Dangerous liver enzyme levels: High, Low & Normal Results, Symptoms & Causes
Alcoholism Definition, Signs, Symptoms, Causes & Treatment
Medically reviewed by Ashraf Ali, MD; Board Certification in Psychiatry and Adolescent & Child Psychiatry
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Liver Test Interpretation – Approach to the Patient with Liver Disease: A Guide to Commonly Used Liver Tests
William D. Carey, MD
Laboratory assessment of the patient with suspected or clinically obvious liver disease is context dependent. For example, the acutely ill jaundiced patient with a history of prolonged alcohol ingestion requires a different laboratory assessment than the well patient in whom one or more standard liver test results are discovered to be abnormal during routine testing. Additionally, the sequence of liver tests depends heavily on the questions being asked. If it is to determine whether this well person whose brother was recently diagnosed with hemochromatosis also has this genetic disease, then a series of tests will be initiated to detect the possibility of iron overload. If it is to determine whether this spouse has been infected with hepatitis B, then blood tests related to hepatitis B will be required. Thus generic algorithms for the evaluation of liver disease need to be considered skeptically.
This chapter is intended to discuss a useful way of thinking about liver tests. It emphasizes limitations of and alternative explanations for isolated abnormalities of common liver test results. It also provides information on the initial screening test to be chosen, their interpretation, and the tests needed to confirm the diagnosis of common liver disorders based on current recommendations. Information in this chapter should be combined with discussions of specific liver diseases. A final caveat relates to terminology. Tests done in clinical laboratories do not measure any functional capacity of the liver. Hence, the commonly used term liver function test is inaccurate, and the term liver tests is used in this chapter. Guidelines on the interpretation and evaluation of abnormal liver test results have been published. Useful algorithms are presented that parallel the recommendations in this chapter.
Isolated Abnormalities in Liver Test Results
A common clinical scenario is the unanticipated discovery of an abnormal liver test result, obtained when a bundle of tests has been done for other reasons. Most clinical laboratories offer bundled blood tests, which often contain all or most of the following:
- Aspartate transaminase (AST, formerly referred to as serum glutamic-oxaloacetic transaminase, SGOT)
- Alanine transaminase (ALT, formerly called serum glutamic-pyruvic transaminase, SGPT)
- Gamma-glutamyl-transpeptidase (GGTP)
- Alkaline phosphatase
- Lactate dehydrogenase (LDH)
Of these tests only the GGTP is liver specific. An isolated elevation of just one of the other test values should raise suspicion that a source other than the liver is the cause (Table 1). When several liver test results are simultaneously out of the normal range, consideration of non-hepatic sources becomes less relevant.
Table 1: Nonhepatic Sources of Abnormalities for Select Laboratory Tests
|Bilirubin||Red blood cells (e. g., hemolysis, intra-abdominal bleed, hematoma)|
|AST||Skeletal muscle, cardiac muscle, red blood cells|
|ALT||Skeletal muscle, cardiac muscle, kidneys|
|LDH||Heart, red blood cells (e.g., hemolysis)|
|Alkaline phosphatase||Bone, first trimester placenta, kidneys, intestines|
ALT, alanine aminotransaminase; AST, aspartate transaminase; LDH, lactate dehydrogenase.
Additional note should be made of the GGTP and LDH as liver tests. The GGTP level is too sensitive, frequently elevated when no liver disease is apparent. A GGTP test is useful in only two instances: (1) It confers liver specificity to an elevated alkaline phosphatase level; (2) In aminotransferase level elevations with AST/ALT ratio greater than 2, elevation of GGTP further supports alcoholic liver disease. In addition, it can be used to monitor abstinence from alcohol. An isolated elevation of the GGTP level does not need to be further evaluated unless there are additional clinical risk factors for liver disease. The LDH assay is insensitive and nonspecific because LDH is present in tissues throughout the body.
Evaluation Based on Enzyme Levels
It is customary and useful to categorize liver diseases into three broad categories: Hepatocellular, in which primary injury is to the hepatocytes; cholestatic, in which primary injury is to the bile ducts; and infiltrative, in which the liver is invaded or replaced by non-hepatic substances, such as neoplasm or amyloid. Although there is a great deal of overlap in liver test result abnormalities seen in these three categories, particularly in cholestatic and infiltrative disorders, an attempt to characterize an otherwise undifferentiated clinical case as hepatocellular, cholestatic, or infiltrative often makes subsequent evaluation faster and more efficient. The AST, ALT, and alkaline phosphatase tests are most useful to make the distinction between hepatocellular and cholestatic disease.
The normal range for aminotransferase levels in most clinical laboratories is much lower than that for the alkaline phosphatase level. Accordingly, when considering levels of elevations, it is necessary to consider them relative to the respective upper limit of normal for each test compared. Consider a patient with an AST level of 120 IU/mL (normal, ≤40 IU/mL) and an alkaline phosphatase of 130 IU/mL (normal, ≤120 IU/mL). This represents a hepatocellular pattern of liver injury because the AST level is three times the upper limit of normal, whereas the alkaline phosphatase level is only marginally higher than its upper limit of normal.
Serum aminotransferase levels—ALT and AST—are two of the most useful measures of liver cell injury, although the AST is less liver specific than is ALT level. Elevations of the AST level may also be seen in acute injury to cardiac or skeletal muscle. Lesser degrees of ALT level elevation may occasionally be seen in skeletal muscle injury or even after vigorous exercise. Thus in clinical practice, it is not uncommon to see elevations of AST, ALT or both in common non-hepatic conditions such as myocardial infarction and rhabdomyolysis. Diseases that primarily affect hepatocytes, such as viral hepatitis, will cause disproportionate elevations of the AST and ALT levels compared with the alkaline phosphatase level. The ratio of AST/ALT is of little benefit in sorting out the cause of liver injury except in acute alcoholic hepatitis, in which the ratio is usually greater than 2.
The current upper limit of serum ALT, though varied among laboratories, is generally around 40 IU/L. However, recent studies have shown that the upper limit threshold of ALT level should be lowered because people who have slightly raised ALT levels that are within the upper limit of normal (35-40 IU/L) are at an increased risk of mortality from liver disease. In addition, it has been suggested that gender-specific thresholds be applied because women have slightly lower normal ALT levels than men. One such study conducted in the U.S. identified an ALT upper limit of 29 IU/L for men and 22 IU/L for women. In asymptomatic patients with minimal elevations of aminotransferases, it is reasonable to repeat the test in a few weeks to confirm elevation. Common causes of mild increases in AST and ALT levels include non-alcoholic fatty liver disease (NAFLD), hepatitis C, alcoholic fatty liver disease, and medication effect (e.g., due to statins).
Serum alkaline phosphatase comprises a heterogeneous group of enzymes. Hepatic alkaline phosphatase is most densely represented near the canalicular membrane of the hepatocyte. Accordingly, diseases that predominately affect hepatocyte secretion (e.g., obstructive diseases) will be accompanied by elevations of alkaline phosphatase levels. Bile-duct obstruction, primary sclerosing cholangitis, and primary biliary cirrhosis (PBC) are some examples of diseases in which elevated alkaline phosphatase levels are often predominant over transaminase level elevations (Table 2).
Table 2: Category of Liver Disease by Predominant Serum Enzyme Abnormality
|Liver Disease Category
|AST, ALT higher than alkaline phosphatase level||Typical||—||—|
|Alkaline phosphatase higher than AST, ALT levels||—||Typical||—|
|Elevation of alkaline phosphatase with near-normal AST, ALT levels||—||Typical||Typical|
ALT, alanine aminotransaminase; AST, aspartate transaminase.
Infiltrative liver diseases most often result in a pattern of liver test result abnormalities similar to those of cholestatic liver disease. Differentiation often requires liver imaging studies. Liver imaging by ultrasound, computed tomography (CT) or magnetic resonance imaging (MRI) most often identify infiltration of the liver by mass lesions such as tumors. Imaging by cholangiography—endoscopic retrograde cholangiography, transhepatic cholangiography, or magnetic resonance cholangiography—identifies many bile duct lesions that cause cholestatic liver disease. Liver biopsy is often needed to confirm certain infiltrative disorders (e.g., amyloidosis) and microscopic biliary disorders such as PBC.
Bilirubin Level Elevations
Bilirubin is produced by the normal breakdown of pigment-containing proteins, especially hemoglobin from senescent red blood cells and myoglobin from muscle breakdown. Bilirubin released from such sources, tightly albumin bound, is delivered to the liver, where it is efficiently extracted and conjugated by hepatic glucuronidation and sulfation. Conjugated bilirubin is rapidly excreted into bile and removed from the body through the gut. Therefore, the amount of conjugated bilirubin present in serum in healthy subjects is trivial (<10% of measured total bilirubin). An elevated level of conjugated serum bilirubin implies liver disease. Also, it is important to note that only conjugated bilirubin appears in urine (unconjugated bilirubin is albumin bound and water insoluble). The presence of bilirubin in urine almost always implies liver disease.
Many laboratories report only the total bilirubin level, the sum of the conjugated and unconjugated portions. It is sometimes useful to determine the fraction of total serum bilirubin that is unconjugated versus that which is conjugated, usually referred to as fractionation of bilirubin. This is most useful when all the standard liver test results are normal, except the total bilirubin. To make matters more confusing, the conjugated bilirubin is sometimes referred to as the direct-reacting bilirubin and the unconjugated as the indirect-reacting bilirubin (Table 3).
Table 3: Bilirubin Fractions Present in Blood and Urine
|Fraction||In Serum As||Measured As||Present in Urine|
|Conjugated||Unbound||Direct-reacting bilirubin||Yes, when serum bilirubin level is elevated|
Normally, 90% or more of measured serum bilirubin is unconjugated (indirect-reacting). When the total bilirubin level is elevated and fractionation shows that the major portion (≥90%) is unconjugated, liver disease is never the explanation. Instead, the clinician should suspect one of two explanations: Gilbert disease or hemolysis. If the patient is young and healthy, an inherited decrease in the inability to conjugate bilirubin is likely and is referred to as Gilbert syndrome. It is seen in about 5% of the general population and causes only mild hyperbilirubinemia without symptoms. It is not associated with liver disease. Interestingly, fasting and intercurrent illnesses such as influenza often make the level of unconjugated bilirubin even higher in those with Gilbert syndrome. This syndrome is easily diagnosed when all standard liver-test results are normal and 90% or more of the total bilirubin is unconjugated. There is no need for an imaging study or liver biopsy in cases of suspected Gilbert syndrome.
Elevations of the unconjugated bilirubin level when the conjugated bilirubin level remains normal may also indicate an increased load of bilirubin caused by hemolysis. Anemia and an elevated reticulocyte count are usually present in such cases (Table 4).
Table 4: Common Causes of Isolated Bilirubin Elevation
|Cause||Direct-Reacting Bilirubin||Indirect-Reacting Bilirubin||Associated Features|
|Liver disease (many types)||Elevated||Elevated or normal||Liver enzyme levels often elevated|
|Hemolysis||Normal||Elevation represents more than 90% of total bilirubin||Anemia usual; increased reticulocyte count; normal liver enzyme levels (although LDH may be elevated)|
|Gilbert’s syndrome||Normal||Elevation represents more than 90% of total bilirubin (common)||No abnormal liver tests; no anemia; onset in late adolescence; fasting makes bilirubin rise|
LDH, lactate dehydrogenase.
Many clinicians mistakenly interpret elevations of direct-reacting bilirubin to indicate that cholestatic (obstructive) liver disease is present. It is apparent from Table 2 that the serum bilirubin level plays no useful role in categorizing a case as hepatocellular, cholestatic, or infiltrative. The bilirubin level may be normal or elevated in each type of disorder. Viral hepatitis A, a prototypic hepatocellular disease, may frequently be associated with bilirubin levels that are high, whereas PBC, a prototypic cholestatic disorder, is associated with a normal serum bilirubin level except in later stage disease. Serum bilirubin levels should be disregarded when trying to decide whether the liver-test pattern is more suggestive of hepatocellular or cholestatic disease.
