Page 1980 - Hematology_ Basic Principles and Practice ( PDFDrive )

1754 Part XI Transfusion Medicine

TABLE Administration of Intravenous Immunoglobulins
115.4
Indicated Solid organ transplantation (kidney)
Ataxia-telangiectasia Systemic lupus erythematosus (refractory, severe, active)
Chronic inflammatory demyelinating polyneuropathy Thrombocytopenia refractory to platelet transfusion
Chronic lymphocytic leukemia Vasculitis (refractory to standard therapy)
Common variable immunodeficiency Investigational
Cytomegalovirus-interstitial pneumonia after bone marrow transplantation Acquired von Willebrand disease
Guillain–Barré syndrome Amyotrophic lateral sclerosis
Graft-versus-host disease after bone marrow transplantation Burn patients
Hemolytic disease of the fetus and newborn Chronic fatigue syndrome
Idiopathic thrombocytopenic purpura Chronic human parvovirus B19 infection
Immunoglobulin G subclass deficiency Chronic idiopathic pericarditis
Inflammatory myopathies (refractory dermatomyositis and polymyositis) Chronic pain syndromes
Myasthenia gravis Congestive heart failure
Mucocutaneous lymph node syndrome (Kawasaki disease) Dilated cardiomyopathy
Neonatal alloimmune thrombocytopenia Graft-versus-host disease
Parvovirus infection Human immunodeficiency virus infection
Pediatric human immunodeficiency virus infection Immune-mediated aplastic anemia
Persistent deficit in antibody production after bone marrow transplantation Inflammatory bowel disease
Posttransfusion purpura Intractable childhood epilepsy
Primary immunodeficiency syndromes Multiple sclerosis
Secondary hypogammaglobulinemia Myocarditis
Severe combined immunodeficiency Necrotizing fasciitis
Stiff-person syndrome Neonatal sepsis
Wiskott-Aldrich syndrome Neonatal hemochromatosis
X-linked agammaglobulinemia Postpartum cardiomyopathy
Possibly Indicated Prevention of nosocomial postoperative infections
Antiphospholipid syndrome in pregnancy Prophylaxis in transplant recipients against cytomegalovirus infection
Autoimmune hemolytic anemia (warm type unresponsive to prednisone) Recurrent unexplained spontaneous abortions
Factor VIII inhibitors (refractory) Rheumatoid arthritis
Graves ophthalmopathy Sepsis and septic shock
Immune neutropenia Toxic epidermal necrolysis/Stevens-Johnson syndrome
Multiple myeloma (stable disease, high risk for infections) Toxic shock syndrome
Pemphigus

Although IVIg has shown equal efficacy with corticosteroids in studies show that infliximab is at least as safe and as efficacious as
pediatric acute ITP and in 75% of adults with chronic ITP, because IVIg in these refractory patients. One retrospective review has even
of the transient responses and high cost, its use is justified only in suggested that infliximab might result in faster resolution of fever and
clinical situations requiring rapid elevation of platelet count or if fewer days of hospitalization in comparison with IVIg. While studies
standard therapy has failed. IVIg is, therefore, indicated in acute are still ongoing, IVIg may soon be replaced by alternative therapies
bleeding episodes or before urgent surgery, including splenectomy; in in this refractory patient population.
patients at high risk of intracranial hemorrhage; and in those in whom With regard to the pathogenesis of Kawasaki disease, decreased
corticosteroids are contraindicated or ineffective. IVIg has also been peripheral blood lymphocyte apoptosis has been demonstrated.
used to treat ITP during pregnancy, postinfectious thrombocytopenia, Therefore, the effect of IVIg in Kawasaki disease has been postulated
ITP associated with HIV infection, and neonatal thrombocytopenia. to partially reverse inhibited lymphocyte apoptosis.
Intravenous anti-D immune globulin (also known as Rh immune
globulin) has demonstrated efficacy in Rh-positive, nonsplenecto-
mized individuals with ITP. It has been suggested that the mechanism Solid Organ Transplantation
of action may involve a shift in the immune-mediated destruction
from platelets to the antibody-coated RBCs (Chapter 131). The presence of high-titer reactive antibodies against incompatible
graft HLA or ABO antigens increases the risk of early solid organ,
antibody-mediated, graft rejection and mortality, especially in kidney
Kawasaki Disease and cardiac transplants. For some patients who have HLA antibodies
to undergo transplantation, these antibodies must be removed or
The mucocutaneous lymph node syndrome (Kawasaki disease) has decreased. While morbidity and mortality can be reduced by selecting
been treated with aspirin with or without concomitant IVIg admin- an adequately cross-matched donor, IVIg with or without plasma
istration. Coronary artery aneurysm, a serious complication of this exchange has also been shown to decrease sensitization of incompat-
disease, was significantly reduced in the IVIg-treated group. However, ible antigens in patients awaiting renal and cardiac transplantations.
in a multicenter retrospective survey of all children treated with In addition, IVIg with or without plasma exchange is used in the
Kawasaki disease, persistent or recrudescent fever after their first treatment of biopsy-proven antibody-mediated rejection. One review
course of IVIg was associated with a statistically significant risk of discussed three randomized control trials which investigated the use
treatment failure. Furthermore, IVIg retreatment in those patients of IVIg for renal transplantation and revealed a trend in improvement
with persistent fever after IVIg treatment failure was approximately in desensitization rates and a statistically significant decrease in time
60%. Current randomized trials are now being done to compare the to transplant for patients treated with IVIg, superior graft survival
efficacy of newer, and perhaps better, therapies, such as infliximab rate in kidney transplant patients desensitized with IVIg, and a lower
(anti-tumor necrosis factor α). To date, these randomized control rate of recurrent acute rejection with IVIg in comparison to OKT3