Anemia of chronic disease overview: Difference between revisions
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==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
The primary goal in the treatment of [[anemia]] of chronic disease it to treat the [[disease]] itself. [[Iron|Supplemental iron]] is recommended, as needed, to keep the [[transferrin]] saturation of above 20 percent and a [[serum]] [[ferritin]] level of above100 ng/mL. [[Intravenous therapy|Intravenous]] [[iron]] is more effective than [[Oral|oral supplementaion.]] Stable patients can be administered synthetically prepared [[erythropoiesis]]-stimulating agent such as [[erythropoietin]]. It is important to give [[oral]] [[iron]] supplementation to all the patients receiving [[erythropoietin]] or [[darbepoetin]], in order to maintain a t[[Transferrin|ransferrin]] [[saturation]] more than 20 percent and a [[serum]] [[ferritin]] more than 100 ng/mL. In case of severe [[disease]], [[blood transfusion]] is recommended. If the case is underlying [[malignancy]], [[chemotherapy]] or [[radiotherapy]] may transiently exacerbate [[anemia]] due to [[Bone marrow suppression|mylesuppressive]] effects, however in the long term, it leads to improvement. If the cause is [[Inflammatory|inflammatory disorder]], such as [[rheumatoid arthritis]] the management of the disease with a [[disease-modifying antirheumatic drug]] [[DMARD|(DMARD]]) improves the [[anemia]] significantly. | |||
=== Interventions === | === Interventions === |
Revision as of 16:20, 3 October 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Historical Perspective
Classification
There is no established classification of anemia of chronic disease.
Pathophysiology
Inflammatory cytokines induce increased amounts of hepcidin by the liver. Hepcidin blocks ferroportin from releasing iron from the body stores. Inflammatory cytokines also decrease ferroportin expression and stops erythropoiesis by increasing bone marrow erythropoietin resistance. Apart from iron sequestration, white blood cells production is promoted by inflammatory cytokines. Bone marrow stem cellsproduce both red blood cells and white blood cells cells. Therefore, the upregulation of white blood cells causes fewer stem cells to differentiate into red blood cells. This may also have a role in inhibition of erythropoiesis ,even when erythropoietin levels are normal, and aside from the effects of hepcidin.
Causes
Conditions that can lead to anemia of chronic disease include autoimmune disorders, such as Crohn's disease, systemic lupus erythematosus, rheumatoid arthritis, and ulcerative colitis, Cancer including lymphoma and Hodgkin's disease, chronic kidney disease, liver cirrhosis, long-term infections, such as bacterial endocarditis, osteomyelitis (bone infection), HIV/AIDS, hepatitis B or hepatitis C, less production of erythropoietin (EPO) by kidneys, resistance of bone marrow to EPO., decreased half life of red blood cells, hospitalized for severe acute infections, trauma, or other conditions that cause inflammation and aging process may cause inflammation and anemia.
Differentiating from Other Diseases
Epidemiology and Demographics
30 to 60 percent of patients in rheumatoid arthritis patients have anemia. More than 30 of cancer patients have anemia. The rate reached 63 percent. In elderly patients, about one third of the cases of anemia are ACD.
Risk Factors
Risk factors for anemia of chronic disease include autoimmune disorders, chronic infection, trauma, major surgery, malignancy, HIV infection, rheumatologic disorders, inflammatory bowel disease, castleman disease, heart failure, older adults, renal insufficiency and chronic obstructive pulmonary disease.
Screening
There is insufficient evidence to recommend routine screening for anemia of chronic disease.
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Study of Choice
There is no single diagnostic study of choice for test that will reliably make the diagnosis of ACD
History and Symptoms
Physical Examination
Laboratory Findings
Mild normocytic and normochromic anemia with a hemoglobin concentration of 10 to 11 g/dL. Less than 25 percent of the cases have microcytic and hypochromic anemia with a mean corpuscular volume (MCV) less than 70 fL. Normal or low mean corpuscular hemoglobin (MHC) similar to the MCV, and normal to increased red cell distribution width (RDW). No significant changes in the mean corpuscular hemoglobin concentration (MCHC). 20 percent of cases have severe anemia, with a hemoglobin concentration <8 g/dL. Absolute reticulocyte count is frequently low (<25,000/microL). There could be an elevation in cytokines (eg, IL-6, interferon-gamma) and acute phase reactants (eg, fibrinogen, erythrocyte sedimentation rate, C-reactive protein, ferritin, haptoglobin, factor VIII)
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
The primary goal in the treatment of anemia of chronic disease it to treat the disease itself. Supplemental iron is recommended, as needed, to keep the transferrin saturation of above 20 percent and a serum ferritin level of above100 ng/mL. Intravenous iron is more effective than oral supplementaion. Stable patients can be administered synthetically prepared erythropoiesis-stimulating agent such as erythropoietin. It is important to give oral iron supplementation to all the patients receiving erythropoietin or darbepoetin, in order to maintain a transferrin saturation more than 20 percent and a serum ferritin more than 100 ng/mL. In case of severe disease, blood transfusion is recommended. If the case is underlying malignancy, chemotherapy or radiotherapy may transiently exacerbate anemia due to mylesuppressive effects, however in the long term, it leads to improvement. If the cause is inflammatory disorder, such as rheumatoid arthritis the management of the disease with a disease-modifying antirheumatic drug (DMARD) improves the anemia significantly.