Primary cystic neuroendocrine tumor of the liver: case report / Tumor neuroendócrino quístico primario de hígado: reporte de un caso

Background: 85% of neuroendocrine tumors (NET) originate in the gastrointestinal tract, which is why their primary hepatic location is very rare; NETs most frequently cause metastases to the liver; so when diagnosed, a hepatic NET is considered initially metastatic. Diagnosis of primary hepatic neuroendocrine tumors (PHNET) should be performed by excluding extrahepatic NETs and through histological confirmation. The objective of this article is to present a case of PHNET. Clinical case: 75-year-old male patient, who presented asthenia, adynamia, abdominal pain in the right hypochondrium, six-month weight loss, with a right subcostal palpable tumor. Imaging studies reported a lesion in the right hepatic lobe, multilobulated, heterogeneous, with poorly defined margins and with cystic areas. It was performed diagnostic laparotomy and then a hepatic tumorectomy, whose product measured 16.0 x 10.0 x 6.5 cm, with two cystic cavities of 13.2 and 11.5 cm of hematic content. Microscopically, cells with neuroendocrine differentiation, with positive immunoreactivity to chromogranin were observed. It was diagnosed well-differentiated neuroendocrine neoplasm, with cystic degeneration. Conclusions: Even though it is excluded a NET from an extrahepatic primary site, the tumor etiology of an important proportion of patients with PHNET will be due to an unknown primary tumor that will become apparent over time; hence, the need to follow up as long as possible.

Introducción: 85% de los tumores neuroendocrinos (TNE) se originan del tracto gastrointestinal, su localización hepática primaria muy rara; los TNE con mayor frecuencia causan metástasis al hígado; por esto, cuando se diagnóstica un TNE hepático es considerado inicialmente metastásico. El diagnóstico de tumor neuroendocrino primario de hígado (TNEPH) debe realizarse mediante la exclusión de tumores neuroendócrinos extrahepáticos y la confirmación histológica. El objetivo de este artículo es presentar un caso con TNEHP. Caso clínico: paciente de sexo masculino, de 75 años de edad, quien presentó astenia, adinamia, dolor abdominal en hipocondrio derecho y pérdida de peso de 6 meses de evolución, con tumor palpable subcostal derecho. Los estudios de imagen reportaron lesión en lóbulo hepático derecho, multilobulada, márgenes mal definidos, heterogénea y con áreas quísticas. Se realizó laparotomía diagnóstica y tumorectomía hepática que midió 16.0 x10.0 x 6.5 cm, con dos cavidades quísticas de 13.2 y 11.5 cm de contenido hemático. Microscópicamente se observaron células con diferenciación neuroendócrina, inmunoreactivas a cromogranina. Se estableció el diagnóstico de neoplasia neuroendócrina bien diferenciada, con degeneración quística. Conclusiones: aunque se excluya un TNE de sitio primario extrahepático, la etiología tumoral de una proporción considerable de pacientes con TNEPH será a causada por un tumor primario no conocido que se hará evidente con el tiempo; de ahí la necesidad de hacer seguimiento el máximo tiempo posible.

Tumor-associated macrophages and angiogenesis: a statistical correlation that could reflect a critical relationship in ameloblastoma.

Neoplasm growth is determined not only by the tumor cells themselves, but also by the tumor microenvironment. Increased densities of macrophages and activation of angiogenesis have been identified as common events in the progression of several neoplasms. Ameloblastoma is one of the most frequent odontogenic tumors and an excellent model for the study of neoplasm progression due to the different clinical variants that it exhibits. Here, by immunohistochemical studies using antibodies against CD68 and CD34, we evaluated the density of macrophages and microvessels associated to 45 paraffin-embedded ameloblastomas. In solid/multicystic ameloblastoma (SMA), we observed significantly higher densities of both macrophages and microvessels than in unicystic (UA) and desmoplastic (DA) ameloblastomas. Likewise, higher densities of macrophages and microvessels were found in UA than in DA. Furthermore, a predominance of intratumoral and peritumoral macrophage infiltrates was seen in SMA, while in UA, both macrophages and microvessels were also detected in the wall of the cysts. In contrast, DA had scant macrophages and microvessels, mainly situated distant from tumoral cells. In addition, a high correlation between macrophage and microvessel densities was observed in the samples (r=0.9623). Our results suggest that these two tumor microenvironmental elements could have an important role during ameloblastoma progression.