Determination of Specific Liver Disorders
Acute Alcoholic Hepatitis
Acute alcoholic hepatitis may be mild or life threatening. The pattern of liver test abnormality is hepatocellular. The AST is typically in the 100 to 200 IU/L range, even in severe disease, and the ALT level may be normal, even in severe cases. The AST level is higher than the ALT level, and the ratio is greater than 2:1 in 70% of patients. A ratio greater than 3 is strongly indicative of alcoholic hepatitis. An important corollary is that an AST greater than 500 IU/L or an ALT greater than 200 IU/L is not likely to be explained by acute alcoholic hepatitis—even in an alcoholic patient—and should suggest another etiology.
The degrees of bilirubin level increase and prothrombin time elevation are better indicators of severity of disease. In alcoholic hepatitis, the Maddrey discriminant function (MDF), a disease-specific prognostic score which indicates the severity of liver injury, has been developed. The formula to calculate the score is as follows:
MDF = 4.6 (patient’s prothrombin time − control prothrombin time) + total bilirubin (mg/dL)
Patients who have a score of 32 or greater have an increased risk of death, with a 1-month mortality rate of 30% to 50%.
Other tools to assess severity of alcoholic hepatitis include the MELD or MELDNA score. Several MELD calculators are available on line (https://optn.transplant.hrsa.gov/resources/allocation-calculators/meld-calculator/ ), and require only four laboratory values: bilirubin, prothrombin time INR, creatinine, and [Na]. A MELD score of > 20 defines patients with severity alcoholic hepatitis and high mortality.
Finally, the Lille score tracks changes in bilirubin over time. Failure of improvement in bilirubin within seven days bodes poorly. Recently, the Lille score using change in bilirubin after only 4 days has been validated. Web-based calculators are available (www.mdcalc.com/lille-model-alcoholic-hepatitis).
Viral hepatitis most often produces a hepatocellular pattern of injury (AST and ALT level elevations predominate). Patients who have no symptoms and in whom aminotransferase levels are normal may still be infected. In addition, a great deal of confusion is caused by abnormal viral markers, many of which do not indicate active infection but rather immunity. These concepts are more fully developed elsewhere in the Cleveland Clinic Disease Management.
Hepatitis A virus (HAV) infection is an acute, self-limited disease in most cases, although it may rarely be fatal. Diagnosis is made through the use of antibody tests (anti-HAV). Positive anti-HAV IgM antibody is diagnostic of acute hepatitis A infection and has a very good sensitivity and specificity.
Three antibody tests are commonly used for diagnosis of hepatitis A:
- Anti HAV IgG
- Anti HAV IGM
- Anti HAV (total)
The IgM antibodies are usually positive at the time of the onset of symptoms and they remain positive for about 3 to 6 months after, and in some cases as long as 1 year. Anti-HAV immunoglobulin G (IgG) antibodies develop later than anti-HAV immunoglobulin M (IgM) but they persist for many years and offer immunity. Anti-HAV IgG antibodies are also seen following vaccination.
The presence of anti-HAV IgM—irrespective of the presence of anti-HAV IgG—suggests acute infection. The presence of anti-HAV IgG in the absence of IgM suggests previous infection or post-vaccination antibodies.
When an acute hepatitis A panel is ordered, the test result that is obtained from the laboratory must be interpreted with caution before making the diagnosis. This is because the standard screening tests performed by most laboratories measure the level of total anti-HAV antibodies. Total anti-HAV antibody tests will be positive in the presence of either anti-HAV IgG or IgM, as the reagents used in this test will react to both anti-HAV IgG and IgM. Therefore, a positive total anti-HAV antibody test alone does not provide the diagnosis of acute hepatitis A. Selective testing of serum IgM anti-HAV is required to establish such a diagnosis (Table 5).
Table 5: Hepatitis A Antibody Testing In Different Clinical States
|State||Total Anti-HAV (IgG, IgM)||Anti-HAV IgM|
|Acute hepatitis A||Positive||Positive|
|Resolved hepatitis A||Positive||Negative|
HAV, hepatitis A virus; IgG, immunoglobulin G; IgM, immunoglobulin M.
Like hepatitis A, hepatitis B in adults produces hepatocellular enzyme level elevations (AST and ALT predominate). In adults who acquire hepatitis B, the infection almost always clears, but antibodies persist. In a few, the disease does not resolve but becomes chronic. These patients retain serum markers of viral infection. Many blood tests are available for hepatitis B antigenic determinants and their antibodies. It is best to separate testing appropriate for the acute hepatitis situation from testing for chronic liver disease caused by hepatitis B. Only a few tests need to be considered by the generalist to determine the status of a patient with possible hepatitis B. A full discussion of hepatitis B can be seen in the Disease Management chapter on Hepatitis B.
Acute Hepatitis B
Hepatitis B surface antigen (HBsAg) emerges within 2 weeks of exposure but can often be delayed for weeks or months. This antigen is present in the blood for a variable period, usually encompassing the time during which the patient is clinically ill and most likely to seek medical attention. In patients with mild symptoms whose testing may be delayed, the HBsAg level may have already declined. In this case, a second chance to make the diagnosis comes from detection of the IgM antibody directed against the hepatitis B core (HBc) antigen, anti HBc-IgM (Table 6). Similar to the testing for acute hepatitis A, selective testing of serum IgM anti-HBc is required to establish a diagnosis of acute hepatitis B in patients whose HBsAg levels have already declined. The total anti-HBc antibody test will be positive in the presence of either anti-HBc IgG or IgM.
Table 6. Common Hepatitis B Testing Results
|HBsAg||Negative||Immune due to natural infection|
|HBsAg||Negative||Immune due to hepatitis B vaccination|
|HBsAg||Negative||Interpretation unclear 4 possibilities:|
|Anti-HBc||Positive||1. Resolved infection (most common)|
|Anti-HBs||Negative||2. False positive|
|3. “Low level” chronic infection|
|4. Resolving acute infection|
From: Interpretation of hepatitis B serologic test results. Centers for Disease Control and Prevention website. www.cdc.gov. Accessed June 27, 2013.
In acute hepatitis B, medical attention is often not sought early, especially if symptoms are mild. In such cases the HBsAg may have already disappeared by the time testing is done. The anti-HBs will not yet have emerged. Thus the sole viral marker may be anti-HBc. This same serologic pattern may be seen years after infection when the titer of anti-HBs is low. Sorting out the difference between late resolved hepatitis B and the period in acute hepatitis B described above can be achieved by testing for anti-HBc IgM which will be positive during this so-called “window period” of acute hepatitis B.
Chronic Hepatitis B
Chronic hepatitis B is characterized by persistence of HBsAg for a period longer than 6 months with positive anti-HBc (IgG), and negative anti-HBs. An additional antigen-antibody system plays a role in patients with chronic hepatitis B and requires mention: the hepatitis B e antigen (HBeAg) and its antibody (anti-HBe). HBeAg positivity in chronic hepatitis B usually indicates active viral replication and significant liver injury. In time, HBeAg may be lost, replaced by its antibody, anti-HBe. This transformation is often associated with lower level infection (less viral replication) or HBV DNA, lower AST and ALT values, and less (or no) hepatic inflammation.
Reactivation Hepatitis B
Hepatitis B reactivation is a sudden increase in hepatitis B virus (HBV) replication or the reappearance of active inflammatory disease of the liver in a patient with previously documented resolved HBV, or with the inactive HBsAg carrier state. Reactivation is usually triggered by immunosuppression in the host, which can occur following the use of chemotherapeutic agents for malignancy and following therapy for autoimmune diseases or organ transplantation.
Reactivation can also occur spontaneously. The extent of clinical manifestation from reactivation HBV can vary from a transient, clinically silent disease to severe or acute liver failure. A chronic infectious state can also be seen following HBV reactivation. Diagnosis of HBV reactivation depends on the HBV disease state before activation. In a patient with resolved infection (negative HBsAg and positive anti-HBs), reactivation is indicated by the decline in anti-HBs and the reappearance of HBsAg. In patients with quiescent HBV with positive HBsAg, reactivation is diagnosed by a rise in the serum HBV DNA (>1 log10 IU/mL) or a rise in the serum ALT levels (>3 times baseline). Reappearance of HBeAg in a patient with previous negative HBeAg also indicates HBV reactivation.
Role of HBV DNA Assays, HBV Genotypes and Liver Biopsy in Chronic Hepatitis B
HBV DNA level plays several important roles in chronic hepatitis B. It is one factor in predicting the progression to cirrhosis, helps to determine the need for treatment in HBeAg negative patients, and also plays a crucial role in estimating the response to treatment.
Up to 8 HBV genotypes, labeled from A to H, have been identified. HBV genotypes are not currently used in contemporary clinical practice.
Resolved Hepatitis B and Immunization Status
As indicated in Table 6, an individual with resolved hepatitis B infection almost always has anti-HBc and anti-HBs. An individual successfully immunized against hepatitis B expresses only anti-HBs. Confusion may occasionally arise in the interpretation of hepatitis B tests in a patient who has recovered from hepatitis B many years ago and who has a low or absent level of measurable anti-HBc.
Because hepatitis C infection usually produces no symptoms, or only mild, nonspecific, flu-like symptoms, it is infrequently diagnosed in the acute phase. The virus clears spontaneously in about 15% of infected patients. Although generally helpful for the diagnosis of chronic infection, antibody tests are often not useful for diagnosis of acute hepatitis C virus (HCV) infection because the emergence of the antibody is delayed for several months after infection.
Three tests are commonly used to define hepatitis C status:
- Anti HCV
- HCV RNA
- HCV Genotype
Most commonly, anti HCV is used for screening. However, for diagnosis of suspected infection HCV RNA is performed.
Table 7: Hepatitis C Testing
|Anti-HCV EIA||Positive indicates infection, past or present|
|HCV RNA PCR||Positive indicates current infection|
|HCV genotype||Genotypes 1-6. Often required for insurance pre-authorization for hepatitis C treatment|
HCV, hepatitis C virus; EIA, enzyme immunoassay; PCR, polymerase chain reaction.
False-positive anti-HCV antibodies are occasionally encountered. Confirmation of chronic hepatitis C infection is obtained by the direct measurement of viral products in serum (HCV RNA). HCV RNA in serum definitively establishes the presence of HCV infection and is recommended in all patients with a positive anti-HCV test. Some clinicians have questioned whether the initial screening test for HCV should be an HCV RNA test or an antibody test. Currently, however, because of cost considerations, the initial test for HCV remains an anti-HCV antibody test.
False-negative anti-HCV tests can occur in two clinical contexts: in a patient with a recent infection, in an immunocompromised individual, or an individual receiving hemodialysis. HCV RNA testing is recommended in patients with negative anti-HCV antibody tests but who have liver disease of unknown etiology and are also immunocompromised. In addition, all potential organ donors should be tested for HCV RNA.
Once the presence of HCV is established, the genotype should be determined. There are 6 major HCV genotypes (1-6). Genotyping continues to gain importance for treatment determinations. This is discussed more fully elsewhere in the Hepatitis C chapter.
Iron and Copper Overload Diseases
Diseases characterized by iron overload and copper overload are discussed in detail in the Disease Management (Inherited Metabolic Liver Diseases: Hemochromatosis, Wilson Disease). A practice guideline has been published.
Excess iron may accumulate in the liver and other organs for a variety of reasons. Some individuals have a genetic disorder while others may accumulate too much iron for other reasons. Among the genetic iron-overload conditions, the most common in individuals of Northern European ancestry is related to an autosomal recessive disorder, hereditary hemochromatosis. Before ordering tests it is important to be clear about what question is being asked. Most of the time the question is: Does my patient have iron overload?
