ABSTRACT
Hypophosphataemia is a metabolic disorder that is commonly encountered in critically ill patients.Phosphate has many roles in physiological functions, thus the depletion of serum phosphate could leadto impairment in multiple organ systems, which include the respiratory, cardiovascular, neurologicaland muscular systems and haematological and metabolic functions. Hypophosphataemia is defined asplasma phosphate level below 0.80 mmol per litre (mmol/L) and can be further divided into subgroupsof mild (plasma phosphate of 0.66 to 0.79 mmol/L), moderate (plasma phosphate of 0.32 to 0.65mmol/L) and severe (plasma phosphate of less than 0.32 mmol/L). The causes of hypophosphataemiainclude inadequate phosphate intake, decreased intestinal absorption, gastrointestinal or renal phosphateloss, and redistribution of phosphate into cells. Symptomatic hypophosphataemia associated withhaematological malignancies has been reported infrequently. We report here a case of asymptomaticsevere hypophosphataemia in a child with acute T-cell lymphoblastic leukaemia.A 14-year-old Chinese boy was diagnosed to have acute T cell lymphoblastic leukaemia (ALL).His serum biochemistry results were normal except inorganic phosphate and lactate dehydrogenaselevels. The serum inorganic phosphate level was 0.1mmol/L and the level was low on repeatedanalysis. The child had no symptoms related to low phosphate levels. The possible causes of lowphosphate were ruled out and urine Tmp/GFR was normal. Chemotherapy regime was started andthe serum phosphate levels started to increase. Hypophosphataemia in leukaemia was attributed toshift of phosphorus into leukemic cells and excessive cellular phosphate consumption by rapidlyproliferating cells. Several reports of symptomatic hypophosphataemia in myelogenous andlymphoblastic leukaemia in adults have been reported. To our knowledge this is the first case ofsevere asymptomatic hypophosphataemia in a child with ALL.
ABSTRACT
Adult T-cell leukaemia/lymphoma (ATLL) is a rare T lymphoproliferative disorder which is aetiologically linked with human T-cell lymphotropic virus type-1 (HTLV-1). HTLV-1 is endemic in Japan, Caribbean and Africa. The highest incidence of ATLL is in Japan although sporadic cases have been reported elsewhere in the world. We describe a case of ATLL with an unusual presentation which we believe is the first reported case of ATLL in Malaysia based on our literature search. A 51-year-old Indian lady was referred to University Malaya Medical Centre for an incidental finding of lymphocytosis while being investigated for pallor and giddiness. Clinical examination revealed bilateral shotty cervical lymph nodes with no hepato-splenomegaly or skin lesions. Laboratory investigations showed absolute lymphocytosis (38 x 10(9)/L) with a mildly increased serum lactate dehydrogenase. The peripheral blood smear showed the presence of predominantly small to medium sized, non-flower lymphocytes. The bone marrow showed similar findings of prominent lymphocytosis. Immunophenotyping of the bone marrow mononuclear cells showed CD3+, CD4+, CD5+, CD7- and CD25+ which is characteristic of ATLL phenotype. HTLV-1 infection was confirmed by the presence of HTLV-1 proviral DNA in the tumor cells using conventional Polymerase Chain Reaction (PCR) and real-time PCR. Here, we discuss the pathogenesis and characteristics of ATLL as well as the detection of HTLV-1 by real time PCR.