The liver plays a central role in cholesterol metabolism. Several studies report an inverse association between low-density lipoprotein cholesterol (LDL-C) and total cholesterol levels with the risk of hepatocellular carcinoma, and reduced LDL-C may reflect underlying liver pathology. Conversely, hypercholesterolaemia is rarely observed in hepatic malignancy, except in uncommon subtypes such as clear cell hepatocellular carcinoma.We report a 58-year-old man with metastatic rectal adenocarcinoma and extensive hepatic involvement who presented with a marked and unexpected rise in LDL-C. During routine follow-up for hyperlipidaemia, his LDL-C increased from 3.23 mmol/L to 8.64 mmol/L over one year. Following complaints of intermittent abdominal bloating and hepatomegaly on physical examination, imaging revealed multiple hypo-enhancing hepatic masses suspicious for hepatic metastases. Alternative secondary causes of hypercholesterolaemia, including hypothyroidism, nephrotic syndrome, and chronic kidney disease, were considered and excluded.While advanced liver disease and malignancy typically reduce cholesterol levels due to impaired hepatic lipid metabolism, hypercholesterolaemia can occur in cholestatic states through accumulation of lipoprotein X (LpX), an abnormal phospholipid-rich, apolipoprotein B (ApoB)-negative lipoprotein. Standard lipid assays may not distinguish LDL from LpX without specialised techniques. In this case, the reported LDL-C, calculated using the Friedewald equation, may be inaccurate if there is significant LpX accumulation, as total cholesterol measurements include LpX.Abrupt or unexpected increases in LDL-C may indicate underlying hepatic pathology, particularly cholestasis. When falsely elevated LDL-C is suspected, additional testing can be considered. ApoB measurement may help to differentiate true LDL-C elevation from LpX-related pseudo-hypercholesterolaemia, as LpX lacks ApoB. A normal ApoB level despite markedly elevated LDL-C strongly supports this diagnosis. Lipid electrophoresis can confirm the presence of LpX, though it may not be routinely available.Our patient’s liver biochemistry demonstrated a cholestatic pattern with elevated alkaline phosphatase (194 U/L) and gamma-glutamyl transferase (334 U/L). We suspect that the abrupt rise in calculated LDL-C reflects LpX accumulation rather than a true increase in LDL-C.There is a growing number of case reports highlighting LpX as a cause of pseudo‑hypercholesterolaemia. Recognition of atypical lipid profiles should prompt consideration of secondary causes, and appropriate confirmatory testing can support timely evaluation and accurate diagnosis.