3 - IV Immunoglobulin Therapy (IVIg) Flashcards
IVIg is derived from a purified human plasma pool of more than 1000 healthy blood donors
True
IVIg contains IgG in supraphysiologic levels, including traces of other immunoglobulins
True
IVIg exerts a variety of immunomodulating activities and is an effective alternative approach for the treatment of many autoimmune immune-mediated inflammatory dermatoses
True
Based on currently available data, the most optimal responses to IVIg appears to be patients with:
(1) Kawasaki’s disease
(2) dermatomyositis
(3) autoimmune blistering diseases - Pemphigus vulgaris, cicatricial pemphigoid, epidermolysis bullous acquisita, pemphigoid gestationis
(4) TEN
True
IVIg can produce favourable clinical outcome, used either as monotherapy or in combination with other immunomodulating agents such as systemic corticosteroids and immunosuppressive agents and allowing for dose reductions of these concomitant therapy and their adverse effects
True
IVIg therapy is appropriate for autoimmune diseases which are progressive, uncontrolled, or rapidly debilitating despite conventional immunosuppressive therapy
True
IVIg therapy is appropriate for autoimmune diseases where there is significant adverse effects from conventional immunosuppressive therapy that are potentially life-threatening, or adverse effects that cause significant morbidity/inability to carry out activities of daily living
True
IVIg therapy is appropriate for autoimmune diseases where there are relative or absolute contraindications to the use of high-dose, long-term systemic corticosteroid therapy or immunosuppressive agents
True
IVIg can be used during pregnancy
True
IVIg can induce long-term remission of various dermatoses
True
IVIg can allow for the reduction or discontinuation of concomitant immunosuppressive treatments
True
Peak serum concentrations of IVIg occur immediately after IV injection
True
Peak serum concentrations of IVIg are dose related
True
Within 24 hours of an IVIg injection, 30% of the dose may be removed by catabolism and distribution
True
IVIg distributes mainly in the intravascular space (60%) than the extravascular space (40%)
True
IVIg crosses the placenta
True
IVIg may be excreted into milk
True
The serum half life of IVIg is 3-5 weeks
True
IVIg causes reduction/suppression of pathogenic autoantibody production due to IgG binding to the corresponding cell surface receptors on B lymphocytes
True (B lymphocytes usually produce antibodies, and IgG binding on its surface receptors causes downregulation of pathogenic autoantibody production)
IVIg causes neutralisation of complement-mediated effects by binding to complement components such as C3 and C5 convertases and so blocking complement activation at an early stage
True
The anti-idiotypic antibodies in IVIg preparations bind to and neutralise circulating pathogenic autoantibodies
True (after IVIg infusions, a marked reduction or even disappearance of these pathogenic autoantibodies could be demonstrated)
IVIg binds to receptors on macrophages, subsequently saturate, alter, and downregulate these receptors leading to inhibition of the pathogenic autoantibody-mediated cellular activation
True
IVIg preparations contain amounts of soluble CD4, CD8, and MHC-I and MHC-II molecules which inhibit autoreactive T-lymphocytes
True
IVIg restores the Th1/Th2 cytokine balance by supplying neutralising antibodies against the pathogenic autoantibodies
True
IVIg may affect the migration of immunocompetent cells from blood to target tissue
True
IVIg preparations contain anti-Fas-receptor antibodies which block molecular Fas ligand-Fas receptor interactions and consequently that of keratinocyte apoptosis
True (this mechanism explains the role of IVIg in the treatment of TEN)
Adjunctive use of IVIg has led to reduced dose requirements for systemic corticosteroids due to the increased glucocorticoid receptor sensitivity as well as because IVIg and corticosteroids cam synergistically suppress lymphocyte activation
True