This question should be entertained in the following situations:
- Any adult with liver disease, especially men and post-menopausal women
- Patients with symptoms suggestive of or having a family history of HH
The initial evaluation for iron overload includes measurement of serum ferritin, iron, iron-binding capacity, and transferrin saturation levels. Transferrin saturation less than 45%, in addition to normal serum ferritin level usually rules out iron overload (negative predictive value of 97%), and no further testing is necessary. Transferrin saturation greater than 45% and/or a serum ferritin above normal level warrants further investigation. However, these thresholds are low, and most patients who exceed these limits will not prove to have iron overload as explained below.
Limitations of Serum-Based Tests of Iron Overload
Because both iron and ferritin are stored in liver cells, any condition that results in hepatocyte injury and release of intracellular contents into the blood will falsely raise iron, transferrin saturation, and ferritin levels. Therefore, in acute hepatic injury these tests will falsely suggest iron overload. Acute inflammation outside the liver may also falsely elevate the results of serum-based iron tests. Tests of serum ferritin levels, iron, iron-binding capacity, and percentage saturation determined in the setting of markedly elevated aminotransferase levels (AST and ALT), such as those seen in acute viral hepatitis or massive hepatic necrosis, will be identical to those seen in hemochromatosis. Iron studies cannot be interpreted in the face of major elevations of transaminase levels.
Normal serum iron studies do not preclude future iron overload in the genetically susceptible individual. In a young patient with this condition who has not yet had enough time to accumulate iron (especially the premenopausal woman), screening tests for iron overload may be normal, even though the individual is at risk for the subsequent development of iron overload.
When iron overload is found or suspected, the question may become:
Does my patient have hereditary hemochromatosis?
This question should be entertained in:
- Any patient with elevated iron/total iron-binding capacity ferritin values
- Those with a family history of liver disease or of hemochromatosis
It has been known for years that many cases of hemochromatosis are inherited as an autosomal recessive trait. In many cases, a defective gene called the HFE gene is implicated. The presence of this inherited gene results in the production of a protein in which a tyrosine amino acid rather than a cysteine amino acid is present at position 282 of the HFE protein. A second missense gene that results in an aspartic acid (instead of histidine) at position 63 of the same protein may increase iron absorption in some patients. The abnormalities are called C282Y and H63D mutations respectively. Most individuals of Northern European descent with hereditary hemochromatosis usually have two abnormal genes (homozygosity). Most often, two C282Y genes are present, but occasionally a compound heterozygote (C282Y-H63D) will also have excess iron. Homozygosity for H63D does not usually result in excess iron absorption (Table 8).
Table 8: Guidance for the Likelihood of Iron Accumulation with Various HFE Patterns
|HFE Finding||Likelihood of Iron Overload|
|Wild type/wild type (no abnormal genes)||Nil|
|C282Y/C282Y (C282Y homozygote)||High|
|H63D/H63D (H63D homozygote)||Low|
|C282Y/H63D (compound heterozygote)||Moderate|
Confirming a Diagnosis of Hemochromatosis and the Role of Liver Biopsy
Homozygosity for C282Y and compound heterozygosity for C282Y/H63D are diagnostic of HH and a liver biopsy with hepatic iron index (HII) estimation, which was previously the criteria for diagnosis, is no longer needed to confirm the diagnosis of HH in these patients. In addition, HFE gene mutation testing is indicated in all first-degree relatives of patients with hemochromatosis. However, it must be remembered that many individuals have iron overload with normal HFE protein. Pre-menopausal women with C282Y homozygosity most often have no iron accumulation. Finally, there is incomplete penetrance of iron overload in many C282Y homozygotes. In other words, expression of disease may not occur despite having the genetic susceptibility.
HFE gene mutation analysis does not establish either the presence or the degree of liver fibrosis or cirrhosis. Studies have shown that patients with serum ferritin less than 1,000 ng/mL are less likely to have cirrhosis in HH. A liver biopsy is thus indicated in patients with elevated ferritin greater than 1,000 ng/mL or having abnormal liver enzymes. This serves two purposes, determining fibrosis and providing an assessment of iron stores. Because there is an age-dependent increase in hepatic iron in normal individuals, it is necessary to create an index that takes this into account. HII is calculated as follows:
HII = hepatic iron concentration(mcmol/g dryweight) ÷ patient age (years)
HII less than 1.9 is normal; values greater than 1.9 are seen in hemochromatosis. A caveat to this would be in cirrhotic livers, which have the tendency to rapidly accumulate iron in liver disease of other etiologies and cause elevation of HII to a level greater than 1.9. Newer techniques, such as the HIC estimation by proton transverse relaxation time determined by MRI, could be an alternative to liver biopsy, and studies have shown good correlation between the tests. It must be remembered that bone marrow iron stores are not adequate to assess total body iron stores. Cases of hemochromatosis with absent stainable bone marrow iron have been reported.
Although copper may accumulate to moderate excess in the liver in any chronic cholestatic liver condition, it does not appear to be injurious in these conditions. Wilson disease is the main disease in which pathologic copper deposition results in serious liver injury, cirrhosis, and death. In Wilson disease, copper also accumulates in the basal ganglia of the brain, where it produces a wide gamut of neurologic abnormalities. Patients may present with liver disease, brain disease, or both. This disorder is discussed in more detail in the Disease Management (Inherited Metabolic Liver Diseases: Wilson’s Disease).
Wilson disease is rare. Untreated, it is usually fatal before the patient is aged 40 years. Therefore, it is most appropriate to consider this potential cause in a child or young adult with otherwise unexplained liver disease. However, a diagnosis of Wilson disease should not be excluded based on age alone. Laboratory diagnosis is most often based on the finding of a low ceruloplasmin level. Serum ceruloplasmin level of less than 5 mg/dL strongly suggests Wilson disease while any subnormal level warrants further evaluation. Most acute and chronic liver diseases cause the ceruloplasmin level to elevate. There are a few exceptions to this. A patient with acute fulminant liver failure of any sort may no longer have a liver capable of ceruloplasmin synthesis, so that patient may have a low serum level. Similarly, the patient with terminal end-stage liver disease may have a falling ceruloplasmin level. Finally, a few individuals have congenital hypoceruloplasminemia without copper accumulation and are healthy. At the same time, it must also be remembered that a normal serum ceruloplasmin level does not exclude Wilson disease.
In patients in whom Wilson disease is suspected, in addition to serum ceruloplasmin, 24-hour urinary copper levels and slit lamp examination to look for Kayser-Fleischer (KF) rings should be obtained. A serum ceruloplasmin level less than 20 mg/dL, 24-hour urine copper greater than 40 mcg, and the presence of KF rings confirms the diagnosis of Wilson disease. No further testing such as a liver biopsy is needed in this setting.
Copper is present in the serum in two forms: copper that is bound to ceruloplasmin, and free copper or the non-ceruloplasmin bound copper. The total serum copper level is the sum of the levels of these two forms of copper and is usually low in those with Wilson disease. This is partly explained by the decrease in the ceruloplasmin bound copper level that results from a reduction in the ceruloplasmin level in Wilson disease. However, the serum free copper level is typically elevated to ≤25 mcg/dL in patients with Wilson disease and may be approximated as follows:
Serum free copper level = Total serum copper level (ug/dl)l − (3 x serum ceruloplasmin level (mg/dL))
A practical algorithm on the diagnostic tests for Wilson disease in shown in Table 9.
Table 9: Diagnostic Tests for Wilson Disease11
|Level 1 Tests||Level 2 Tests||Level 3 Tests|
|Low serum ceruloplasmin level (<20 mg/dL)||Liver histopathology and stainable copper||Ultrastructural study of hepatocytes|
|Kayser-Fleischer rings||Liver copper concentration (>250 µg/g dry weight)||Mutational gene analysis for Wilson disease|
|Raised serum-free copper level (non-ceruloplasmin-bound) (>25 µg/dL)||Incorporation of radiocopper into ceruloplasmin|
|24-hr urinary copper (>100 µg/24 hr)|
Autoimmune Liver Diseases
The two most common forms of autoimmune liver disease are autoimmune chronic hepatitis and PBC. Ninety percent of those with each disorder are women. Autoimmune hepatitis (AIH) is characterized by very high serum aminotransferase (ALT and AST) levels, whereas PBC is a cholestatic disorder with predominant elevations of the alkaline phosphatase level. Each is associated with autoantibodies in the serum. The treatment for each is different, so accurate diagnosis is essential. Table 10 contrasts the laboratory findings of these two autoimmune liver disorders.
Table 10: Contrasting Features of Two Autoimmune Liver Diseases
|Feature||Autoimmune Chronic Hepatitis||Primary Biliary Cirrhosis|
|AST, ALT||7-10 times upper limit of normal (ULN)||1-3 times ULN|
|Alkaline phosphatase||1-3 times ULN||2-10 times ULN|
|Anti-smooth muscle antibody positive||90% (usually high titer)||10%-20% (usually low titer)|
|Anti-mitochondrial antibody positive||10%-20% (usually low titer)||90%-100% (usually high titer)|
|Liver-kidney microsomal antibody positive||Positive in some cases in which smooth muscle antibody is negative (rare in North America)||Negative|
ALT, alanine aminotransaminase; AST, aspartate transaminase.
Interpretation of autoimmune markers in a patient with liver disease is highly context-dependent. Autoantibodies are common in low titer in a number of acute and chronic liver conditions, such as viral hepatitis. Therefore, the finding of autoantibodies in low titer is not sufficient evidence with which to make a diagnosis of autoimmune chronic hepatitis or PBC. At the same time, low titers do not exclude the diagnosis.
AIH should be rapidly recognized by its propensity to occur in women (90%) and to be associated with high transaminase levels (200 IU/mL or higher). In this disease, elevations of the gamma globulins (especially IgG) are pronounced. A myriad of autoimmune markers may be positive in autoimmune chronic hepatitis, but only a few serological markers have to be assessed: anti-smooth muscle antibody, antinuclear antibody, liver-kidney microsomal antibody and anti-liver cytosol type 1 antibody. High titers of antibodies are suggestive of but on their own they do not establish a diagnosis of AIH.
The diagnosis of AIH can be difficult at times and various factors need to be taken into account. Clinical criteria are usually sufficient to make a diagnosis of or to exclude AIH. Scoring systems have been developed to assist in establishing a diagnosis of AIH. Exclusion of other liver diseases should be undertaken as part of the work up. A liver biopsy at presentation is recommended to establish the diagnosis of AIH and to make treatment decisions.
Primary Biliary Cirrhosis
Primary biliary cholangitis (PBC) is an autoimmune liver disease that involves the intrahepatic small bile ducts. In this condition, serum-based liver tests reveal a predominant elevation of the alkaline phosphatase level. It is associated with the elevation of an autoantibody in high titer known as the anti-mitochondrial antibody (AMA). It has a high sensitivity and a very high specificity. It is reported to be seen in less than 1% of normal people. However AMA has been shown to be present in increased frequency in relatives of patients with PBC. One study showed that the frequency of positive AMA among first-degree relatives of patients with PBC was 13% as compared with 1% in controls. Though positive AMA antibodies may suggest susceptibility to development of PBC, they, on their own even in high titers, do not establish a diagnosis of PBC. Ultrasound or other imaging techniques are necessary in all patients to exclude bile duct obstruction as the cause of cholestasis. Presence of predominant alkaline phosphatase elevation and positive AMA antibody establishes the diagnosis of PBC. Liver biopsy is indicated if the AMA is negative or is in low titers and if associated AIH or NAFLD is suspected. Occasionally, a patient may have features of both autoimmune chronic hepatitis and PBC known as AIH/PBC overlap syndrome.
