PATHOLOGIC RBC FORMS.

TYPE	PATHOLOGY	BRIEF REVIEW
Biconcave		Normal
Spherocytes	Hereditary spherocytosis Autoimmune hemolysis	Spheroid erythrocytes due to spectrin or ankyrin defect; hemolytic anemia; ↑ MCHC, ↑ RDW. Associated with splenomegaly, aplastic crisis (B19 infection). Splenectomy is curative. Howell-Jolly bodies present after splenectomy.
Elliptocyte	Hereditary elliptocytosis	inherited disorders of erythrocytes that have the common feature of elliptical RBCs,the most frequent mode of inheritance is autosomal dominant. Most patients are asymptomatic and do not have any obvious physical signs. Patients with clinically significant hemolysis have splenomegaly, pallor, scleral icterus, and (in rare cases) leg ulcers.
Macro-ovalocyte	Megaloblastic anemia Marrow failure	Vitamin B12/folate deficiency
Helmet cell, schistocyte	DIC TTP/HUS Traumatic hemolysis	Activation of coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors. Platelets abnormalities. Deficiency of vWF-cleaving metalloproteinase → excess large vWF multimers, leading to ↑ platelets aggregation, thrombosis and schistocyte formation, ↑ LDH, neurologic and renal symptoms, fever.
Sickle cell	Sickle cell anemia	Autosomal recessive diseases. HbS mutation is a single amino acid replacement in β chain (substitution of normal glutamic acid with valine). Hair-on-end (crew-cut) appearance on x-ray.
Bite cell	G6PD deficiency	X-linked recessive disorder, most common human enzyme deficiency, ↑ malaria resistance. Heinz bodies.
Teardrop cell	Myeloid metaplasia with myelofibrosis
Acanthocyte (spur cell)	Spiny appearance in liver disease and abetalipoproteinemia
Target cell	HbC disease Asplenia Liver disease Thalassemia	HbC defect is a different β chain mutation.
Burr cell	TTP/HUS
Basophilic stippling	Thalassemias Anemia of chronic diseases Iron deficiency Lead poisoning	Inherited disorders of hemoglobin (Hb) synthesis. Their clinical severity widely varies, ranging from asymptomatic forms to severe or even fatal entities.
Heinz bodies	α–thalassemia G6PD deficiency	Oxidation of iron from ferrous to ferric form leads to denatured hemoglobin precipitation and damage to RBC membrane. Leads to formation of bite cell
Howell-Jolly bodies	Functional hyposplenia or asplenia	Basophilic nuclear remnants found in RBCs.

MCHC=mean corpuscular hemoglobin concentration

RDW  =red-cell distribution width

DIC    =disseminated intravascular coagulation

TTP    =thrombotic thrombocytopenic purpura

HUS   =hemolytic-uremic syndrome