Melanoma metastasis is one of the most common hypervascular metastasis types in the liver. It develops through hematogenous spread from primary cutaneous or ocular melanoma. Due to melanin pigment, it demonstrates T1 hyperintensity — this finding is pathognomonic and distinguishes it from other metastases. Autopsy series reveal liver metastases in 50-80% of patients with malignant melanoma. Prognosis is poor with median survival of 4-6 months, but significant improvement is achievable with immunotherapy (anti-PD-1, anti-CTLA-4).
Age Range
30-75
Peak Age
55
Gender
Equal
Prevalence
Uncommon
Melanoma cells synthesize melanin pigment — this pigment has paramagnetic properties (chelates stable free radicals and metal ions). Paramagnetic melanin shortens T1 relaxation time, creating T1 hyperintensity on MRI. Melanoma cells exhibit high VEGF expression and form hypervascular metastases. Tumor cells reaching the liver through hematogenous spread lodge in sinusoids and grow from millimetric micrometastases to centimeter-sized masses. Amelanotic melanoma (10-20%) does not produce melanin and does not show T1 hyperintensity — this variant complicates diagnosis.
The paramagnetic effect of melanin pigment shortens T1 relaxation time, creating T1 hyperintensity on MRI. The combination of T1 bright + T2 dark is pathognomonic for melanoma among liver metastases. This finding must be distinguished from subacute hemorrhage (methemoglobin): melanoma lesions show homogeneous and consistent T1 hyperintensity, while hemorrhagic lesions display heterogeneous and variable patterns. This finding is absent in amelanotic melanoma.
Marked hyperintensity on T1 — due to paramagnetic effect of melanin pigment. This finding is pathognomonic for melanoma metastasis. Amelanotic melanoma (10-20%) does not show T1 hyperintensity.
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Lesion(s) demonstrating hyperintense signal on T1-weighted sequences are seen in the liver, consistent with melanin-containing metastasis in the context of known melanoma history.
T2 hypointensity in melanotic lesions — T2 shortening effect of melanin. Amelanotic lesions show T2 hyperintensity. In mixed melanoma metastasis, both patterns may coexist.
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The lesions demonstrate hypointense signal on T2-weighted sequences, consistent with melanin content.
Intense arterial phase enhancement — melanoma metastases are hypervascular in character. Enhancement may be homogeneous or heterogeneous. Rim enhancement may be seen in large lesions due to central necrosis.
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Multiple hypervascular lesions demonstrating intense arterial phase enhancement are seen in the liver, consistent with melanoma metastasis.
Portal venous phase washout — after arterial enhancement, lesions become hypodense relative to surrounding parenchyma. Typical dynamic pattern of hypervascular metastases.
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The lesions demonstrate washout in the portal venous phase, consistent with hypervascular metastasis dynamics.
On non-contrast CT, melanotic lesions may appear slightly hyperdense (40-60 HU) — due to melanin accumulation. Amelanotic lesions may be isodense or hypodense. When combined with hemorrhage, attenuation increases further.
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Slight hyperdensity is seen in the liver lesions on non-contrast CT, suggesting melanin accumulation.
On US, melanoma metastases typically show hyperechoic or mixed echogenicity. Target pattern is common: hyperechoic periphery + hypoechoic center. Heterogeneous echogenicity predominates in large lesions.
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Multiple lesions with hyperechoic/mixed echogenicity are seen in the liver, consistent with metastasis.
Criteria
Melanin-producing tumor cells (80-90%). T1 hyperintense, T2 hypointense signal pattern.
Distinct Features
Classic T1 bright + T2 dark pattern. Slight hyperdensity on non-contrast CT. Diagnosis is readily made.
Criteria
Non-melanin-producing tumor cells (10-20%). T1 hyperintensity is ABSENT — nonspecific signal like other metastases.
Distinct Features
On MRI T1 isointense/hypointense, T2 hyperintense — indistinguishable from other hypervascular metastases. Diagnosis relies on primary melanoma history. Biopsy may be needed.
Criteria
Hepatic metastasis of uveal melanoma. Liver is the most common metastatic site for uveal melanoma (>90%). Different biology from cutaneous melanoma.
Distinct Features
Hematogenous spread via hepatic artery rather than portal vein — metastases are therefore more hypervascular. Diffuse millimetric pattern is common. Immunotherapy response is lower than cutaneous melanoma.
Distinguishing Feature
RCC metastasis is hypervascular but does not show T1 hyperintensity (unless hemorrhage). Melanoma metastasis has consistent T1 bright signal from melanin. Primary tumor history (kidney vs skin) is distinguishing.
Distinguishing Feature
Neuroendocrine metastasis is also hypervascular and enhances in arterial phase. However, it does not show T1 hyperintensity on MRI. Clinical context (carcinoid syndrome, 5-HIAA, chromogranin A) and primary tumor location are distinguishing.
Distinguishing Feature
Hemangioma is markedly T2 hyperintense (light bulb sign), T1 hypointense — the opposite of melanoma metastasis. Hemangioma shows peripheral nodular enhancement with centripetal fill-in; melanoma shows diffuse arterial enhancement.
Distinguishing Feature
HCC develops in cirrhotic liver, usually solitary or oligofocal. Generally T1 hypo/isointense (T1 bright HCC is rare — fat or copper accumulation). Melanoma metastasis occurs as mostly multiple lesions in non-cirrhotic liver. Melanoma history is critical.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
3-monthLiver melanoma metastasis indicates systemic disease. Biopsy is generally unnecessary — known melanoma history and characteristic MRI findings (T1 hyperintensity) suffice for diagnosis. Treatment is systemic immunotherapy (anti-PD-1: nivolumab/pembrolizumab, anti-CTLA-4: ipilimumab) and/or targeted therapy (vemurafenib/dabrafenib if BRAF mutant). Surgical resection or ablation may be considered in oligometastatic disease. Treatment response should be evaluated with CT/MRI at 3-month intervals.
Melanoma liver metastasis indicates metastatic disease (stage IV) and is associated with poor prognosis. Immunotherapy (pembrolizumab, nivolumab + ipilimumab) and targeted therapy (BRAF/MEK inhibitors) are treatment options. T1 hyperintensity may complicate treatment response assessment.