32 Sideroblastic Anemia

Michelle To and Valentin Villatoro

Cause(s): Development of sideroblastic anemia can be due to hereditary or acquired causes that lead to abnormal heme synthesis.1,2

 

Hereditary: Sex-linked or autosomal recessive mutations

 

Acquired: Idiopathic, MDS and other malignancies, drugs, lead toxicity

 

Laboratory Features of Sideroblastic Anemia:1-3

CBC:

RBC: Decreased

WBC: Variable

PLT: Variable

Hb: Decreased

MCV, MCH, MCHC: Normal to Decreased (as they are averages of the RBC appearance)

RDW: Increased

RETIC: Decreased

PBS:

Dimorphic population (Normochromic/Normocytic alongside Hypochromic/Microcytic )

Tears

Schistocytes

Pappenheimer bodies

Basophilic stippling

BM:

M:E Ratio: Decreased

Erythroid hyperplasia (ineffective erythropoiesis)

Ringed sideroblasts

Macrophages have increased iron (Increased iron stores)

Iron Studies:

Serum Iron: Increased

Ferritin: Increased

Transferrin: Normal to Decreased

Transferrin Saturation: Increased

TIBC: Normal to Decreased

Other Tests:

Bilirubin: Increased

Haptoglobin: Decreased

LD: Increased

Prussian blue stain of BM shows increased iron levels and ringed sideroblasts


References:

1. McKenzie SB. Anemias of disordered iron metabolism and heme synthesis. In: Clinical laboratory hematology. 3rd ed. New Jersey: Pearson; 2015. p. 198-230.

2. Doig K. Disorders of iron kinetics and heme metabolism. In: Rodak’s hematology clinical applications and principles. 5th ed. St. Louis, Missouri: Saunders; 2015. p. 297-313.

3. Finnegan K. Iron metabolism and hypochromic anemias. In: Clinical hematology and fundamentals of hemostasis. 5th ed. Philadelphia: F.A. Davis Company; 2009. p. 117-37.

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A Laboratory Guide to Clinical Hematology by Michelle To and Valentin Villatoro is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.

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