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MCHC can be normal even when hemoglobin production is decreased (such as in iron deficiency) due to a calculation artifact. MCHC can be elevated ("hyperchromic") in hereditary spherocytosis, sickle cell disease and homozygous hemoglobin C disease, depending upon the hemocytometer. [4] [5] MCHC can be elevated in some megaloblastic anemias. MCHC ...
Macrocytic anemias have several causes but with the implementation of folic acid fortification in North America, folate deficiency has become a rare cause of megaloblastic macrocytic anemia in that part of the world. [1] In this region, Vitamin B 12 deficiency is a far more common cause of megaloblastic macrocytic anemia. [1]
As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B 6, folic acid (vitamin B 9), and vitamin B 12 can lead to high homocysteine levels. [2] Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases.
Polycythemia is defined as serum hematocrit (Hct) or hemoglobin (HgB) exceeding normal ranges expected for age and sex, typically Hct >49% in healthy adult men and >48% in women, or HgB >16.5 g/dL in men or >16.0 g/dL in women. [8] The definition is different for neonates and varies by age in children. [9] [10]
Decreased red blood cell (RBC) count and hemoglobin levels [7] Increased mean corpuscular volume (MCV, >100 fL) and mean corpuscular hemoglobin (MCH) Normal mean corpuscular hemoglobin concentration (MCHC, 32–36 g/dL) Decreased reticulocyte count due to destruction of fragile and abnormal megaloblastic erythroid precursor. The platelet count ...
The most common causes of microcytic anemia are iron deficiency (due to inadequate dietary intake, gastrointestinal blood loss, or menstrual blood loss), thalassemia, sideroblastic anemia or chronic disease. In iron deficiency anemia (microcytic anemia), it can be as low as 60 to 70 femtolitres.
Treatment may vary depending on the cause of the condition. In the case of hereditary spherocytosis, although research is ongoing, at this point there is no cure for the genetic defect that causes hereditary spherocytosis. [5] Current management focuses on interventions that limit the severity of the disease.
Hemoglobin C is produced when a point mutation in the HBB gene causes amino acid substitution of glutamic acid to lysine at the 6th position of the β-globin chain of the hemoglobin. The mutation can be homozygous, occurring on both the chromosomes (alleles), or heterozygous, affecting only one allele. [ 1 ]