future clinical studies need to address the risk of other disease states within “normal” GGT ranges.

Conditions Associated with Low GGT Levels

Rarely are low levels of GGT dangerous. However, a few conditions are associated with abnormally low levels of GGT. Whether this is cause for concern depends on other factors.

1) Inherited Disorders

Familial Intrahepatic Cholestasis (FIC) includes inherited (genetic) disorders, usually observed in infants and children. It is characterized by the decreased flow of bile from the liver. It can be:

Mutations in the ATP8B1 gene are related to both the mild and severe forms of the disease. This gene controls the bile salt export pump, which drives bile flow [94].

2) Mid to Late Pregnancy

Women in their second and third trimesters may have lower levels of GGT in comparison to non-pregnant women. There is no indication that this is a cause for concern [95].

Genetics of GGT

GGT levels are influenced by your genes.

Many genetic and environmental factors can influence GGT levels. Genetic factors affect GGT levels, dependent on age, and contribute to about 1/3 to 2/3 of GGT levels [96, 97, 98].

The GGT gene family consists of 13 members, with 6 considered to be “active,” The gene responsible for most of the GGT throughout the body is GGT1 [99].

Takeaway

Early animal and cell-based studies suggest fullerene (buckminsterfullerene or C60) may be an antioxidant that removes toxic metabolic waste. According to these early studies, C60 may promote longevity and reduce oxidative stress. However, it showed the potential to damage DNA. Additionally, fullerene has not yet been studied in humans. Thus, its short- and long-term risk and safety profile remain unknown. We recommend against taking this compound until proper clinical trials are completed.

Liver Function Test normal range chart : (ALT, AST, Albmin)

A liver function test (LFT test) is an important test for measuring the particular biomarker in the blood. It helps in the (1) diagnosis of liver disease,(2) monitor therapy, (3) and assesses the prognosis.

Serum total Bilirubin 3-17 micromol/litter
Alanine aminotransferase (ALT) up to 42 u/l
Asparatate amino transferase(AST) up to 37 u/l
Serum Alkaline Phosphatase (ALP) 60-306 u/l
Total Protein 60-80 g/l
Albumin 40-50 g/l
Gamma Glutamyltransferase GGT 11- 60 u/l

liver function test normal range chart

There are two groups of tests used to assess the liver disease.

  1. Routine LFT
  2. Special LFT

What are the

Routine Liver Function Test name

Routine LFTs include six serum (S) tests.

  1. Serum alanine aminotransferase (ALT or SGPT )
  2. Serum Alkaline phosphatase (ALP)
  3. Serum Bilirubin
  4. Total protein and Albumin
  5. S. Gamma glutamyl transperase (GGT)
  6. S. 5-Nucleotidase
  7. Serum Amonia

NOTE: Serum albumin range shows the synthetic function of the liver. while bilirubin indicated the excretory function of the liver. ALT and AST directly link to liver damage. The rest of the test, GGT, ALP, and 5- nucleotidase relates to liver obstruction.

What are the

Special LFT Test name

Following are the six special LFT tests.

  1. Serum iron and copper
  2. Alpha feto protein
  3. Hepatitis Markers
  4. Prothrombine time
  5. Blood amonia
  6. Liver biopsy

when to worry about alt levels?

Liver function tests rise when the hepatocyte is damaged by the pathogen. When is mid-damage, there will be a mild change in ALT, AST, and bilirubin. But when their severe damage, the owing changes in result will occur.

  1. ALT will be more than 42 U/litter.
  2. AST will be higher than 37 U/litter.
  3. Serum Albumin is less than 65 g/l.

Can a liver function test detect cancer?

A liver function test can detect damage liver cells. When there is a malignancy or infiltration, following LFT test value alter.

  1. Aminotransferase (ALA) will increase
  2. Alkaline Phosphatase (ALP) will raise.
  3. Albumin can be decrease or normal
  4. Porthrombine, Bilirubin, GGT all these test will be normal.

Why is liver function elevated?

Liver function tests range (serum bilirubin, ALT, AST, GGT, ALP) directly link hepatocyte function. When liver cells are damaged due to the virus (HBV, HCV ) results in the elevation of liver function test.

will liver function test show liver damage?

