Acute Lymphoblastic Leukemia Presenting with Liver Infiltration and Severe Lactic Acidosis

Abstract

Patient: Male, 58Final Diagnosis: Acute lymphoblastic leukemiaSymptoms: Chest pain • fatigue • loss of appetite • shortness of breathMedication: —Clinical Procedure: Liver biopsy and bone marrow biopsySpecialty: HematologyObjective:Rare diseaseBackground:Type-B lactic acidosis is a rare complication of solid tumors and hematological malignancies. It occurs secondary to Warburg effect, when glucose metabolism in cancer cells switches from the oxidative pathway to the glycolytic pathway. Malignant lactic acidosis is a life-threatening condition if not promptly diagnosed and treated urgently.Case Report:We report the case of a 58-year-old male patient who presented with severe chest pain, dyspnea, systemic symptoms, leukopenia, normocytic anemia, and severe lactic acidosis. He was admitted with a possible diagnosis of acute pericarditis and lactic acidosis. Sodium bicarbonate replacement did not improve the lactic acidosis. Liver biopsy was performed because of persistently elevated alkaline phosphatase and gamma-glutamyl transferase; the biopsy showed atypical lymphoblasts and bone marrow biopsy confirmed the diagnosis of precursor B acute lymphoblastic leukemia. Lactic acidosis normalized after initiation of chemotherapy.Conclusions:Cancer, particularly hematological malignancy, should be considered as an etiology and differential diagnosis of type-B lactic acidosis. Prompt recognition and urgent initiation of specific therapy to control the underlying malignancy are critical to manage this serious metabolic complication.

Effect of A20 on glucose dependent cell migration in acute lymphoblastic leukemia

“…Cancer cells including leukemic blasts use glucose to produce a severely elevated level of lactic acid by switching the oxidative pathway to the glycolytic pathway even in the presence of oxygen, whereas in normal cells glucose generates lactate in anaerobic conditions (Warburg, 1956). Accumulation of lactic acid is associated with poor prognosis of ALL (Sayyed et al, 2018), and hyperglycemia is found in about 10% ALL patients during chemotherapy treatment, who are associated with risk of infection and poorer survival (Panigrahi et al, 2016). In this study, we used high glucose to stimulate this activation in the blasts.…”

A Rare Case of Severe Lactic Acidosis in a Patient With Mantle Cell Lymphoma

“…In most cases the liver can utilize the Cori cycle to counteract lactic acidosis. 6 The development of persistent lactic acidosis may indicate neoplastic liver infiltration 7,8 ; however, in patients with intact liver function with no evidence of metastases there is still much to explore about what predisposes these patients to lactic acidosis. Also the presence of high levels of lactate may reflect the poor prognostic outcome of the malignancy.…”

FtH-Mediated ROS Dysregulation Promotes CXCL12/CXCR4 Axis Activation and EMT-Like Trans-Differentiation in Erythroleukemia K562 Cells

“…In solid tumors, the EMT process enhances the metastatic potential converting polarized epithelial cells into non-polarized mesenchymal cells thus promoting cell mobility, invasion and resistance to apoptotic stimuli (48)(49)(50). In hematological malignancies, the blasts move from BM into peripheral blood and colonize distant sites such as liver and spleen, a process reminiscent of EMT in metastatic solid tumors (51)(52)(53). Moreover, it has been recently demonstrated that EMT transcription factors are critical in promoting leukemia and lymphoma progression (6, 18).…”