Complications Of Aplastic

Anemia
 Heart Failure
Hb < 13 gr% untuk laki-laki,
dan < 12 gr% untuk
perempuan.
Risk Factors
Old age, female gender, a
decrease in body mass index, use
of angiotensin converting
enzyme–inhibitor (ACE-
inhibitor) drugs and angiotensin
receptor blockers (ARBs), as well
advanced heart failure
- Abnormality heart function and
structure
- Peripheral ischemia
- Activates the renin-angiotensin
aldosterone system
- Increased volume of extracellular fluid
due to retention fluid
- Plasma overloads
Etiology
The reduced tolerance for
workload, exacerbate functional
class heart failure based on the
New York Heart Association
(NYHA) functional class, as well
leading to increased hospitalization
and death from heart failure
 - Inflammation
- Proinflammatory cytokines such as
TNF-ά, interleukin-1 and interleukin-6 : increased in heart failure, and cause impaired aspects of erythropoiesis
- Proinflammatory cytokines also increase hepcidin levels
- Hepcidin causes impaired absorption of iron in the duodenum: increases iron uptake into the macrophages and inhibits iron release from
macrophages.
- This leads to iron trapped in macrophages thereby reducing the bioavailability of stored iron for hemoglobin synthesis

- The renin-angiotensin system plays an important role in the regulation of plasma and erythrocyte volume.
- Coding improvements Angiotensin II in the kidney changes blood pressure peritubular oxygen is a factor important regulation of erythropoietin
secretion.
- Decreased peritubular oxygen tension in the adrenal cortex causes increased hypoxia inducible factor-1 (HIF-1) activity and expression of the
erythropoietin gene.
-Angiotensin II increases erythropoietin secretion by decreasing blood flow kidneys and increase sodium reabsorption in the proximal tubule
- Angiotensin II too has a direct stimulating effect on erythrocyte precursors in the bone marrow.
- Inhibition of the renin-angiotensin system with ACE inhibitors or ARBs associated with decreased production erythrocytes, causing anemia

—Heart Failure
 Leukimia
Chronic Lymphocytic
Leukimia Leukimia ( CLL )
Abnormal leukocyte Bone marrow : ↑producing too
production abnormal lymphocytes

Reduced body's ability to produce new Acute Myeloid

red blood cells. Because red blood cells, Leukimia ( AML )
white blood cells, and platelets are made
in the bone marrow, other blood cells are Bone marrow : ↑ produces too
affected immature myeloid cells or
myeloblasts.
Akute Lymphoblastic Chronic Myeloid
Leukimia ( ALL ) Leukimia ( CML )
Bone marrow : ↑ produces Bone marrow is unable to
too immature white blood produce mature myeloid cells.
cells (lymphocytes).
 Febrile Neutropenia and Bleeding
Febrile
Neutropenia is a common complication in
patients receiving immunosuppressive therapy
for various reasons such as with leukemia
acute and other hematology, malignancy, post
bone marrow transplant and anemia
aplastic
A marked state
by anemia, leukopenia, and
thrombocytopenia in the peripheral blood
caused by a primary abnormality of the marrow
bone in aplastic or hypoplastic form
without infiltration, suppression or
bone marrow suppression
Hemochromatosis
- An autosomal recessive disorder that is carried on a closely
related chromosome 6
with HLA-A3
- More homozygous prone to iron overload. However, 10% of the
heterozygotes will also show signs excessive iron production

In the patient there is a process absorption and storage of iron become

unbalanced due to the inheritance of an abnormal gene, HFE, a gene
that regulates the amount of iron absorbed from food

Because iron is constantly loaded inside

storage sites and cause symptoms and multiorgan damage for
many years.
  
1. Putra M, Aprijadi H. Anemia Aplastik Berat dengan Komplikasi Febril
Neutropenia dan Perdarahan pada Perempuan Usia 20 Tahun. J
Agromedicine. 2019;6(1):226–30.
2. Andika A. Buku Ajar Mata Kuliah Hematologi. Buku Ajar Mata Kuliah
Hematologi. 2019.
3. Hendrata C, Lefrandt RL. Anemia Pada Gagal Jantung. J Biomedik.
2013;2(3):133–9.
 

—Reference