Effect of septoplasty on inferior turbinate hypertrophy.

OBJECTIVE: To measure the effect of septoplasty on the volume of inferior turbinate in patients with a deviated nasal septum. DESIGN: In this retrospective analysis, patients who underwent septoplasty without turbinate surgery from May 1, 2003, through April 30, 2006, were studied. The thicknesses and cross-sectional areas of mucosa and conchal bones were measured with computed tomography before the operations and at least 1 year after the operations. SETTING: University hospital. PATIENTS: A total of 20 patients who presented with a chief concern of nasal obstruction. MAIN OUTCOME MEASURES: The thicknesses of the medial mucosa, bone, and lateral mucosa and the cross-sectional area of turbinate before and after septoplasty were compared using the Wilcoxon signed rank test. P < .05 was considered statistically significant. RESULTS: The medial mucosa and cross-sectional area of the inferior turbinate on the concave side of the septum were significantly decreased by septoplasty (both, P = .01), and the medial mucosa and cross-sectional area of the inferior turbinate on the convex side of the septum were significantly increased by septoplasty (P = .01). The thicknesses and cross-sectional areas of the conchal bone on the concave and convex sides of the septum were not affected by septoplasty. CONCLUSION: After septoplasty, inferior turbinate hypertrophy, especially in the medial mucosa, may reverse.

Serum hepatocyte growth factor as a marker of tumor activity in head and neck squamous cell carcinoma.

Hepatocyte growth factor (HGF) has previously been reported to be elevated in the serum of patients with malignancy, including breast, colorectal and gastric cancers. Here, we evaluated the correlation between serum HGF and the progression of head and neck squamous cell carcinoma (HNSCC). The mean serum HGF levels in 71 healthy control subjects, 78 patients with primary HNSCC, and eight patients with recurrent HNSCC were 0.538+/-0.163, 0.701+/-0.252, and 0.925+/-0.349ng/ml, respectively. The increase in the HGF level was significantly correlated with tumor stage progression. The HGF level had decreased to normal at 1 month after curative resection of the tumors. During follow-up for several months, the HGF level significantly increased in recurrent HNSCC patients, whereas there was no increase in nonrecurrent patients. Our data suggest that serum HGF is significantly corrected with tumor progression and may be a strong predictor of recurrence in HNSCC.

Expression of the gap junction proteins connexin 26 and connexin 43 in human middle ear cholesteatoma.

CONCLUSION: The results of this study showed upregulated expression and a change in localization of both connexin 43 (Cx43) and Cx26 in human middle ear cholesteatoma compared to those in normal retroauricular skins (RASs) and ear canal skins (ECSs). This suggests that perturbations of intercellular communication through gap junctions may be associated with the pathology of human cholesteatomas. OBJECTIVE: Cholesteatomas in the middle ear require intercellular signal exchange through gap junctions as well as intracellular signal pathways for the hyperproliferation and differentiation of epithelial cells. Cx is a gap junction protein involved in intercellular communication. The objective of this study was to analyze the expression and possible roles of Cx43 and Cx26 in human cholesteatoma compared to normal epithelium. MATERIAL AND METHODS: Ten RASs, 10 ECSs and 10 cholesteatomas were obtained during middle ear operations. Immunohistochemical staining, Western blotting and reverse transcriptase polymerase chain reaction (RT-PCR) were used to detect Cx43 and Cx26. The expression patterns of Cx43 and Cx26 were also compared with that of the proliferation marker Ki67. RESULTS: In human cholesteatomas, Cx43 was expressed in whole suprabasal layers, except in the basal layer, and Cx26 was usually expressed in the suprabasal and basal layers. However, normal RASs showed weak expression of Cx43 in the upper spinosal and granular layers (with no expression in the basal layers) and restricted localization of Cx26 in the basal layer. The expression of Cx43 and Cx26 in ECSs was weak but showed similar patterns to that of cholesteatoma. RT-PCR and Western blotting showed that the expression of Cx43 and Cx26 was higher in cholesteatoma than in RASs. Epithelial cells expressing Cx43 and Cx26 in cholesteatoma were not exactly identical to Ki67-expressing cells on immunohistochemical staining.