Non-Alcoholic Fatty Liver Disease
NAFLD is the most common cause of mildly elevated liver enzymes. Please see the chapter on Non-Alcoholic Fatty Liver Disease in Disease Management. NAFLD is defined as the accumulation of fat in the liver in the absence of conditions that cause secondary fat accumulation such as alcoholic hepatitis, medications, metabolic disorders or viral hepatitis. Two types of NAFLD have been described, non-alcoholic fatty liver and non-alcoholic steatohepatitis. The latter has evidence of hepatocellular injury in addition to fat accumulation. Patients with NAFLD are non-alcoholic, usually obese, and have a high BMI.
Liver tests are unreliable guides to the presence or absence of fatty liver disease. When elevated, enzymes show hepatocellular pattern, often with an AST/ALT ratio of less than 1. However, they can be normal. Therefore, liver tests are not useful to make a diagnosis of NAFLD. A history of significant alcohol intake can reliably distinguish between alcoholic fatty liver disease and NAFLD. Imaging is performed to demonstrate the presence of fat in the liver. Liver biopsy is indicated if competing etiologies cannot be ruled out, if a co-existing liver disease is suspected, and for patients at risk of developing cirrhosis.
A scoring system has been developed to identify patients with liver fibrosis in NAFLD. This scoring system comprises of six variables namely: age, hyperglycemia, body mass index, platelet count, albumin, and AST/ALT ratio. The system has been shown to distinguish patients with NAFLD and with or without advanced fibrosis accurately. Certain biomarkers such as serum CK18 have been shown to predict the presence of hepatocellular injury in NAFLD, but further studies are needed to establish their utility.
Noninvasive Tests for Liver Fibrosis and Cirrhosis
Liver biopsy is the gold standard for determining the stage of liver fibrosis and cirrhosis. However, it is invasive and can cause significant complications and sampling error, the latter due to the non-uniform distribution of fibrosis in the liver. In recent years, a number of noninvasive tests have been developed and are being studied to assess liver fibrosis and cirrhosis. Among these, the most widely studied and promising noninvasive tests are hepatic elastography and the serologic markers of fibrosis. Serologic markers can be further divided into direct markers and indirect markers. Direct serologic markers are those that are associated with the deposition of matrix and include procollagen type III amino-terminal peptide (P3NP), type I and IV collagens and matrix metalloproteinases among others. P3NP is found to be the most promising among these markers. It is elevated in both acute and chronic liver disease. Studies have also shown that the serum levels of P3NP reflect the degree of fibrosis in chronic liver disease. However, the test is currently not readily available in commercial laboratories and has not yet been validated for use.
Hepatic elastography is a noninvasive imaging technique used to determine the degree of fibrosis of the liver. Most frequently, ultrasound-based elastrography is performed. It uses a device called Fibroscan which transmits low-frequency waves into the liver. The waves’ velocities are then recorded and are shown to correlate with the liver stiffness. It can be performed either by an ultrasound or MRI. Studies have shown that ultrasound elastography has excellent diagnostic accuracy to diagnosing cirrhosis but does not perform as well to assess fibrosis. Magnetic resonance elastography has been shown to be the most promising noninvasive test as studies have shown that it can assess both the degree of fibrosis in addition to diagnosing cirrhosis. However, its use may be limited by its high cost. In addition, these tests are not yet FDA-approved to be used in the United States. Therefore, liver biopsy still remains the most important tool in the assessment of liver fibrosis and cirrhosis, though the need for it may be significantly decreased in the future with the further development and validation of noninvasive tests.
Elevated Liver Enzymes: Causes & Symptoms
Liver and other organs in the abdomen
What does the liver do and what are elevated liver enzymes?
The liver is the body’s largest internal organ. It is located below the diaphragm on the right side of the abdomen. The liver performs many functions, including the following:
- Produces most of the proteins the body needs.
- Metabolizes (breaks down) nutrients from food to produce energy.
- Prevents shortages of nutrients by storing certain vitamins, minerals, and sugar.
- Produces bile, a substance that helps digest fat and absorb vitamins A, D, E and K.
- Produces substances that help with blood clotting.
- Helps your body fight infection by removing bacteria from the blood.
- Removes potentially poisonous byproducts of certain medications.
What are liver enzymes?
An enzyme is a chemical that accelerates (speeds up) chemical reactions within the body. There are several enzymes in the liver, including alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transpeptidase (GGT). Elevated liver enzymes, found with a blood test, indicate inflamed or injured liver cells.
Why does a doctor check for elevated liver enzymes?
A doctor may order a liver enzyme test if a patient is being treated for liver disease or has a higher risk for liver disease. For instance, if the liver is injured, ALT is released into the bloodstream, and levels of this enzyme would be elevated.
What causes elevated liver enzymes?
Certain diseases or situations can cause a rise in liver enzymes, including:
- Hepatitis (inflammation, or swelling, of the liver).
- Fatty liver disease (a buildup of certain fats in the liver).
- Metabolic syndrome (a collection of heart disease risk factors that increase the chance of developing heart disease, stroke, and diabetes).
- Cirrhosis (the liver tissue is filled with scar tissue).
- Drug abuse.
What are the signs and symptoms of elevated liver enzymes?
Elevated liver enzymes usually have no signs or symptoms on their own. The doctor may check for elevated liver enzymes in patients who might have hepatitis. The symptoms of hepatitis include:
- Jaundice (a yellowing of the skin, whites of the eyes, and mucous membranes caused by liver problems).
- Pain or swelling in the abdomen.
- Nausea and vomiting.
- Dark urine.
- Pale-colored stools.
- Poor appetite.
The doctor may also order a liver enzyme test for patients who:
- Drink a great deal of alcohol or abuse drugs.
- Have a family history of liver disease.
- Are overweight.
- Have diabetes.
Care and Treatment
What is the treatment for someone who has elevated liver enzymes?
Depending on what is causing the rise in liver enzymes, your doctor may advise you to stop drinking alcohol or using certain drugs, lose weight, or eat a healthier diet. If your liver enzymes remain elevated, your doctor may order other tests, or may refer you to a specialist in liver diseases.
Overview of ALT and AST Liver Enzymes
Liver enzymes are substances produced by the liver that can be measured with a blood test. Any elevation in an enzyme level may be a sign of a liver problem, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are two of the enzymes central to such an investigation. When used comparatively, AST and ALT can help identify liver toxicity, liver disease, or liver damage.
Verywell / Elise Degarmo
Roles of AST and ALT
Aminotransferases are chemicals that the liver uses to make glycogen. Glycogen is the stored form of glucose, a sugar that the body uses for energy. Any glucose not immediately used will be converted into glycogen and stored in cells for future use. Most will be stored in the liver, while the remainder will be warehoused in skeletal muscles, glial cells of the brain, and other organs.
Aspartate aminotransferase (AST) is found in a variety of tissues, including the liver, brain, pancreas, heart, kidneys, lungs, and skeletal muscles. If any of these tissues are damaged, AST will be released into the bloodstream. While increased AST levels are indicative of a tissue injury, it is not specific to the liver per se.
By contrast, alanine aminotransferase (ALT) is found primarily in the liver. Any elevation of the ALT is a direct indication of a liver injury, whether minor or severe. Occasional increases may occur in association with a short-term infection or illness. Sustained increases are more problematic as they suggest an underlying disease and a greater likelihood of liver damage.
Normal Lab Values
AST and ALT are measured in international units per liter (IU/L). The normal levels vary based on a person’s body mass index (BMI) as well as the individual lab’s reference value. Generally speaking, the normal reference value for adults is:
- AST: 8 to 48 IU/L
- ALT: 7 to 55 IU/L
The high end of the reference range is referred to as the upper limit of normal (ULN). This number is used to establish how elevated your liver enzymes are.
Mild elevations are generally considered to be two to three times the ULN. With some liver diseases, the level can exceed 50 times the ULN. Levels this high are described as deranged.
While it may seem that a high ALT is all that is needed to diagnose liver disease, its relationship to AST can provide valuable clues as to what exactly is going on and whether the issue is acute (occurring suddenly and progressing rapidly) or chronic (long-standing or persistent).
If the liver sustains an acute injury, you can expect to see a sudden spike in the ALT. On the other hand, if a liver disease is slowly progressing, the damage incurred by the liver will gradually affect other organs as well. As these organs are damaged, the AST will begin to rise.
This occurs with diseases like hepatitis C in which long-term liver damage will trigger an ever-expanding array of symptoms involving the kidneys, brain, eyes, skin, and joints (referred to as extra-hepatic symptoms).
This enzyme relationship can be described diagnostically with the AST/ALT ratio. This is a calculation that compares the levels of AST and ALT in your blood. Depending on which value is elevated and the extent of that elevation, doctors can often get a pretty strong indication as to what disease is involved.
What the AST/ALT Ratio Reveals
The AST/ALT ratio is important insofar as the pattern of elevation can tell a lot about the condition involved. Among the general guidelines used to diagnose liver disease:
- An AST/ALT ratio of less than one (where the ALT is significantly higher than the AST) is suggestive of non-alcoholic fatty liver disease.
- An AST/ALT ratio equal to one (where the ALT is equal to the AST) is suggestive of acute viral hepatitis or drug-related liver toxicity.
- An AST/ALT ratio higher than one (where the AST is higher than ALT) is suggestive of cirrhosis.
- An AST/ALT ratio higher than 2:1 (where the AST is more than twice as high as the ALT) is suggestive of alcoholic liver disease.
However, a disease cannot be diagnosed by the pattern of elevation alone. The magnitude of elevation described in multiples of the ULN also needs to be evaluated. It is only when the magnitude is above a certain threshold that the ratio can be considered diagnostic.
When Testing Is Recommended
AST and AST are part of a comprehensive testing panel known as the liver function test (LFT). An LFT may be ordered:
- If you have symptoms of liver disease, including jaundice, dark urine, nausea, vomiting, and fatigue
- To monitor the progression of a liver disease
- To determine when certain drug treatments should be started
- To assess your response to a liver treatment
Even beyond the scope of liver disease, an LFT can assess whether a drug (prescription or over-the-counter) or an herbal remedy is causing liver injury.
If the lab test is processed on-site, the results can be returned within hours. Otherwise, your doctor will usually receive the results in anywhere from one to three days.
Abnormal Liver Enzymes | Digestive Care Physicians
Abnormal liver enzymes can be a sign of chronic and acute alcohol use, chronic hepatitis B and hepatitis C and possibly liver cancer.
The liver is one of the most important organs in the body, and is responsible for a number of functions that keep the body working as it is designed. The liver detoxifies your blood, produces proteins that help with clotting, handles cellular waste, processes nutrients, stores vitamins, and helps your body make glucose. Liver Enzymes are proteins within the liver that help to speed up certain chemical reactions. If any of these processes are inhibited it could lead to serious complications. Elevated liver enzymes may indicate inflammation or damage to cells in the liver. Inflamed or injured liver cells leak higher than normal amounts of certain chemicals, including liver enzymes.
Abnormal Liver Enzymes Symptoms
Symptoms of mild to moderate elevation of liver enzymes may vary from no symptoms to the following:
- Nausea and Vomiting
- Upper right quadrant abdominal pain and tenderness
- Mental changes
Elevated liver enzymes most commonly found:
- Alanine Transaminase (ALT): In most types of liver disease, the ALT level is higher than AST and the AST/ALT ratio will be low (less than 1). There are a few exceptions; the AST/ALT ratio is usually increased in Alcoholic Hepatitis, Cirrhosis, and in the first day or two of Acute Hepatitis or injury from bile duct obstruction. With heart or muscle injury, AST is often much higher than ALT (often 3-5 times as high) and levels tend to stay higher than ALT for longer than with liver injury. AST is often performed together with the ALT test or as part of a liver panel.
