Vertebral metastasis with spinal cord compression as the first manifestation of hepatocellular carcinoma: a case report

Abstract

Background

Hepatocellular carcinoma, typically linked to chronic hepatitis B or C, usually presents with liver-related symptoms, mainly jaundice, abdominal pain, and weight loss, and rarely spreads beyond the liver. Bone metastases and their complications are uncommon and seldom the initial sign.

Case presentation

We report the case of a North African (Tunisian) man in his 70s with undiagnosed chronic hepatitis B who presented with back pain and was subsequently diagnosed with multifocal hepatocellular carcinoma. His clinical course was complicated by acute paraplegia due to spinal cord compression caused by vertebral metastases.

Conclusion

This case highlights the variability in hepatocellular carcinoma presentations and underscores the need for heightened clinical vigilance in patients presenting with unexplained bone or neurological symptoms, even in the absence of overt hepatic signs. Skeletal metastases are rare in this tumor compared with other cancers. The diagnosis can be even more challenging when bone metastases are the predominant initial manifestation, particularly when neurological complications emerge early in the course of disease.

Introduction

Hepatocellular carcinoma (HCC) accounts for approximately 90% of primary liver cancers and most often develops in the setting of chronic liver disease, particularly after progression to cirrhosis [1]. Despite advances in surveillance and imaging, HCC is often diagnosed at an advanced stage due to its insidious onset and the absence of specific early symptoms. As a result, extrahepatic metastases are increasingly recognized at the time of diagnosis [2]. Bone metastasis as the initial manifestation of HCC is uncommon [3]. We report an unusual case of spinal cord compression due to vertebral metastases, unveiling an unknown HCC.

Case presentation

A North African (Tunisian) man in his 70s, with a 20-year history of chronic obstructive pulmonary disease managed with inhaled corticosteroids and bronchodilators, had no personal or family history of hepatobiliary or metabolic disease and denied exposure to hepatotoxic risk factors including alcohol, illicit drugs, or high-risk sexual behavior. He presented with new-onset inflammatory thoracolumbar back pain over the past 3 weeks, described as a dull, persistent aching sensation that did not radiate. It was initially rated 5/10 on a visual analog scale, progressively worsened, and became refractory to analgesic therapy. He reported associated fatigue, weight loss, and anorexia in the preceding weeks but denied any abdominal pain, jaundice, abdominal distension, or gastrointestinal bleeding. Upon physical examination, the patient had an Eastern Cooperative Oncology Group Performance Status (ECOG PS) of 1, with no hepatomegaly, jaundice, collateral circulation, or palpable tenderness noted. Laboratory studies revealed moderately elevated liver enzymes [aspartate transaminase (AST) 72 U/L, alanine aminotransferase (ALT) 85 U/L], hypoalbuminemia (32.4 g/L), and hypocholesterolemia (3.64 mmol/L). Prothrombin level was low at 60% and complete blood count was within normal limits. As an initial investigation for suspected referred back pain, abdominal ultrasound showed a hepatic mass. Contrast-enhanced abdominal computed tomography (CT) confirmed a 68 × 48 mm irregular lesion at the junction of liver segments V, VI, and VIII. The lesion exhibited intense arterial phase enhancement, washout in the portal venous phase, and a peripheral capsule, imaging characteristics consistent with Liver imaging reporting and data system (LI-RADS) 5 (Fig. 1), highly suggestive of HCC. A second 2.4 cm arterially enhancing nodule in segment IV was classified as LI-RADS 4. The liver appeared dysmorphic, suggestive of chronic liver disease, but without evidence of intraabdominal collateral venous circulation. Viral serology showed positive HBs antigen and anti-HBc antibodies, and polymerase chain reaction (PCR) confirmed active hepatitis B virus replication with hepatitis B virus (HBV) DNA viral load of 2.1 × 10⁶ IU/mL. Alpha-fetoprotein (AFP) was significantly elevated at 288 ng/mL. Upper gastrointestinal endoscopy revealed grade II esophageal varices, confirming portal hypertension. A diagnosis of multifocal HCC in the setting of HBV-related cirrhosis was confirmed and antiviral therapy was started. Shortly after admission, the patient developed sudden paraplegia. Neurological examination confirmed flaccid paralysis of the lower limbs without preserved sensation. Urgent magnetic resonance imaging of the spine revealed a pathological fracture of the T11 vertebra with collapse of the vertebral body exceeding 50%, consistent with metastatic involvement. The lesion appeared hypointense on T1, heterogeneously hyperintense on T2, and showed marked contrast enhancement after gadolinium administration. There was an associated epidural mass compressing the spinal cord with more than 50% canal stenosis and bilateral dilatation of the intervertebral foramina with invasion of the surrounding soft tissue and loss of the fat pad between the mass and the descending thoracic aorta (Fig. 2). The radiological pattern of this lesion was highly consistent with spinal metastasis from the primary liver tumor, negating the need for a confirmatory biopsy. Thus the diagnosis of HCC vertebral metastases with epidural spinal cord compression was established. The tumor was classified as Barcelona Clinic Liver Cancer (BCLC) stage D; indicating a poor prognosis and no curative options, primarily due to the rapid deterioration of the patient’s general condition leading to an ECOG PS of 3 despite preserved hepatic function with a Child–Pugh score of 6. Emergency management included intravenous high-dose corticosteroids (dexamethasone 8 mg three times daily for 5 days, followed by gradual tapering) and urgent radiotherapy for spinal cord decompression (30 Gy in 10 fractions over 2 weeks), resulting in complete recovery from the motor deficit. The patient was referred to palliative care focused on symptom control, quality of life, and psychosocial support. Unfortunately, he passed away a few weeks after his discharge from the hospital. The timeline of key clinical events, from initial presentation to outcome, is illustrated in Fig. 3.

