What is selective IgA deficiency and how common is it?

Selective IgA deficiency is defined as serum IgA below 7 mg/dL in adults aged 4 and older with normal IgG and IgM and no identifiable cause. It is the most common primary immunodeficiency in populations of European descent, occurring in approximately 1 in 300–500 individuals. Most affected patients are asymptomatic, but a significant proportion experience recurrent sinopulmonary infections, gastrointestinal infections (particularly Giardia), autoimmune conditions, and — if transfused or given IVIG containing IgA — risk anaphylactic reactions from anti-IgA antibodies.

What does a markedly elevated serum IgA result suggest?

Markedly elevated serum IgA — particularly above 500–600 mg/dL — or an elevated IgA with concurrent low IgG and IgM (immunoparesis pattern) raises suspicion for IgA myeloma or other monoclonal plasma cell disorders. SPEP and immunofixation electrophoresis are required to distinguish monoclonal from polyclonal IgA elevation. Moderately elevated IgA with normal IgG and IgM is more commonly polyclonal — reflecting alcoholic liver disease, chronic liver inflammation, IBD, or chronic mucosal infection — and does not independently require haematological referral.

Can serum IgA be normal when mucosal immune function is impaired?

Yes. Serum IgA and secretory IgA (sIgA) — the dimeric form present at mucosal surfaces — are distinct compartments that can diverge significantly. Some patients have adequate serum IgA but reduced mucosal secretory IgA, presenting with recurrent mucosal infections despite a normal serum result. Conversely, patients with low serum IgA may retain some mucosal secretory IgA production. Salivary or stool secretory IgA testing is required to assess mucosal immune function specifically.

Do medications affect serum IgA levels?

Yes. Systemic corticosteroids suppress immunoglobulin production, including IgA. Rituximab (anti-CD20 B-cell depletion therapy) can cause profound and prolonged hypogammaglobulinaemia affecting IgA, IgG, and IgM. Other B-cell-suppressive DMARDs used in rheumatoid arthritis and autoimmune conditions may also reduce IgA over time. Current and recent immunosuppressive therapy must be documented on the requisition form for accurate interpretation of low IgA results.

Is fasting required before the serum IgA test?

No. Fasting is not required for serum IgA quantification. The specimen can be collected at any time of day without dietary preparation.

How long does it take to receive serum IgA results from Quest Diagnostics?

Results are typically available within 1–3 business days from specimen receipt at the Quest Diagnostics processing laboratory. Serum immunoglobulin quantification by nephelometry is a high-throughput assay with rapid processing.

When should serum IgA be ordered alongside IgG and IgM rather than as a standalone test?

A full quantitative immunoglobulin panel — IgG, IgA, and IgM together — is indicated for comprehensive immunodeficiency evaluation (CVID workup, hypogammaglobulinaemia investigation), characterisation of immunoparesis pattern in plasma cell dyscrasia monitoring, and complete humoral immune status assessment. IgA alone is sufficient when the clinical question is specifically coeliac serology validation or selective IgA deficiency screening. Standalone IgA is diagnostically incomplete for immunodeficiency evaluation because the IgG:IgA:IgM ratio and the pattern of deficiency across all three isotypes determines the classification of the immunodeficiency.

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Immunoglobulin A (IgA), Serum

The Immunoglobulin A (IgA) Serum test quantifies total serum IgA concentration by nephelometry, providing critical diagnostic information across multiple clinical domains — validating IgA-based coeliac serology (IgA below 7 mg/dL renders tTG-IgA and DGP-IgA false-negative), diagnosing selective IgA deficiency (the most common primary immunodeficiency), characterising immunoparesis in IgA…

Biomarkers

Blood (serum)

Sample

1–3 business days

Turnaround

No — fasting is not required for serum IgA quantification. However, if IgA is collected as part of a fasting lipid or metabolic panel, the fasting requirement of companion tests applies.

Fasting

What is the Serum IgA test?

The Immunoglobulin A (IgA) Serum test quantifies the total concentration of IgA in serum by nephelometry or turbidimetry, providing a direct measurement of the systemic IgA pool. It is a fundamental immunoglobulin panel component and a mandatory prerequisite for multiple downstream diagnostic pathways. The most clinically critical application is as the obligatory first step before ordering IgA-based coeliac disease serology — because IgA deficiency is both 10–15 times more prevalent in coeliac disease patients than in the general population and causes complete false-negative results on tTG-IgA and DGP-IgA assays, which constitute the standard coeliac antibody screening panel. Ordering coeliac IgA-based serology without a concurrent or prior serum IgA quantification is a significant diagnostic error that will miss coeliac disease in IgA-deficient patients. Beyond its coeliac diagnostic gating role, serum IgA is ordered as a component of quantitative immunoglobulin panels (IgG, IgA, IgM) in the evaluation of primary and secondary immunodeficiency presenting with recurrent sinopulmonary infections, gastrointestinal infections, or unexplained poor vaccine responses; in the investigation and monitoring of IgA myeloma and other plasma cell dyscrasias, where serum IgA quantification tracks monoclonal IgA protein burden alongside serum protein electrophoresis (SPEP) and immunofixation electrophoresis (IFE); in the assessment of alcoholic liver disease and chronic liver disease, where polyclonal IgA elevation is a characteristic finding; and in the evaluation of IgA nephropathy, where serum IgA is elevated in a proportion of patients alongside galactose-deficient IgA1 and anti-IgA1 antibodies. Serum IgA is typically ordered as part of a quantitative immunoglobulin panel rather than in isolation, providing interpretive context from concurrent IgG and IgM levels.

