Abstract
Peribiliary inflammatory phlegmon arising from chronic portal venous thrombosis can produce a morphological replica of periductal cholangiocarcinoma at the hepatic hilum. We report a 68-year-old woman referred with an outside magnetic resonance imaging diagnosis of cholangiocarcinoma, in whom multimodality imaging reassessment demonstrated a 68 mm × 37 mm × 32 mm porta hepatis soft-tissue lesion encasing the biliary confluence. The common bile duct measured only 5 mm despite circumferential encasement, disproportionately limited for malignant transmural invasion. Color Doppler ultrasonography with pulsed-wave spectral analysis demonstrated low-velocity continuous venous waveforms within intralesional channels, confirming patent cavernous collateral vessels and excluding tumor neovascularity. Triphasic contrast-enhanced computed tomography (CT) showed absent arterial-phase enhancement, near-homogeneous portal-phase uptake, and mild delayed washout, in contrast to the progressive delayed enhancement of fibrotic periductal cholangiocarcinoma. Tumor markers were normal. Blood count showed thrombocytosis, neutrophilia, and anemia; Janus kinase 2 (JAK2) V617F mutation was confirmed in peripheral blood. Bone marrow trephine biopsy demonstrated grade III reticulin fibrosis with megakaryocytic hyperplasia, establishing primary myelofibrosis as the driver of chronic multivessel splanchnic venous thrombosis and cavernous transformation. The oncology referral was cancelled, and the patient commenced on ruxolitinib. Follow-up sonography at 3 months showed stable lesion morphology with identical Doppler characteristics, inconsistent with untreated malignancy. Spectral Doppler confirmation of venous intralesional flow, disproportionately limited biliary obstruction relative to ductal encasement, and an atypical CT enhancement profile can reliably distinguish peribiliary phlegmon from cholangiocarcinoma. When cavernous transformation is identified on CT, JAK2 V617F testing for myeloproliferative neoplasm should follow.
Keywords: Cavernous transformation, cholangiocarcinoma mimic, janus kinase 2 V617f, peribiliary phlegmon, portal biliopathy, portal vein thrombosis, primary myelofibrosis
Résumé
Un phlegmon péribiliaire inflammatoire découlant d’une thrombose veineuse portale chronique peut produire une réplique morphologique du cholangiocarcinome périductal au niveau du hile hépatique. Nous rapportons le cas d’une femme de 68 ans adressée avec un diagnostic IRM extérieur de cholangiocarcinome, chez qui une réévaluation par imagerie multimodalité a démontré une lésion tissulaire de 68 mm × 37 mm × 32 mm au niveau du hile portal encerclant la confluence biliaire. Le canal cholédoque ne mesurait que 5 mm malgré un encerclement circonférentiel, de façon disproportionnément limitée pour une invasion transmurale maligne. L’échographie Doppler couleur avec analyse spectrale en onde pulsée a démontré des formes d’ondes veineuses continues à basse vélocité dans les canaux intralésionnels, confirmant des vaisseaux collatéraux caverneux perméables et excluant une néovascularisation tumorale. La tomodensitométrie (TDM) triphasique avec injection de contraste a montré une absence de rehaussement en phase artérielle, une prise de contraste quasi homogène en phase portale et un lavage retardé discret, contrastant avec le rehaussement retardé progressif du cholangiocarcinome périductal fibrotique. Les marqueurs tumoraux étaient normaux. L’hémogramme montrait une thrombocytose, une neutrophilie et une anémie ; la mutation JAK2 V617F a été confirmée dans le sang périphérique. La biopsie ostéomédullaire tréphine a démontré une fibrose réticulinique de grade III avec hyperplasie mégacaryocytaire, établissant la myélofibrose primitive comme facteur prothrombotique. Le bilan oncologique a été annulé et la patiente a commencé le ruxolitinib. La confirmation Doppler spectral du flux veineux intralésionnel, l’obstruction biliaire disproportionnément limitée et un profil de rehaussement TDM atypique permettent de distinguer de manière fiable le phlegmon péribiliaire du cholangiocarcinome. Lorsqu’une transformation caverneuse est identifiée au scanner, un test JAK2 V617F pour néoplasie myéloproliفérative doit être réalisé.
