[Case of skull metastasis from hepatocellular carcinoma at the site of skull fracture].
ABSTRACT It has occasionally been reported that mechanical trauma and posttraumatic inflammation may promote metastasis from a primary tumor to the site of the trauma. However, the etiologies that contribute to the metastasis formation at the trauma site remain unknown. We describe here the first case of skull metastasis from hepatocellular carcinoma (HCC) revealing a growing subcutaneous mass at the site of skull fracture. A 58-year-old man had undergone surgical resection of a primary tumor in the liver 2 years previously and was in clinical remission. The patient fell head first off his bicycle and suffered a skull fracture in the squamous portion of the left temporal bone without ostelysis. Three months after the head trauma, he presented at our department with a growing lump on the left side of his head, and magnetic resonance (MR) imaging revealed an osteolytic tumor extending into the adjacent subcutaneous and epidural space. The tumor was at the same location as the skull fracture sustained in the bicycle accident. The mass lesion was radically resected with surrounding normal bone. The tumor formed a well-demarcated mass with osteolysis of the inner and outer skull tables, and the inner layer of the dura mater was intact. The histological diagnosis for the surgical specimen from the skull tumor was a HCC identical to the primary tumor. Immunohistochemically, the tumor cells were diffusely and strongly positive for vascular endothelial growth factor (VEGF) and basic fibrous growth factor (bFGF). It is well known that the extracellular matrix and cytokines are involved in the processes of not only bone healing but also metastasis formation. The present case suggests that several processes involved in bone healing modified the microenvironment and represent a possible cause of skull metastasis from primary tumor.
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ABSTRACT: Cases with subcutaneous metastasis of differentiated hepatocellular carcinoma to the abdominal wall without prior seeding as a consequence of local interventions with a negative or normal alpha-fetoprotein level in the serum are extremely rare. This is the first report of a case with AFP-negative, differentiated hepatocellular carcinoma metastasis to the abdominal wall within a pre-existing subcutaneous lipoma since childhood after antiandrogen therapy with leuprorelin and buserelin acetate for prostate cancer without seeding. Clinical features including histology, immunohistochemistry, clinical course and surgical approach are presented. Histological examination revealed a hepatocellular carcinoma with a trabecular and pseudoglandular growth pattern with moderately atypical hepatocytes with multifocal bile formation within a lipoma. The postoperative course of abdominal wall reconstruction with a monocryl-prolene mesh and a local flap after potentially curative resection was uncomplicated. It may be that previous antiandrogen treatment for prostate carcinoma contributed to the fact that our patient developed alpha-fetoprotein-negative and androgen receptor-negative subcutaneous abdominal wall metastasis within a pre-existing lipoma since childhood.World Journal of Surgical Oncology 05/2012; 10:98. · 1.09 Impact Factor
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ABSTRACT: The relationship between inflammation and tumorigenesis has been established. Recently, inflammation is also reported to be a drive force for cancer metastasis. Further evidences show that various stimuli directly induced-injury in a specific organ can also promote metastasis in this organ, which include epidemiological reports, clinical series and experimental studies. Each type of cancer has preferential sites for metastasis, which is also due to inflammatory factors that are released by primary cancer to act on these sites and indirectly induce injuries on them. Host factors such as stress,fever can also influence distant metastasis in a specific site through stimulation of immune and inflammatory effects. The five aspects support an idea that specific-organ injury directly induced by various stimuli or indirectly induced by primary tumor or host factors activation of proinflammatory modulators can promote metastasis in this organ through a spatiotemporal regulation, which has important implications for personalized prediction, prevention and management of cancer metastasis.Pathology & Oncology Research 12/2013; · 1.56 Impact Factor
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ABSTRACT: Skull metastasis from hepatocellular carcinoma (HCC) is reported rarely. In addition, solitary skull metastasis as the first symptom of HCC is reported even less. Here, we reported a case of solitary skull metastasis as the first symptom of HCC and reviewed the literature on skull metastasis. A 49-year-old male patient was admitted to Jinjiang Hospital of Quanzhou Medical College with a painless parietal-occipital scalp mass, and he denied any history of hepatic disease. A cranial computed tomography demonstrated a hypervascular enhancement with osteolytic change in the right parietal-occipital region, cranial magnetic resonance imaging indicated a highly enhanced and osteolytic skull tumor, and abdominal computed tomography showed a huge tumor in the liver. The other examinations showed no other metastases. Laboratory data showed no liver dysfunction while hepatitis B surface antigen was positive, and alpha fetal protein level was high. A craniectomy was performed and the mass was totally removed. The histological diagnosis was skull metastasis from HCC. The patient was subsequently treated by transcatheter arterial chemoembolization. In a review of published literature, the incidence of skull metastasis from HCC in the period between 1990 and 2011 has significantly increased. The misdiagnosis rate of skull metastases as the first symptom from HCC was high. Therefore, it is necessary to give each patient with a scalp mass that has invaded the skull a liver ultrasound or computed tomography scan. On the other hand, we found that metastases that occurred in the calvaria site were more frequent than those that occurred in the skull base and facial skeleton. This may be worthy of further investigation in the future.Neuropsychiatric Disease and Treatment 01/2014; 10:681-686. · 2.00 Impact Factor