RESUMO
Silent somatotroph tumors (sSTs) are pituitary neuroendocrine tumors (PitNETs) which do not give rise to the clinical syndrome of acromegaly. Differently to their functioning counterparts, the adjuvant medical treatment with somatostatin analogues (SSAs) or dopamine receptors agonists (DAs) has been scarcely addressed in these tumors. As preliminary results of an ongoing research on silencing mechanisms involved in the pathogenesis of sSTs, we have characterized by qRT-PCR the expression of SSTRs and DRDs in a large series of 18 silent and 68 functioning STs. Although the expression of SSTR2 and SSTR5 was lower in sSTs than in functioning ones, we found a negative correlation between SSTR2 and the tumor size of the sSTs. Additionally, levels of expression of DRD2 were similar between the two subtypes suggesting a possible basis for the treatment of these tumors with SSAs and DAs.
Assuntos
Adenoma/metabolismo , Tumores Neuroendócrinos/metabolismo , Neoplasias Hipofisárias/metabolismo , Receptores de Dopamina D2/biossíntese , Receptores de Somatostatina/biossíntese , Somatotrofos/metabolismo , Adenoma/diagnóstico , Adenoma/genética , Adulto , Biomarcadores Tumorais/biossíntese , Biomarcadores Tumorais/genética , Gerenciamento Clínico , Feminino , Perfilação da Expressão Gênica/métodos , Humanos , Masculino , Pessoa de Meia-Idade , Tumores Neuroendócrinos/diagnóstico , Tumores Neuroendócrinos/genética , Neoplasias Hipofisárias/diagnóstico , Neoplasias Hipofisárias/genética , Receptores de Dopamina D2/genética , Receptores de Somatostatina/genética , Somatotrofos/patologiaRESUMO
Amyloid goiter (AG) is characterized by the presence of deposits of amyloid protein in the thyroid tissue in sufficient amounts to produce enlargement of the gland, accompanied by fat deposition or thyrolipomatosis. It can be seen in long-standing inflammatory disorders, with the common characteristic of amyloidotic renal failure. In daily practice, practitioners should pay attention to the differential diagnosis in patients with suggestive co-morbidities for amyloidosis. The clinic is a progressive increase of the thyroid gland with compressive symptomatology (dyspnea, dysphagia, and changes in the voice). The main imaging finding is diffuse fatty infiltration of the thyroid. The amyloid goitre was most probably in the general context of amyloidosis, regardless of the other complications. We present a case of a 48-years-old female with amyloid goiter secondary to rheumatoid arthritis and renal failure.
