Serum transcobalamin II level in a malarial patient with ceftriaxone-induced haemolyic anaemia.

Cephalosporins have rarely been reported as the cause of immune haemolytic anaemia (IHA). The case history of a patient who had elevated serum transcobalamin II (TCII) levels due to a ceftriaxone-induced haemloytic anaemia is presented in this study. The patient was admitted because of high fever due to P.falciparum. The fever subsided after treatment with anti-malarial drugs. However, two days later, the fever recurred and ceftriazone was given. On the next day, the patient had haemolysis with haemoglobinuria and renal insufficiency which resolved after withdrawal of the drug. Serum TCII levels were elevated during the haemolytic episode and the period of renal impairment. The mechanisms of increased serum TCII are probably due to the acute haemolysis and nephrotoxicityinduced by ceftriaxone, leading to the impaired catabolism and clearance of TCII. Therefore, intravascular THII survival is prolonged. Resulting in elevated serum TCIIlevels.

Persistently elevated serum transcobalamin II in a patient with reactive haemophagocytic syndrome.

A 24-year-old man was admitted to the hospital with a history of prolonged fever, peripheral blood neutropenia and bone marrow showing benign haemophagocytic histiocytosis. He presented with symptoms and manifestations over a brief duration until death, with the progressive development of multi-organ dysfunction. His serum TCII levels were persistently elevated throughout the disease duration in the hospital. Available evidence indicates that macrophages, mononuclear cells and histiocytes can produce TCII. Serum TCII levels in patients with reactive haemophagocytic syndrome are therefore elevated due to the increased be helpful in making the diagnosis in these patients.

Elevated serum transcobalamin II levels in patients with prolonged fever.

Serum transcobalamin II levels were determined in 70 patients with prolonged fever. Twelve patients were found to have elevated serum TCII levels, i.e., 8 patients with salmonellosis, 3 patients with scrub typhus and 1 patient with pyrexia of unknown origin. There were no relationships between serum TCII levels and white blood cells, lymphocytes or monocytes. The possible mechanism producing increased serum TCIII levels in patients with salmonellosis and scrub typhus is the increased synthesis and release of TCII by the proliferative mononuclear phagocytic cells of the reticuloendothlial tissues such as spleen, liver, bone marrow and lymph nodes. This study gives the additional data that elevated serum TCII may occur not only in inflammatory disorders, autoimmune diseases, lymphoproliferative disorders, malignant histiocytosis and neoplasms, but also in infection with salmonellosis and scrub typhus.