No abstract

Biopsies from 25 juvenile nasopharyngeal angiofibromas (JNAs) and respective normal inferior turbinates were examined and compared. The expression patterns of the messenger RNAs (mRNAs) for various growth factors possibly involved in the growth of mesenchymal cells, as well as angiogenesis and fibrosis, were also compared. These growth factors included insulin-like growth factor II (IGF-II), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), transforming growth factors-beta1 (TGF-beta1) and platelet-derived growth factors (PDGF-A and PDGF-B). Quantification of mRNA coding for proto-oncogenes and suppressor genes related to proliferation (i.e., c-myc, c-fos, p53) was also undertaken. Tumor and turbinates expressed similar levels of bFGF, VEGF, TGF-beta1, c-myc, c-fos, and PDGF-A mRNAs. The presence of TGF-beta1 protein was confirmed by immunohistochemistry in several structures that characterize the lesions of JNA, which suggests that TGF-beta1 may play a role in the development of the fibrous component of this tumor. PDGF-B and p53 were overexpressed (i.e., twice the mean level found in turbinates) in 50% and 32% of JNAs, respectively but there was no statistical significance when compared with controls. Statistically significant increased expression of IGF-II mRNA was observed in JNA (P = .04). IGF-II mRNA levels were correlated to p53 (P = .05) and PDGF-B (P = .034), indicating a possible synergistic action of such factors in JNA. The results of this study suggest that IGF-II might be a potential growth regulator of nasopharyngeal angiofibromas.

Brown tumor, an uncommon focal giant-cell lesion, arises as a direct result of the effect of parathyroid hormone on bone tissue in patients with hyperparathyroidism. The initial treatment involves the correction of hyperparathyroidism, which usually leads to tumor regression. We report a case of brown tumor of the right nasal fossa in a 71-year-old woman. The tumor had caused nasal obstruction and epistaxis. Laboratory evaluation revealed that the patient had primary hyperparathyroidism. Anatomicopathologic investigation revealed the presence of a giant-cell tumor. We performed a partial parathyroidectomy, but the tumor in the right nasal fossa failed to regress. One year later, we performed surgical resection of the lesion. The patient recovered uneventfully, and she remained asymptomatic and recurrence-free at the 1-year follow-up. Facial lesions with histologic features of a giant-cell tumor should be evaluated from a systemic standpoint. Hyperparathyroidism should always be investigated by laboratory tests because most affected patients are asymptomatic. Surgical resection of a brown tumor should be considered if the mass does not regress after correction of the inciting hyperparathyroidism or if the patient is highly symptomatic.

The nasal surgeries are clean contamined and do not need antibioticprophilaxy because of the low infection risk.

Endonasal endoscopic ligature of the sphenopalatine artery has been an effective surgical technique for treating severe posterior epistaxis.