Mots-clés: Transformation caverneuse, simulateur de cholangiocarcinome, Janus kinase 2 V617F, phlegmon péribiliaire, biliopathie portale, thrombose de la veine porte, myélofibrose primitive
INTRODUCTION
A porta hepatis soft-tissue mass in adult cross-sectional imaging carries a strong prior probability for cholangiocarcinoma, particularly when it encases the biliary confluence and produces upstream ductal dilatation. The reflexive nature of this association means that less common entities sharing these morphological features are frequently misclassified, sometimes with serious clinical consequences, including unnecessary oncologic workup, misdirected surgical intervention, and an underlying systemic disorder remaining undiagnosed.
Chronic portal venous thrombosis with cavernous transformation produces a distinct complication termed portal biliopathy, referring to the spectrum of biliary ductal changes that arise from extrinsic compression of the periductal biliary plexus by portosystemic collateral vessels.[1,2] In its most advanced form, the organised fibroinflammatory peribiliary reaction consolidates into a focal soft-tissue mass at the hepatic hilum that can genuinely simulate periductal cholangiocarcinoma on cross-sectional imaging.[3] Janus kinase 2 (JAK2) V617F-positive myeloproliferative neoplasms are the leading identifiable cause of noncirrhotic splanchnic venous thrombosis, accounting for approximately 17%–40% of such cases across published series.[4]
We report a case in which multimodality imaging (color Doppler ultrasonography with pulsed-wave spectral analysis, triphasic contrast-enhanced computed tomography [CT], and magnetic resonance imaging [MRI]) provided a coherent argument against cholangiocarcinoma in a patient referred with that active working diagnosis. Hematological evaluation subsequently confirmed JAK2 V617F-positive primary myelofibrosis (PMF) as the prothrombotic driver, and the patient was managed without oncologic intervention. The case illustrates the role of structured multimodality imaging in the diagnosis of a cholangiocarcinoma mimic at the hepatic hilum and highlights the importance of recognising cavernous transformation as a pointer toward systemic disease.
CASE REPORT
A 68-year-old female with no prior abdominal surgery, known liver disease, or hematological disorder presented with a 1-month history of dull right hypochondrial discomfort, low-grade fever, and unintentional weight loss. There was no jaundice, hematemesis, or melena. Physical examination revealed no stigmata of chronic liver disease and no palpable abdominal mass. She had been referred from an outside institution with a working diagnosis of cholangiocarcinoma, established on MRI that identified a signal-abnormal enhancing periportal lesion measuring approximately 3.6 cm × 5.4 cm × 9.1 cm extending along both hepatic ducts and encasing the extrahepatic common bile duct (CBD), with inferior extension toward the ampulla of Vater. The portal vein was not adequately evaluated on that study.
Initial laboratory evaluation revealed hemoglobin of 6.7 g/dL with microcytic hypochromic morphology, leukocyte count of 15,500/µL with 84% neutrophilia, and platelet count of 550,000/µL. Cancer antigen 19-9 was 16.75 U/mL (reference: ≤37 U/mL), and carcinoembryonic antigen was 3.0 ng/mL (reference: ≤5 ng/mL). Serum immunoglobulin G4 (IgG4) measured 120 mg/dL (reference: ≤140 mg/dL). Lupus anticoagulant screen by dilute Russell’s viper venom time was negative.
Imaging findings
Color Doppler ultrasonography was performed using a Samsung HS50 machine with a curvilinear transducer (1–8 MHz) and a high-frequency linear transducer (5–15 MHz). Grayscale imaging demonstrated an ill-defined hypoechoic soft-tissue lesion at the porta hepatis traversed by multiple linear anechoic channels [Figure 1]. Color Doppler mapping revealed dense bidirectional flow within these channels, and pulsed-wave spectral analysis confirmed low-velocity continuous venous waveforms without arterial pulsatility [Figure 2], which directly documented patent cavernous collateral vessels within the peribiliary tissue. This finding is structurally incompatible with solid tumor neovascularity. The main portal vein, splenic vein, and proximal superior mesenteric vein were nonvisualized on Doppler, confirming chronic thrombosis with cavernous transformation. A 7-mm anechoic cystic focus adjacent to the CBD represented liquefactive necrosis [Figure 3]. Splenomegaly was present at 17.2 cm.
