IgA blood test: what high and low immunoglobulin A levels mean
Immunoglobulin A (IgA) · Quantitative immunoglobulins (IgG, IgA, IgM); also ordered with tTG-IgA celiac testing · reported in mg/dL (outside the US, g/L; 1 g/L = 100 mg/dL)
Immunoglobulin A (IgA) is the antibody that defends the body's surfaces. Most of it is made by plasma cells lining the gut, airways and glands and secreted into saliva, tears, breast milk and intestinal mucus as 'secretory IgA', where it coats bacteria and viruses before they can attach. The blood test measures the smaller pool of IgA circulating in serum, which for adults is normally about 70 to 400 mg/dL (0.7 to 4 g/L), with lower, age-specific ranges in children. Labs vary in their exact limits.
IgA is tested for two different reasons. The first is as part of quantitative immunoglobulins when infections are frequent or a blood protein abnormality is suspected, where a low IgA may point to selective IgA deficiency (the commonest primary immunodeficiency, affecting roughly 1 in 300 to 1 in 700 people of European ancestry, most of whom are healthy) and a high IgA may point to liver disease, chronic infection, inflammatory bowel disease, IgA nephropathy or, rarely, an IgA-producing myeloma. The second reason is celiac screening: the standard test, tissue transglutaminase IgA (tTG-IgA), is an IgA antibody, so a person who cannot make IgA will test falsely negative, and total IgA is checked alongside to catch this.
A low IgA is far more common than a low IgG and usually far less serious: most people with selective IgA deficiency never know they have it. A high IgA, by contrast, is almost always a reaction to something else, and the useful question is what. As with the other immunoglobulins, the pattern across IgG, IgA and IgM and the shape of the gamma region on protein electrophoresis tell you more than the single number.
IgA at a glance
- What it is: the antibody of mucosal surfaces (gut, airways, saliva, tears, breast milk); the blood test measures serum IgA, about 10 to 15 percent of circulating antibody.
- Normal (adults): about 70–400 mg/dL (0.7–4 g/L). Children: lower and rising with age, reaching adult values in the teens. Labs differ.
- Low IgA: selective IgA deficiency is defined as under 7 mg/dL at age 4 or older with normal IgG and IgM; partial deficiency is between 7 mg/dL and the lower limit. Most people are asymptomatic; some get sinus and chest infections, allergies, autoimmune disease or celiac disease.
- High IgA: alcohol-related and other chronic liver disease, chronic infections (HIV, bronchiectasis), inflammatory bowel disease, rheumatoid arthritis and other autoimmune disease, IgA nephropathy, or an IgA monoclonal protein (MGUS or myeloma).
- Celiac testing: a low IgA makes the tTG-IgA test unreliable; an IgG-based test (deamidated gliadin IgG or tTG-IgG) is used instead.
- Next step: for low IgA, IgG and IgM plus a check of infections, allergies and celiac disease; for high IgA, liver tests, protein electrophoresis with immunofixation, urine for blood and protein, and tests for the suspected cause.
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What IgA measures
In serum, IgA circulates mostly as a single Y-shaped unit (monomer) of about 160 kilodaltons, made largely by plasma cells in the bone marrow. At mucosal surfaces, two IgA units are joined and wrapped in a 'secretory component' that lets them pass through the lining and survive digestive enzymes; this secretory IgA is produced in far larger amounts (several grams a day) than any other antibody but does not enter the blood in quantity. The serum test therefore reflects the marrow-derived pool, and a normal serum level does not guarantee normal secretory IgA, nor vice versa.
The lab measures serum IgA by nephelometry or turbidimetry and reports it in mg/dL in the US (g/L elsewhere; 1 g/L = 100 mg/dL). The subclasses IgA1 (about 85 percent of serum IgA) and IgA2 are rarely measured separately. For selective IgA deficiency, the assay's lower detection limit matters: a result of 'under 7 mg/dL' or 'under 5' defines the deficiency, and some labs use more sensitive assays to confirm it.
Serum IgA has a half-life of about 6 days, so it responds faster than IgG to changes in production. It is lowest in infancy (newborns make almost none, and breast milk supplies secretory IgA instead), rises slowly through childhood and reaches adult levels in adolescence, then increases gradually with age. Alcohol intake raises it in a dose-dependent way, smoking lowers it modestly, and it is not affected by food, so fasting is unnecessary.