The answer to this question is YES. ALT and AST enzyme range in the serum is directly linked to hepatocytes. When liver cells are attacked by any kind of pathogen like HBV or HCV, alanine aminotransferase and aspartate aminotransferase rises.

Can a liver function test detect cirrhosis?

Yes, a liver function test (LFT test) can detect cirrhosis. Cirrhosis is the end stage of liver disease. At this stage, the liver stops its synthesis and neutralizing functions.

At this stage, albumin decrease, ALT, AST, bilirubin, ALP, GGT range will increase.

Can liver function tests be normal with liver disease?

Liver function tests can be normal with liver disease, but IF disease is at its initial stage and it did not damage more liver cells, But in the late stage, ALT (SGPT), AST, will raise in the blood.

Liver function test ALT

ALT is the short-term for alanine aminotransferase. ALT is a special test for detecting hepatic cell damage. ALT and AST levels tend to increase during the onset of viral attacks.

Liver function test ALT normal range

Aspartate aminotransferase (AST) normal is between 0 to 37 micro/litter.

Does a liver function test require fasting?

In most cases, no fasting is required for liver function tests (LFT test). But some laboratories asked for fasting before collecting LFT test samples.

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90,000 Diagnosis of “Cirrhosis of the liver” – what you need to know and do?

What is liver cirrhosis?

Liver cirrhosis is a stage of many chronic liver diseases. Cirrhosis is the result of prolonged damage to liver cells, which results in the replacement of living, functioning liver tissue with fibrous scar tissue. Violation of the normal structure of the liver leads to a decrease in the ability of the liver to perform its functions and the development of a number of complications.

Cirrhosis to cirrhosis – strife!

Usually people think that if a diagnosis of cirrhosis of the liver is made, then this is a sentence.This is not always the case. There are various causes, forms and stages of liver cirrhosis. And depending, mainly, on the cause of the disease, the prognosis of the disease can be different. In some forms of cirrhosis, elimination of the cause of the disease leads not only to the cessation of progression, but also to the restoration of liver function. Such patients can live long, fulfilling lives even if the disease was diagnosed at a very young age. Of course, in cases where the cause of the disease cannot be eliminated, and the diagnosis is made at a very late stage (doctors call it decompensated cirrhosis), the prognosis is not favorable.In such cases, liver transplant surgery may be required.

The main thing is to establish and eliminate the cause of liver cirrhosis!

Establishing the cause of the development of the disease is the primary task of the doctor, since in most cases it allows eliminating the factor that caused the disease, preventing the progression of cirrhosis and the development of complications.
The most common causes of cirrhosis are alcohol, hepatitis B and C viruses, and metabolic disorders with fat deposition in the liver.Less common are autoimmune (autoimmune hepatitis) and cholestatic diseases (primary biliary cholangitis, primary sclerosing cholangitis), hereditary diseases with accumulation of copper in the liver (Wilson-Konovalov disease) or iron (hemochromatosis), and drug damage to the liver.

An infection caused by the hepatitis C virus is a completely removable cause of liver damage. Currently, medicine has safe and highly effective drugs that allow for a short course of therapy to completely eliminate the hepatitis C virus from the body. Elimination of the hepatitis C virus, even at the stage of liver cirrhosis, prevents the progression of the disease, improves and restores liver function.

There is also effective treatment for liver cirrhosis in the outcome of chronic hepatitis B. This infection cannot be completely eliminated from the body, but there are drugs that can steadily suppress the infection, stabilize the disease, preventing its progression and the development of complications. Unlike in cases of liver cirrhosis caused by hepatitis C virus, people with hepatitis B virus should be treated with antiviral medication continuously throughout their lives.

Complete cessation of alcohol consumption is the main treatment for alcoholic cirrhosis of the liver, which leads to restoration of the liver and prevention of complications. Therefore, the prognosis for this disease depends not only on the doctor, but also to a large extent on the patient himself.

