Serum transcobalamin II level in glucose-6-phosphate dehydrogenase deficient subjects with typhoid fever.

ABSTRACT

Transcobalamin II (TCII) is the vitamin B12 binding protein which is responsible for delivery of this vitamin to the tissues. High values for serum TCII have been reported in many clinical conditions. This paper describes the elevated serum TCII levels in three G-6-PD deficient patients with typhoid fever. They had severe hemolysis with hemoglobinuria associated with slight liver dysfunctions but without obvious increased serum creatinine and BUN concentrations. A remarkable increase in serum TCII level was observed during active hemolysis and decreased to the normal level within 2-3 days after hemolysis ceased. The mechanism of increased serum TCII during hemolysis is probably due to hemoglobinuria secondary to excessive hemolysis. As Hb is known to be efficiently reabsorbed by the proximal tubule cells and can competitively inhibit the tubular uptake of TCII-B12. It is possible that excess Hb interferes with TCII uptake and degradation at renal tubular cells. Therefore, the circulating TCII survival is prolonged resulting in the elevated TCII level. Furthermore, lysosomal degradation of newly synthesized TCII is a normal process that regulates the TCII secretion. Therefore, a reduced lysosome-mediated uptake of TCII-B12 by renal tubular cell may stimulate the TCII secretion as has been shown experimentally in vitro.