- Aspartate Transaminase (AST): Very high levels of AST (more than 10 times normal) are usually due to Acute Hepatitis, sometimes due to a viral infection. With acute Hepatitis, AST levels usually stay high for about 1-2 months but can take as long as 3-6 months to return to normal. Levels of AST may also be markedly elevated (often over 100 times normal) as a result of exposure to drugs or other substances that are toxic to the liver as well as in conditions that cause decreased blood flow (ischemia) to the liver. With Chronic Hepatitis, AST levels are usually not as high, often less than 4 times normal, and are more likely to be normal than are ALT levels. AST often varies between normal and slightly increased with Chronic Hepatitis, so the test may be ordered frequently to determine the pattern. Such moderate increases may also be seen in other diseases of the liver, especially when the bile ducts are blocked, or with cirrhosis or certain cancers of the liver. AST may also increase after heart attacks and with muscle injury, usually to a much greater degree than ALT.
The human liver contains thousands of enzymes, which are special types of protein cells that help necessary chemical reactions to take place. Liver enzymes trigger activity in the body’s cells, speeding up and facilitating naturally occurring biochemical reactions, and maintaining various metabolic processes within the liver. A wide range of health problems can lead to elevated liver enzymes:
When the liver is damaged, cells release higher levels of the two major enzymes, Alanine Transaminase (ALT) and Aspartate Transaminase (AST), into the bloodstream. To determine if your liver is damaged, several blood tests will be conducted to check the type and amount of Liver Enzymes in the blood. If elevated abnormal liver enzymes are present, it could indicate liver damage, as these enzymes are normally only found within the liver. In most cases, liver enzyme levels are only mildly or temporarily elevated and don’t signal a serious liver problem.
- Physical Examination
- CAT scan (computed axial tomography)
- Liver Biopsy
- Liver Blood tests – Alanine Transaminase (ALT) and Aspartate Transaminase (AST)
The liver helps maintain good health and is important for many body functions including digestion, metabolism, detoxification and blood clotting. Liver Enzymes are proteins that help to speed up reactions, and elevated levels are signs of a liver impairment that must be treated. While a variety of conditions and some medications can cause enzyme imbalances in the liver, diet also plays a crucial role.
|Lifestyle Changes||Food to Add||Food to Avoid|
|Stop drinking alcohol||Garlic||Sugar|
|Limit caffeine||Eggs||White bread|
|No non-prescription drugs||Broccoli||Pasta|
|No fast food||Spinach||Pastries|
|Take fish oils||Brown Rice||Desserts|
|Increase fiber intake||Mustard Greens||Fried food|
|Eat whole foods||Fruit||Processed food|
Are You Drinking Too Much? How Alcohol Consumption Can Affect Your Health
Many people enjoy a drink now and then. But how is that alcohol affecting your body? The liver is where a lot of your metabolism lives. It filters out harmful substances, like alcohol and toxins, from your blood. But its duties don’t end there. It processes what you eat and drink into energy and nutrients for your body, produces bile to help you digest those nutrients, stores blood sugar in the form of glycogen, and performs many other essential functions. So a healthy liver is critical to your overall well-being and performance. But how can you find out whether your liver is healthy, or whether you may have pushed it too far? Well, the best way to monitor your liver health is through a blood test for liver damage biomarkers, such as ALT.
Found primarily in your liver cells, ALT is an enzyme that plays a role in converting stored glucose into usable energy. When liver cells are damaged, ALT can leak out into your bloodstream. Normally, there is only a small amount of ALT in your blood; higher levels of ALT typically indicate liver injury or inflammation
The normal range for ALT is 10-40 units per liter (U/L) of blood for men and 7-35 U/L for women. Blood tests from InsideTracker will tell you your optimal range for ALT based on your age, gender, ethnicity, athletic activity, alcohol consumption, BMI, and smoking history. And if your levels of ALT are elevated, InsideTracker will recommend diet, lifestyle, and supplement changes that can help to reduce your ALT levels. Since high levels of ALT indicate liver damage or disease, it’s important to consult your physician if you have elevated ALT.
Many lifestyle factors can influence your ALT levels, including:
One of the more frequent causes of high ALT levels is a condition commonly referred to as a fatty liver, which is a reversible condition that occurs when large amounts of triglycerides (the type of fat typically found in food) accumulate in liver cells. In the United States, alcohol abuse is one of the largest contributors to fatty liver, but other causes include elevated blood glucose and excess body weight. Disease and certain medications can also increase ALT.
The good news is that many people can lower their elevated ALT with changes in their lifestyle and exercise:
InsideTracker will recommend personalized lifestyle changes to help you decrease your ALT.
What you eat also has an effect on ALT. Limiting high-fat foods, especially ones that are derived from animal sources, may help decrease elevated ALT levels. High-fat foods increase fat levels in your blood, which may end up being deposited in the liver.
Helpful changes can include:
- Choosing lean proteins, such as chicken breast, fish, or beans, and low-fat dairy products.
- Reducing the refined carbohydrates and sugars in your diet. Instead, eat whole foods like beans, whole grains, berries, oatmeal, and vegetables, which provide fiber, vitamins and antioxidants.
- Eating foods high in folate, which studies have shown can help to reduce ALT and improve liver health. Foods include black-eyed peas, fortified breakfast cereals, Brussels sprouts, and avocado.
With an InsideTracker Ultimate test you can easily check whether you have elevated ALT, and learn how to improve your liver health using simple interventions such as food, supplement, exercise, and lifestyle changes.
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Elevated Liver Enzymes in Children: Symptoms, Diagnosis and Treatment
How Are Elevated Liver Enzymes Diagnosed in a Child?
High liver enzymes may show up on a routine blood test during a child’s yearly checkup. A health care provider may also test for elevated liver enzymes when a child is feeling unwell. This is especially true if a child has abdominal pain, vomiting, diarrhea, or jaundice (yellowish color of the eyes or skin).
What Does a Diagnosis of Elevated Liver Enzymes in a Child Mean?
Liver enzyme levels alone are not enough to tell exactly what is wrong with the liver. This is why it is very important to follow up with a child’s health care provider. If high levels of liver enzymes are found, more tests can help determine the cause.
The reason for elevated liver enzymes sometimes appears to be fairly clear. For example, your child’s health care provider may decide that the elevated liver enzymes are probably due to a virus. In these cases, your child’s health care provider may want to wait and see what happens. As the illness clears up, elevated liver enzymes should return to normal levels.
Seeing a Specialist
It is rare for a primary health care provider to not be able to explain why liver enzymes are elevated. However, occasionally your child’s health care provider may suspect something more serious. If so, a doctor who specializes in liver diseases (hepatologist) can help.
Specialized care starts with taking a careful history, and then a physical exam to check for outward signs of liver disease. Such signs may include jaundice or an enlarged liver or spleen.
If liver trouble seems likely, additional tests may include:
- Other liver tests to compare levels of ALT and AST with alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), bilirubin, albumin, prothrombin time etc.
- Specialized lab tests to look for specific diseases, such as celiac disease, autoimmune hepatitis, alpha-1 antitrypsin deficiency, Wilson disease, and viruses such as hepatitis B, hepatitis C, EBV or cytomegalovirus (CMV)
- Imaging tests, such as ultrasound, computerized tomography (CT) or magnetic resonance imaging (MRI), to examine the liver, blood vessels, and nearby organs – especially the spleen.
- Liver biopsy (under anesthesia) to remove a tiny piece of the liver that will be examined under a microscope
Once complete, all of these tests help paint a more complete picture of a child’s liver. This can point the way to the correct diagnosis.
Secondary iron overload syndrome
Early detection and treatment of secondary iron overload syndrome in patients with chronic liver disease prevents the progression of liver disease to cirrhotic stage and significantly reduces the risk of liver cancer. We successfully treat patients with obesity and non-alcoholic fatty hepatosis (non-alcoholic fatty liver disease) and chronic hepatitis C in combination with secondary iron overload syndrome.
The center’s gastroenterologists have created an author’s method of identifying and treating secondary overload syndrome in patients with chronic liver diseases.Our gastroenterologists share their experience in scientific and practical seminars and in scientific articles.
Treatments for secondary iron overload syndrome in chronic liver disease include :
- treatment of the underlying disease;
- adherence to a diet with limited iron content to 8-10 mg / day;
- therapeutic phlebotomy in the absence of contraindications;
- use of antioxidants.
90,011 strict abstinence from alcohol;
Specializes in the diagnosis and treatment of secondary iron overload syndrome in patients with chronic diseases in our center, Candidate of Medical Sciences, Associate Professor of the Department of Hospital Therapy, St. Petersburg State Medical University. Academician I.P. Pavlova, hepatologist Mekhtieva Olga Alexandrovna .
Once diagnosed with iron overload syndrome, treatment options are fairly straightforward for most people . However, without treatment for this condition, life-threatening damage to organs and tissues, and above all to the liver, can develop.Thus, it is important to detect iron overload before organ and tissue damage due to iron accumulation occurs.
There are a number of laboratory tests that are used to detect iron overload. These are, first of all, the level of ferritin and the percentage of saturation of transferrin with iron in the blood serum. All patients with elevated values of these indicators should undergo genetic testing to exclude the primary syndrome of iron overload – hereditary hemochromatosis. All tests for the diagnosis of iron overload syndrome can be taken at our center .
The patient will receive
as a result of treatment
- No symptoms and improved quality of life.
- Prevention of complications and improvement of well-being.
- Normalization of laboratory analysis indicators.
- Elimination of risk factors for the development of dangerous diseases.
Tips and tricks
With iron overload syndrome, it will help to reduce the amount of excess iron in the liver diet with limited intake of iron .
Iron overload diet
Secondary iron overload syndrome is a pathological condition in which the level of iron in the body increases above the permissible norm, excess iron begins to accumulate in organs and tissues, which leads to their damage. Most often, secondary iron overload syndrome develops in liver disease, obesity and metabolic syndrome and is characterized by an increased level of serum ferritin.
How does liver health affect performance – Society
Have you noticed weakness, drowsiness, irritability, decreased attention and low mood? These symptoms are often attributed to a sleepless night, the result of a busy day at work, or vitamin deficiency. And, as a rule, you do not pay attention to them until some trouble happens. Then there is a reason to think about what is really going on.
One of the probable causes is an increase in ammonia in the blood.This happens due to a violation of the liver, which ceases to cope with cleansing the body of toxins. Let’s figure out where this molecule known from school comes from in the body and how its presence affects the performance and well-being of a person.
What’s going on?
Ammonia is formed in our body in the course of life and is a toxin, its excess is removed by the liver. If something is wrong with the liver, the main filter of the body, detoxification processes are disturbed and the level of toxic ammonia in the blood rises, ammonia reaches the brain and inhibits its work.Ammonia is dangerous for the liver itself, as it can aggravate its condition.
No matter how strange it may sound, we ourselves may be to blame for the fact that a large amount of ammonia accumulates in our body. The protein diet, which is so loved by lovers of a healthy lifestyle and athletes who want to build muscle or get rid of excess fat, is often one of the reasons. This also includes the regular use of alcohol, fatty foods, as well as active physical activity and systematic intake of medications.All this creates additional and sometimes excessive stress on the liver, which reduces its ability to cleanse from toxins.
Fans of a sports lifestyle should remember that increased ammonia reduces endurance during sports training, slows down the recovery process between classes. Stiffness and pain in muscles after jogging or playing, feeling tired are also partly his fault.
The toxin inhibits the functions of the brain, which negatively affects concentration and reaction speed.This should be paid attention to employees of large enterprises, financiers, managers and other office workers who may have a drop in performance.