What does the Serum IgA test measure?

IgA(Immunoglobulin A, Serum (Total))

Range: Adult (18+): 70–400 mg/dL (0.70–4.00 g/L) # REVIEWER FLAG: Confirm Quest Diagnostics age-stratified reference ranges for serum IgA — values are substantially lower in infants and children and increase progressively to adult levels by approximately age 10–14 years. Confirm adult range and whether Quest applies age-band stratification for paediatric patients on the same test code. Confirm assay methodology — nephelometry or turbidimetry — as platforms have slightly different reference intervals.Optimal: 120–250 mg/dL (functional medicine mid-reference-range optimal for adequate mucosal and systemic humoral immune function). # REVIEWER FLAG: No standardised functional medicine optimal range exists for serum IgA beyond the laboratory reference interval — reviewer to confirm whether a functional optimal range is clinically appropriate to document for this marker, or whether the reference range alone should be cited.mg/dL / g/L

Immunoglobulin A is the second most abundant immunoglobulin in serum (after IgG) and the dominant immunoglobulin at mucosal surfaces — the gastrointestinal, respiratory, and urogenital tracts — where it exists primarily as secretory IgA (sIgA), a dimeric form complexed with a secretory component produced by epithelial cells. Serum IgA is predominantly monomeric, produced by plasma cells in the lamina propria of mucosal tissues and in peripheral lymphoid organs, and represents the systemic pool of IgA rather than the secretory mucosal pool. IgA has a serum half-life of approximately 5–7 days. Two subclasses exist — IgA1 (predominant in serum, approximately 80–85%) and IgA2 (predominant in mucosal secretions) — which can be quantified separately in specialist haematological investigations but are not distinguished by standard total serum IgA quantification. IgA mediates mucosal immune defence primarily through immune exclusion — binding and trapping pathogens and antigens at epithelial surfaces — and through FcαRI-mediated phagocyte activation.

Serum IgA quantification carries several distinct clinical applications spanning immunodeficiency, autoimmune disease serology interpretation, haematological malignancy, hepatology, and coeliac disease diagnostics. It is the mandatory prerequisite test before ordering tissue transglutaminase IgA (tTG-IgA) or deamidated gliadin peptide IgA (DGP-IgA) coeliac serology — IgA deficiency (serum IgA below 7 mg/dL in adults) renders these IgA-based coeliac antibody tests falsely negative and requires alternative IgG-based coeliac testing. Selective IgA deficiency — the most prevalent primary immunodeficiency in populations of European descent, occurring in approximately 1 in 300–500 individuals — is defined by serum IgA below 7 mg/dL with normal IgG and IgM, and is associated with recurrent sinopulmonary infections, gastrointestinal infections, autoimmune diseases, and anaphylactic transfusion reactions. Elevated IgA is characteristic of IgA myeloma, alcoholic liver disease, and certain autoimmune and chronic inflammatory conditions.

Why is the Serum IgA test ordered?

