27 June 2026
: Case report 
Depicting Characteristic Staghorn Vessels in Solitary Fibrous Tumor of the Liver With Contrast-Enhanced Ultrasound and Ultrasound Localized Microscopy: A Case Report
Challenging differential diagnosis, Diagnostic / therapeutic accidents, Unusual setting of medical care, Rare disease, Educational Purpose (only if useful for a systematic review or synthesis)
Xue Lu
ABCDEFG 1, Yuanqiang Xiao BCDE 2, Lili Wu BCD 1, Jianning Chen BCD 3, An Liu BF 1,4, Jie Ren CDFG 1, Yinglin Long AEFG 1*
DOI: 10.12659/AJCR.952355
Am J Case Rep 2026; 27:e952355
Table 2 The differential diagnosis of SFTL, HCC, FNH and AML.
| Characteristics | SFTL | HCC | FNH | AML |
|---|---|---|---|---|
| Pathology | The tumor consists of irregularly arranged (fascicular) spindle or ovoid cells with oval nuclei and scant cytoplasm. Collagen-rich stroma and abundant staghorn (branching) thin-walled vessels (hemangiopericytoma-like vascular pattern) are present. Gene fusion, particularly the characteristic NAB2–STAT6 fusion, serves as a defining molecular feature of SFT | Exhibits structural and cytologic atypia (such as disorganized trabecular arrangement and increased nuclear-to-cytoplasmic ratio), and is often accompanied by stromal or vascular invasion. | Composed of a proliferative growth of morphologically normal hepatocytes but lacks normal portal tract development. Characteristic central fibrovascular scar and radiating fibrous septa are present, containing aberrant feeding arteries and their branches. Bile ductular proliferation is typically seen at the edges of the fibrous septa | It is primarily composed of 3 tissue components mixed in varying proportions: smooth muscle cells, adipose tissue, and blood vessels, with some cases containing hematopoietic tissue. Among these, smooth muscle cells (often epithelioid, with clear or eosinophilic cytoplasm) are the only specific diagnostic component, while the abnormal blood vessels are typically tortuous and thick-walled |
| Epidemiologic features | Rare mesenchymal tumor; wide age range (median, 57 y); affects men and women | Adults, more common in men (60–70 y) | Adults, more common in women (30–50 y) | Adults, more common in women (50–60 y) |
| Clinical history | Mostly asymptomatic (incidental); large mass → abdominal discomfort, pain, weight loss, fatigue; rare Doege-Potter syndrome (IGF-II); 10–20% malignant potential | Chronic liver disease (HBV, HCV, alcoholic, NAFLD) in most cases; cirrhosis in vast majority | Normal/near-normal liver; asymptomatic (incidental); rare bleeding/rupture | Most asymptomatic (incidental); large lesions → discomfort, mild fever; sporadic or with tuberous sclerosis |
| Laboratory examination | Tumor markers negative/normal; diagnosis: histology + IHC (CD34+, STAT6+, Vimentin+) + NAB2-STAT6 fusion | Frequently elevated serum AFP; linked to increased mortality and recurrence | Tumor markers (AFP, etc.) typically unremarkable | LFTs and tumor markers (AFP, CEA, CA19-9) usually normal/negative |
| US | Well-defined heterogeneous mass, hypo- or mildly hyperechoic; rare calcification; color Doppler: often no obvious internal or peripheral flow | Solid nodules on US; combined with AFP for high-risk monitoring | Often nearly isoechoic to normal liver (subtle differences); color/power Doppler: central feeding artery with characteristic “spoke-wheel” branches | Heterogeneous hyperechoic nodule (fat content) with shadowing/refraction artifacts; may mimic hemangioma |
| CEUS | Intrinsic and extensive intratumoral small-vessel proliferation, arterial phase hyperenhancement; arterial phase: peripheral/internal hyperenhancement, rapid centripetal filling; possible wash-out (hypoenhancement) on portal/delayed phases, possible central defect; mimic HCC | Disorganized external feeders; arterial non-rim hyperenhancement with subsequent washout | Central scar and spoke-wheel enhancement; portal/delayed phases: mild hyperenhancement or isoenhancement | Heterogeneous enhancement and irregular vascular morphology; arterial early: hyperenhancement, persists to portal/late phases; Approximately 25% may exhibit wash-out |
| CT | Plain scan: heterogeneous low density (solid soft tissue; necrotic/cystic areas lower); rare calcification and hemorrhage; after contrast: arterial phase marked heterogeneous enhancement; portal/delayed phases: persistent/progressive enhancement (“fast-in slow-out”) | Early arterial marked hyperenhancement, delayed washout; may have peripheral enhancing pseudocapsule | Plain scan: iso- or slightly hypodense; arterial: homogeneous arterial phase hyperenhancement; central scar: hypo- in arterial/portal, hyper- in delayed (2–5 min) | Plain scan: heterogeneous low density, macroscopic fat (−100 to −10 HU); arterial: soft tissue markedly enhances; portal phase: persistent in most (some washout); common internal vessels and early draining veins |
| MRI | T1: intermediate/low; T2: mixed high/low (low = fibrous/collagen), flow voids from vessels; Post-contrast: arterial heterogeneous; delayed progressive enhancement (fibrous) | Arterial enhancement + delayed washout; coating appearance; With hepatobiliary contrast, most HCCs are hypointense on HPB | T1 iso-/slightly hypointense; T2 slightly hyperintense (“invisible nodule”); arterial marked enhancement; central scar (T2 hyper/T1 hypo) enhances delayed; hepatobiliary contrast: nearly uniform HBP hyperintensity (characteristic) | T2 heterogeneous hyperintense; T1 variable; in/opposed-phase: fat signal drop; Arterial hyperenhancement; possible washout on venous/delayed; HBP: hypointense |
| SFTL, solitary fibrous tumor of the liver; HCC, hepatocellular carcinoma; FNH, focal nodular hyperplasia; AML, angiomyolipoma; AFP, alpha-fetoprotein; HVB, hepatitis virus B; HVC, hepatitis virus C; CT, computed tomography; MRI, magnetic resonance imaging; NAFLD, nonalcoholic fatty liver disease; HPB, hepatobiliary phase; LFT, liver function tests; IHC, immunohistochemistry. | ||||