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* Can be autosomal dominant or recessive
* Can be autosomal dominant or recessive
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|[[Thalassemia]]
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* [[Genetic defect]] with alpha- or [[beta-globin]] production
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* [[Microcytic]] (<80 femtoliter)
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* Abnormal [[hemoglobin]] [[electrophoresis]] (in [[beta-thalassemia]])
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* [[Irritability]]
* [[Growth retardation]]
* [[Jaundice]]
* [[Hepatomegaly]]
* [[Splenomegaly]]
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* [[Blood transfusion|Transfusion]] support
* [[Iron]] chelation
* [[Gene therapy]] if available
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* [[Extramedullary hematopoiesis]]
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|[[Iron deficiency anemia]]
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* Loss of [[iron]] from [[gastrointestinal]] blood loss or [[menstrual]] [[blood loss]]
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* [[Microcytic]] (<80 femtoliter)
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* Low serum [[iron]]
* Elevated [[transferrin]]
* Low [[transferrin saturation]]
* Low [[ferritin]]
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* [[Pallor]]
* [[Weakness]]
* Positive [[occult blood]] testing (if [[Gastrointestinal bleeding|GI bleeding]])
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* Intravenous or oral iron supplementation
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* [[Blood loss|Chronic blood loss]]
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|-
|[[Pernicious anemia]]
|[[Pernicious anemia]]

Revision as of 01:14, 2 April 2018

Autoimmune hemolytic anemia Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assosciate Editor(s)-In-Chief: Prashanth Saddala M.B.B.S; Shyam Patel [2]

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Overview

Differentiating Autoimmune hemolytic anemia from other Diseases

Diagnosis is made by first ruling out other causes of hemolytic anemia, such as G6PD, thalassemia, sickle-cell disease, etc.


Characteristic Causes Pathophysiology Laboratory abnormalities Physical examination Therapy Other associations
Autoimmune hemolytic anemia
  • Polyclonal antibody production that binds to and targets red blood cells for destruction intravascurly or extravascularly[1]
  • Removal of offending agent
  • Corticosteroids
  • Cyclophosphamide
  • Cyclosporine A
  • Azathioprine
  • Rituximab
  • Splenectomy
  • Hemolysis can occur at warm or cold temperatures
Paroxysmal cold hemoglobinuria
  • Biphasic hemolysin (IgG) that binds red blood cells and low temperatures and triggers complement-mediated intravascular hemolysis at warm temperatures[2]
  • Associated with syphilis[2]
  • Maternal IgG can cross the placenta and affect the fetus[2]
Hereditary spherocytosis[3]
  • Mutation in ankyrin[3]
  • Mutation in alpha- or beta-spectrin[3]
  • Mutation in band 3[3]
  • Mutation in protein 4.2[3]
  • Positive eosin-5-maleimide binding to red blood cells[3]
  • Positive osmotic fragility testing[3]
  • Spherocytes on peripheral blood smear
  • Can be autosomal dominant or recessive
Pernicious anemia
  • Vitamin B12 deficiency
  • Low vitamin B12 level
  • Presence of anti-intrinsic factor or anti-parietal cell antibody
Chronic lymphocytic leukemia
  • Mutations in hematopoietic stem cells and B lymphocytes
  • Clonal proliferation of malignant B lymphocytes
  • Elevated absolute lymphocyte count
  • Anemia (Rai stage III) and thrombocytopenia (Rai stage IV)
  • Secondary autoimmune hemolytic anemia occurs in advanced CLL; treatment with corticosteroids or anti-leukemic therapy will correct the underlying anemia

References

  1. ↑ 1.0 1.1 1.2 Berentsen S, Sundic T (2015). "Red blood cell destruction in autoimmune hemolytic anemia: role of complement and potential new targets for therapy". Biomed Res Int. 2015: 363278. doi:10.1155/2015/363278. PMC 4326213. PMID 25705656.
  2. ↑ 2.0 2.1 2.2 2.3 Akpoguma AO, Carlisle TL, Lentz SR (2015). "Case report: paroxysmal cold hemoglobinuria presenting during pregnancy". BMC Hematol. 15: 3. doi:10.1186/s12878-015-0023-7. PMC 4334594. PMID 25699184.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Gallagher PG (2013). "Abnormalities of the erythrocyte membrane". Pediatr Clin North Am. 60 (6): 1349–62. doi:10.1016/j.pcl.2013.09.001. PMC 4155395. PMID 24237975.

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