Discussion

PUO, defined as fever exceeding 38.3°C (101°F) for over three weeks without an identifiable cause despite thorough evaluation, posed a significant diagnostic challenge [1]. In this patient, the combination of prolonged fever, weight loss, negative basic microbiology, and preserved liver stiffness initially obscured the diagnosis. However, marked leukocytosis, neutrophilia, and very high C‐reactive protein supported a significant systemic inflammatory process, while the concurrent elevation of alkaline phosphatase with mild–moderate aminotransferase rise suggested a cholestatic‐hepatitic pattern, thereby increasing suspicion for an occult hepatobiliary source. This constellation is consistent with the Tokyo Guidelines framework, in which systemic inflammation together with abnormal liver biochemistry should prompt targeted biliary imaging even when classic localizing symptoms are absent [2].

Although acute cholangitis is classically associated with Charcot's triad, many patients do not present with all three components, and atypical or subacute disease may manifest chiefly as fever [2]. This explains why initial ultrasonography showing only non‐specific biliary dilatation was insufficient. In such cases, MRCP and CECT may reveal occult biliary infection and its vascular consequences [3, 4]. Pylephlebitis secondary to cholangitis appears to be distinctly uncommon; published biliary‐source cases are largely limited to isolated reports, including those of Ozawa and Shikino and Zardi et al. [3, 8]. This is consistent with larger reviews in which diverticulitis and appendicitis, rather than cholangitis, predominate as the infective source of pylephlebitis [4, 5].

Pylephlebitis is thought to arise from local infectious spread to the portal venous system, endothelial injury, and a systemic prothrombotic inflammatory state [4, 5]. Once portal vein thrombosis becomes chronic, cavernous transformation and portal hypertension may follow, leading to portal cavernoma cholangiopathy from extrinsic compression and ischaemic injury to the bile ducts [6, 7]. Current reviews support anticoagulation for at least 3–6 months in acute or recent portal vein thrombosis when bleeding risk is acceptable, together with treatment of the underlying cause [6]. Our patient's favorable short‐term course and partial recanalisation on follow‐up support the value of timely recognition, antibiotics, anticoagulation, and multidisciplinary surveillance.

A limitation of this report is the absence of microbiological confirmation of the biliary source. Nevertheless, the inflammatory profile, cholestatic liver test abnormalities, biliary imaging findings, and subsequent clinical response together make occult cholangitis the most plausible explanation. Overall, this case highlights that occult cholangitis should remain in the differential diagnosis of PUO when fever coexists with cholestatic liver biochemistry, even in the absence of abdominal pain or jaundice, and that early advanced biliary imaging may reduce the risk of chronic portal hypertensive and biliary sequelae [2, 3, 4, 5, 6, 7].