Normal range for IgA
Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.
| Group | Typical range (mg/dL (outside the US, g/L; 1 g/L = 100 mg/dL)) | Notes |
|---|---|---|
| Adults | About 70–400 mg/dL (0.7–4 g/L) | Labs differ; some quote 60–350 or 80–450 mg/dL. Rises slightly with age and alcohol use. |
| Newborns | About 0–10 mg/dL | IgA does not cross the placenta; the infant's own production starts over the first months. |
| Infants 6–12 months | About 10–50 mg/dL | IgA deficiency cannot be diagnosed before age 4 because levels are normally low and still rising. |
| Children 2–12 years | About 20–200 mg/dL, rising with age | Adult levels are reached by about 16 years. Pediatric labs use age-specific ranges. |
| Partial IgA deficiency | 7 mg/dL up to the lab's lower limit | Common and usually harmless; celiac testing still needs an IgG-based test if the level is very low. |
| Selective IgA deficiency | Below 7 mg/dL (often reported as 'under 5' or 'undetectable') at age 4 or older, with normal IgG and IgM | Affects about 1 in 300 to 1 in 700 people of European ancestry; much rarer in East Asian populations. Most are healthy. |
| Mild to moderate high IgA | About 400–800 mg/dL | Liver disease, chronic infection, inflammatory bowel disease, autoimmune disease or IgA nephropathy; electrophoresis shows a broad band. |
| Monoclonal IgA (M-protein) | MGUS: M-protein under 3,000 mg/dL; smoldering or active myeloma: 3,000 mg/dL or more, or any level with organ damage | IgA myeloma is about 20 percent of myelomas; hyperviscosity is more common than with IgG because IgA forms dimers. |
High IgA
A high serum IgA almost always means sustained stimulation of the mucosal and marrow plasma cells by something chronic. The classic association is alcohol-related liver disease: alcohol increases gut permeability and the damaged liver clears less of the IgA-containing immune complexes from the portal blood, so IgA rises in rough proportion to intake, and in cirrhosis the electrophoresis shows a characteristic 'beta-gamma bridging' pattern. Chronic infections of mucosal surfaces (bronchiectasis, chronic sinusitis, HIV), inflammatory bowel disease, celiac disease and autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis and Sjögren's syndrome raise it in the same polyclonal way.
IgA nephropathy, the commonest form of glomerulonephritis worldwide, is caused by deposits of abnormally glycosylated IgA1 in the kidney filters. Serum IgA is raised in only 30 to 50 percent of patients, so a normal level does not exclude it and a high level does not diagnose it; a high IgA with blood or protein in the urine is what prompts referral and, ultimately, a kidney biopsy. Henoch-Schönlein purpura (IgA vasculitis) in children and adults is the same process affecting skin, joints and gut as well.
A monoclonal IgA is less common than a monoclonal IgG but behaves somewhat differently. IgA MGUS progresses to myeloma at a slightly higher rate (around 1.5 percent a year) than IgG MGUS, and IgA myeloma, about 20 percent of all myelomas, is more likely to cause hyperviscosity because IgA circulates partly as dimers. Any high IgA without an obvious liver, gut or infection explanation, and certainly any IgA above about 600 to 800 mg/dL, should be followed by serum protein electrophoresis with immunofixation to settle whether it is polyclonal or monoclonal.
Common causes
Alcohol-related liver disease and other cirrhosis
The most characteristic cause. IgA rises with the amount of alcohol consumed, even without liver damage, and reaches 2 to 3 times normal in alcoholic cirrhosis; non-alcoholic fatty liver disease, hepatitis C and primary biliary cholangitis also raise it, less markedly.
Chronic infections, especially of mucosal surfaces
Bronchiectasis, cystic fibrosis, chronic sinusitis, HIV, tuberculosis and chronic urinary infection drive mucosal plasma cells; HIV often raises IgA and IgG together.
Inflammatory bowel disease and celiac disease
Crohn's disease and ulcerative colitis raise IgA in proportion to gut inflammation; untreated celiac disease often produces a modestly high IgA that falls on a gluten-free diet.
Autoimmune and inflammatory diseases
Rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, Sjögren's syndrome and lupus commonly raise IgA; in rheumatoid arthritis a high IgA rheumatoid factor is linked to more erosive disease.
IgA nephropathy and IgA vasculitis (Henoch-Schönlein purpura)
Serum IgA is raised in 30 to 50 percent of IgA nephropathy and about half of IgA vasculitis, with blood and protein in the urine; the diagnosis is made on biopsy, not on the blood level.
