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IgG in serum

Reference values: age MEAN mg/dL RANGE mg/dL Adult 1204 723-1685 CORD BLOOD 1121 636-1606 1 month 503 251-906 2 months 365 206-601 3 months 334 176-581 4 months 343 196-558 5 months 403 172-814 6 months 407 215-704 7-9 months 475 217-904 10-12 months 594 294-1069 1 year 679 345-1213 2 years 685 424-1051 3 years 728 441-1135 4-5 years 780 463-1236 6-8 years 915 633-1280 9-10 years 1007 608-1572 Clinical significance: The major Ig produced by plasma cells is IgG, which makes up 70-75% of the total IgG. Of this amount, 65% is extravascular; the remainder is mainly present in plasma. Its major function appears to be neutralization of toxins in tissue spaces. Antibodies of the IgG class are produced in response to most bacteria & viruses; they aggregate & coat small soluble foreign proteins such as bacterial toxins. IgG level in a neonate represents IgG transferred across the placenta from the mother. Immunoglobulin synthesis is stimulated by environmental antigens so that serum IgG reaches adult levels in 3 years. IgG deficiency is commonly secondary to protein loss or to failure of synthesis, but may be due to a primary congenital disorder. The diagnosis of a deficiency state is important because replacement therapy with gamma-globulin can be provided. Some primary deficiencies involve only one of two Ig classes; some clinically immunodeficient patients have normal IgG levels, yet the antibodies appear incompetent when the patient is challenged with antigen. 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 parallelled by a decrease of maternal IgG, so that in the infant's blood, IgG falls to a minimum at about 3 months of age. Two groups of newborns are at risk: premature babies, because they start with less than the full-term amount of maternal IgG, & babies in whom initiation of IgG synthesis is transiently delayed. IgG determinations are invaluable 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. IgG tends to predominate in skin, gut, respiratory, & renal infections. Chronic bacterial infections cause an increase in serum levels of all Igs. Individual Igs are of value in the differential diagnosis of liver disease & of intrauterine infections. 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. Increases: - polyclonal gammopathy - recurrent or chronic infections - autoimmune disorders - rheumatoid arthritis - sarcoidosis - Sjogren's syndrome - systemic lupus erythematosus - autoimmune pacreatitis - autoimmune hepatitis - idopathic portal hypertension - some intrauterine contraceptives - monoclonal gammopathy - multiple myeloma - solitary plasmacytoma - gamma-heavy chain disease - MGUS - lymphoma - chronic lymphocytic leukemia Decreases: - primary immunodeficiency - severe-combined immunodeficiency - X-linked agammaglobulinemia - common variable immunodeficiency - hyper-IgM syndrome - Nijmegen breakage syndrome - secondary causes - protein-losing enteropathy - nephrotic syndrome - thermal burns - myotonic dystrophy - immunosuppressive therapy Principle: - see IgG [Nephelometry] in serum/CSFurine Specimen: - minimum volume 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 - see IgG [Nephelometry] in serum/CSF/urine

Related

IgG subclasses in serum

Specific

IgG1 in serum IgG2 in serum IgG3 in serum IgG4 in serum

General

immunoglobulin in serum IgG in body fluid

References

  1. Beckman Array Protein System Operating Manual.
  2. Kaplan, Lawrence A. & Amadeo, J. Pesce: Clinical Chemistry, pp. 1304-1306, 1984.
  3. Tietz, Norbert W: Textbook of Clinical Chemistry, pp. 563-573, 1986.
  4. Immunoglobulin G Laboratory Test Directory ARUP: 50350
  5. Panel of 10 tests Laboratory Test Directory ARUP: 50615
  6. Panel of 3 tests Laboratory Test Directory ARUP: 50630
  7. Panel of 8 tests Laboratory Test Directory ARUP: 50676
  8. Panel of 24 tests Laboratory Test Directory ARUP: 50980
  9. Panel of 17 tests Laboratory Test Directory ARUP: 51223
  10. Panel of 16 tests Laboratory Test Directory ARUP: 51225
  11. Panel of 10 tests Laboratory Test Directory ARUP: 80440
  12. Panel of 10 tests Laboratory Test Directory ARUP: 2002715

Component-of

IgG/Albumin in serum IgG/beta-tubulin in serum immunoglobulin classes in serum (gammaglobulin classes in serum)