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Hemolytic jaundice information


Hemolytic jaundice, also known as prehepatic jaundice, is a type of jaundice arising from hemolysis or excessive destruction of red blood cells, when the byproduct bilirubin is not excreted by the hepatic cells quickly enough.[1] Unless the patient is concurrently affected by hepatic dysfunctions or is experiencing hepatocellular damage, the liver does not contribute to this type of jaundice.[1]

As one of the three categories of jaundice, the most obvious sign of hemolytic jaundice is the discolouration or yellowing of the sclera and the skin of the patient, but additional symptoms may be observed depending on the underlying causes of hemolysis. Hemolytic causes associated with bilirubin overproduction are diverse and include disorders such as sickle cell anemia,[2] hereditary spherocytosis,[3] thrombotic thrombocytopenic purpura,[4] autoimmune hemolytic anemia,[5] hemolysis secondary to drug toxicity,[6] thalassemia minor,[7] and congenital dyserythropoietic anemias.[8] Pathophysiology of hemolytic jaundice directly involves the metabolism of bilirubin, where overproduction of bilirubin due to hemolysis exceeds the liver's ability to conjugate bilirubin to glucuronic acid.[9]

Diagnosis of hemolytic jaundice is based mainly on visual assessment of the yellowing of the patient's skin and sclera, while the cause of hemolysis must be determined using laboratory tests.[10] Treatment of the condition is specific to the cause of hemolysis, but intense phototherapy and exchange transfusion can be used to help the patient excrete accumulated bilirubin.[11] Complications related to hemolytic jaundice include hyperbilirubinemia and chronic bilirubin encephalopathy, which may be deadly without proper treatment.[12][13]

  1. ^ a b Hall J (2015). Pocket Companion to Guyton and Hall Textbook of Medical Physiology. Saunders. ISBN 978-1455770069.
  2. ^ Rees DC, Williams TN, Gladwin MT (December 2010). "Sickle-cell disease". Lancet. 376 (9757): 2018–31. doi:10.1016/S0140-6736(10)61029-X. PMID 21131035. S2CID 29909566.
  3. ^ "Hereditary spherocytosis | Genetic and Rare Diseases Information Center (GARD) – an NCATS Program". rarediseases.info.nih.gov. Retrieved 2021-04-01.
  4. ^ Page EE, Kremer Hovinga JA, Terrell DR, Vesely SK, George JN (April 2017). "Thrombotic thrombocytopenic purpura: diagnostic criteria, clinical features, and long-term outcomes from 1995 through 2015". Blood Advances. 1 (10): 590–600. doi:10.1182/bloodadvances.2017005124. PMC 5728353. PMID 29296701.
  5. ^ Brodsky RA (August 2019). "Warm Autoimmune Hemolytic Anemia". The New England Journal of Medicine. 381 (7): 647–654. doi:10.1056/NEJMcp1900554. PMID 31412178. S2CID 199662490.
  6. ^ Dausset J, Contu L (1967). "Drug-induced hemolysis". Annual Review of Medicine. 18: 55–70. doi:10.1146/annurev.me.18.020167.000415. PMID 5337612.
  7. ^ Robinson S, Vanier T, Desforges JF, Schmid R (September 1962). "Jaundice in thalassemia minor: a consequence of "ineffective erythropoiesis"". The New England Journal of Medicine. 267: 523–9. doi:10.1056/NEJM196209132671101. PMID 14492944.
  8. ^ Kamiya T, Manabe A (October 2010). "Congenital dyserythropoietic anemia". International Journal of Hematology. 92 (3): 432–8. doi:10.1007/s12185-010-0667-9. PMID 20820969. S2CID 71018193.
  9. ^ Billing BH (June 1978). "Twenty-five years of progress in bilirubin metabolism (1952-77)". Gut. 19 (6): 481–91. doi:10.1136/gut.19.6.481. PMC 1412033. PMID 98394.
  10. ^ Cite error: The named reference :2 was invoked but never defined (see the help page).
  11. ^ Cite error: The named reference :1 was invoked but never defined (see the help page).
  12. ^ Cite error: The named reference :13 was invoked but never defined (see the help page).
  13. ^ Cite error: The named reference :14 was invoked but never defined (see the help page).

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