Figure 1.
68-year-old female with JAK2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon at the porta hepatis. FINDINGS: Split-screen transabdominal ultrasound at the porta hepatis. Left panel (grayscale): ill-defined hypoechoic lesion (arrow) with multiple linear anechoic channels traversing its substance (arrowheads), representing intralesional collateral venous pathways. Right panel (colour Doppler): dense mixed red-blue bidirectional flow signals within the intralesional channels confirm venous flow within the lesion structurally incompatible with tumour neovascularity. Absence of a discrete portal vein lumen at this level confirms cavernous transformation. TECHNIQUE: Transabdominal grayscale and colour Doppler ultrasound. Samsung HS50, curvilinear transducer, 11 cm depth, 14 Hz. Colour Doppler pulse repetition frequency (PRF) 1.0 kHz, gain 45. No intravenous contrast. 07 October 2025.
Figure 2.
68-year-old female with JAK2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Color Doppler with simultaneous pulsed-wave spectral trace. Upper image: mixed bidirectional color signals within intralesional channels; pulsed-wave gate positioned within the color-defined region. Lower spectral display: low-velocity continuous venous waveform without cardiac pulsatility or arterial components. This spectral pattern confirms collateral venous flow within the lesion and directly excludes tumor arterial neovascularity. This is the single most discriminating finding in this case. Technique: Pulsed-wave spectral Doppler. Samsung HS50, curvilinear transducer, 10 cm depth. Sample gate 2.5 mm; spectral pulse repetition frequency 2.5 kHz; wall filter 90 Hz; angle 0° at 4.3 cm depth. 07 October 2025
Figure 3.
68-year-old female with JAK2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Split-screen ultrasound with a linear high-frequency transducer. Left panel (grayscale): the encased common bile duct (labeled CBD) is visible within the lesion with closely apposed walls. A small anechoic cystic focus (labeled CYST, approximately 7 mm), representing liquefactive necrosis, is identified inferomedial to the duct and separate from its lumen. Right panel (color Doppler): venous flow signals within intralesional channels adjacent to the biliary structures are confirmed. Technique: Transabdominal grayscale and color Doppler ultrasound. Samsung HS50, linear transducer, 7.5 cm depth, 42 Hz. Color Doppler pulse repetition frequency 1.0 kHz. 07 October 2025.
Triphasic contrast-enhanced CT confirmed nonopacification of the portal, splenic, and superior mesenteric veins with extensive portosystemic collateral formation at the splenic hilum and perigastric and perisplenic regions [Figure 4]. The porta hepatis lesion measured 68 mm × 37 mm × 32 mm and extended from the hepatic hilum to the superior pancreatic head, encasing the common hepatic duct, CBD, and cystic duct [Figure 5]. Coronal multiplanar reconstruction confirmed the craniocaudal extent of the lesion and the massively enlarged spleen occupying the left hemiabdomen [Figure 6]. Despite circumferential ductal encasement, the CBD measured only 5 mm. Mild central intrahepatic biliary radicular dilatation was present bilaterally [Figure 7], representing a degree of obstruction disproportionately limited for a lesion of this size. The enhancement profile demonstrated absent arterial-phase uptake, near-homogeneous portal-phase enhancement, and mild delayed washout [Figure 8], which was contrary to the progressive delayed enhancement expected in the desmoplastic stroma of fibrotic periductal cholangiocarcinoma. Diffuse central hepatic hypoattenuation with peripheral sparing on portal-phase imaging, resolving on delayed sequences, was consistent with altered hepatic perfusion from chronic portal venous occlusion.
Figure 4.