Increased ammonia in the body is a great danger for motorists. Several years ago, in the course of an independent Smart Radar study, in which 42 drivers aged 20 to 45 with at least three years of experience took part, Russian scientists proved the relationship between an increase in the frequency of traffic violations and the presence of liver diseases.It turned out that all participants in the study with the initial stages of liver disease had an increased level of ammonia in the blood, which negatively affected concentration and led to traffic violations and accidents.
How to protect the liver?
In order not to accumulate ammonia in the body, do not overload the liver – to abuse fatty foods, alcohol and protein supplements when playing sports. Simple rules to follow to make your liver healthy. If problems have already arisen, then you can use a proven remedy – the German hepatoprotector-detoxifier “Hepa-Merz”.It contains the active substance L-ornithine-L-aspartate, which decomposes into natural amino acids ornithine and aspartate 20-25 minutes after ingestion and begins to solve the problem.
The drug reduces the increased level of ammonia in the body, improves liver performance and test parameters, restores metabolism. The standard course “Hepa-Merz” lasts one month, but the manufacturer promises the first results in 10 days. “Hepa-Merz” is the winner of the Russian Pharma Awards in the category “A drug that has a positive effect on liver function”.
How do you know when it’s time to check your liver health?
Liver diseases are difficult to detect in the early stages, therefore, the presence of symptoms characteristic of an increased level of ammonia in the body may be a reason to see a doctor. Another way to find out about the problem is to take a test, which in just 40 seconds will help you know if you should be worried. For the result to be accurate, it is better to be tested several times, in the morning, at intervals of a couple of days.
If the test fails several times in the allotted time, you should consult a doctor and make an analysis to determine the activity of the liver enzymes ALT, AST, GGTP.And for prevention, experts recommend taking biochemical blood tests and doing an ultrasound of the liver at least once a year. This is especially important for people whose work requires maximum concentration.
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Enzymes and their functions
A number of chemical transformations of substances coming from the outside constantly take place in the body. These reactions can only take place in the presence of certain catalysts.The latter, in turn, are presented in the form of substances of a protein nature – enzymes. They speed up the metabolic process and help to achieve balance. Thanks to the action of enzymes, the reactions taking place in the body are accelerated hundreds of times. A change in the concentration of these substances in the body indicates the development of very dangerous diseases. In this case, the activity of enzymes decreases much earlier than more obvious signs of the disease appear. This type of analysis allows you to accurately diagnose the presence of a particular disease and start treatment in a timely manner.In our laboratory you can go through all the necessary research.
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Properties of enzymes:
- First of all, as mentioned above, enzymes directly affect the rate of chemical reactions taking place inside the body.
- Specificity of action. Since a huge number of reactions constantly occur in the body, to accelerate each of them, its own special enzyme is produced, which cannot act on other processes. Due to the specificity of the action, two groups of enzymes are distinguished:
- relative – the enzyme catalyzes a certain type of reaction;
- absolute – when the enzyme is responsible for the course of only one reaction.
- The activity of enzymes characterizes their ability to speed up reactions in the body to varying degrees.This indicator depends on the following factors: temperature, pH of the medium, etc.
Types of tests for enzymes
Alanine aminotransferase (ALT) is a liver enzyme and is involved in the exchange of amino acids. When the cells of the kidneys, liver, skeletal muscles and heart muscle are destroyed, the concentration of ALT in the blood increases. Test results may indicate the following diseases:
- viral hepatitis A and other types of hepatitis;
- cirrhosis or liver cancer;
- liver damage to toxins;
- chronic alcoholism;
- myocardial infarction;
Amylase is produced in the pancreas and salivary glands. Provides the breakdown of carbohydrates entering the body along with food. An increased content of alpha-amylase is a symptom of the following diseases: cyst, peritonitis, pancreatitis, mumps, diabetes mellitus, renal failure. Also, an increase in alpha-amylase occurs with abortion or abdominal trauma. Pancreatic amylase is synthesized in the pancreas. Its level increases with injuries of the pancreas, acute pancreatitis, renal failure, alcoholism, ulcers.
Aspartate aminotransferase (AST) – an enzyme that is found in the nervous, skeletal tissues, as well as in the cells of the heart, kidneys, liver and other organs. The results of the analysis can give both increased values (with liver cancer, hepatitis, heart failure, angina pectoris), and also show a low level due to rupture of the liver and serious diseases.
Creatine kinase is part of the cells of the brain, lungs, thyroid gland, skeletal muscles, heart muscle.An increase in creatine kinase is noted when there is a disruption in the work of any of the listed organs. Most often, an increase in activity is observed in acute myocardial infarction, diseases of skeletal muscles, brain, hypothyroidism.
Lipase is synthesized by the organs for the breakdown of fats. The analysis is carried out to detect and diagnose diseases. An increased lipase content in the blood indicates the presence of the following diseases:
- gallbladder disease;
- breast cancer;
- renal failure;
A decrease in level occurs in the case of oncological diseases.
Cholinesterase is produced in the liver. A cholinesterase test is done to assess liver function or in case of insecticide poisoning. The enzyme content decreases sharply in severe liver diseases, myocardial infarction, cirrhosis, oncological diseases, hepatitis (for example, in hepatitis B). A decrease in the level of this enzyme is characteristic in the last stage of pregnancy, while its increase is noted at the initial stage.Increased cholinesterase is a symptom of the following diseases: obesity, breast cancer, tetanus, diabetes mellitus, alcoholism, manic-depressive psychosis, neuroses.
Alkaline phosphatase takes part in the exchange of phosphoric acid. An analysis is carried out to diagnose diseases of the liver, skeletal system. An increase in alkaline phosphatase occurs in myeloma, rickets, infectious mononucleosis, bone lesions, liver diseases, decrease in is a sign of a lack of vitamins, magnesium, zinc, anemia.When monitoring pregnancy, an alkaline phosphatase test is also performed. A decrease in its activity occurs in case of insufficient development of the placenta.
Failed while taking blood. The girl-laboratory assistant reacted very quickly and correctly, brought her to her senses, encouraged me. It’s nice when they treat you carefully)
Sincerely, I want to thank the doctor Azizov Magomed Alievich For many years I suffered from varicose veins I did not know which doctor to turn to. I started looking for specialists on the Internet. it was to this doctor that the treatment was painless.and accurately explained everything clearly, commented on every movement I answered all my questions Thank you for your professionalism and sensitive attitude towards patients
Nikolaev Arseny Vitalievich
Good afternoon! I would like to thank the traumatologist Riahi Aymena for his professionalism and high responsibility in his work! Damaged ligaments, for the first time in my life, I was very worried.At the very first visit, I received qualified help and recommendations for a speedy recovery. I am a very curious person and I was pleasantly pleased with the fact that I was able to get answers to all my questions related to stretching (like an injury), materials for fixing the leg, etc. This is a very important quality of a doctor when he can explain processes from his sphere in a professional, but at the same time understandable language for a common man in the street.
Thank you MediCenter for your attitude towards recruiting!
In July 2020, he broke his arm, turned to the traumatology department at the Meditsentr on Okhtinskaya Alley, d18 for help. A month and a half was observed in this traumatology. I want to express my deep gratitude to traumatologists working in trauma for the qualified and timely treatment. I was very pleased! The center is modern, very qualified and friendly staff, modern equipment, very good organization of treatment, attached under the compulsory medical insurance.Thank you!
Saibel Olga Evgenievna
I, Saibel Olga Evgenievna, born on 05.04.1976, I earnestly ask you to reward all doctors, junior medical personnel and administrators of the clinic LLC “Medicenter YuZ”, St.Murino, Okhtinskaya alley, 18, for a huge contribution to saving my life.
I have been diagnosed with cancer of the sublingual region of the oral cavity. Absolutely all the medical staff of this clinic provided me not only with qualified medical care at the highest level, but also went beyond the scope of official duties, showing human sympathy, correct attitude and sincere interest in providing me with maximum assistance on the path to my recovery.
Thank you very much!
Thank you very much!!!
Good afternoon! I would like to thank the MediCenter Clinic (on Polikarpov alley) and the ENT doctor Tatyana Viktorovna Ershova for their work.I first came to Tatyana Viktorovna’s appointment in 2016. From that moment on, if I have problems with my throat or nose, I turn only to Tatiana Viktorovna. Always attentive to the described symptoms and a thorough examination, referrals for tests that clarify the condition and, as a result, correct treatment.
Anesthesia and your pet | Vedeneev’s veterinary clinic
Anesthesia and your pet
There are three main reasons for examining your pet prior to anesthesia:
1.Helps to create the safest anesthesia protocol
If the results are normal, then the anesthesia can be started without any hesitation. If not, then the anesthesia should be discontinued or other precautions taken to keep your pet healthy.
2. Helps to reveal hidden diseases
Animals can look quite healthy even if there is an underlying disease or ailment.The study helps to identify the disease before clinical signs appear. Early detection will allow timely medical intervention and improve the result of treatment.
3. Keeps your pet healthy in the future
The test results are saved in the medical record of the animal and serve as a source material for further examination. This helps to more accurately identify violations in the study of blood in the future.
1.Blood tests help you create the best anesthesia protocol for your pet
In addition to taking a detailed history, we will conduct a physical examination of your pet. Since the condition of internal organs and blood cells cannot be assessed in other ways, we recommend that you carry out a blood test when assessing the health of your pet. The blood test will include various indicators depending on the age and disease of the pet.
Complete blood count (CBC) The CBC contains detailed information about red and white blood cells and platelets.The total white blood cell count, along with the differential formula, helps to detect hidden pathologies, including stress response, inflammation, inability to fight infection, and leukemia.
A low platelet count indicates a possible clotting disorder. It is recommended to postpone the operation in case of anemia, inflammation and, especially, with a low platelet count, since these pathologies can lead to the development of dangerous postoperative complications.
Alkaline Phosphatase (ALP) An enzyme found in many tissues, including liver and bone. Increased importance occurs with liver disease, Cushing’s syndrome, or steroid hormone therapy.
Total protein (OB) The value of OB changes in many conditions, including dehydration, inflammation, and liver, kidney, or bowel disease.
Blood urea nitrogen (BUN) BUN is produced in the liver and excreted by the kidneys.Excessively elevated levels indicate kidney disease or dehydration. Low levels may be due to liver disease.
Creatinine (CREA) Creatinine is a byproduct of muscle metabolism and is excreted by the kidneys. An elevated level indicates kidney disease, urinary obstruction, or dehydration.
Blood glucose (GLU) An increase occurs in diabetes mellitus. In cats, an increase also occurs with stress, which may be caused by visiting a veterinary clinic.Low levels occur with liver disease or certain tumors.
Albumin (ALB) A protein that is formed in the liver. A decrease in the concentration of this protein indicates chronic liver, kidney, intestinal disease, or inflammation.
Cholesterol (COL) Increased cholesterol has been reported in many pathologies, including hypothyroidism and liver or kidney disease.
Total bilirubin (OBIL) Bilirubin is a breakdown product of hemoglobin and is part of bile.It is important to measure the level of bilirubin in the blood to rule out liver disease and some types of anemia.
Amylase (AMYL) An enzyme that is produced in the pancreas. The pancreas produces amylase to aid in the digestion of food. An increase in the concentration in the blood indicates its pathology.
Lipase (LIP) An increase in the concentration of lipase in the blood, combined with the clinical picture, to a large extent confirms pancreatitis, gastrointestinal tract pathology or the intake of certain medications.
Phosphorus (Phos) An increase in phosphorus occurs in kidney disease.
Calcium (Ca2 +) An increase in calcium is observed in diseases of the parathyroid glands and kidneys, as well as in some types of tumors.
Sodium, Potassium, Chlorine (Na +, K +, Cl-) The balance of these electrolytes is extremely important for your pet’s health. Deviations may be due to life-threatening conditions.Electrolyte testing is especially important for symptoms such as vomiting, diarrhea, and heart failure.
