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At least 433 records · Page 24Linked to original sources
PubMed1996

Abnormal hemoglobins with high oxygen affinity and erythrocytosis.

More than 200 hemoglobin variants with high oxygen affinity have been reported since 1966. In about one third of these, the increase in oxygen affinity is responsible for a compensatory erythrocytosis. The degree of erythrocytosis depends primarily upon the molecular defect of the hemoglobin molecule. Measurement of the oxygen binding properties of the blood (or of the stripped lysate) is a convenient test both for the diagnosis of these variants and for evaluation of their severity. In the severe cases the affinity of the abnormal hemoglobin is identical to that of isolated subunits and the heme heme interaction is abolished; erythrocythemia is usually observed. Conversely, when the increase in oxygen affinity is moderate no clinical abnormal features are noticed. A high oxygen affinity variant has to be suspected when the hemoglobin level is at the upper limits of the normal in females or individuals with a mild iron deficiency. Several high oxygen affinity hemoglobins are also unstable and a hemolytic process may mask the increase of the Hb level. These patients, despite Hb levels close to the normal, are anemic from a functional view point. Examples have been reported in the literature in which the high oxygen affinity hemoglobin was found in coincidence with another red cell abnormality: such a situation lead usually to a more severe syndrome than the simple heterozygous state.

Erythrocytes↗
PubMed1975

Abnormal hemoglobin synthesis in some leukemic patients.

Hemoglobin chain synthesis during leukemic processes has been studied on patients having fetal hemoglobin. All cases showed the following abnormalities : (1) a relatively increased synthesis of the beta chain ; (2) an important increase of the free dimeric precursors pool, with, most of the time, a predominance of alpha chain. If the first point suggests an alpha-thalassemia feature, the presence of free alpha chains shows evidence for a more complex mechanism not only due to a decrease of messenger RNA. The hypothesis of a clonal disorder could neither be demonstrated nor ruled out. The observed abnormalities could be due to a defect in a alpha chain depending regulation mechanism.

Carbon Radioisotopes↗
PubMed2006

[Hemoglobinopathies--clinical symptoms and diagnosis of thalassemia and abnormal hemoglobins].

Haemoglobinopathies constitute entities that are generated by either an abnormal haemoglobin or thalassaemias. While abnormal haemoglobins are caused by a qualitative structural abnormality of the haemoglobin molecule, thalassaemias result by diminished synthesis of the globin chain. Due to increased immigration from Asia, Africa and the Mediterranean to Northern Europe, haemoglobin S, haemoglobin C, haemoglobin E are also encountered commonly in Switzerland, while other abnormal haemoglobins are rare, yet can cause clinically relevant symptoms. This include haemolysis, polyglobulia, cyanosis or a combination thereof Thalassaemia-syndroms constitute with two million affected individuals to the most prelevant monogenetic diseases worldwide. Due to migration into Switzerland, they are also found quite commonly among our patients with 10-15 per cent of all hypochromic, microcytic, anemia second only to iron deficiency. Importantly, thalassaemias and haemoglobinopathies can occur concomitantly sometimes even with a normal haemoglobin variant. This results in wide-spread presentations, making diagnosis and clinical judgement difficult. We describe in this article not only physiological mechanisms and clinical presentation but also propose a step-wise diagnostic algorithm including selective use of molecular biology methods.

Hematologic Tests↗