Warm autoimmune hemolytic anemia: Difference between revisions

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Revision as of 17:15, 21 September 2012

Template:DiseaseDisorder infobox For patient information, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Warm autoimmune hemolytic anemia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Treatment

Case Studies

Case #1

Template:Hematology

Template:WikiDoc Sources

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-==Overview==
+==[[Warm autoimmune hemolytic anemia overview|Overview]]==
-'''Warm Antibody Autoimmune Hemolytic Anemia''' (AIHA) is the most common of the [[Autoimmune diseases|autoimmune]] [[Hemolysis|hemolytic]] diseases.  About half of the cases are [[idiopathic]], with the other half attributable to a predisposing condition or medications being taken.
-==Pathophysiology==
+==[[Warm autoimmune hemolytic anemia historical perspective|Historical Perspective]]==
-The most common [[antibody]] involved in warm antibody AIHA is [[IgG]], though sometimes [[IgA]] is found.  The IgG antibodies attach to a red blood cell, leaving their F<sub>C</sub> portion sticking out.  The F<sub>C</sub> region is recognized and grabbed onto by F<sub>C</sub> receptors found on monocytes and macrophages in the [[spleen]].  These cells will pick off portions of the red cell membrane, almost like they are taking a bite.  The loss of membrane causes the red blood cells to become spherocytes.  Spherocytes are not as flexible as normal RBCs, and will be singled-out for destruction in the red pulp of the spleen as well as other portions of the reticuloendothelial system.  The red blood cells trapped in the spleen cause the spleen to enlarge, leading to the splenomegaly often seen in these patients.
-The cause of the autoantibody formation is unknown, but the mechanism for drug-induced destruction is better understood.  There are two models for this: the [[hapten]] model and the autoantibody model.  The hapten model proposes that certain drugs, especially [[penicillin]] and [[cephalosporins]], will bind to the red cell membrane and act as haptens.  Antibodies are created against the cell-drug complex, leading to the destructive sequence described above.  The autoantibody model proposes that, through a mechanism not yet understood, certain drugs will cause antibodies to be made against red blood cells which again leads to the same destructive sequence.
+==[[Warm autoimmune hemolytic anemia classification|Classification]]==
-==Clinical Findings==
+==[[Warm autoimmune hemolytic anemia pathophysiology|Pathophysiology]]==
-Laboratory findings include severe [[anemia]], increased mean corpuscular volume (MCV, due to the presence of a large number of young erythrocytes), and [[hyperbilirubinemia]] (from increased red cell destruction) that can be of the conjugated or unconjugated type.
+==[[Warm autoimmune hemolytic anemia causes|Causes]]==
+==[[Warm autoimmune hemolytic anemia differential diagnosis|Differentiating Warm autoimmune hemolytic anemia from other Diseases]]==
+==[[Warm autoimmune hemolytic anemia epidemiology and demographics|Epidemiology and Demographics]]==
+==[[Warm autoimmune hemolytic anemia risk factors|Risk Factors]]==
+==[[Warm autoimmune hemolytic anemia screening|Screening]]==
+==[[Warm autoimmune hemolytic anemia natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
 ==Diagnosis==
-Diagnosis is made by a positive direct [[Coombs test]], other lab tests, and clinical examination and history.  The direct Coombs test looks for antibodies attached to the surface of red blood cells.
+[[Warm autoimmune hemolytic anemia history and symptoms|History and Symptoms]] | [[Warm autoimmune hemolytic anemia physical examination|Physical Examination]] | [[Warm autoimmune hemolytic anemia laboratory findings|Laboratory Findings]] | [[Warm autoimmune hemolytic anemia electrocardiogram|Electrocardiogram]] | [[Warm autoimmune hemolytic anemia chest x ray|Chest X Ray]] | [[Warm autoimmune hemolytic anemia CT|CT]] | [[Warm autoimmune hemolytic anemia MRI|MRI]] | [[Warm autoimmune hemolytic anemia ultrasound|Ultrasound]] | [[Warm autoimmune hemolytic anemia other imaging findings|Other Imaging Findings]] | [[Warm autoimmune hemolytic anemia other diagnostic studies|Other Diagnostic Studies]]
 ==Treatment==
-[[Corticosteroids]] and immunoglobulins are two commonly used treatments for warm antibody AIHA. Initial Tx consists of prednisone. If ineffective, [[splenectomy]] should be considered. If refractory to both these therapies, consider rituximab, danazol, cyclosphosphamide, azathioprine, or cyclosporine, High dose intravenous immune globulin may be effective in controlling hemolysis, but the benefit is short lived (1-4 weeks), and the therapy is very expensive.
+[[Warm autoimmune hemolytic anemia medical therapy|Medical Therapy]] | [[Warm autoimmune hemolytic anemia surgery|Surgery]] | [[Warm autoimmune hemolytic anemia primary prevention|Primary Prevention]] | [[Warm autoimmune hemolytic anemia secondary prevention|Secondary Prevention]] | [[Warm autoimmune hemolytic anemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] |  [[Warm autoimmune hemolytic anemia future or investigational therapies|Future or Investigational Therapies]]
+==Case Studies==
-==References==
+[[Warm autoimmune hemolytic anemia case study one|Case #1]]
-*Sacher, Ronald A. and Richard A. McPherson. "Wildman's Clinical Interpretation of Laboratory Tests, 11th edition."
-*Kumar, Vinay, Abul Abbas, and Nelson Fausto. "Robbins and Cotran Pathologic Basis of Disease."
 {{Hematology}}

Warm autoimmune hemolytic anemia: Difference between revisions

Revision as of 17:15, 21 September 2012

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