RT Book, Section
A1 Ganz, Tomas
A2 Kaushansky, Kenneth
A2 Prchal, Josef T.
A2 Burns, Linda J.
A2 Lichtman, Marshall A.
A2 Levi, Marcel
A2 Linch, David C.
SR Print(0)
ID 1178739771
T1 Anemia of Chronic Disease
T2 Williams Hematology, 10e
YR 2021
FD 2021
PB McGraw-Hill Education
PP New York, NY
SN 9781260464122
LK accessmedicine.mhmedical.com/content.aspx?aid=1178739771
RD 2024/04/19
AB SUMMARYMost  patients  who  experience  chronic  infections  or  chronic  inflammation,  or  some  patients  with  various  malignancies,  will  also  have  mild  to  moderate  anemia.  This  anemia,  designated  anemia  of  chronic  disease  or  anemia  of  inflammation,  is  characterized  by  a  low  serum  iron  level,  a  low  to  normal  transferrin  level,  and  a  high  to  normal  ferritin  level.  The  anemia  is  caused  by  the  direct  and  indirect  inhibitory  effects  of  inflammatory  cytokines  on  erythrocyte  production.  Among  the  cytokines,  interleukin-6  has  a  central  role,  acting  by  increasing  hepatocyte  production  of  the  iron-regulatory  hormone  hepcidin.  Hepcidin  then  blocks  the  release  of  iron  from  macrophages  and  hepatocytes,  causing  the  characteristic  hypoferremia  associated  with  this  anemia  and  limiting  the  availability  of  iron  to  the  developing  erythrocytes.  Effective  treatment  of  the  underlying  disease  restores  normal  erythropoiesis.  When  this  is  not  possible,  and  treatment  is  necessary,  therapeutic  trials  have  revealed  that  the  anemia  is  often  responsive  to  pharmacologic  doses  of  erythropoietin  combined  with  intravenous  iron.Anemia  of  chronic  kidney  disease  presents  similarly  to  anemia  of  inflammation  but,  because  the  kidneys  are  the  predominant  site  of  erythropoietin  production,  the  pathogenesis  of  this  anemia  is  frequently  dominated  by  relative  erythropoietin  deficiency,  where  erythropoietin  concentrations  in  serum  are  lower  than  expected  for  the  severity  of  anemia.  Systemic  inflammation  from  underlying  renal  disease,  or  that  induced  by  dialysis  treatments  and  their  complications,  contributes  to  pathogenesis  in  a  manner  similar  to  anemia  of  inflammation.  Circulating  hepcidin  concentrations  may  also  rise  because  of  its  decreased  renal  clearance.  Suppressive  effects  of  uremia  on  erythropoiesis  and  blood  losses  from  hemodialysis  may  contribute  to  anemia  in  end-stage  renal  disease.  A  combination  of  erythropoiesis-stimulating  agents  and  intravenous  iron  is  usually  effective  in  reversing  anemia,  but  overtreatment  may  worsen  overall  outcomes.