Comparative Study Of Electrolyte Patterns In Sickle Cell Disease Patients In Owerri
ABSTRACT
A study on the comparative study of electrolyte patterns in sickle cell disease patients in Owerri was carried out. A total of 60 subjects between the ages of 18 and 40 years were randomly selected.
30 subjects were sickle cell disease patients while 30 subjects who served as the control were not suffering from sickle cell disease. Serum electrolyte were measured using colorimetric method and manufactures standard operating procedure were strictly adhered to.
Data were compared between Sickle cell patients and control. Comparism was also done according to patients various age groups.
Statistical analyses were done using student independent t-test and anova. Results obtained from the study showed that sickle cell anaemia patients has a significant (P<0.05) decrease in serum sodium (102.93 ± 10.91mEq/L) concentration compared to the control subjects (139.10 ± 5.01mEq/L).
Sodium level was lower among the older patient. Potassium concentration of patient (5.53 ±0.37 mEq/L) was significantly in control subjects (4.17 ± 0.49mEq/L).
Potassium level was higher among the older patients. Results also gathered from the study showed that sickle cell anaemia resulted in significant (P<0.05) decreased in serum chloride concentration compared to the control subjects.
Chloride concentration was 103.07 ± 12.41 and 73.77 ± 8.06 mEqL in control subjects and sickle cell patients respectively. Chloride level was lower among the older patients.
Bicarbonate concentration of patient (17.57±2.47mEq/L) was significantly lower when compared to the control subjects (24.17±2.49mEq/L). Bicarbonate was lower among patients of age group 27-33 (17.82± 1.24 mEq/l) and higher in those of age group 18-26 (20.43±2.18 mEq/l).
In conclution decrease electrolyte in patients with sickle cell disease probably depends on dehydration accelerated influx and efflux of sodium and potassium ion respectively. The regular measurement of sodium and potassium is necessary in the management of sickle cell patient.
INTRODUCTION
Sickle cell disease (SCD) is a group of inherited disorders of the beta-hemoglobin chain. Normal hemoglobin has 3 different types of hemoglobin – hemoglobin A, A2, and F. Hemoglobin S in sickle cell disease contains an abnormal beta globin chain encoded by a substitution of valine for glutamic acid on chromosome 11 (Bunn,2007). This is an autosomal recessive disorder.
Sickle cell disease refers to a specific genotype in which a person inherits one copy of the HbS gene and another gene coding for a qualitatively or quantitatively abnormal beta globin chain.
Sickle cell anemia (HbSS) refers to patients who are homozygous for the HbS gene, while heterozygous forms may pair HbS with genes coding for other types of abnormal hemoglobin such as hemoglobin C, an autosomal recessive mutation which substitutes lysine for glutamic acid.
In addition, persons can inherit a combination of HbS and β-thalassemia. The β-thalassemias represent an autosomal recessive disorder with reduced production or absence of β-globin chains resulting in anemia. Other genotype pairs include HbSD, HbSO-Arab and HbSE (Meremiku, 2008).
Sickle hemoglobin in these disorders cause affected red blood cells to polymerize under conditions of low oxygen tension resulting in the characteristic sickle shape.
Normal red cells live about 120 days in the blood stream but sickled red cells die after about 10 – 20 days. Because they cannot be replaced fast enough, the blood is chronically short of red blood cells, a condition called anaemia.
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