Coeliac disease serology prerequisite — serum IgA must be measured before or alongside tTG-IgA or DGP-IgA testing to validate IgA-based coeliac serology results; IgA-deficient patients require IgG-based coeliac antibody substitution (tTG-IgG, DGP-IgG, or EMA-IgG)
Suspected selective IgA deficiency — patients with recurrent sinopulmonary infections (otitis media, sinusitis, bronchitis, pneumonia), recurrent gastrointestinal infections (Giardia, cryptosporidium), unexplained chronic diarrhoea, or a personal or family history of autoimmune conditions including coeliac disease, SLE, or inflammatory bowel disease
Primary immunodeficiency evaluation — quantitative immunoglobulin panel (IgG, IgA, IgM) as part of the workup for suspected common variable immunodeficiency (CVID), X-linked agammaglobulinaemia (XLA), or other primary antibody deficiencies presenting with recurrent bacterial infections and poor vaccine responses
Suspected IgA myeloma or plasma cell dyscrasia — elevated serum IgA identified on SPEP as an M-protein spike in the beta-gamma region, requiring quantification alongside immunofixation to characterise and monitor the monoclonal IgA protein burden
Alcoholic liver disease and chronic liver disease evaluation — polyclonal IgA elevation is a characteristic hepatological finding in alcoholic liver disease (predominantly IgA elevation), cirrhosis, and chronic hepatitis, providing immunological context alongside hepatic function markers
IgA nephropathy (Berger's disease) investigation — elevated serum IgA occurs in approximately 50% of IgA nephropathy cases; its measurement complements complement levels, urinalysis, and renal biopsy findings in the investigation of haematuria and proteinuria with glomerulonephritis pattern
Monitoring IgA replacement therapy or immunoglobulin treatment adequacy — assessment of IgA levels in patients with documented IgA deficiency or CVID as part of ongoing immunological monitoring, noting that IgA-deficient patients who receive intravenous immunoglobulin (IVIG) containing IgA traces are at risk of anaphylactic anti-IgA antibody reactions
Integrative and functional medicine immune system baseline — serum IgA as part of a comprehensive immunological profile alongside IgG, IgM, complement levels, and lymphocyte subsets in patients with chronic infections, autoimmune tendencies, or immune dysregulation

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

No — fasting is not required for serum IgA quantification. However, if IgA is collected as part of a fasting lipid or metabolic panel, the fasting requirement of companion tests applies.

Collection method

Venipuncture at patient service centre

Turnaround

1–3 business days

Collection notes

Standard venipuncture into a serum separator tube (SST / gold top). No special preparation, fasting, or dietary restrictions required. Document on the requisition form: (1) current immunosuppressive medications — corticosteroids, rituximab, DMARDs — as these significantly suppress IgA; (2) whether IgA is being ordered as a coeliac disease prerequisite, to ensure the result is reported concurrently with or before coeliac antibody results; (3) known or suspected IgA deficiency — particularly relevant if blood product or IVIG exposure is anticipated, warranting concurrent anti-IgA antibody testing; (4) history of IgA myeloma or plasma cell dyscrasia, if IgA quantification is being used for monitoring. # REVIEWER FLAG: Confirm Quest Diagnostics tube type, minimum serum volume, and any special handling requirements for this assay before publication.

Specimen requirements

Minimum 0.5 mL serum. Centrifuge and separate serum from cells within 2 hours of collection. Stable at 2–8°C for up to 7 days; stable frozen at −20°C for extended storage. # REVIEWER FLAG: Confirm minimum volume and stability data with Quest Diagnostics assay documentation.

What can affect Serum IgA results?

variableAge

Serum IgA rises progressively from birth — where levels are near-zero (infants rely on maternal IgA from breast milk for mucosal protection) — through childhood and adolescence, reaching adult reference range levels by approximately age 10–14 years. IgA levels are also lower in the elderly due to declining B-cell function. Age-stratified paediatric reference ranges are essential for accurate interpretation in children; adult reference ranges should not be applied to paediatric specimens.

reducesImmunosuppressive therapy (corticosteroids, rituximab, DMARDs)

Systemic corticosteroids suppress immunoglobulin production by reducing plasma cell activity and B-cell differentiation. Rituximab (anti-CD20) depletes B-cells and can cause profound and prolonged hypogammaglobulinaemia including IgA reduction. Other B-cell-suppressive DMARDs may reduce IgA over time. Current immunosuppressive therapy must be documented when interpreting low IgA results — drug-induced hypogammaglobulinaemia should be distinguished from primary IgA deficiency.

elevatesIgA myeloma and B-cell malignancies

Malignant plasma cell clones in IgA myeloma produce large quantities of monoclonal IgA, substantially elevating total serum IgA. Paradoxically, IgA myeloma also causes immunoparesis — suppression of normal polyclonal immunoglobulin production — resulting in low IgG and IgM despite high total IgA. When markedly elevated IgA is identified (particularly above 1000 mg/dL), SPEP and IFE should be performed to characterise whether the elevation is polyclonal (reactive, inflammatory) or monoclonal (consistent with a plasma cell dyscrasia).

elevatesAlcoholic liver disease and chronic hepatic inflammation

Chronic ethanol consumption stimulates polyclonal IgA production through multiple mechanisms — hepatic Kupffer cell activation, gut microbiome alteration producing increased antigen exposure, and direct stimulation of gut-associated lymphoid tissue IgA production. IgA elevation in alcoholic liver disease is characteristically polyclonal and is often the dominant immunoglobulin elevated relative to IgG and IgM. The degree of IgA elevation broadly correlates with severity of hepatic inflammation.

