Presentations

Abstract

Introduction:

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. We present a case of a patient with persistent lactic acidosis despite appropriate treatment for sepsis believed to be secondary to prostate cancer.

Case Information:

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 or tachycardic but his bicarb was low at less than 8 and his lactic acid was elevated at 7.8mmol/l. He had a 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. Review of his prior to admission labs showed that his prostate-specific antigen (PSA) was markedly elevated 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 acidosis persisted between 6 and 12 mmol/l. Follow up thiamine and riboflavin levels did not show deficiencies. The patient received degarelix prior to discharge, a gonadotropin-releasing hormone (GnRH) antagonist which reversibly binds to GnRH receptors in the anterior pituitary gland, blocking the receptor and decreasing secretion of luteinizing hormone (LH) and follicle stimulation hormone (FSH). This results in rapid androgen deprivation by decreasing testosterone production, thereby decreasing testosterone levels. With degarelix, testosterone levels do not exhibit an initial surge, or flare, as is typical with GnRH agonists

Discussion/Clinical Findings:

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, 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 poor prognosis. Regardless of the mechanism, treatment of the tumor (by chemotherapy, irradiation, or surgery) usually corrects the lactic acidosis.

Conclusion:

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.