There are some forms of liver cirrhosis in which treatment is successfully applied that is not directed at the cause, but at the mechanism of damage. So, with genetically determined liver diseases, we cannot change genetics.But, for example, in Wilson-Konovalov’s disease, liver damage occurs due to excessive accumulation of copper in it, and the removal of copper from the body by special drugs leads to the restoration of the liver. This is one of the few hereditary diseases with very successful treatment. In such patients, cirrhosis of the liver is diagnosed more often in childhood and adolescence. Without treatment, they die at a young age. Under the condition of constant therapy with drugs that remove copper from the body, they live a full life (they study, work, give birth and raise children).With hereditary hemochromatosis, cirrhosis of the liver develops due to an excess of iron, therefore, the removal of iron (by simple bloodletting) changes the prognosis of the disease.

In case of liver cirrhosis as a result of autoimmune hepatitis, doctors also act on the mechanism of damage – they suppress pathological immune reactions with the help of corticosteroid hormones, azathioprine, and other drugs. Treatment allows you to stop or significantly slow down the progression of the disease. In primary biliary cirrhosis, it is also possible to significantly slow down the progression of the disease with the help of ursodeoxycholic acid preparations.

The same patient may have two or more causes of liver damage. For example, viral hepatitis can be combined with alcohol abuse, metabolic disorders, etc. It is very important to establish and eliminate all factors damaging the liver. This is the key to a good prognosis of the patient’s life.

Liver cirrhosis has its own developmental stages

When making a diagnosis of liver cirrhosis, in addition to the causes of liver damage, a doctor always evaluates the degree of disease activity and the severity of liver damage.Depending on the severity of the liver dysfunction, there are three stages, or a class of liver cirrhosis:

  • class A is a fully compensated cirrhosis (there is fibrosis, but liver functions are not impaired).
  • class B – there are initial moderate signs of liver dysfunction (a slight increase in bilirubin, a decrease in albumin levels, a small accumulation of fluid in the abdomen, treatable, etc.).
  • class C – severe disorders (or severe decompensation) of liver function and the presence of complications of liver cirrhosis.These patients usually have jaundice, edema, ascites, a tendency to bleed, impaired consciousness (hepatic encephalopathy).

It is clear that the diagnosis of cirrhosis at the “class A” stage is more favorable for the prognosis, but to a greater extent the prognosis depends on the possibility of eliminating the cause of liver damage. So, for example, with autoimmune, viral genesis of the disease, with Wilson-Konovalov disease, successful treatment is possible even in the later stages, and it can lead to compensation for liver cirrhosis (transition to class A).In the same rare cases when treatment is absent or ineffective (for example, with primary sclerosing cholangitis, hepatitis delta virus infection, and some others), the prognosis may not be so favorable in the initial class A cirrhosis.

Patients with liver cirrhosis should undergo regular examination, including assessment of liver function and prognosis, to select adequate treatment and prevent complications.

Cirrhosis is dangerous for its complications

Danger to life in patients with liver cirrhosis are complications.The main complications include bleeding, hepatic encephalopathy and coma, ascites, and the development of liver cancer.

Bleeding. Fibrous scars in the liver squeeze intrahepatic blood vessels, which leads to an increase in pressure in the vessels that bring blood to the liver, and their expansion. This is called portal hypertension. In the dilated portal vessels, saccular protrusions form – the so-called varicose veins. Most often, varicose veins are observed in the esophagus, stomach, rectum.Rupture of these vessels leads to severe and life-threatening bleeding.

The most dangerous bleeding from varicose veins of the esophagus and stomach. Therefore, all patients with a diagnosis of liver cirrhosis are shown to undergo esophagogastroduodenoscopy (EGDS) at least once a year to clarify the presence of varicose veins, assess the risk of bleeding and, if necessary, carry out preventive ligation of these veins. This is a small operation performed through an endoscope and consists of compressing varicose veins using latex ligatures.Such an operation is performed urgently in cases of bleeding to stop it, but if there is a risk of bleeding, it is better to carry out it prophylactically. In addition, adherence to a certain diet is of great importance. The doctor may also recommend medications that reduce pressure in the portal vessels, as well as erosions and ulcers of the mucous membrane.

