Serum transcobalamin II levels in patients with acute and chronic renal failure.

Serum TCII levels were determined in 57 patients with acute and chronic renal failure. They were divided into 3 groups, group I was malarial patients with acute renal failure, group II and III were patients with acute renal failure and chronic renal failure from other underlying causes, respectively. All patients in group I had serum TCII over 2000 pg/ml while these values were within the normal limits in the other 2 groups. These findings indicated that elevated serum TCII occurred only in malarial patients with acute renal failure. The clearance and urinary excretion of TCII in malarial patients were found to be lower and increased to the normal levels after recovery from azotemia, indicating that the failure of excretion of TCII by the kidneys may be responsible for elevated serum TCII levels. The pathophysiological changes in the kidneys in malarial patients may reduce the amount of filtered TCII-B12 through the glomeruli and decrease TCII-B12 uptake by the renal tubules resulting in the decreased TCII degradation by tubular cells. Therefore, the intravascular TCII survival is prolonged with elevated serum TCII levels in these patients.

Serum transcobalamin II levels in patients with malaria infection.

Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1% infection). Elevated serum TCII values were found only in patients with severe malaria infection. These values correlated directly with parasitemia, blood urea nitrogen and creatinine, but were not correlated with alkaline phosphatase. As 17 patients with azotemia had elevated serum TCII levels while other 3 patients with normal BUN and creatinine concentrations had serum TCII levels within the normal limits. These findings indicated that malarial patients with renal insufficiency had increased serum TCII. A possible mechanism is the reduced TCII-B12 that filtered through the glomeruli due to the reduced renal blood flow with the decreased its uptake by proximal tubular cells resulting in the decreased degradation of TCII by the tubular lysosomal enzymes. Determination of serum TCII level may be used as an indicator of renal function in malarial patients with renal insufficiency.

Persistently elevated serum transcobalamin II in a patient with cerebral malaria and typhus infections.

A 25-year-old man presented with a history of fever, chills and vomiting for three days. The parasite count was 207 ring-forms of P. falciparum per 1000 red cells. He developed hemoglobinuria and excreted hemoglobin in the urine 0.20-0.30 g/dl for 14 days during admission. Many blood transfusions were administered for correcting anemia. Although the malarial parasites disappeared one week after anti-malarial therapy, however, the fever and hemoglobinuria persisted. The Weil-Felix reaction OXK was positive with a titre of 1:40 on admission and increased to 1:160 on the second week. Chloramphenical and prednisolone were given for treatment of typhus fever and all symptoms subsided. Serum TCII levels were found to be increased and persisted high during the hemoglobinuria. The clearance of TCII was lower and increased relatively slowly to the normal level on day 30. On the other hand, TCII excretion in the urine was found to be increased during hemoglobinuria. These findings indicate that the catabolism and clearance of TCII in this patients is impaired with increased TCII excretion in the urine in parallel to the hemoglobinuria. Serum TCII level is, therefore, increased and persistently high in a patient with malaria and typhus fever infections with hemoglobinuria.

Estudio de la vitamina B12 y sus transportadores en la leucemia aguda y síndrome mieloproliferativo / Study of vitamin B12 and its carriers in acute leukemia and myeloproliferative syndrome

Se realizaron determinaciones de la vitamina B12 y sus proteínas transportadoras en un grupo de pacientes con leucemia aguda y síndrome mieloproliferativo y los resultados se compararaon con un grupo control. El grupo con policitemia vera se compara con 5 pacientes que padecen de policitemia secundaria. Se encontró un aumento de la capacidad latente de unión (UBBC) dependiente de la transcobalamina II en los pacientes con leucemia aguda. Igual resultado se encontró en aquéllos con leucemia mieloide crónica y policitemia vera, pero en éstos dicha elevación se debió a un aumento conjunto de los niveles de transcobalamina I y II (ARBC). Los resultados obtenidos en los pacientes con leucemia mieloide crónica, que fueron estudiados evolutivamente, sugieren que la vitamina B12 y sus proteínas transportadoras pueden ser un elemento que se deba considerar para decidir la duración del tratamiento de esta enfermedad

Studies on the effect of folic acid supplement on folate and vitamin B12 status in children.

The effect of folic acid supplement (15 mg folic acid per day) for 5 weeks was studied on a group of 5 children aged 8-12 years who were admitted to hospital. The result was compared to a control group of 5 children who were given a placebo. After supplementation, both serum and red cell folate levels in the experimental group significantly increased, i.e., 15 fold (82.0 ng/ml) and 4 fold (880 ng/ml), respectively. Serum UFBP decreased considerably while TFBP showed no significant alteration which resulted in the elevation of the % saturation to its maximum value. These findings indicated that the supplementary folic acid not only increased both serum and red cell folate levels and saturated nearly all serum UFBP but also elevated the % saturation markedly. There were no definite changes of serum vitamin B12, UBBC, TBBC and TC levels of the experimental group from those of the control group. There were slightly but not significantly increased blood haemoglobin and haematocrit levels in both groups of children. This indicated that folic acid supplement had no definite effect on vitamin B12 and haematological findings in this study.

Vitamin B12 and vitamin B12 binding proteins in liver diseases.

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.