(OAM) Urine contains byproducts of many organs, including the kidneys, liver and pancreas. Changes in the concentration of these by-products occur in diabetes mellitus, as well as in diseases of the liver or urinary tract.
Thyroxine (T4) Measurement of thyroid
hormone in the blood to detect thyroid disease.Thyroid disease can occur in both cats and dogs and can be serious without timely treatment. It is especially important to conduct this study in cats over seven years of age.
1. Study of coagulation for the assessment of thrombus formation
2. Cardiopet proBNP: heart overload rate
3. Electrocardiogram (ECG): assessment of the electrical activity of the heart
four.Feline Immunodeficiency Virus (FIV) and Feline Leukemia Virus (FLV)
5. SBK: assessment of renal function
2. Helps to reveal latent disease
A blood test helps to assess the state of internal organs, which cannot be determined using the senses (eyes, ears) or fingers during a clinical examination.
Biochemical research helps to determine:
– dehydration (in cats)
– Cushing’s syndrome (in dogs)
– obstruction of the biliary tract (in cats)
– violations against the background of prolonged use of drugs
Heart and lungs
Immunological analysis helps to identify heartworms – an infectious pathogen that leads to damage to the heart and lungs.
A T4 test can help identify thyroid disease.
Examination of the teeth reveals the pathology of the teeth and soft tissues of the oral cavity. Diseases of the oral cavity can occur secondarily with another pathology.
Examination of the teeth reveals the pathology of the teeth and soft tissues of the oral cavity.Diseases of the oral cavity can occur secondarily with another pathology.
Blood and urine tests can reveal:
– early kidney disease
– renal failure
– violations against the background of long-term use of drugs
Urinalysis and urine protein-to-creatinine ratio are also used to determine:
– functioning of the kidneys and urinary tract
– kidney infection
Pancreas and intestines
Biochemical research helps to determine:
– pancreatitis (inflammation of the pancreas)
– diabetes mellitus
– violations against the background of long-term use of drugs
Fecal examination reveals parasites that cause:
– weight loss
– blood loss
– infections in humans (zoonoses)
UAC is used to determine:
– anemia (decrease in red blood cells)
– bleeding disorders
– inability to fight infection
– water balance
3.Keeps your pet healthy in the future
When performing a diagnostic examination, veterinary surgeons usually compare the results with the values of the reference interval in order to detect possible deviations.
The reference interval (or range) corresponds to most normal blood values in a healthy animal. However, since the range of these values is quite wide, significant differences are possible within one reference interval, which correspond to a certain dynamics.
Dynamics provides valuable insight into hidden abnormalities that may not be clinically apparent. Sometimes the nature of changes can be identified only in dynamics. Early diagnosis and treatment increases the chances of your pet having a positive prognosis. Examination before anesthesia allows you to determine the initial level and then monitor its change in order to maintain the health of the animal.
Like humans, the health of cats and dogs changes with age.Since animals age faster than humans, changes in basic health indicators can also occur quickly.
The main laboratory of the body: everything about the liver
How to help the main filter of our body – the liver, and why we harm it without even knowing it, Ekaterina Stepanova, a specialist in preventive medicine, told Sputnik Belarus.
Depression? Check the liver
The liver is called the main laboratory of the body, it is supplied with blood, which it receives from two sources.About 80% of blood with prepared nutrients, but also with poisons, medicines, processed products, comes through the portal vein, collecting from the small and large intestines and other participants in digestion. The remaining 20% of blood traffic is arterial oxygenated blood that comes from the heart.
In addition to the general filtration of everything that we have consumed, another task of the liver is the production of bile, which is indispensable for digestion, including for the emulsification of fats. Bile is stored in a small reservoir under the liver – the gallbladder.
Every minute, if an adult is healthy and active, about 1 liter of blood flows through the liver. There it is filtered and enters the systemic circulation.
If the blood is good and the liver is healthy – we are active, happy and cheerful! This is important because a damaged or diseased liver can cause a wide variety of diseases, including depression.
How the liver works
The liver is the best nutritionist for the body. She participates in all exchange functions.We know only the approximate norms of proteins, fats, carbohydrates, etc., and our liver verifies everything for us individually. The excess is stored or converted. For example, if we go too far with carbohydrates, the liver processes them into proteins or fats, and stores excess glucose in the form of glycogen, suddenly the body will have to starve.
And if she feels a lack of nutrients, she will open her bins, and urgently will enter the blood: glucose, vitamins A, B, D, iron. This mechanism is used by all living things in nature.In many animals, for example, a bear and a frog, the liver enlarges by autumn, they go into hibernation, while spending the accumulated liver reserves in winter or during a hunger period.
What the liver can suffer from
Modern man does not always fit into the norms of the physiology of life and is often the most dangerous enemy for himself and his liver.
Alcohol. No matter how much a person drinks alcohol – a glass, a glass, half a bottle, this amount will be distributed over the total volume of blood.Once alcohol has entered the bloodstream, the liver slows down to pick up the alcohol. Additional resource filtration mechanisms are included in order to have time to neutralize alcohol. In the liver, as a result, blood flow slows down, and problems begin.
For example, a liter of blood entered the liver, but only half a liter came out, since blood flows to the liver from below, the rest of it is waiting in the wings below the liver, in the pelvic organs, the veins of the lower extremities. The blood flow rate is impaired and the volume of waiting blood increases.
Over time, varicose veins form. We have veins not only in the legs, but also in the small pelvis, in the rectum – the expansion of its veins, for example, causes hemorrhoids.
Small vessels – capillaries – also swell, a vascular mesh appears on the body, more often on the legs (where the blood stagnates in anticipation). Therefore, when this happens, you should not look for a problem in the vessels – you should take care of the liver and the speed of blood flow in it.
What factors slow down blood flow in the liver
First of all – a change in the cells of the liver itself – cirrhosis.There are no voids in the body. If a liver cell has died (melted) from toxins or alcohol, then a connective tissue cell will take its place. Such a cell has no filtering function. The liver becomes like a filter with a broken cartridge – connective tissue instead of filtering cells. There is a redistribution of blood and again there are problems with the veins below the liver.
What are the symptoms that indicate that the liver is suffering:
- nausea; headache, sometimes migraines;
- temperature rise; dizziness;
- dry, bitter mouth;
- intolerance to fatty foods;
- light or fatty feces; heaviness in the right hypochondrium;
- yellowness of any part of the body; anger;
- irritability, it is not for nothing that such people were previously called “bilious”;
- rapid intoxication; vomiting; smell from the mouth;
- skin pigmentation, uneven tan; vascular red asterisks.
- But the most important symptom that should alert you is weakness, because the liver is the main energy organ!
How to examine the liver
To understand how to help yourself, you need to know that negative things can happen in the liver: parasites can live: lamblia and opisthorchias (protozoa), worms – toxacaras and pinworms; there may be viruses A, B, C cytomegalovirus; fungi, bacteria – staphylococci, which cause inflammation; chemical and toxic damage to cells.
All this is called chemical, physical or biological poisoning, in which liver cells are affected. It is impossible to help the liver without a diagnosis. In this case, it is more important than with any other organ!
To examine the state of the liver you need:
1. Make an ultrasound of the liver.
2. Pass a biochemical blood test, which should contain bilirubin – (reflects the level of intoxication, its norm is 19-21, while there should be no direct bilirubin), ALT, AST (indicators of destruction of liver cells, norm 21-24)
3.Get tested for viruses A, B, C, lamblia, opisthorchis, toxacara and echinococcus by blood ELISA.
These three points are a mandatory set of liver examinations, the subsequent ones can be done at will, they will significantly increase the likelihood of the effectiveness of treatment. 4. Radioisotope scanning of the liver. 5. MRI or tomogram. Cytomegalovirus contributes to the development of an autoimmune disease – vitiligo. All pigments on the skin are also the cause of liver cell damage.
How to help the liver
First of all, control the power supply.It is better to do it voluntarily, until the illness resolves it for you. Try to exclude from the diet foods with dyes, preservatives, genetically modified ingredients. Try to eat a low-calorie diet for 7-10 days each month. The liver produces allergies well, so try to eat as simple as possible. Best of all – without the use of flavors, and this even applies to tea.
It is also necessary to undergo antiparasitic cleansing, but first you need to pass tests in order to understand how and with whom to fight.Depending on which parasite is detected, you will have to behave with it differently. In the presence of lamblia and opisthorchus, for example, low-calorie diets are contraindicated, because if these protozoa do not receive food, they will begin to feed on liver cells.
In case of any changes or diseases of the liver, alcohol is strictly prohibited. If you went through all the procedures sequentially – you were examined, you removed intoxication, including with tyubages, you follow a diet, drink herbal decoctions and lecithin, then the liver cells will begin to recover.This is the great strength of our body – the cells of all tissues, except perhaps the lens of the eye, are capable of renewing.
So, if you want to have a beautiful tan, be always in a good mood, full of energy and not suffer from varicose veins and hemorrhoids – take care of your liver, do not irritate it. After all, only by living in unison with our body, we extend our life.
Take care of the liver!
“No body can be so strong,
that wine cannot defeat it”
Drinking regularly is harmful – anyone knows this, even a person infinitely far from medicine.And when it comes to diseases caused by excessive consumption of intoxicating drinks, as a rule, the first thing to remember is cirrhosis of the liver. Indeed, the doctor is faced with a difficult task when the patient comes to him already with “ready” cirrhosis, manifested by a violation of the structure and function of the organ. You can help at this stage, but still you should not bring the disease to cirrhosis. It is much better for both the doctor and the patient when the liver changes are still minimal and reversible.
Of all foods that a person has ever consumed, alcohol is the most frequently associated with the development of addiction.Alcoholism is a widespread disease in many countries.
The actual problem, which narcologists are increasingly talking about, is beer alcoholism. The barley from which beer is made is a healthy product. It contains proteins, fats, carbohydrates and vitamins. But fermentation microbes in beer wort kill all these beneficial properties, using them for their own growth and reproduction. They treat beer much more easily than vodka. In situations where “drinking vodka” means “being an alcoholic,” beer is often perceived as harmless entertainment.
The liver is most susceptible to the negative effects of alcohol, since it metabolizes most of the ethanol. This was the reason for the allocation of alcoholic liver damage into a separate nosological form – alcoholic liver disease (ABD).
Alcoholic liver disease is a combination of clinical symptoms and pathological changes in the liver caused by alcohol (ethanol).
ABP risk factors
There are specific risk factors for the development of alcoholic liver damage.
First, the average daily dose of ethanol, the duration and continuity of its use, matters. Alcohol is classified as a direct hepatotoxic agent and its dangerous and safe doses have long been determined:
Dangerous risk mode:
- daily consumption> 40 g / day ethanol – for men> 20 g / day ethanol – for women
Low Risk Mode:
- – not> 20 g (men) and not> 10 g (women) ethanol / day
- – no more than 5 days a week
- – Recommended 2 days abstinence from alcohol
1 drink (10-13 g ethanol) = standard alcohol dose:
- 1 can of beer (330 ml 5% ethanol)
- 1 glass of wine (140 ml 12% ethanol)
- 1 shot of vodka (40 ml of 40% ethanol)
The development of ABP does not depend on the type of alcoholic beverages and is determined by the dose of ethanol entering the body.However, no direct correlation was found between the degree of liver damage and the amount of alcohol consumed. Less than 50% of people who drink alcohol in dangerous doses suffer from severe liver damage – hepatitis and cirrhosis. This indicates that, in addition to the direct toxic effect of ethanol, other factors are involved in the pathogenesis of alcoholic illness.