Fig. 1.

Axial abdominal computed tomography demonstrating cirrhotic liver with hepatic mass: axial contrast-enhanced abdominal computed tomography scan with mediastinal window settings, obtained during the late arterial (A) and portal venous (B) phases, demonstrating a cirrhotic liver with irregular contours (black arrowheads) and a 68 × 48 mm (axial plane) heterogeneous mass spanning segments V, VI, and VIII (black arrows, A/B) with arterial phase hyperenhancement (white arrow, A) and early washout during the portal phase (white arrow, B)

Fig. 2.

Dorsolumbar spine magnetic resonance imaging demonstrating T11 vertebral pathology: sagittal T1-weighted (A) and post-contrast T1-weighted (B) images showing complete marrow replacement causing T11 vertebral collapse exceeding 50% (white arrows, A/B), T1 hypointense signal with heterogeneous T2 signal, and intense heterogeneous gadolinium enhancement. Axial T2-weighted image at T11–T12 level (C) reveals epidural extension with posterior wall bulging, resulting in more than 50% spinal canal stenosis (short white arrows) and early cord compression without cord signal abnormality, bilateral foraminal extension (dotted white arrows), and posterior element involvement: posterior arch, pedicles, laminae (white arrowheads)

Fig. 3.

Timeline summarizing the key clinical events, diagnostic procedures, and therapeutic interventions

