Persistent lactic acidosis in ALK-positive anaplastic large cell lymphoma: a case report and literature review

Lactic acidosis is common in the ICU, but malignancy-associated type B lactic acidosis mediated by the clinical Warburg effect (CWE) is uncommon and easily missed when infection or organ dysfunction dominates the presentation. We report a 35-year-old man with a month of fever and progressive dyspnea who presented with persistent hyperlactatemia (peak 15.46 mmol/L) and markedly elevated LDH despite stable hemodynamics. Imaging revealed generalized lymphadenopathy, multifocal osteolytic lesions, and bilateral pleural effusions; infectious studies were unrevealing apart from chronic hepatitis B. Cervical node biopsy (CD30 + , ALK-L + , EMA + ; Ki-67 ~80%; EBER–; pan-B/T and epithelial markers negative) established ALK-positive anaplastic large-cell lymphoma. In the absence of shock or sustained hypoperfusion, CWE/type B lactic acidosis was diagnosed. An etoposide-containing CHOP variant (ECHOP/CHOEP, days 1–5) was initiated with parallel continuous renal replacement therapy (CVVHDF) to stabilize acid–base and electrolytes as a bridge to chemotherapy. Lactate declined from 13.30 mmol/L immediately before chemotherapy to 2.88 mmol/L by day 3, 1.33 mmol/L by day 8, and normalized (0.6 mmol/L) by day 17, closely tracking clinical improvement. The patient was extubated, CRRT discontinued, transferred out of the ICU, and discharged; chemotherapy-related myelosuppression and ICU-acquired weakness were managed with G-CSF, transfusions, and early rehabilitation, and a femoral deep-vein thrombosis was treated with anticoagulation. A focused review of 18 recent case reports (2021–2025) suggests that timely, standardized antitumor therapy is frequently followed by a rapid, time-locked fall in lactate, whereas the absence of definitive oncologic treatment portends uniformly poor short-term outcomes. This case underscores that, in hemodynamically stable patients with refractory hyperlactatemia, early consideration of CWE and prompt tumor-directed therapy—supported by targeted organ support such as CRRT—offer the most reliable path to metabolic reversal and recovery.