IgA monoclonal gammopathy (MGUS) and IgA myeloma
A single plasma-cell clone producing IgA; other immunoglobulins are often suppressed. IgA myeloma is about 20 percent of myelomas and more often causes hyperviscosity and kidney involvement than IgG myeloma.
Smoking-related and occupational lung disease
Chronic bronchitis and COPD with recurrent infections raise IgA modestly; asbestos exposure has also been associated with higher IgA.
Hyper-IgA states in skin disease and allergy
Severe atopic dermatitis, chronic urticaria and some drug reactions produce mild polyclonal rises; IgE is the more informative antibody in allergy.
Lymphoma and chronic lymphocytic leukemia
Can raise IgA polyclonally through IL-6 and other cytokines, or produce an IgA M-protein; CLL more often lowers immunoglobulins with time.
Symptoms that can go with it
- Often none; a mildly high IgA is usually an incidental finding that reflects an underlying condition rather than the antibody itself
- Fatigue, jaundice, abdominal swelling, easy bruising or spider veins with chronic liver disease, often with a history of heavy drinking
- Chronic cough with sputum and repeated chest infections with bronchiectasis or COPD
- Diarrhea, abdominal pain, blood in the stool or weight loss with inflammatory bowel disease or celiac disease
- Cola-colored or visibly bloody urine, often during or just after a sore throat, or foamy urine and ankle swelling, with IgA nephropathy
- Joint pain and morning stiffness, or a purple rash on the legs and buttocks with joint and abdominal pain (IgA vasculitis)
- Bone pain, anemia, excessive thirst, kidney problems, or headache, blurred vision and nosebleeds (hyperviscosity) with IgA myeloma
Low IgA and IgA deficiency
A low serum IgA with normal IgG and IgM is most often selective IgA deficiency, the commonest primary immunodeficiency, defined as a serum IgA below 7 mg/dL in someone aged 4 or older with normal other immunoglobulins and normal vaccine responses. It affects roughly 1 in 300 to 1 in 700 people of European ancestry and is often discovered by chance, for example when total IgA is checked alongside a celiac test. Between 7 mg/dL and the lower limit of the lab range is 'partial IgA deficiency', which is even more common and rarely causes problems. In most people secretory IgM and IgG compensate at mucosal surfaces, which is why the majority are perfectly well.
A minority, perhaps 10 to 30 percent of those with complete deficiency, have consequences. The commonest are recurrent sinus, ear and chest infections and giardiasis of the gut. Allergic disease (asthma, hay fever, eczema, food allergy) is more frequent. Autoimmune diseases, particularly celiac disease (found in 2 to 3 percent of people with celiac disease, about 10 to 15 times the general rate), type 1 diabetes, thyroid disease, lupus, rheumatoid arthritis and immune thrombocytopenia, are all over-represented. A small proportion, especially those with low IgG2 as well, have more serious infections, and in a few people IgA deficiency evolves over years into common variable immunodeficiency, so a repeat immunoglobulin panel every few years is reasonable.
Two practical consequences matter even in the healthy majority. First, all IgA-based tests are unreliable: a tTG-IgA for celiac disease will be falsely negative, so an IgG-based test must be used, and IgA-based tests for some infections have the same problem. Second, a few people with complete IgA deficiency make anti-IgA antibodies and can have severe allergic reactions to blood products containing IgA; the risk is low but real, and anyone with complete deficiency should mention it before a transfusion or IVIG. Low IgA can also be secondary: some medications (phenytoin, carbamazepine, sulfasalazine, penicillamine, gold) and a few chronic conditions reduce it, and it is low alongside IgG and IgM in CVID, X-linked agammaglobulinemia, protein-losing states and myeloma.
Common causes
Selective IgA deficiency
Serum IgA under 7 mg/dL with normal IgG and IgM at age 4 or older; a failure of B cells to switch to IgA production, often with a genetic contribution shared with CVID. Most people are asymptomatic.
Partial IgA deficiency
IgA between 7 mg/dL and the lab's lower limit; very common, usually of no consequence, though IgA-based celiac tests may still read low.
Age under 4
IgA is normally low in infants and toddlers because production matures slowly; the deficiency cannot be diagnosed until age 4, and many low values in young children normalize.