Discussion

HCC ranks as the sixth most common cancer and the fourth leading cause of death from cancer worldwide. It is considered one of the most lethal and rapidly progressive tumors [1]. Portal and hepatic vein invasion by the tumor is a common manifestation, thus explaining the rising frequency of distant metastases at the time of diagnosis [2]. Extrahepatic involvement is rare in early HCC [4] and is mainly associated with advanced tumors with a size exceeding 5 cm. Extrahepatic metastases are reported in approximately 14–36.7% of cases, with skeletal metastases being the third most common site after the lung and lymph nodes [3]. Recent data indicate that bone metastasis is present in 16.1–38.5% of patients with HCC at the initial diagnosis, while 11.7% of those receiving curative resections develop it later [5]. Bone metastases as the initial manifestation of HCC are less common, occurring in 3.3–5.1% of cases, though their overall incidence has notably increased in the last decade, primarily attributed to the improved overall survival of these patients [6–8]. The most affected bones are vertebrae, pelvis, ribs, skull, humerus, and sternum [9], exceptionally the calcaneus and calvarium [10, 11]. On CT imaging, metastases typically appear as expansile, lytic lesions with prominent hypervascularity, creating diagnostic challenges in distinguishing them from renal cell carcinoma or thyroid carcinoma metastases [12]. The distribution of lesions is helpful since HCC metastases frequently involve the lower thoracic and lumbar spine [13]. On magnetic resonance imaging (MRI), HCC metastases usually have heterogeneous contrast enhancement and associated soft tissue masses compressing the spinal cord, paralleling renal cell carcinoma lesions. However, an early washout has been described as a specific finding for HCC bone metastases noted in 56% of cases [13]. Thyroid metastases, on the contrary, may show mixed lytic–sclerotic changes and possibly calcifications, which can aid differentiation [5, 14]. Given radiological similarities, correlation with clinical, biochemical, and other imaging findings is essential for an accurate diagnosis. While skeletal metastases typically develop during advanced stages of HCC, our case highlights the rare but clinically significant phenomenon of osseous metastasis as the index presentation. This unusual presentation pattern underscores the importance of considering HCC in the differential diagnosis of lytic bone lesions, particularly in patients with risk factors for chronic liver diseases [15]. In the present case, the vertebral metastasis was complicated by spine compression. This entity remains uncommon since only some similar cases of spinal compression as a first manifestation of HCC have been reported in the literature [6, 7, 11, 16–18]. A study reported spinal compression from hepatocellular carcinoma vertebral metastasis in less than 2% of cases, highlighting its very rare and infrequent occurrence as a feature of HCC [7]. It occurs due to the invasion of the epidural space, most often as a direct extension of vertebral body metastases. There are various routes of the epidural invasion by tumor cells, hematogenous being the most common mode of spread. Hematogenous spread occurs directly or via the involvement of Batson’s venous plexuses [5]. Overall, HCC is usually associated with a poor prognosis, with a 5-year survival rate of less than 20% [3]. The prognosis further deteriorates in the presence of metastases, which preclude any curative treatment [19]. Radiotherapy is an effective therapeutic option for bone metastases, providing significant pain relief in approximately 60–90% of patients, with up to 33% achieving complete pain resolution during or shortly after treatment [8]. Other authors reported a significant effect of systemic chemotherapy, as well as targeted therapies [7, 8, 12]. In our case, despite the advanced-stage disease at diagnosis, immediate therapeutic intervention comprising intravenous high-dose corticosteroids and emergency radiotherapy resulted in complete restoration of motor function and complete pain resolution. To minimize patient burden and improve outcomes, this case emphasizes the critical need for heightened clinical suspicion of HCC in patients with atypical musculoskeletal symptoms, especially those with risk factors for chronic liver disease, enabling earlier diagnosis and less invasive management strategies.

Conclusion

This case highlights a rare and clinically significant presentation of HCC, initially revealed by vertebral metastasis with cord compression in the absence of typical liver-related symptoms. This underscores that new onset back pain and neurological deficits in patients with risk factors for chronic liver disease should trigger urgent imaging and early intervention. Prompt recognition is essential to initiate appropriate diagnostic workup and timely palliative interventions, which can significantly improve patient quality of life.

Abbreviations

AFP

Alpha-fetoprotein

BCLC

Barcelona Clinic Liver Cancer

CT

Computed tomography

HCC

Hepatocellular carcinoma

LI-RADS

Liver imaging reporting and data system

Author contributions

Patient management: HH; data collection: WK, HH and AG; manuscript drafting: WK and HH; and manuscript revision: HY, DC, HK, HD, and NM. All authors have read and approved the final manuscript.

Funding

No funds, grants, or other support were received.

Data availability

All data generated or analyzed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

The institutional review board of our institution waived the need for ethics approval because this report describes a single patient.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

Authors declared they have no conflicts of interest.