Hepatic encephalopathy and coma. With the progression of cirrhosis, the liver’s ability to neutralize toxic substances is impaired.The brain is especially sensitive to the effects of toxic substances, primarily ammonia, which is formed in the intestines as a result of the digestion of protein foods (the so-called “nitrogenous waste”). As a result, disorders of the function of the central nervous system are observed in the form of memory loss, slowing down of reactions, drowsiness, lethargy, hand tremors, impaired coordination, etc. With the progression of encephalopathy, a life-threatening coma develops.

Therefore, patients with liver cirrhosis should undergo regular examination aimed at assessing the presence and degree of hepatic encephalopathy, and the appointment of adequate treatment.Patients are advised to adhere to a diet with varying degrees of restriction of the use of animal protein (mainly red meat), depending on the severity of liver dysfunction. Prescribed drugs that eliminate constipation and reduce the toxicity of “nitrogenous waste”, drugs that bind ammonia in the blood, etc.

Ascites, edema. Ascites refers to the accumulation of fluid in the abdominal cavity. Ascites is a consequence of portal hypertension, as well as a decrease in the synthesis of albumin in the liver. At the same time, fluid can accumulate in the chest (in the pleural cavity), edema is observed.There is an increase in the abdomen, a decrease in the amount of urine, shortness of breath. Ascites can be complicated by the development of infection of the abdominal cavity, impaired renal function, etc. The doctor prescribes to such patients a diet with limited salt, diuretic therapy, which is based on the use of spironolactone, drugs for the prevention of bacterial infection and other complications. The patient should avoid excessive prescription of diuretics, massive urine flow (more than 2-2.5 liters per day), regularly monitor fluid secretion, blood tests and be monitored by a doctor.

Primary liver cancer is a malignant tumor that, unlike liver metastases from cancer of other localizations, develops directly in the liver tissue. Liver cirrhosis is a precancerous condition. The highest risk of liver cancer is in patients with viral and alcoholic cirrhosis of the liver. After eliminating the cause of liver cirrhosis, the risk of developing liver cancer decreases tenfold, but still it remains.

Since the early stages of primary liver cancer are successfully treated, all patients with liver cirrhosis should regularly (at least once every 6 months) undergo examination, including mandatory ultrasound and a study of the level of the liver tumor marker – alphafetoprotein. In some cases, additional studies are required (magnetic resonance imaging, etc.).

Insidious liver disease

Many human diseases can proceed imperceptibly, without vivid manifestations. But liver diseases are distinguished by a particularly long asymptomatic course, and this is their insidiousness. There are no nerve endings in the liver, so even in the presence of liver cirrhosis, it does not hurt. Jaundice usually develops in the late stages of cirrhosis. Therefore, the disease is often detected during clinical examination or random examination already at the stage of cirrhosis, and not hepatitis.

You need to know that the first manifestations are different for everyone, which depends on the cause and stage of the disease. Often it is only weakness, increased fatigue and discomfort in the right hypochondrium. The first manifestations may be an increase in the volume of the abdomen, edema in the legs, that is, complications of cirrhosis. Sometimes it is itchy skin, bleeding from the nose and gums, slight bruising on the skin, yellowing of the sclera of the eyes, joint pain, skin rashes, etc.

When should I see a hepatologist?

For a timely diagnosis of liver disease, you need to contact a specialist

  • if you feel unwell, the cause of which is not clear
  • if there is any of the above manifestations of the disease
  • if you regularly drink alcohol
  • if you have had jaundice or have had operations, blood transfusions, intravenous drug use, tattoos (all of these are risk factors for infection with hepatitis viruses)
  • if you suffer from metabolic disorders (diabetes mellitus, obesity, gout, high cholesterol)
  • if during the prophylactic medical examination you were found to have abnormalities in the biochemical blood test or markers of hepatitis viruses
  • if your ultrasound examination revealed an enlarged liver

Diseases of the liver in dogs and cats

The liver is a vital organ that participates in many processes in the body. The uniqueness of this organ is that liver cells are able to regenerate.

