Abstract
Specific antibody deficiency (SAD) is a primary immunodeficiency disease characterized by normal immunoglobulins (Igs), IgA, IgM, total IgG, and IgG subclass levels, but with recurrent infection and diminished antibody responses to polysaccharide antigens following vaccination. There is a lack of consensus regarding the diagnosis and treatment of SAD, and its clinical significance is not well understood. Here, we discuss current evidence and challenges regarding the diagnosis and treatment of SAD. SAD is normally diagnosed by determining protective titers in response to the 23-valent pneumococcal polysaccharide vaccine. However, the definition of an adequate response to immunization remains controversial, including the magnitude of response and number of pneumococcal serotypes needed to determine a normal response. Confounding these issues, anti-polysaccharide antibody responses are age- and probably serotype dependent. Therapeutic strategies and options for patients with SAD are often based on clinical experience due to the lack of focused studies and absence of a robust case definition. The mainstay of therapy for patients with SAD is antibiotic prophylaxis. However, there is no consensus regarding the frequency and severity of infections warranting antibiotic prophylaxis and no standardized regimens and no studies of efficacy. Published expert guidelines and opinions have recommended IgG therapy, which are supported by observations from retrospective studies, although definitive data are lacking. In summary, there is currently a lack of evidence regarding the efficacy of therapeutic strategies for patients with SAD. We believe that it is best to approach each patient as an individual and progress through diagnostic and therapeutic interventions together with existing practice guidelines.
Highlights
Specific antibody deficiency (SAD) mimics the deficient immune response often seen in healthy young children and infants who are unable to mount a robust response to pure unconjugated polysaccharide antigens such as Streptococcus pneumoniae polysaccharide and Haemophilus influenzae type b capsular polysaccharide
Specific antibody deficiency is characterized by an abnormal IgG antibody response to a pneumococcal vaccine, which was developed to protect against the Gram-positive cocci S. pneumoniae [12]
The practice parameter from the American Academy of Allergy, Asthma and Immunology (AAAAI), American College of Allergy, Asthma and Immunology (ACAAI), and Joint Council of Allergy, Asthma and Immu nology (JCAAI) recommends that for patients who have previously received at least one dose of conjugate vaccine, normal antibody levels against serotypes in the conjugate vaccine do not exclude the diagnosis of SAD; at least six serotypes should be tested that are present in 23-valent pneumococcal polysaccharide vaccine (PPSV23) only [12]
Summary
Specific antibody deficiency (SAD) is a primary immunodeficiency disease (PIDD) characterized by normal immunoglobulins (Igs), IgA, IgM, total IgG, and IgG subclass levels, but with recurrent. Specific Antibody Deficiency infection and diminished antibody responses to polysaccharide antigens following vaccination [1,2,3]. There is some confusion concerning the relationship between SAD and IgG subclass levels and the controversial diagnosis of IgG subclass deficiency These diagnoses are considered distinct, and the designation of SAD is reserved for impaired polysaccharide vaccine responsiveness with completely normal Ig isotype levels [11, 12]. The diagnosis should not be conferred until after 2 years of age [11, 12] It should be noted that some children under the age of 2 years (as young as 1 year) are able to mount robust responses to polysaccharide vaccines [14]. We will discuss current evidence and challenges regarding the diagnosis and treatment of SAD
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