RESUMO
A case of osteosarcoma in pelvic bone following radiation therapy for prostate cancer is reported. A 74-year-old patient was diagnosed with prostate cancer 10 years ago and started on the endocrine therapy with LH-RH agonist. He had no apparent distant metastasis, and received radiation therapy 8 years ago. He has complained of low back pain since several months ago. A high uptake on bone scintigram and osteolytic and osteoblastic damages on CT were noted in pubic bone and sacrum. The PSA level was less than 0.2 ng/ml. Pathohistological diagnosis by biopsy of the pubic bone was chondroblastic type osteosarcoma, showing an atypical cell proliferation with osteoid. Immunostaining for nonepithelial marker vimentin was positive. He underwent heavy ion radiation therapy for osteosarcoma at the National Institute of Radiological Sciences. Osteosarcoma is one of the rare delayed complications after radiation therapy and requires biopsy for correct diagnosis.
Assuntos
Neoplasias Ósseas/etiologia , Neoplasias Induzidas por Radiação , Osteossarcoma/etiologia , Ossos Pélvicos , Neoplasias da Próstata/radioterapia , Sacro , Idoso , Neoplasias Ósseas/diagnóstico por imagem , Neoplasias Ósseas/patologia , Hormônio Liberador de Gonadotropina/agonistas , Humanos , Masculino , Neoplasias Induzidas por Radiação/patologia , Osteossarcoma/diagnóstico por imagem , Osteossarcoma/patologia , Ossos Pélvicos/diagnóstico por imagem , Neoplasias da Próstata/tratamento farmacológico , Cintilografia , Radioterapia/efeitos adversos , Sacro/diagnóstico por imagemRESUMO
We examined the effects of human alpha(1)-acid glycoprotein on isometric tension of mouse aortic rings. alpha(1)-Acid glycoprotein (7.5-75 microM) produced a transient, concentration-dependent relaxation of the phenylephrine-precontracted preparation. Although N(G)-nitro-L-arginine methyl ester or removal of endothelium rarely affected the alpha(1)-acid glycoprotein-induced relaxation, extracellular heparin inhibited the alpha(1)-acid glycoprotein-induced relaxation. In 10 mM Ca(2+)-containing external solutions, the alpha(1)-acid glycoprotein-induced relaxation was significantly potentiated. In the 60 mM KCl-precontracted preparation, alpha(1)-acid glycoprotein produced weaker relaxation than in the phenylephrine-precontracted preparation. These results suggest that the vasorelaxant effect of alpha(1)-acid glycoprotein is mainly achieved by block of Ca(2+) entry in the vascular smooth muscle cells. The interaction between alpha(1)-acid glycoprotein molecules and plasmalemmal Ca(2+) entry channels may be modified by extracellular Ca(2+) and heparin.