Basic functions of the liver:

  1. Neutralization of hazardous substances. The liver can be called a kind of “filter”, it neutralizes both harmful substances formed in the body as a result of metabolism, and toxic substances coming from outside.
  2. Participates in the metabolism of proteins, fats and carbohydrates
  3. Accumulation of vitamins, iron, glycogen
  4. Synthesis of bile, which is involved in the breakdown of fats

What liver diseases do pets suffer from more often?

Hepatitis

Most common liver disease in cats or dogs.Hepatitis causes inflammation and death of hepatocytes, replacement of normal connective tissue. Cholestasis is often observed when the outflow of bile is impaired. In this case, the inflammatory process often affects the spleen, and hepatolienal syndrome occurs.

As a rule, hepatitis is toxic or infectious in nature.

Toxic hepatitis often occurs when:

– poisoning with poisons, chemicals, rodent poison;

– drug overdose;

– overdose of vitamin A;

– feeding with poor quality feed;

– gastroenteritis, enterocolitis.

Infectious hepatitis occurs as a complication in a number of infectious diseases of a bacterial or viral nature. Most often hepatitis occurs against the background of adenovirus, leptospirosis, salmonellosis.

For parasitic diseases, for example, with piroplasmosis in dogs, toxoplasmosis in cats.

In addition, hepatitis occurs with neoplasms.

Fatty hepatosis

Fatty hepatosis is the collective name for a whole group of pathological liver disorders, in which the liver parenchyma degenerates and the hepatocytes are destroyed.

More often occurs in cats, often after prolonged fasting or feeding with poor quality food. Often occurs in overweight cats over 8 years of age. Amyloidosis, one of the varieties of hepatosis, is more common in cats of the Abyssinian and Siamese breeds, so it makes sense to talk about a breed predisposition. Hepatosis is asymptomatic for a long time. A characteristic sign is a sharp decrease in body weight, apathy and lethargy.

Most of the liver diseases have a latent course, so the owners are not always able to recognize the disease in time.

Symptoms

What should alert your pet in the first place?

1. Indigestion accompanied by vomiting, diarrhea or constipation, weight loss, decreased appetite.

2. Jaundice, when the visible mucous membranes and white of the eyes turn yellow.

3. Feces are whitish or grayish in color. This happens because the production of bile decreases or it stops flowing into the digestive tract.

4. The urine is bright yellow. With liver diseases, a large amount of bilirubin begins to be excreted in the urine.

5. Apathy. With liver disease, hepatodepressive syndrome develops, in which the animal is depressed and inactive.

6. Increase in the volume of the abdominal cavity. Dropsy or ascites may develop.

7. Skin itching. It is a common symptom of liver disease.

Treatment

Treatment is impossible without an accurate diagnosis in a veterinary clinic.It is necessary to thoroughly examine the animal: collect anamnesis, conduct a clinical examination, do a general clinical and biochemical blood test, ultrasound diagnostics, and, if necessary, a liver biopsy.

After the diagnosis is made, the veterinarian prescribes treatment, which should include:

  1. Diet.
  2. Detoxification therapy, which consists in the introduction of special solutions to replenish the lack of fluid and energy intravenously.Sometimes it is even required to place the animal in a hospital.
  3. Antibacterial and antiviral drugs are prescribed for bacterial infections.
  4. Symptomatic therapy is used: antispasmodics, antiemetic drugs.
  5. Hepatoprotectors are used to restore the structure and function of the liver.

An effective and safe drug for the treatment of liver diseases is Covertal , which combines the properties of the main groups of hepatoprotectors.

Covertal has a hepatoprotective, anti-inflammatory, antispasmodic and anticholestatic effect. Promotes the activation and protection of phospholipid-dependent enzyme systems of hepatocytes, improves the detoxification function of the liver.

Indications for use:

– Acute and chronic hepatitis;

– Toxic liver damage;

– Hepatosis;

– Infectious and invasive diseases (as concomitant therapy).

90,000 Signs of liver disease – liver disease: symptoms and early signs

Liver – “biochemical laboratory” of the body

The liver is the largest digestive gland and one of the largest human organs. The weight of the liver reaches 1.5-1.6 kg. The liver is called the body’s “biochemical laboratory” because it performs many vital functions.