Medications
Phenytoin, carbamazepine, valproate, sulfasalazine, penicillamine, gold, captopril, thyroxine in rare cases and some chemotherapy can reduce IgA; levels often recover after the drug is stopped.
Common variable immunodeficiency and other primary immunodeficiencies
IgA is low together with IgG and sometimes IgM in CVID, absent with all other immunoglobulins in X-linked agammaglobulinemia, and low with IgG in hyper-IgM syndromes; ataxia-telangiectasia is another cause of absent IgA in children.
Protein loss and malnutrition
Nephrotic syndrome, protein-losing enteropathy, severe burns and protein-energy malnutrition lower all immunoglobulins, including IgA.
Multiple myeloma and chronic lymphocytic leukemia
The malignant clone suppresses normal plasma cells, so the uninvolved immunoglobulins fall; a low IgA with a high IgG spike is typical of IgG myeloma.
Immunosuppressive treatment
Rituximab, glucocorticoids, mycophenolate and chemotherapy lower IgA along with IgG, though IgA tends to be affected later and less than IgG.
Symptoms that can go with it
- Usually none; most people with IgA deficiency are found incidentally and stay healthy
- Recurrent sinus infections, ear infections, bronchitis or pneumonia, particularly in childhood
- Chronic or recurrent diarrhea, bloating and weight loss, sometimes from Giardia or from undiagnosed celiac disease
- Asthma, hay fever, eczema or food allergies, which are more common than in the general population
- Symptoms of associated autoimmune disease: joint pain, thyroid symptoms, easy bruising from low platelets
- Severe allergic reactions (flushing, wheeze, low blood pressure) during a blood transfusion or IVIG infusion, from anti-IgA antibodies (rare)
Read it alongside
- IgG and IgM — normal IgG and IgM with a very low IgA is selective IgA deficiency; all three low is a global antibody deficiency; one high with the others suppressed suggests a monoclonal protein.
- tTG-IgA and deamidated gliadin IgG — total IgA is checked with celiac serology because a low IgA makes the IgA-based test falsely negative.
- Serum protein electrophoresis with immunofixation — distinguishes a polyclonal rise from an IgA M-protein and is the next test for any unexplained high IgA.
- GGT, AST, ALT and liver function — a high IgA with raised GGT and an AST higher than ALT points toward alcohol-related liver disease.
- Urinalysis for blood and protein, and creatinine — a high IgA with microscopic hematuria or proteinuria raises the question of IgA nephropathy.
- IgG subclasses — people with IgA deficiency plus low IgG2 have more infections and are followed more closely.
- Vaccine antibody titers — normal responses to tetanus and pneumococcal vaccines confirm the deficiency is selective rather than part of a broader problem.
- Complete blood count and calcium — anemia, high calcium or kidney impairment with a monoclonal IgA point to myeloma.
What usually happens next
- A low IgA in someone who feels well is usually repeated with IgG, IgM and, in children, age-adjusted ranges; the deficiency is only labelled after age 4 and when the level is confirmed below 7 mg/dL.
- If IgA deficiency is confirmed: expect celiac screening with an IgG-based test, a check of IgG subclasses and vaccine responses if infections are frequent, and advice to mention the deficiency before any transfusion or IVIG. Immunology referral is for those with recurrent infections, autoimmune complications or a falling IgG.
- Ask for a repeat immunoglobulin panel every 2 to 3 years, or sooner if infections increase, because a small proportion of IgA deficiency progresses to CVID.
- For a high IgA: expect liver tests and an honest discussion about alcohol, a urinalysis, and serum protein electrophoresis with immunofixation to exclude a monoclonal protein; further tests follow the leading cause (hepatitis serology, HIV test, stool calprotectin, celiac serology, autoimmune screen).
- A high IgA with blood or protein in the urine, or with raised creatinine, is referred to a kidney specialist; a kidney biopsy is the only way to confirm IgA nephropathy.
- An IgA MGUS is monitored with electrophoresis and blood tests every 6 to 12 months; a rising M-protein, anemia, kidney impairment or bone pain prompts a myeloma work-up.
Diet, lifestyle and natural levers with evidence
What can move IgA once the cause is known. Nothing here replaces finding the cause.
