LIVER-KIDNEY MICROSOME IGG ANTIBODY BY IFA
- LIVER-KIDNEY MICROSOME IGG ANTIBODY BY IFA
- Start Date
- Expiration Date
- LKM IgG Ab
- CPT Codes
- Reference Test
- Transport Info
Centrifuge and immediately transfer serum to separate plastic tube
- Fasting Required?
- Patient Instructions
- Reference Range
< 1:20 Normal
Indirect Fluorescent Antibody (IFA)
This assay should be used to test patients with suspected autoimmune disorders with liver involvement. In 1973, liver-kidney microsomal (LKM) antibodies were first identified in a subgroup of patients with idiopathic autoimmune chronic hepatitis. These autoantibodies are divided into three specific subtypes depending on the specificity of the antigen binding site: LKM-1, LKM-2, or LKM-3. LKM-1 antibody reacts uniformly with cytochrome P450 2D6, a 50 kDa protein found in the cytoplasm of all hepatocytes and renal proximal tubular cells. Studies in the early 1990s identified less than three percent of patients infected with hepatitis C virus have related antibodies that also recognize antigenic sites on P4502D6. LKM-2 antibody is associated with ticrynafen (tienilic acid)-induced hepatitis. The target antigen for this antibody is cytochrome P450 2C9. LKM-3 antibody is associated with chronic hepatitis D. The target antigen for this autoantibody is UDP-1 glucuronosyl transferase. Although the specific LKM antigenic sites differ from one another, LKM-1 and LKM-2 antibodies cannot be differentiated using indirect fluorescent antibody (IFA) techniques. LKM-3 antibody is identified by IFA that employs human or primate tissue sections. Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease, characterized by the presence of autoantibodies produced against antigens expressed within hepatocytes. AIH can be categorized into three separate disease groups based on the presence of marker antibodies in the serum of affected patients. AIH Type I is the most common disease group (60-70%) and is characterized by the presence of autoantibodies against nuclear (ANA) and smooth muscle (ASM) antigens. AIH Type II is less prevalent than AIH Type I, with only 10-20 cases per million. AIH Type II has an acute onset with a rapid progression to cirrhosis and liver failure. AIH Type II is characterized by the presence of specific antibodies (LKM-1) against LKM antigens (P450IID6) and the absence of ANA and ASM. AIH Type III is characterized by the presence of antibodies against soluble liver antigens (SLA), which react with liver cytokeratins. Patients with LKM IgG IFA titers of less than 1:20 are considered to be negative for LKM-1 and LKM-2 antibody. Significant antibodies are present when titers are ł 1:20. Testing LKM positive patients for ANA and ASM may be helpful in distinguishing between Type I and Type II AIH. Other abnormalities of the immune system often found in patients with AIH include hypergammaglobulinemia and an increased CD4/CD8 ratio in peripheral blood and liver. Test results in and of themselves are not diagnostic. Assay results are to be interpreted in conjunction with other laboratory tests, as well as with the clinical presentation of the patient. LKM antibodies react with specific proteins localized in the smooth endoplasmic reticulum of liver and kidney cells. IFA methods that employ rodent liver and kidney tissue sections detect only LKM-1 and LKM-2 antibodies and cannot differentiate which antibody is present.