Signs of abnormal liver function

The liver performs various functions every day, and we do not even notice how hundreds of complex biochemical processes are going on in the body.However, the liver is a very fragile organ that is susceptible to the influence of internal and external factors. The causes of liver dysfunction are poor ecology, unhealthy diet, low level of physical activity, excess weight, alcohol consumption, viruses, medication and genetic and immune disorders 5 .

How to understand if the liver is malfunctioning?
  1. Pain or heaviness in the right hypochondrium
  2. The liver is surrounded by a shell, the so-called capsule, which is sensitive to changes in the size of the organ.Inflammation of the liver caused by alcohol or excess fat intake leads to enlargement of the liver. In response, the liver capsule stretches, causing pain, heaviness and discomfort 6 .

  3. Weight gain
  4. The liver is involved in the metabolism of fats and carbohydrates. Insufficient physical activity and too high-calorie food lead to the fact that the liver does not have time to process fats and carbohydrates 7 . The excess is deposited as fat in the liver (fatty hepatosis develops) and in the subcutaneous fat, especially in the abdomen and thighs.Both are reflected in the extra pounds on the scales.

  5. Nausea or vomiting
  6. When the liver cannot cope with toxins, their amount in the blood rises. An excessive amount of endogenous toxins (formed as a result of the metabolism of various substances) and exogenous toxins (coming from the outside) lead to the development of such unpleasant symptoms as nausea and vomiting 8 .

  7. Increased fatigue
  8. Increased fatigue, accompanied by low performance, is closely associated with liver disease and is the most frequent and early symptom in liver disease 9 . Inflammatory substances produced in liver cells can affect the transmission of nerve signals in the brain. This leads to the development of increased fatigue and decreased mood 9 .

  9. Bad breath
  10. Bad breath may indicate a malfunctioning digestive system. A sweetish “mouse aroma” can appear when liver cells cannot cope with the processing of toxic substances 10 .

  11. Yellowness of the skin and eyes
  12. A change from the normal color of the eyes, skin and mucous membranes to yellow is called jaundice.This condition is explained by the ingestion of excess bilirubin, a yellow pigment that is formed as a result of the destruction of hemoglobin, into the bloodstream. For example, hemoglobin can be released when red blood cells (erythrocytes) in the liver die. Jaundice can indicate liver cell malfunction and be a symptom of alcohol-related liver disease. In addition, jaundice can occur with viral hepatitis and medicinal liver damage 11 .

  13. Discoloration of urine and feces
  14. Bilirubin, a yellow pigment and one of the main components of bile, is present not only in the blood, but also in urine and feces.Bilirubin is excreted in the bile into the duodenum and, under the influence of intestinal bacteria, changes its color to brown. It is this brown pigment that gives the stool its characteristic color. In the urine, however, there is another product of the metabolism of bilirubin, which gives the urine a light yellow color 12 .

    Certain liver diseases can interfere with its ability to process bilirubin, causing significant amounts of it to be excreted through the urine, which becomes darker as a result.On the other hand, insufficient bile supply is accompanied by fecal discoloration 12 .

  15. Swelling of the legs
  16. Liver diseases sometimes make themselves felt only in late stages, for example, in cirrhosis, when normal liver tissue is replaced by connective tissue.

    Swelling of the legs occurs as a result of increased pressure in the vessels of the liver (portal hypertension) and insufficient production of albumin protein 13 . With albumin deficiency, fluid is not retained in the bloodstream and fills the tissue.

  17. Rapid bruising
  18. The most important function of the liver is the production of proteins. In response to chronic alcohol use or viruses, the liver ceases to cope with its work and begins to synthesize fewer proteins that regulate blood clotting 14 . As a result, hemorrhagic syndrome develops. Its manifestations are unreasonable bruising, bleeding gums and nosebleeds 14 .

  19. Itching
  20. Itchy skin is a symptom of allergic diseases and liver problems.Itching occurs in response to the irritation of excess bile acids on the skin 15 . Often, itching and jaundice go hand in hand, or itching precedes jaundice.

