Case Presentation: A 91-year-old male with a known history of benign prostatic hyperplasia (BPH), diastolic heart failure, pulmonary embolism, hypertension, and previous extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli (E. coli) urinary tract infection (UTI) presented with encephalopathy. He was not tachypneic nor tachycardic, but his bicarbonate was low at less than 8, and his lactic acid was elevated at 7.8mmol/l. He had leukocytosis, and the patient was started on meropenem and vancomycin due to concern for sepsis from a UTI, and he received thiamine supplementation. The patient’s leukocytosis resolved, and his mental status improved. His hepatic function and liver imaging were normal. A review of his prior-to-admission labs showed markedly elevated prostate-specific antigen (PSA) at 481ng/ml (normal range up to 4.4). Urine culture eventually grew pansensitive Enterococcus faecalis. Despite normal hemodynamics, appropriate antibiotics, and thiamine supplementation, his lactic acid was persistently elevated, ranging between 6 and 12 mmol/l. Follow-up thiamine and riboflavin levels did not show deficiencies. The patient received degarelix prior to discharge, which reversibly binds to and blocks gonadotropin-releasing hormone (GnRH) receptors, which results in rapid androgen deprivation by decreasing testosterone production.
Discussion: Lactic acidosis is the leading cause of metabolic acidosis in hospitalized patients. Three types of lactic acidosis exist: Type A lactic acidosis is usually associated with impaired tissue oxygenation. Type B lactic acidosis occurs in patients without overt systemic hypoperfusion. D-lactic acidosis occurs in settings of GI malabsorption, diabetic ketoacidosis, and receiving rapid and high-dose infusions of propylene glycol.Causes of type B lactic acidosis include toxin-induced impairment of cellular metabolism, regional areas of tissue ischemia, high levels of metformin, malignancy-associated lactic acidosis, alcoholism, and drug-induced mitochondrial dysfunction, often in HIV-infected patients. We believe that our patient had type B lactic Acidosis due to his underlying malignancy. Type B lactic acidosis is more commonly reported in hematologic malignancies, while it is a rare finding in solid tumors without hepatic metastasis. Underperfusion of tumor clusters, hepatic metastases, and increased rates of lactate production by the neoplastic cells that shift to primarily anaerobic glycolysis (Warburg effect) are possible mechanisms. Thiamine and/or riboflavin deficiency could also contribute to the pathophysiology of cancer-related type B lactic acidosis. Although type B lactic acidosis is an uncommon metabolic complication in prostate cancer, it is a significant finding that indicates a poor prognosis. Regardless of the mechanism, treatment of the tumor (by chemotherapy, irradiation, or surgery) usually corrects the lactic acidosis. We generally encounter lactic acidosis in the context of sepsis, and this case highlights the importance of having a good differential diagnosis for the various types of lactic acidosis to deliver the right treatment.
Conclusions: Although type B lactic acidosis is a rare finding in prostate cancer, it indicates a significant tumor burden and poor prognosis. As we generally encounter lactic acidosis in the context of sepsis, identifying the underlying cause of lactic acidosis is very important to deliver the right treatment.