68-year-old female with Janus kinase 2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Axial contrast-enhanced computed tomography (CT) at the level of the porta hepatis, portal venous phase. The 68 mm × 37 mm × 32 mm (craniocaudal × anteroposterior × transverse) ill-defined heterogeneous lesion (yellow arrow) occupies the periportal region and encases the common hepatic duct. Multiple small enhancing foci within and around the lesion represent cavernous collateral channels replacing the thrombosed portal vein. The common hepatic artery is displaced anteriorly (pink arrow) without luminal compromise, serving as a vascular landmark and confirming the extrinsic rather than infiltrative nature of the periportal mass. Mild central intrahepatic biliary radicular dilatation is visible bilaterally. Technique: Triphasic contrast-enhanced CT, portal venous phase (~70 s after intravenous contrast injection). Siemens SOMATOM 256-slice scanner; 120 kV, 200–250 mAs (CARE Dose4D automated modulation); 5 mm axial sections with 1.5 mm multiplanar reconstructions; 100 mL Omnipaque 350 administered intravenously at 3 mL/s via antecubital vein. October 7, 2025.
Figure 5.
68-year-old female with Janus kinase 2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Axial CT at a caudal level, portal venous phase. Arrow indicates multiple small enhancing collateral channels in the perisplenic region, forming part of the extensive portosystemic collateral network secondary to chronic splenic vein thrombosis. The massively enlarged spleen (17.8 cm craniocaudal) causes extrinsic compression of the anterior surface of the left kidney. Mild perisplenic ascites is present. Technique: Triphasic contrast-enhanced CT, portal venous phase. Siemens SOMATOM 256-slice scanner; 120 kV, 200–250 mAs (CARE Dose4D automated modulation); 5 mm axial sections with 1.5 mm multiplanar reconstructions; 100 mL Omnipaque 350 administered intravenously at 3 mL/s via antecubital vein. October 7, 2025
Figure 6.
68-year-old female with Janus kinase 2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Coronal multiplanar reconstruction, portal venous phase. The arrow indicates the porta hepatis lesion with periportal cavernous collateral channels spanning from the hepatic hilum superiorly to the superior pancreatic head inferiorly. Despite circumferential ductal encasement, the intrahepatic biliary radicals show only mild central dilatation, which is characteristic of extrinsic peribiliary compression with preserved ductal wall compliance rather than malignant transmural infiltration. The massively enlarged spleen occupies the left hemiabdomen. Near-homogeneous portal-phase uptake without progressive delayed enhancement supports fibro-inflammatory tissue vascularised by the portal circulation. Technique: Coronal multiplanar reconstruction from contrast-enhanced computed tomography dataset, portal venous phase (~70 s after intravenous contrast injection). October 7, 2025
Figure 7.
68-year-old female with Janus kinase 2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Axial contrast-enhanced computed tomography (CT) at the level of the upper liver, portal venous phase. The two yellow arrows indicate mildly dilated intrahepatic biliary radicals in both lobes, consistent with central portal biliopathy secondary to extrinsic compression of the biliary plexus by periportal collateral vessels. In the context of a 68 mm × 37 mm × 32 mm porta hepatis mass with circumferential ductal encasement, this mild dilatation reflects preserved ductal wall compliance, a key discriminating feature from cholangiocarcinoma. Diffuse subtle hypodensity of the central hepatic parenchyma with relative peripheral sparing, representing altered portal perfusion, was also noted and normalised on delayed-phase imaging. Technique: Triphasic contrast-enhanced CT, portal venous phase (~70 s after intravenous contrast injection). Siemens SOMATOM 256-slice scanner; 120 kV, 200–250 mAs (CARE Dose4D automated modulation); 5 mm axial sections with 1.5 mm multiplanar reconstructions; 100 mL Omnipaque 350 administered intravenously at 3 mL/s via antecubital vein. October 7, 2025.
Figure 8.
