Abstract
<title>Abstract</title> <p> <bold>Introduction</bold> : AKT inhibition is an effective anticancer strategy because AKT is a key serine/threonine kinase in the PI3K/AKT pathway that promotes tumor cell survival, growth, and metabolic adaptation; however, AKT inhibitors such as capivasertib can disrupt glucose metabolism and cause hyperglycemia, while associated hyperlactatemia remains underrecognized. We report a case of life-threatening type B hyperlactatemia preceding ketosis and emphasize early lactate monitoring. <bold>Case Presentation:</bold> A 79-year-old woman with metastatic breast cancer received capivasertib (400 mg/day) plus capecitabine. Glucose levels was monitored using intermittently scanned continuous glucose monitoring, with venous measurements of glucose, lactate, and ketones. On day 11, severe hyperglycemia (334 mg/dL) developed with minimal ketonemia but marked hyperlactatemia, prompting hospitalization. Capivasertib was discontinued, and transient insulin therapy rapidly normalized glucose. After discharge, capivasertib was reintroduced at a reduced dose (200 mg/day). Recurrent, asymptomatic lactate elevations occurred early in subsequent cycles without ketosis, resolving with brief treatment interruptions and gradually attenuating over three months. <bold>Conclusions</bold> : Capivasertib can induce type B hyperlactatemia independent of ketosis, likely via impaired glucose utilization and altered pyruvate metabolism. Notably, lactate elevation may precede symptoms and ketogenesis, posing an immediate metabolic risk. These findings underscore the need for early and concurrent monitoring of lactate and ketones during capivasertib-associated hyperglycemia. Prompt recognition and intervention may prevent progression to severe lactic acidosis while enabling continuation of effective oncologic therapy. </p>