Successful reversal of hepatic visceral crisis in HER2-positive metastatic breast cancer: a case report.

Introduction: Hepatic visceral crisis (HVC) in the setting of HER2-positive metastatic breast cancer (mBC-HER2+) is an infrequent but often catastrophic presentation. Management remains particularly challenging, largely because patients with marked hepatic dysfunction are routinely excluded from clinical trials, leaving clinicians with little prospective evidence to guide decisions. For this reason, observations from well-documented cases continue to offer practical insights when conventional pathways fall short. Case presentation: A 51-year-old woman with HER2-positive metastatic breast cancer (mBC) and widespread bilobar liver metastases, BRCA wild-type, presented with rapidly progressive jaundice and a marked decline in performance status. Initial laboratory tests revealed severe hepatic dysfunction-total bilirubin 31.4 mg/dL, AST 462 U/L, ALT 185 U/L, and LDH >1800 U/L-meeting criteria for hepatic visceral crisis (HVC). Given the clinical severity, inpatient treatment was promptly initiated with trastuzumab and pertuzumab every three weeks, combined with weekly paclitaxel at a 50% dose reduction. During this initial phase, the patient showed early clinical and biochemical improvement; however, paclitaxel was discontinued after the second dose due to grade 2 toxicities, while anti-HER2 therapy was maintained without interruption. Discussion: Over the following cycles, liver function normalized, CA15-3 levels fell from 893 to 39.5 U/mL, and imaging demonstrated a sustained partial response. Radiologic assessment also revealed changes consistent with pseudocirrhosis-hepatic contour remodeling, capsular retraction, and venous alterations-findings that, in this context, were interpreted as treatment-related rather than evidence of progression. The patient's course suggests that, when HER2 dependence is strong, rapid and continuous HER2-targeted therapy may restore organ function even from a state of profound hepatic failure. The brief exposure to dose-reduced paclitaxel likely served only as an initial cytoreductive step while avoiding further hepatic strain. Conclusion: This case illustrates that HVC in mBC-HER2+ is not uniformly irreversible. In carefully selected patients, early and sustained HER2-directed therapy can lead to meaningful clinical recovery when options appear limited. Such cases help bridge the evidence gap for this high-risk group and may inform future therapeutic considerations.