INTRODUCTION TO NEONATAL JAUNDICE (RED BLOOD CELL)

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The major function of red blood cells, also known as erythrocytes, is to transport hemoglobin, which in turn carries oxygen from the lungs to the tissues. In some lower animals, hemoglobin circulates as free protein in the plasma not enclosed in red blood cells. When it is free in the plasma of the human being, about 3 percent of it leaks through the capillary membrane into the tissue spaces or through the glomerular membrane of the kidney into the glomerular filtrate each time the blood passes through the capillaries. Therefore for hemoglobin to remain in the blood stream, it must exist inside the red blood cells (Guyton et al, 1994).

          Bilirubin is derived from the haem moiety of the hemoglobin of  red cells, and to a much lesser extent, from the haem content of haemoproteins such as cytochrome P₄₅₀, myoglobin, catalase and peroxidases. It is known that bilirubin is not the only breakdown product of haem, but the alternative, metabolic pathway is unknown (Guyton et al,1994). The fact that such an alternative pathway exists, however, helps explain why the blood bilirubin, a pigment derived mainly from breakdown of hemoglobin, becomes stable even when excretion by the liver is completely stopped.

          Neonatal jaundice is a clinical description of the yellowish discoloration of the sclera and mucous membranes. It is due to increased serum levels of bilirubin. Jaundice in the newborn infant is a very common problem. The prevalence in hospital practice is estimated at between 23-60% (Azubuike et al, 1999). Jaundice in the newborn child is unique because it is only in the neonatal period that serum bilirubin per se poses a threat to the well being of the infant. Neonatal jaundice is of two types; physiological and pathological jaundice. Under normal circumstances, the umbilical corSd serum is 1-3 mg/dl. Jaundice appears by the 2^nd day of life, peaks by the 3^rd – 4^th day at a level of 10 -12mg/dl and disappears by the 4^th – 5^th day. Jaundice associated with these changes is designated as physiological jaundice and any thing outside this is pathological (Azubuike et al, 1999). 

          Regardless of cause, the goal of therapy is to prevent concentrations of unconjugated bilirubin from reaching toxic levels. Treatment strategies include; phototherapy, pharmacotherapy and Exchange blood transfusion. Poor management of Jaundice in a newborn can have dire consequences. Where death does not result, varying forms of cerebrial damage like kernicterus and acute bilirubin encephalopathy may occur.

SEMINAR SUBMITTED TO THE DEPARTMENT OF BIOCHEMISTRY/BIOTECHNOLOGY, EBONYI STATE UNIVERSITY (NIGERIA) IN PARTIAL FULFILLMENT  FOR  THE  AWARD  OF  THE  DEGREE  OF  MASTERS  OF  SCIENCES  IN  MEDICAL  BIOCHEMISTRY

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