variableAnti-IgA antibodies in IgA-deficient patients

Approximately 20–40% of patients with selective IgA deficiency develop anti-IgA antibodies — most commonly IgG anti-IgA — as a consequence of alloimmunisation from blood product exposure or prior IVIG infusions containing IgA traces. These antibodies do not affect the serum IgA quantification result (which will remain undetectable or very low) but are critically important to identify before blood product transfusion or IVIG therapy, as exposure to IgA-containing products in sensitised patients carries risk of anaphylactic reaction. Anti-IgA antibody testing should be requested when IgA deficiency is confirmed and blood product or IVIG use is anticipated.

elevatesAutoimmune conditions and chronic mucosal antigen stimulation

Chronic mucosal antigen stimulation — from inflammatory bowel disease, coeliac disease with ongoing gluten exposure, chronic respiratory infections, or autoimmune mucosal conditions — drives polyclonal IgA production from gut-associated and respiratory lymphoid tissue plasma cells. Elevated IgA in the context of IBD or untreated coeliac disease reflects chronic mucosal immune activation rather than a primary IgA overproduction disorder and should resolve or reduce with effective disease control.

What do Serum IgA results mean?

Elevated

Elevated serum IgA above the upper reference limit (>400 mg/dL in adults) is most commonly polyclonal in origin — reflecting chronic mucosal antigen stimulation from alcoholic liver disease, chronic hepatitis, cirrhosis, inflammatory bowel disease, chronic mucosal infections, or systemic autoimmune conditions. A markedly elevated IgA — particularly above 500–600 mg/dL — or an elevated IgA associated with low IgG and low IgM (immunoparesis pattern) raises suspicion for a monoclonal IgA disorder (IgA myeloma, smouldering myeloma, or monoclonal gammopathy of undetermined significance — IgA-MGUS) and should prompt SPEP and IFE to characterise monoclonal vs polyclonal elevation. IgA elevation in the context of known liver disease, IBD, or autoimmune disease in the absence of immunoparesis is typically polyclonal and does not independently require haematological referral.

Normal

A serum IgA within the adult reference range (70–400 mg/dL) confirms that IgA-based coeliac serology results are analytically valid — tTG-IgA and DGP-IgA results can be interpreted at face value without concerns about false-negative IgA deficiency. In the context of an immunodeficiency evaluation, a normal IgA with normal IgG and IgM effectively excludes common variable immunodeficiency and selective IgA deficiency as causes of recurrent infection. In a patient with known IBD, autoimmune disease, or liver disease, a normal IgA does not exclude these diagnoses but suggests the degree of mucosal immune activation is not reflected in the systemic serum IgA pool at the time of testing.

Reduced

The clinically most significant low IgA finding is selective IgA deficiency — defined as serum IgA below 7 mg/dL (0.07 g/L) in adults aged 4 years and older with normal IgG and IgM and no other identifiable cause. This is the most common primary immunodeficiency in European populations (prevalence approximately 1:300–500) and has critical clinical implications: it invalidates all IgA-based coeliac serology (tTG-IgA, DGP-IgA, EMA-IgA), which must be replaced with IgG-based coeliac antibody testing; it predisposes to recurrent sinopulmonary and gastrointestinal infections; it is associated with higher rates of autoimmune disease including coeliac disease, SLE, rheumatoid arthritis, and IBD; and it requires anti-IgA antibody assessment before blood product or IVIG exposure. Low-normal IgA (7–70 mg/dL) represents partial IgA deficiency and warrants clinical monitoring and IgG-based coeliac serology substitution.

Note: The most operationally important caveat is that serum IgA below 7 mg/dL renders all IgA-based coeliac antibody assays clinically invalid — a result that is frequently missed when IgA quantification is not performed concurrently with coeliac serology. This is the most impactful analytical pitfall in routine clinical practice for this analyte. A second important caveat is the distinction between monoclonal and polyclonal IgA elevation — SPEP and IFE are required to make this distinction, as total serum IgA quantification alone cannot identify monoclonal proteins. Practitioners should also note that secretory IgA — measured in saliva or stool — reflects mucosal immune function and is not equivalent to serum IgA; the two compartments can diverge significantly, and low serum IgA does not necessarily imply low mucosal secretory IgA.

Frequently asked questions

The standard coeliac disease antibody tests — tissue transglutaminase IgA (tTG-IgA) and deamidated gliadin peptide IgA (DGP-IgA) — are IgA-based assays that produce completely false-negative results in patients with IgA deficiency, as there is insufficient IgA to generate a detectable antibody response. IgA deficiency is 10–15 times more prevalent in coeliac disease patients than the general population. Serum IgA must be measured concurrently or before coeliac serology — if IgA is below 7 mg/dL, IgG-based coeliac antibody testing (tTG-IgG or DGP-IgG) must be substituted.

How to access the Serum IgA test

The Serum IgA reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.

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About this page

Published: May 23, 2026

Last reviewed: May 23, 2026

References:

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.