68-year-old female with Janus kinase 2 V617F-positive primary myelofibrosis and peribiliary inflammatory phlegmon. Findings: Three-phase computed tomography (CT) at the porta hepatis level. (a) Arterial phase (~30 s): no appreciable enhancement of the lesion (green arrow); collateral channels faintly opacified. (b) Portal venous phase (~70 s): near-homogeneous enhancement of the lesion (red arrow); collateral channels prominently opacified, confirming their venous nature. (c) Delayed phase (~180 s): mild washout of the lesion (red arrow) without progressive accumulation. This enhancement sequence contrasts with the pattern of fibrotic cholangiocarcinoma, in which delayed-phase intensity exceeds portal-phase intensity due to desmoplastic stroma. Technique: Triphasic CT: arterial phase (~30 s), portal venous phase (~70 s), delayed phase (~180 s) after intravenous contrast injection. Siemens SOMATOM 256-slice scanner; 120 kV, 200–250 mAs (CARE Dose4D automated modulation); 5 mm axial sections with 1.5 mm multiplanar reconstructions; 100 mL Omnipaque 350 administered intravenously at 3 mL/s via antecubital vein. October 7, 2025
JAK2 V617F mutation was detected in peripheral blood. Bone marrow trephine biopsy demonstrated a hypercellular marrow with megakaryocytic hyperplasia and grade III reticulin fibrosis, confirming PMF as the hematological driver of the chronic multivessel splanchnic venous thrombosis.[5]
The key imaging and biochemical discriminators between peribiliary phlegmon and periductal cholangiocarcinoma in this case are summarised in Table 1
Table 1.
Imaging and biochemical discriminators between peribiliary phlegmon from chronic portal venous thrombosis and periductal cholangiocarcinoma
| Parameters | Peribiliary phlegmon (present case) | Periductal cholangiocarcinoma |
|---|---|---|
| Biliary obstruction versus encasement | Disproportionately mild; CBD 5 mm despite circumferential encasement | Marked upstream dilatation; CBD typically >8 mm |
| CT arterial phase | Absent enhancement | Variable; may be absent or mild |
| CT delayed phase | Mild washout; does not exceed the portal phase | Progressive enhancement exceeding portal phase (desmoplastic stroma) |
| Spectral Doppler | Low-velocity continuous venous waveforms in intralesional channels | Absent or arterial-pattern neovascularity |
| Portal venous patency | Absent; cavernous transformation present | Usually patent (may be invaded in advanced disease) |
| CA 19-9/CEA | Normal | Often elevated (not pathognomonic) |
| Hematological evaluation | JAK2 V617F mutation; bone marrow fibrosis | Not contributory |
CA 19-9=Cancer antigen 19-9, CBD=Common bile duct, CEA=Carcinoembryonic antigen, CT=Computed tomography, JAK2=Janus kinase 2
Management and follow-up
The oncology referral was cancelled upon integration of the imaging and hematological findings. The patient was commenced on ruxolitinib for intermediate-risk PMF and a nonselective beta-blocker for primary variceal hemorrhage prophylaxis. Therapeutic anticoagulation was deferred, given coexisting thrombocytosis and portal hypertension-related bleeding risk. Follow-up sonography at 3 months demonstrated stable lesion morphology with identical venous Doppler characteristics and no interval growth.
DISCUSSION
The working diagnosis of cholangiocarcinoma in this case was challenged by findings on three imaging modalities. The CBD measured only 5 mm despite a 68-mm mass encasing it circumferentially along its entire length. Periductal cholangiocarcinoma invades transmurally and does not merely compress; this transmural invasion produces progressive luminal obliteration and marked upstream dilatation, with CBD diameters typically exceeding 8 mm once circumferential encasement is established.[6] Extrinsic inflammatory compression is anatomically different: the ductal wall remains pliable, and the lumen holds its caliber far better than the surrounding mass would suggest. The CT enhancement pattern was equally discordant with carcinoma. Portal-phase uptake was near-homogeneous, and the lesion showed mild washout on delayed imaging, which contrasts with the progressive contrast accumulation seen in the desmoplastic stroma of fibrotic cholangiocarcinoma.[7] The most direct evidence against malignancy, however, came from pulsed-wave spectral Doppler. Low-velocity continuous venous waveforms were recorded within multiple intralesional channels, with no arterial component detected anywhere in the lesion. Tumor neovascularity generates arterial signals; portal collateral veins embedded in peribiliary connective tissue generate exactly this venous-only pattern. No solid malignancy produces this spectral finding, irrespective of lesion size or degree of portal involvement. Spectral Doppler interrogation of a porta hepatis lesion is widely available, does not require intravenous contrast, and, in this case, provided the clearest single argument against carcinoma.