Reduce or stop alcohol
Moderate evidenceSerum IgA rises with alcohol intake in a dose-dependent way: in a population study of about 460 adults, heavy drinkers had IgA levels around 30 to 50 percent higher than non-drinkers, and in people with alcohol-related liver disease IgA is often 2 to 3 times normal. Levels fall over weeks to months of abstinence as gut permeability and liver clearance recover, and a falling IgA alongside a falling GGT is one of the markers clinicians use to confirm reduced drinking. This is the only lifestyle change with a clear effect on serum IgA.
Stopping suddenly after heavy daily drinking can cause withdrawal seizures; people who drink heavily every day should reduce under medical supervision.
Probiotics and fermented foods (for secretory IgA)
Preliminary evidenceSeveral randomised trials have found that specific probiotic strains (Lactobacillus and Bifidobacterium species, typically 1 to 10 billion CFU a day for 4 to 12 weeks) raise salivary or fecal secretory IgA in infants, athletes and older adults by roughly 20 to 50 percent, and some trials report fewer respiratory infections. These effects are on mucosal IgA, not the serum level, and do not apply to people with selective IgA deficiency, who cannot make IgA at any surface. Fermented foods such as yogurt and kefir provide similar organisms with weaker evidence.
Avoid live probiotics in people with severe immunodeficiency, central venous catheters or critical illness, where rare bloodstream infections have been reported.
Vitamin A, if intake is low
Preliminary evidenceRetinoic acid, the active form of vitamin A, is the signal that directs B cells in the gut to switch to IgA production and to home to mucosal tissue; vitamin A deficiency in animal and human studies lowers secretory IgA and increases diarrheal and respiratory infections. Vitamin A supplementation in deficient children in low-income countries reduces mortality from diarrhea and measles. In well-nourished adults there is no evidence that extra vitamin A raises IgA.
Preformed vitamin A above 3,000 mcg (10,000 IU) a day is toxic to the liver and causes birth defects; do not supplement in pregnancy beyond a prenatal vitamin. Beta-carotene from food is safe.
Moderate regular exercise, not exhaustive training
Preliminary evidenceModerate exercise training (for example, 30 to 45 minutes of brisk walking most days for 12 weeks) has raised salivary secretory IgA by around 20 to 30 percent in trials of older adults and sedentary people, and is associated with fewer upper respiratory infections. Prolonged exhaustive exercise does the opposite, with salivary IgA falling for hours to days after a marathon or heavy training block. Serum IgA changes little either way.
When to see a clinician promptly
- IgA deficiency and a transfusion or IVIG is planned: tell the team beforehand so IgA-depleted or washed products can be considered.
- Any flushing, wheeze, swelling or faintness during a blood or immunoglobulin infusion: stop the infusion and get immediate help; anaphylaxis is an emergency.
- Recurrent chest or sinus infections (two or more pneumonias, or four or more sinus infections a year), or persistent diarrhea and weight loss, with a low IgA: ask for immunology and celiac evaluation.
- A high IgA with visible blood in the urine, foamy urine, ankle swelling or rising blood pressure, which may indicate IgA nephropathy.
- A high IgA with jaundice, abdominal swelling, vomiting blood or confusion, which suggests advanced liver disease and needs urgent assessment.
- A high IgA with bone pain, anemia, excessive thirst, confusion, blurred vision or nosebleeds, which can indicate myeloma or hyperviscosity and needs same-day assessment.
Frequently asked questions
What is a normal IgA level?
For adults, roughly 70 to 400 mg/dL (0.7 to 4 g/L), with the exact range varying between labs. Children have much lower, age-specific ranges: newborns have almost none, levels rise slowly through childhood, and adult values are reached in the teens. A value slightly above the range is common with age, alcohol use or any chronic inflammation and is usually repeated rather than acted on.
What does high immunoglobulin A mean?
Most often chronic stimulation of the immune system by liver disease (classically alcohol-related), a chronic infection of the lungs, sinuses or gut, inflammatory bowel disease, celiac disease, or an autoimmune condition such as rheumatoid arthritis. It is also raised in a third to a half of people with IgA nephropathy. Rarely it is a monoclonal protein from MGUS or IgA myeloma, which is why an unexplained high IgA is followed by protein electrophoresis. The level itself does no harm; the cause is what matters.
What is IgA deficiency and is it serious?
Selective IgA deficiency is a serum IgA below 7 mg/dL with normal IgG and IgM, in someone aged 4 or older. It affects about 1 in 300 to 1 in 700 people of European descent and is the commonest primary immunodeficiency. For most it is harmless and found by chance. Some have more sinus and chest infections, allergies, or autoimmune disease, especially celiac disease, and a few make antibodies against IgA that can cause reactions to blood products. It is not treated with immunoglobulin, because standard products contain little IgA and the risk of reaction outweighs any benefit.
