An imbalance of protective SIgA can result in a compromised mucosal immunity and eventual gastrointestinal, immunological and neurological disorders.
A deficiency of SIgA may be an indication of chronic stress, adrenal insufficiencies, bacterial colonization on molar surfaces, recurrent tonsillitis, adenoid hyperplasia, cutaneous candidiasis, intestinal barrier dysfunction, nutritional deficiencies, recurrent herpes infection, celiac, crohn’s or ulcerative colitis. Patients presenting with low levels of SIgA are at greater risk of gastrointestinal infections, dysbiosis and autoimmune disorders. Such a patient may have increased IgG responses to multiple foods, or may be asympomatic.
Known Causes of Low SIgA:
Anti-inflammatory drugs
Cyclosporine Fenclofenac Gold
Hydantoin Sodium valproate Sulfasalazine
Although Selective IgA Deficiency is usually
one of the milder forms of immunodeficiency,
it may result in severe disease in some people. Therefore, it is difficult to predict the long-term outcome in a given patient with Selective IgA Deficiency. In general, the prognosis in Selective IgA Deficiency depends on the prognosis of the associated diseases. It is important for physicians to continually assess and reevaluate patients
with Selective IgA Deficiency for the existence of
associated diseases and the development of more extensive immunodeficiency. For example, rarely, IgA deficiency will progress to become Common Variable Immunodeficiency with its deficiencies of IgG and/or IgM. The physician should be notified of anything unusual, especially fever, productive cough, skin rash or sore joints. The key to a good prognosis is adequate communication with the physician and the initiation of therapy as soon as disease processes are recognized.
Selective deficiency of IgA is the most common immune deficiency disorder. Persons with this disorder have low or absent levels of a blood protein called immunoglobulin A.
Causes, incidence, and risk factors
IgA deficiency is usually inherited, which means it is passed down through families. However, cases of drug-induced IgA deficiency have been reported.
It may be inherited as an autosomal dominant or autosomal recessive trait. It is found in approximately 1 in 700 individuals of European origin. It is less common in people of other ethnicities.
See also: Celiac disease - sprue
Symptoms
Many people with selective IgA deficiency have no symptoms.
Symptoms include frequent episodes of:
Bronchitis
Chronic diarrhea
Conjunctivitis (eye infection)
Gastrointestinal inflammation including ulcerative colitis, Crohn's disease, and a sprue-like illness
Mouth infection
Otitis media (middle ear infection)
Pneumonia
Sinusitis
Skin infections
Upper respiratory tract infections
Other symptoms include:
Bronchiectasis (a disease in which the small air sacs in the lungs become damaged and enlarge)
Unexplained asthma
Signs and tests
There may be a family history of IgA deficiency. Tests that may be done include:
IgA
IgG
IgG subclass measurements
IgM
Quantitative immunoglobulins
Serum immunoelectrophoresis
Treatment
No specific treatment is available. Some people gradually develop normal levels of IgA without treatment.
Low serum IgA levels in children aged 6 months to 4 years should be confirmed to be persistently low at age 4 years before making a lifetime diagnosis of IgAD. Some children with a low level when aged 6 months to 4 years progress to common variable immunodeficiency (CVID), whereas others completely normalize.
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Below 5 is considered IgA deficient .