Portal biliopathy refers to the biliary ductal changes arising from extrinsic compression of the periductal biliary plexus by portosystemic collateral vessels, occurring in up to 80% of patients with longstanding portal vein thrombosis.[3] When the fibroinflammatory peribiliary reaction consolidates into a focal hilar mass, as in the present case, it can produce a convincing morphological replica of periductal cholangiocarcinoma on cross-sectional imaging.[3] Among the recognized causes of noncirrhotic splanchnic venous thrombosis, JAK2 V617F-positive myeloproliferative neoplasms are the most common identifiable driver, accounting for 17%–40% of cases in published series.[4] PMF carries a particularly high thrombotic burden because constitutive JAK-STAT pathway activation sustains thrombocytosis and promotes platelet-endothelial adhesion, often silently occluding multiple splanchnic vessels before any clinical presentation.[8] In this patient, thrombocytosis, neutrophilia, and anemia were all present on the admitting full blood count and provided the trigger for JAK2 V617F testing.
IgG4-related sclerosing cholangitis was considered, given the periductal distribution without an obvious primary mass. Serum IgG4 was within the normal range, the pancreas was uninvolved, and the hematological findings provided a complete mechanistic explanation for all imaging abnormalities without requiring a second diagnosis.[9] Antiphospholipid syndrome was excluded on the basis of a negative lupus anticoagulant screen. At the 3-month review, the lesion was unchanged in size, morphology, and Doppler characteristics on ruxolitinib alone, with no oncologic intervention. Untreated cholangiocarcinoma would be expected to show progression and worsening biliary obstruction over this interval. Radiological stability on disease-specific treatment was, in retrospect, a further confirmation of the diagnosis.
The practical implications of this case extend beyond tertiary referral centers. In settings where MRI, advanced molecular diagnostics, and specialist oncology services are not always immediately accessible, the full blood count provides the hematological signal that should redirect the diagnostic pathway before an oncology referral is committed to. Thrombocytosis with unexplained anemia in a patient presenting with a porta hepatis mass and cavernous transformation on CT is sufficient to justify JAK2 V617F testing. Had this patient proceeded to surgery or chemotherapy on the basis of the outside report, she would have been treated for a disease she did not have while PMF remained undiagnosed. The diagnostic sequence in this case did not require MRI or biopsy of the hilar lesion. Recognizing cavernous transformation on CT, confirming venous intralesional flow on spectral Doppler, noting the blood count abnormalities, and testing for JAK2 V617F is a practical approach that can be applied at most institutions with CT and Doppler capability.
CONCLUSION
Organised peribiliary phlegmon arising from chronic portal venous thrombosis with cavernous transformation can closely simulate periductal cholangiocarcinoma at the hepatic hilum. Spectral Doppler confirmation of venous intralesional flow, absent progressive delayed enhancement on CT, and disproportionately limited biliary obstruction relative to ductal encasement are reliable discriminating features that can prevent misclassification as malignancy. When cavernous transformation is identified on CT, evaluation for JAK2 V617F-positive myeloproliferative neoplasm should be undertaken before any oncologic referral or biopsy of the hilar lesion.
Ethics statement
This case report was conducted in accordance with the ethical principles of the Declaration of Helsinki (1975, as revised in 2013). Formal institutional review board approval was not required per institutional policy for a deidentified single-patient case report with written informed consent obtained. Written informed consent for publication of clinical details and imaging findings was obtained from the patient before submission. No identifying information appears in the manuscript text or figures.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.
Conflicts of interest
There are no conflicts of interest.
Acknowledgments
The authors would like to acknowledge the technical staff of the Department of Radiodiagnosis, Dr. D.Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, for their assistance with CT and sonographic imaging acquisition.
Funding Statement
Nil.
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