Why is total IgA tested with a celiac test?
The standard celiac screening test, tissue transglutaminase IgA (tTG-IgA), measures an IgA antibody. Someone who cannot make IgA will test negative even with active celiac disease, and IgA deficiency is 10 to 15 times more common in people with celiac disease than in the general population. Checking total IgA at the same time tells the lab whether the tTG-IgA result can be trusted; if IgA is low, an IgG-based test (deamidated gliadin peptide IgG or tTG-IgG) is used instead.
Can IgA deficiency be treated or does it go away?
There is no treatment that restores IgA, and in adults it is lifelong; in children under 4 a low level often normalizes as the immune system matures, which is why the diagnosis waits until that age. Management is practical: prompt treatment of infections, standard vaccinations (which work normally), screening for celiac and other autoimmune disease if symptoms appear, a repeat immunoglobulin panel every few years because a small minority progress to CVID, and a note on your record about the small risk of reactions to blood products.
Does alcohol raise IgA?
Yes, and it is the single most consistent lifestyle influence on the test. IgA rises with the amount of alcohol consumed, even before any liver damage, because alcohol makes the gut lining more permeable to bacterial products and the liver clears IgA complexes less efficiently. In alcohol-related cirrhosis it is commonly 2 to 3 times the upper limit. A high IgA with a raised GGT and an AST higher than ALT is a recognizable pattern, and both fall with abstinence.
Is high IgA a sign of cancer?
Rarely. The great majority of high IgA results are polyclonal responses to liver disease, infection, gut inflammation or autoimmune disease. A monoclonal IgA is found in a small number of people, mostly as IgA MGUS, which progresses to myeloma at roughly 1.5 percent a year. IgA myeloma itself accounts for about 20 percent of myelomas and is suspected when the M-protein is large or there is anemia, kidney impairment, high calcium or bone pain. Protein electrophoresis with immunofixation is the test that distinguishes the two.
What is the difference between serum IgA and secretory IgA?
Serum IgA is the antibody circulating in the blood, mostly made in the bone marrow, and is what the blood test measures. Secretory IgA is a double unit with a protective coat, made by plasma cells in the gut and airway lining and released into saliva, tears, breast milk and mucus, where it does most of the work of mucosal defence. The two pools are produced separately, so lifestyle measures that raise salivary IgA (exercise, probiotics) do not change the serum result, and a normal serum IgA does not guarantee normal secretory IgA.
References
- Immunoglobulins blood test. MedlinePlus, US National Library of Medicine (2023)View source
- Selective IgA deficiency. Merck Manual Professional Version (2024)
- Yel L. Selective IgA deficiency. Journal of Clinical Immunology (2010)
- Yazdani R, Azizi G, Abolhassani H, Aghamohammadi A. Selective IgA deficiency: epidemiology, pathogenesis, clinical phenotype, diagnosis, prognosis and management. Scandinavian Journal of Immunology (2017)
- Bonilla FA, Khan DA, Ballas ZK, et al.. Practice parameter for the diagnosis and management of primary immunodeficiency. Journal of Allergy and Clinical Immunology (2015)
- Rubio-Tapia A, Hill ID, Semrad C, et al.. American College of Gastroenterology guidelines update: diagnosis and management of celiac disease. American Journal of Gastroenterology (2023)
- Gonzalez-Quintela A, Alende R, Gude F, et al.. Serum levels of immunoglobulins (IgG, IgA, IgM) in a general adult population and their relationship with alcohol consumption, smoking and common metabolic abnormalities. Clinical and Experimental Immunology (2008)
- Wyatt RJ, Julian BA. IgA nephropathy. New England Journal of Medicine (2013)
- Rajkumar SV, Dimopoulos MA, Palumbo A, et al.. International Myeloma Working Group updated criteria for the diagnosis of multiple myeloma. Lancet Oncology (2014)
- Mora JR, Iwata M, von Andrian UH. Vitamin effects on the immune system: vitamins A and D take centre stage. Nature Reviews Immunology (2008)
- Kyle RA, Therneau TM, Rajkumar SV, et al.. Prevalence of monoclonal gammopathy of undetermined significance. New England Journal of Medicine (2006)
- Celiac disease. Mayo Clinic (2023)View source
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