World Library  
Flag as Inappropriate
Email this Article

Drug-induced autoimmune hemolytic anemia

Article Id: WHEBN0021438687
Reproduction Date:

Title: Drug-induced autoimmune hemolytic anemia  
Author: World Heritage Encyclopedia
Language: English
Subject: Acquired hemolytic anemia, Nutritional anemia, Delta-thalassemia, Hexokinase deficiency, Hereditary persistence of fetal hemoglobin
Collection: Acquired Hemolytic Anemia
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Drug-induced autoimmune hemolytic anemia

Drug-induced autoimmune hemolytic anemia
Classification and external resources
ICD-10 D59.0
ICD-9 283

Drug-induced autoimmune hemolytic anemia is a form of hemolytic anemia.

In some cases, a drug can cause the immune system to mistakenly think the body's own red blood cells are dangerous, foreign substances. Antibodies then develop against the red blood cells. The antibodies attach to red blood cells and cause them to break down too early. Drugs that can cause this type of hemolytic anemia include:

Cephalosporins (a class of antibiotics) -- most common cause

Dapsone

Levodopa

Levofloxacin

Methyldopa

Nitrofurantoin

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Phenazopyridine (pyridium)

Quinidine [1]

Penicillin in high doses can induce immune mediated hemolysis[2] via the hapten mechanism in which antibodies are targeted against the combination of penicillin in association with red blood cells. Complement is activated by the attached antibody leading to the removal of red blood cells by the spleen.

The drug itself can be targeted by the immune system, e.g. by IgE in a Type I hypersensitivity reaction to penicillin, rarely leading to anaphylaxis.

See also

References

  1. ^ http://www.nlm.nih.gov/medlineplus/ency/article/000578.htm
  2. ^ Stroncek D, Procter JL, Johnson J (May 2000). "Drug-induced hemolysis: cefotetan-dependent hemolytic anemia mimicking an acute intravascular immune transfusion reaction". Am. J. Hematol. 64 (1): 67–70.  
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.