Avascular necrosis

Sudipa Sarkar, M.D., Todd T. Brown, M.D., Ph.D.

PATHOGENS

  • In the general population in the U.S., ethanol use and glucorticoid use account for the majority of cases of avascular necrosis (AVN).[4] In particular, glucocorticoid use in the setting of systemic lupus erythematosis and organ transplantation has been associated with AVN. Other associated conditions include sickle cell disease, trauma, and radiation.[5]
  • In people with HIV (PWH), the incidence of AVN has been reported to be about 45 to 100 times greater than in the general population.[17][10]
  • The principal mechanism contributing to AVN is compromised local blood flow, with resultant necrosis.[6]
  • The pathophysiology of AVN in PWH is felt to be multifactorial, but the complete pathophysiology is unknown. Risk factors include traditional risk factors, such as glucocorticoids and dyslipidemia, HIV infection, nadir CD4 cell count, and prior AIDS-defining illness.[7][2][12]
  • The direct role of ART is controversial.[7]

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Last updated: March 7, 2020