The causes of increase and decrease in hemoglobin
Last reviewed: 19.10.2021
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The concentration of hemoglobin in the blood can increase (up to 180-220 g / l and above) with myeloproliferative diseases (erythremia) and symptomatic erythrocytosis accompanying various conditions. The study of hemoglobin concentration in dynamics gives important information about the clinical course of the disease and the effectiveness of treatment. A false increase in the concentration of hemoglobin in the blood is observed with hypertriglyceridemia, leukocytosis above 25.0 × 10 9 / L, progressive liver disease, the presence of hemoglobin C or S, myeloma or Waldenström disease (the presence of readily precipitating globulins).
Diseases and conditions, accompanied by a change in the concentration of hemoglobin in the blood
Increase in hemoglobin concentration |
Decreased hemoglobin concentration |
Primary and secondary erythrocytosis Erythremia Dehydration Excessive physical activity or agitation Long stay at high altitudes Smoking |
All kinds of anemia related:
Hyperhydration |
There are several types of hemoglobin in human blood: HbA1 (96-98%), HbA2 (2-3%), HbF (1-2%), differing in amino acid composition of globin, physical properties and oxygen affinity. HbF prevails in newborns - 60-80%, by the 4-5th month of life its quantity decreases to 10%. HbA appears in a 12-week-old fetus, in an adult it is the bulk of hemoglobin. HbF in a concentration of up to 10% can be detected with aplastic, megaloblastic anemia, leukemia; with a large beta-thalassemia, it can be 60-100% of the total hemoglobin, with a small - 2-5%. Increase of HbA2 fraction is characteristic for beta-thalassemia (for large beta-thalassemia - 4-10%, for small - 4-8%). An increase in HbA2 is observed in malaria, acute lead poisoning and chronic lead intoxication. However, in these conditions, a change in the ratio of hemoglobin fractions is not a defining symptom.
The appearance of pathological forms of hemoglobin is due to a disruption in the synthesis of globin chains (hemoglobinopathy). The most common hemoglobinopathy is S-sickle-cell anemia. The main method of detecting pathological forms of hemoglobin is the method of electrophoresis.
Methemoglobin is formed upon exposure to hemoglobin of a number of substances that transfer bivalent iron of hemoglobin into a trivalent one. Methemoglobin is unable to enter into a reversible bond with oxygen and can not carry oxygen. From the tissues and intestines, substances causing methemoglobin formation constantly enter the blood, but the amount of methemoglobin in the blood of healthy people remains small - 0.4-1.5% of the total hemoglobin content.
Methemoglobinemia (the content of methaemoglobin is more than 1.5% of the total hemoglobin content) can result from hereditary diseases or exposure to toxic agents. These can be various substances (potassium chlorate, benzene derivatives, aniline, nitrogen oxides, some synthetic paints, methylnitrophos, nitrates of well water, etc.). Methemoglobinemia can develop with enterocolitis.
At low degrees of methemoglobinemia (less than 20% of total hemoglobin), clinical and hematologic symptoms may be absent. Expressed methemoglobinemia causes a decrease in the oxygen capacity of the blood, which develops with a sufficient or even compensatory increase in the amount of hemoglobin and erythrocytes. In erythrocytes, pathological inclusions (Heinz body) can be detected. Sometimes a small reticulocytosis is possible.