Restoration of the liver with the hepatoprotector Heptral

®

In case of liver problems, the level of an amino acid vital for its function drops. This amino acid is involved in more than 100 biochemical reactions and is essential for the liver to function properly and to restore it.This amino acid is called ademetionine, and it is impossible to get it from food 16 . Ademetionine is produced in the liver itself. However, an unhealthy liver cannot provide itself with a sufficient level of ademetionine to function properly 16 . This is where Heptral ® comes to the rescue.

Heptral ® is an active amino acid source that triggers the natural regeneration of liver cells from the inside. Replenishing the level of ademetionine in the liver, Heptral ® stimulates important processes inside the liver cells.Heptral ® helps to normalize metabolic processes in the liver, eliminate toxins, restore hepatic cell membranes, improve bile excretion and replenish the energy of liver cells 17.18 .

The drug Heptral ® helps to remove toxins and restore liver function after the 1st week of administration. And the effect of taking Heptral ® can persist for 3 months after the end of therapy 18 . Also, Heptral ® is a hepatoprotector that helps to cope with one of the first and most common symptoms of liver disease – increased fatigue 19 .Taking Heptral ® can help restore vigor and give a surge of vitality.

Liver segments: scheme, structure, characteristics

The liver is considered the second largest human organ, the structure of which includes liver segments. For each segment, there is a special network of blood supply and innervation. In addition, in each lobe of the liver there is a central middle channel through which bile is excreted. The liver is an important organ that is associated with digestive and metabolic processes, with the immune system and the preservation of compounds necessary for the body.The organ regenerates rapidly and grows in order to restore normal functioning and average normal size. Therefore, it is necessary to know the organ structurally.

Features of the structure of the liver, in many respects, predetermine the methods of examination for certain diseases.

The structure of the liver: lobes, sectors and segments

The internal hepatic structure includes a small functional unit called the hepatic lobule. The structural particle of the lobules is a beam. Each of the beams contains central hepatic veins, around which there are 6 portal veins and 6 hepatic arteries.They all communicate using sinusoids – small capillary tubes. Structurally, an organ has two types of cells. The first type is Kupffer cells, which destroy unusable red blood cells that pass through the tubules. Cells of the second type are hepatocytes, characterized as cuboidal epithelial cells, which are considered the main constituent of the hepatic cell composition. Cells are responsible for functions such as metabolic processes and fully functioning digestive tracts, and are also involved in the production of bile.In this case, the bile capillaries are located in parallel with the sinusoids.

Thanks to the development of medicine, scientists have managed to divide the organ into liver segments, which are directly connected with the organ’s flow system. When studying the ducts, attention is paid to the arteries, vessels of the lymphatic system, branches of the portal system, bile ducts and hepatic branches. The first three points grow together into the vascular-sector bundles. The hepatic segments are characterized by a pyramidal shape, and thanks to the vessels, the organ triad is formed.Each segment is enriched with a blood supply system and provides bile outflow. The first to describe the structure of the liver was Claude Quinot.

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Table: lobes, sectors and segments

There are 8 segments in the human liver, which are located around the gate zone along the radius. The development of segmental formations is facilitated by the hepatic veins and their structure. Hepatic segments are formed even before a person is born, while segmentation, as well as the lobular division of the liver, can be seen when examining the developing fetus.

Left lobe Right lobe
The structure of the left lobe of the liver includes four hepatic segments:

  • the caudate, characterized as a multi-segmental dorsal region, which is located closer to the dorsal region;
  • posterior element entering the left lateral zone;
  • anterior part, which is part of the structure of the paramedian sector;
  • square segment related to the structure of the paramedian sector, like the previous element.
The structure of the right hepatic lobe of the liver includes the lateral and paramedian zones, which have two segments each.

The lateral sector consists of the lower posterior and upper posterior segments. The structure of the paramedian sector includes the middle anteroposterior and middle anteroposterior parts of the liver.

Due to segmental hepatic division, the ability to better describe the spread of the problem area or tumor formations in the organ has emerged. Also, anatomy has been associated with manifestations of hepatic activity, and the segments are considered a functional structural unit. Due to the fact that there are membranes between the segments, it is possible to carry out an operation on the organ with a lesser likelihood of complications. The membranes are segmental and sectoral boundaries, in the structure of which there are no large vessels and ducts.

