Lactic acidosis in a patient with acute lymphoblastic leukemia

Abstract

To the Editor:Ali et al.1Ali AA Flombaum CD Brochstein JA Gillio AP Bussel JB Boulad F. Lactic acidosis and renal enlargement at diagnosis and relapse of acute lymphoblastic leukemia.J PEDIATR. 1994; 125: 584-586Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar report an interesting clinical observation in a patient with acute lymphoblastic leukemia who had lactic acidosis. Several aspects of the acid-base abnormalities observed in this patient require clarification. The authors state that the “lactate values again returned to normal (4.0 mmol/L).” A normal serum lactate concentration is less than 2.0 mmol/L. There was therefore continuing evidence of lactic acidosis in their patients. Is it possible that the continuing lactic acidosis was a sign of persistent acute lymphoblastic leukemia?The authors state that the urine pH was inappropriately low at 5.0. This urine pH is appropriately low for a patient with systemic acidemia. With chronic acidemia, the kidney responds by increasing the excretion of hydrogen ions including free hydrogen ions, ammonium, and titratable acid. The authors mention that a contributing factor to the metabolic acidosis “may have been high doses of alkaline therapy,” which does not cause metabolic acidosis. The authors may be referring to the modest increase in serum lactate observed in patients with alkalemia. The anion gap was elevated at 32 mmol/L. The elevation in serum lactate concentration explained only 12 mmol/L of the elevated anion gap; there was 8 mmol/L of further unexplained anions.9/35/64044 To the Editor:Ali et al.1Ali AA Flombaum CD Brochstein JA Gillio AP Bussel JB Boulad F. Lactic acidosis and renal enlargement at diagnosis and relapse of acute lymphoblastic leukemia.J PEDIATR. 1994; 125: 584-586Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar report an interesting clinical observation in a patient with acute lymphoblastic leukemia who had lactic acidosis. Several aspects of the acid-base abnormalities observed in this patient require clarification. The authors state that the “lactate values again returned to normal (4.0 mmol/L).” A normal serum lactate concentration is less than 2.0 mmol/L. There was therefore continuing evidence of lactic acidosis in their patients. Is it possible that the continuing lactic acidosis was a sign of persistent acute lymphoblastic leukemia?The authors state that the urine pH was inappropriately low at 5.0. This urine pH is appropriately low for a patient with systemic acidemia. With chronic acidemia, the kidney responds by increasing the excretion of hydrogen ions including free hydrogen ions, ammonium, and titratable acid. The authors mention that a contributing factor to the metabolic acidosis “may have been high doses of alkaline therapy,” which does not cause metabolic acidosis. The authors may be referring to the modest increase in serum lactate observed in patients with alkalemia. The anion gap was elevated at 32 mmol/L. The elevation in serum lactate concentration explained only 12 mmol/L of the elevated anion gap; there was 8 mmol/L of further unexplained anions. Ali et al.1Ali AA Flombaum CD Brochstein JA Gillio AP Bussel JB Boulad F. Lactic acidosis and renal enlargement at diagnosis and relapse of acute lymphoblastic leukemia.J PEDIATR. 1994; 125: 584-586Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar report an interesting clinical observation in a patient with acute lymphoblastic leukemia who had lactic acidosis. Several aspects of the acid-base abnormalities observed in this patient require clarification. The authors state that the “lactate values again returned to normal (4.0 mmol/L).” A normal serum lactate concentration is less than 2.0 mmol/L. There was therefore continuing evidence of lactic acidosis in their patients. Is it possible that the continuing lactic acidosis was a sign of persistent acute lymphoblastic leukemia? The authors state that the urine pH was inappropriately low at 5.0. This urine pH is appropriately low for a patient with systemic acidemia. With chronic acidemia, the kidney responds by increasing the excretion of hydrogen ions including free hydrogen ions, ammonium, and titratable acid. The authors mention that a contributing factor to the metabolic acidosis “may have been high doses of alkaline therapy,” which does not cause metabolic acidosis. The authors may be referring to the modest increase in serum lactate observed in patients with alkalemia. The anion gap was elevated at 32 mmol/L. The elevation in serum lactate concentration explained only 12 mmol/L of the elevated anion gap; there was 8 mmol/L of further unexplained anions. 9/35/64044