Potential predispositions and etiologies of immune thrombocytopenic purpura (ITP).
Predispositions . |
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1. hypogammaglobulinemia: combined variable immunodeficiency (CVI), severe combined immunodeficiency disease (SCID), IgA and IgG2 deficiency, but not x-linked agammaglobulinemia (XLA) |
2. deficiency of classical pathway of complement components, C4, C2 |
3. ? certain HLA types, e.g. B8DR3 |
4. abnormalities of CD95 (Fas pathway) |
5. ? other failure of autoimmune lymphocytes |
6. ? certain Fc receptor polymorphisms |
Predispositions . |
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1. hypogammaglobulinemia: combined variable immunodeficiency (CVI), severe combined immunodeficiency disease (SCID), IgA and IgG2 deficiency, but not x-linked agammaglobulinemia (XLA) |
2. deficiency of classical pathway of complement components, C4, C2 |
3. ? certain HLA types, e.g. B8DR3 |
4. abnormalities of CD95 (Fas pathway) |
5. ? other failure of autoimmune lymphocytes |
6. ? certain Fc receptor polymorphisms |
Etiologies . |
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1. Persistent antigen exposure |
2. ? selection of certain heavy chain genes in antibody production |
3. unknown tendency to develop autoimmunity: systemic lupus erythematosus (SLE), Evans syndrome |
4. abnormal antigen presentation, e.g. in lymphoproliferative states such as chronic lymphocytic leukemia (CLL) |
5. persistent infections: see Table 4 |
Etiologies . |
---|
1. Persistent antigen exposure |
2. ? selection of certain heavy chain genes in antibody production |
3. unknown tendency to develop autoimmunity: systemic lupus erythematosus (SLE), Evans syndrome |
4. abnormal antigen presentation, e.g. in lymphoproliferative states such as chronic lymphocytic leukemia (CLL) |
5. persistent infections: see Table 4 |