Secondly, the female sex is a risk factor for the development of alcoholic liver damage. There is a hypothesis that this is due to a lack of gastric alcohol dehydrogenase (ADH), as a result of which a greater amount of ethanol enters the hepatocyte of a woman, while in men some of it is metabolized in the stomach.Currently, it is believed that the Kupffer cells of women under the influence of estrogens are more sensitive to endotoxins, the transport of which against the background of alcoholism through the intestinal wall is increased.
Third, genetic factors are important, namely, hereditary polymorphism of enzymes that metabolize alcohol (ADH and aldehyde dehydrogenase – ALDH). For example, persons of Asian descent often inherit the “slow” isoenzyme of ADH, and therefore, they have an increased level of acetaldehyde (the main metabolite of ethanol) in the blood serum.When drinking alcohol, these people often have dysphoria, severe nausea, facial flushing. This may explain the rare development of alcohol addiction in this group.
Fourth, overweight is currently an independent risk factor for ABD. The likely cause is additional fat deposition in hepatocytes in obese people, which increases oxidative stress.
Fifth, it should be noted that regular alcohol consumption increases the risk of infection with the hepatitis C virus, which affects the severity of alcoholic liver damage.In alcohol-dependent individuals infected with the hepatitis C virus, the liver is damaged at a younger age, with lower cumulative alcohol doses, with more severe morphological changes and higher mortality.
There are four main forms of ABD: steatosis, hepatitis – acute and chronic, fibrosis and cirrhosis. The most common form of liver damage is steatosis. Alcoholic hepatitis and cirrhosis develop in approximately 25% of patients with chronic alcoholism.Many experts believe that most patients with liver cirrhosis go through the alcoholic hepatitis stage. In some patients, cirrhosis develops due to the occlusion of terminal hepatic venules, i.e. development of perivenular fibrosis, which may already be at the stage of steatosis and lead to the formation of cirrhosis of the liver, bypassing the stage of hepatitis.
Clinical presentation of ABP
Clinical signs of ABD range from the complete absence of any symptoms to the classic picture of severe forms of liver damage with symptoms of liver failure and portal hypertension.At the stage of steatosis, an enlarged liver of a soft consistency is detected either accidentally or with complaints of recurrent pain in the right hypochondrium. The diagnosis is confirmed by a biochemical blood test and an ultrasound scan. At the stage of hepatitis and cirrhosis, patients often complain of weakness, lack of appetite, nausea and vomiting, disturbances in the rhythm of sleep and wakefulness, decreased libido, increased body temperature, etc. There are no physical signs pathognomonic for ABP. Most often, when examining a patient, gynecomastia, testicular atrophy, decreased muscle mass, Dupuytren’s contracture, white nails, peripheral polyneuropathy, “spider veins”, redness of the palms, ascites, enlarged liver and spleen, jaundice, and enlargement of the saphenous veins of the abdominal wall can be detected.
Physical data alone cannot differentiate ABP from other forms of liver damage.
Criteria for the diagnosis of ABP
First of all, the doctor must know in what quantities and for how long the patient has been drinking alcohol. This is a very difficult problem, as patients often tend to hide their alcohol abuse. It is advisable to ask relatives and use special questionnaires.
Laboratory diagnostic methods
General blood test
A clinical blood test reveals macrocytosis (mean erythrocyte volume> 100 μm 3) associated with an increased blood alcohol content and toxic effects on the bone marrow.
Anemia (B 12 and iron deficiency), leukocytosis, accelerated ESR are often found. Thrombocytopenia can be mediated as a direct toxic effect of alcohol on the bone marrow, and be the result of hypersplenism due to portal hypertension.
Biochemical blood test
Approximately 30% of patients with alcoholic liver disease have elevated levels of aminotransferases (AST, ALT) and bilirubin, which may reflect hemolysis caused by prolonged systematic alcohol consumption.
The activity of AST is more than 2 times higher than that of ALT. Moreover, the absolute values of these indicators do not exceed 500 U / ml.
In 70% of patients with alcoholic liver disease, the level of gamma-glutamyl transpeptidase is within the normal range.
Latent alcoholic hepatitis can be diagnosed by an increase in the activity of aminotransferases.
A decrease in serum albumin is observed with a moderate increase in the level of gamma globulins.
Immunological blood test
Alcoholic liver disease is characterized by an increase in the concentration of immunoglobulin A.
Determination of antibodies to chronic hepatitis viruses.
Determination of the content of transferrin (depleted in carbohydrates) in the blood serum. An increase in transferrin (depleted in carbohydrates) is characteristic of alcoholic liver disease. It is observed with an average daily alcohol consumption of more than 60 g.
Determination of serum iron content.
Serum iron levels may be elevated in patients with alcoholic liver disease.
Determination of the content of alpha-fetoprotein.
Patients with alcoholic cirrhosis of the liver are at increased risk of developing liver cancer. For the purpose of its detection, the content of alpha-fetoprotein is determined (in liver cancer, this indicator is? 400 ng / ml).
Determination of lipid profile disorders.
The triglyceride content increases in patients with alcoholic liver disease.
Instrumental diagnostic methods
With the help of this study, hepatic steatosis can be diagnosed: the characteristic hyperechoic structure of the parenchyma is revealed. In addition, gallstones can be identified. Ultrasound examination of the abdominal cavity allows visualization of the biliary tract, liver, spleen, pancreas, kidneys; helps in the differential diagnosis of cystic and masses in the liver, more sensitive in the diagnosis of ascites (visualized from 200 ml of fluid in the abdominal cavity).
Doppler ultrasound of hepatic and portal veins
This study is performed when signs of portal hypertension appear.
Computed tomography – CT, magnetic resonance imaging – MRI
These studies allow you to obtain information about the size, shape, state of the vessels of the liver, the density of the parenchyma of the organ. Visualization of intrahepatic vessels of the liver depends on the ratio of their density to the density of the liver parenchyma.
In radionuclide scanning, colloidal sulfur labeled with technetium (99mTc) is used, which is captured by Kupffer cells.Using this method, it is possible to diagnose diffuse hepatocellular diseases (hepatitis, steatosis or cirrhosis), hemangiomas, carcinomas, abscesses, the rate of hepatic and biliary secretion.
Performed to confirm the diagnosis of alcoholic liver disease. Allows you to establish the degree of tissue damage and the severity of fibrosis.
Carried out in order to detect varicose veins of the esophagus and stomach and determine its degree, identify portal gastropathy and assess the risk of bleeding.
It is used to identify anorectal varicose veins.
Refusal from alcohol
The main method of therapy for alcoholic liver disease is a complete rejection of alcohol. At any stage, this measure contributes to a favorable course of the disease. Signs of steatosis may disappear with abstinence from alcohol for 2-4 weeks.
Restriction of animal fats.With ascites – limited consumption of sodium chloride and liquid. In severe hepatitis, it is necessary to provide the patient with adequate nutrition with a sufficient amount of carbohydrates, proteins and fats. The caloric content of the daily diet should be calculated on the basis of 40 kcal / kg and 1.5-2.0 protein per kilogram (in the absence of hepatic encephalopathy, the protein dose is selected individually, depending on tolerance).
For anorexia, tube or parenteral nutrition is used.
Carrying out detoxification measures is necessary for all stages of alcoholic liver disease.The course of detoxification measures is usually 5 days.
The use of these drugs is justified in patients with severe acute alcoholic hepatitis in the absence of infectious complications and gastrointestinal bleeding.
Has a stabilizing effect on the membranes of hepatocytes, has an anti-cholestatic effect. The drug is prescribed at a dose of 10-15 mg / kg / day.
The mechanism of action of these drugs is to restore the structure of cell membranes, normalize molecular transport, cell division and differentiation, stimulate the activity of various enzyme systems, antioxidant and antifibrotic effects.
It is used intravenously (jet or drip), 5-10 ml. The course consists of 15-20 injections with simultaneous ingestion of 2 capsules 3 times a day for 3 months.
It is prescribed in a dose of 400-800 mg intravenously drip or jet (slowly) in the morning; only 15-30 injections. Then you can continue taking the drug, 2 tablets 2 times a day for 2-3 months.
An important effect of this drug is its antidepressant effect.
Treatment of complications of alcoholic liver disease
Complications are diagnosed in patients with alcoholic hepatitis and liver cirrhosis and are the result of the development of portal hypertension.
Treatment of ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy and bleeding from varicose veins is carried out by medical and surgical methods.
Liver transplantation is performed in patients with terminal stage of alcoholic liver disease.
The main condition for performing liver transplantation is at least 6 months of alcohol withdrawal.
The operation allows to achieve 5-year survival in 50% of patients with acute alcoholic hepatitis.
Alcoholic liver disease is not just a disease of a single person, it is a disease of the whole society. To solve this problem, it is necessary to carry out special government programs aimed at promoting a healthy lifestyle among the population. The fact is that avoiding alcohol at any stage of liver disease greatly contributes to its treatment.
Is it safer to induce labor immediately or wait if the mother has high but not persistent high blood pressure after 34 weeks of pregnancy?
What is the problem?
Women with high blood pressure (hypertension) during pregnancy or if they develop preeclampsia (high blood pressure with protein in the urine or involvement of other systems and organs or both) can develop serious complications.Possible complications in the mother are worsening of preeclampsia, development of seizures and eclampsia, HELLP syndrome (hemolysis, elevated liver enzymes and low platelet count), placental abruption, liver failure, renal failure, and breathing problems due to fluid accumulation in the lungs …
Childbirth usually prevents an increase in hypertension, but a baby born prematurely has other health problems, such as breathing problems due to immaturity of the lungs.Induction of labor can lead to overstimulation of contractions and fetal distress syndrome. Another option is to wait for a natural birth, carefully observing the condition of the mother and child.
Why is this important?
Since there are benefits and risks to both planned early delivery and expectant management, where the mother has high blood pressure towards the end of pregnancy, we wanted to know which tactic is the safest.We reviewed clinical trials comparing planned early labor by induction of labor or caesarean section versus expectant management.
What evidence have we found?
We searched for evidence as of January 12, 2016 and found five randomized trials involving 1819 women. The two studies were large and high quality, involving 704 women with hypertension during pregnancy, mild preeclampsia or worsening existing hypertension at 34-37 weeks, and 756 pregnant women with hypertension or mild preeclampsia at 36-41 weeks …Few women who had planned early births experienced serious adverse outcomes (1,459 women, high-quality evidence). There was insufficient information to draw any conclusions about the number of infants born in poor health conditions and there was a high level of variability between the two studies (1495 infants, low quality of evidence). No difference was found between planned early labor and delayed labor in terms of the number of caesarean sections (four studies, 1728 women, moderate quality evidence), or length of hospital stay for mothers postpartum (two studies, 925 women, moderate quality evidence) (or child (one study, 756 infants, moderate quality of evidence).
Most children born prematurely had respiratory problems (respiratory distress syndrome, three studies, 1511 infants) or were admitted to the neonatal unit (four studies, 1585 infants). A small number of women who gave birth prematurely developed HELLP syndrome (three studies, 1628 women) or severe kidney problems (one study, 100 women).
Two studies compared women with preterm labor at 34-36 weeks and 34-37 weeks with a comparison group that was observed up to 37 weeks, when labor was induced artificially if it did not start spontaneously.Three studies compared women with induced labor with normal or near-normal gestation at 37 completed weeks and between 36 and 41 weeks and women followed up to 41 weeks when induced labor was they did not start spontaneously. Inclusion and exclusion criteria also differed across the five studies.
Information regarding which study group the women belonged to was not hidden from both women and clinicians.Women and staff were aware of this intervention, which could have implications for care and decision-making. Most of the evidence was of moderate quality, so we can be relatively confident in the results.
What does this mean?
Overall, if labor was triggered immediately after 34 weeks of gestation, the risk of complications for the mother was lower and overall there was no obvious difference in the incidence of complications for the baby, but information was limited.