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Scheme of segmental structure

The scheme of organ structure includes: caudate lobe of the liver, left lateral segments, left medial particle, right anterior and posterior segments.The caudate hepatic lobule is 1 segment that has clearly defined boundaries with other segments. In this case, particles are separated from 2 and 3 due to the venous ligament, and the 4th segment disconnects the hepatic gate. The inferior vena cava and the right hepatic vein zone separate 1 segment from the 7 segment area.

The left lobe of the liver in the structure has 2 and 3 segments, the boundaries of which correspond to the boundaries of the site. The square lobe of the liver corresponds to the 4th segment, which has no clear boundaries separating it and the right hepatic lobules.Behind the gallbladder there is a 5th segment, and below it is 6. The segment reaching the beginning of the diaphragm has a value of 7. The segmental structure of the liver consists of 8th segment, which is also called “reed”.

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Blood supply and innervation of the hepatic structures

The liver is supplied with blood through the portal vein and the hepatic artery. Although only a third of the blood travels through the hepatic artery, it plays an important role. Providing the organ with blood, the artery also carries oxygen masses, which are necessary to maintain the vital functions of the organ.Thanks to the blood supply, the main biological roles of the liver are realized, namely, the protection of the body and the detoxification of hazardous substances. Venous blood flows are necessary for the organ, as it destroys harmful substances that have entered the liver.

Through the liver, all blood of the human body undergoes functional “filtration”.

The blood supply processes in the liver are unique processes in which the entire blood composition of the human body passes through the organ in a minimum period of time. With the help of venous blood, the human body is cleansed of slag accumulations, and also carries additional useful compounds throughout the body. Due to the presence of hemocapillaries, the liver implements protective, barrier-biosynthetic and secretory functions.

The innervation of the liver occurs due to the solar connection located between the sheets of the duodenal-hepatic junction. The structure of the solar plexus includes branches of the nerve plexus of the womb and individual vagus nerves. An important additional role belongs to the branches of the diaphragmatic node, in particular, its right side. Some of the plexus particles are located near the vena cava and get inside the organ thanks to the particles of the hepatic ligaments.

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Characteristics and significance of bile capillaries

Bile vessels are the transporters of bile through the liver and bladder.

Bile capillaries are tubular formations that carry bile through the liver and gallbladder. Together, these capillaries form the bile-flow system. Thanks to the liver cells, it produces bile, which flows out through small channels. Capillaries act as such channels, which later grow into a large bile duct.Further, the process of accretion of the bile ducts into the left and right branches takes place, carrying bile formations from the right and left hepatic parts. Then these branches grow together into one duct of the liver, through which all the bile masses flow down.

Further, the duct is connected to the inflow of the bladder, which is related to the gall bladder. The result is a single large bile duct that carries bile to the small intestine duodenum. Due to peristalsis, the process of moving bile masses to the cystic duct takes place, where it remains until it is needed for the digestive process.

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Implications for non-invasive examinations

By dividing the organ into zones, the chance of obtaining accurate results from a non-invasive hepatic examination method increases. Such methods make it possible to examine the vessels and grooves, determine the place where the violation occurred, and notice the development of tumor formations in the organ in time. The central role in the ultrasound scan is assigned to large vessels and bile ducts, which are landmarks. There are such forms of ultrasound slices as subcostal, transverse and longitudinal.With the help of ultrasound, changes in hepatic size, the development of poor digestion of fatty compounds, and the appearance of carcinomas are determined.

With the help of MRI, it is possible to see the division of the liver into zones using furrows and blood vessels. To assess parenchymal inflammation, blood supply in different liver segments is assessed. The most reliable in the MRI results are the portal phases, in which the parenchyma can be located, during which the results change significantly. During the portal phase, you can see the difference between the normal state of the parenchyma and during the period of inflammation.

To determine the exact localization of the neoplasm in the liver, the CT method is used, thanks to which the chances of severely damaging the liver during surgery are reduced. To give more contrast, a special hepatic window is used during the study.