Biochemical diagnosis in sickle cell disease

Ghana Medical Journal
|March 1, 1971
PubMed

Seventy-four sicklers with bone pain had blood taken for biochemical analysis of the haemoglobins carried. Sixty-five patients with sickle cell disease diagnosed as Hb S/S disease, five patients diagnosed as Hb A/S and four patients with three haemoglobin bands corresponding to Hb's A, S and C were used in this quantitative reassessment on cellulose acetate. Haemoglobin A2 level was determined in all cases and alkali resistant haemoglobin level in twenty-nine cases. The significance of raised Hb A2 levels in some of these cases is discussed with relation to the possible existence of Hb S/beta-Thalassaemia in the sickle cell disease patients examined.

Related Concept Videos

Pedigree Analysis01:35

Pedigree Analysis

Overview
Glucose Transporters01:27

Glucose Transporters

Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
Disorders of Erythrocytes01:27

Disorders of Erythrocytes

Disorders of erythrocytes, or red blood cells (RBCs), include a range of conditions affecting their number, shape, or function.
Erythrocyte disorders can be broadly categorized into two main types: anemic and polycythemic conditions.
A low oxygen-carrying capacity of the blood due to the loss, lower production, or destruction of erythrocytes is termed anemia. Hemorrhagic anemia, for example, occurs when bleeding from an external wound or internal ulcer reduces erythrocyte counts.
On the other...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...