Evidence map›Paper›PMID 42633160›Full record

ArticleClinical case reports2026

Septic Pylephlebitis and Cavernous Transformation Presenting as Pyrexia of Unknown Origin: A Diagnostic Challenge.

Aditi Sarker, Prodipta Chowdhury, Md Razibul Alam

Abstract read
In one paragraph

Article in Clinical case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Aditi SarkerDepartment of Gastroenterology Bangabandhu Sheikh Mujib Medical University Dhaka Bangladesh.ORCID https://orcid.org/0009-0006-5443-8392
Prodipta ChowdhuryDepartment of Endocrinology Bangabandhu Sheikh Mujib Medical University Dhaka Bangladesh.ORCID https://orcid.org/0000-0001-9300-2950
Md Razibul AlamDepartment of Gastroenterology Bangabandhu Sheikh Mujib Medical University Dhaka Bangladesh.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute cholangitis classically presents with fever, jaundice, and right upper quadrant pain, but atypical or subacute disease may present as pyrexia of unknown origin (PUO) and remain unrecognized until vascular complications develop. We report a 45-year-old man referred for weight loss, malaise, and suspected non-cirrhotic portal hypertension after upper gastrointestinal endoscopy showed esophageal varices despite a normal FibroScan. Detailed history revealed intermittent fever for 2 months. Laboratory evaluation demonstrated marked systemic inflammation, with leukocytosis, neutrophilia, ferritin 1095 ng/mL, and C-reactive protein > 200 mg/L, together with a cholestatic-hepatitic liver enzyme pattern and preserved liver synthetic function. Blood and urine cultures were negative. Initial ultrasonography showed bile duct dilatation without a definite obstructing lesion, delaying diagnosis. Subsequent magnetic resonance cholangiopancreatography and contrast-enhanced computed tomography demonstrated biliary abnormality with portal vein thrombosis and periportal collateralization, consistent with septic pylephlebitis, cavernous transformation, and portal biliopathy secondary to occult cholangitis. The patient was treated with intravenous broad-spectrum antibiotics and anticoagulation, with clinical improvement and partial portal vein recanalisation on follow-up ultrasonography at 3 months. This case highlights that occult cholangitis should be considered in patients with PUO and cholestatic liver biochemistry, even in the absence of classic biliary symptoms, and that early cross-sectional biliary imaging may allow timely recognition of pylephlebitis before chronic portal hypertensive and biliary sequelae become established.

Indexed as

cholangitisfever of unknown originportal biliopathyportal hypertensionportal vein thrombosispylephlebitis

Identifiers

PMID42633160
PMCPMC13498970

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