IgM in serum
Reference interval
Table
age | MEAN mg/dL | Range mg/dL |
---|---|---|
Adult | 170 | 63-277 |
CORD BLOOD | 13 | 6.3-25 |
Newborn | 17.5 | 5.0-30 |
1 month | 45 | 20-87 |
2 months | 46 | 17-105 |
3 months | 49 | 24-89 |
4 months | 55 | 27-101 |
5 months | 62 | 33-108 |
6 months | 62 | 35-102 |
7-9 months | 80 | 34-126 |
10-12 months | 82 | 41-149 |
1 year | 93 | 43-173 |
2 years | 95 | 8-168 |
3 years | 104 | 47-200 |
4-5 years | 99 | 43-196 |
6-8 years | 107 | 48-207 |
9-10 years | 121 | 52-242 |
Principle
See IgM by nephelometry in serum/CSF/urine
Clinical significance
IgM is the most primitive & least specialized Ig & the only Ig that a newborn synthesizes. In adult serum it is the third most abundant Ig & accounts for 5-10% of the total circulating Ig.. IgM continues, however, to be synthesized against antigens confined to the blood, such as erythrocyte surface antigens & tropical parasites. IgM is not transported across the placenta & is therefore not involved in hemolytic disease of the newborn. It is an efficient complement activator.
Immunoglobulin synthesis is stimulated by environmental antigens so that serum IgM reaches adult levels at about 9 months.
Immunodeficiency is a risk for infants. Levels of maternal IgG, transferred across the placenta, rise in the fetus during the last 3 months of pregnancy. Contact of the neonate with environmental antigens causes B lymphocytes to begin to multiply, IgM levels to start to rise, & plasma cells producing IgG & IgA to increase in number. These developments, however, are paralleled by a decrease of maternal IgG, so that in the infant's blood, IgG falls to a minimum at about 3 months of age. 2 groups of newborns are at risk; premature babies, because they start with < the full-term amount of maternal IgG, & babies in whom initiation of IgG synthesis is transiently delayed. IgG determinations are usefup in these cases since levels may fall dangerously low if the baby is not treated. Rising IgM & normal salivary IgA concentrations at 6 weeks of age suggest a good prognosis.
Polyclonal increases in serum Igs are the normal response to infections IgM tends to predominate in primary viral infections & bloodstream infections such as malaria. Chronic bacterial infections cause an increase in serum levels of all Igs. They are of value, however, in the differential diagnosis of liver disease & of intrauterine infections. In primary biliary cirrhosis, the IgM level is markedly increased; in chronic active hepatitis, IgG & sometimes IgM are increased, & in portal cirrhosis, IgA & sometimes IgG are increased. In intrauterine infections, production of IgM by the fetus increases & at birth the IgM level in cord blood is increased.
Should a paraprotein be identified in blood, or urine, or both, its heavy & light chains should be typed & the concentrations of polyclonal IgG, IgA, & IgM should be determined. These studies confirm whether the spike on the electrophoretic pattern is indeed a paraprotein; they help to decide the probable prognosis, & they show whether the polyclonal Igs are so low as to make the patient vulnerable to infections. Prognosis is based on the class of the paraprotein found, its concentration at the time of diagnosis, & the rate at which its concentration increases. The concentration at the time of diagnosis must correlate with the current extent of the disease process. The rate of increase in concentration, when compared with the average doubling time for the concentration of the particular class of paraprotein, should correlate with the rate of growth of the neoplasm.
Lymphoid tumors, presenting as lymphomas or chronic lymphocytic leukemias, arise from less mature stages in B lymphocyte development; ~ 1 in 5 produce paraproteins, usually of the IgM class. Waldenstrom's macroglobulinemia, however, arises from the most mature B lymphocytes & invariably produces IgM; in fact, it is the presence of this very high molecular weight protein that produces the disease - an increase in viscosity of the blood. Bence Jones proteinuria occurs in 80% of these cases, but the condition is much less malignant than multiple myeloma. Lymph nodes & spleen are enlarged, but the lymphoid infiltration is slow-growing & the symptoms are treatable by exchange transfusion.
Increases
- polyclonal increase
- acute infection
- chronic inflammatory conditions
- nephrotic syndrome
- hyper-IgM syndrome
- monoclonal gammopathy
- Waldenstrom's macroglobulinemia
- lymphoma
- chronic lymphocytic leukemia
- mu-heavy chain disease (rare)
- multiple myeloma (rare)
- Schnitzler's syndrome
- cold agglutinin syndrome
- MGUS Decrease:
- selective IgM deficiency (uncommon)
- immunosuppressive therapy
- splenectomy
- monoclonal gammopathy
- protein deficiency
- thermal burns
Specimen
200 uL. Store sample in freezer until ready for assay. Highly lipemic samples may result in inaccurate determination & should be redrawn on a fasting patient. Plasma is not recommended.
More general terms
More specific terms
Additional terms
Component of
References
- ↑ Clinical Guide to Laboratory Tests, 4th edition, HB Wu ed, WB Saunders, Philadelphia, 2006
- ↑ Immunoglobulin M Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050355.jsp
- ↑ Panel of 10 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050615.jsp
- ↑ Panel of 3 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050630.jsp
- ↑ Panel of 24 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050980.jsp
- ↑ Panel of 17 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0051223.jsp
- ↑ Panel of 16 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0051225.jsp
- ↑ Panel of 10 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0000000.jsp