Radiofrequency is a safe surgical procedure capable of reducing turbinate volume without altering the nasal mucosa, and causing minimal discomfort for the patient.
Myofibroblasts that express alpha-smooth muscle actin (alpha-SMA) are detected in many chronic inflammatory diseases. Transforming growth factor-beta (TGF-beta) is a potent inducer of myofibroblast accumulation in tissues. In this study, scattered myofibroblasts and TGF-beta were quantified and localized in nasal polyps (NPs) and normal nasal mucosa (NM). NPs were sampled in 16 patients during ethmoidectomy and NM was obtained from 10 control subjects during rhinoplasty. alpha-SMA and TGF-beta were detected using immunohistochemistry and the numbers of labeled cells were quantified (alpha-SMA and TGF-beta indices) and compared between NPs and NM. In eight NPs, in which the pedicle was preserved, alpha-SMA and TGF-beta were evaluated and compared in the pedicle, central, and tip areas. Finally, TGF-beta expression was compared between low (zone 1), moderate (zone 2), and high (zone 3) zones of alpha-SMA positivity. alpha-SMA and TGF-beta indices were significantly higher in NPs than in NM. In the eight selected NPs, alpha-SMA-positive cells were significantly more abundant in the pedicle than in the central and tip areas, whereas TGF-beta-positive cells were significantly more numerous in the pedicle than in the tip area. The number of TGF-beta-positive cells was significantly higher in zone 3 than in zone 1 of alpha-SMA positivity. Myofibroblasts, which are abundant in NPs but rare in NM, could be involved in the growth of NPs by inducing extracellular matrix accumulation. The local development of myofibroblasts in NPs could be controlled by TGF-beta, locally produced by inflammatory cells.
These results suggest that smell recognition is impaired in patients with diabetes mellitus. Smell dysfunction is associated with age and degenerative complications of diabetes, suggesting a degenerative mechanism related to diabetes.
To study taste in type I (insulin-dependent) diabetes mellitus, 57 consecutive diabetic outpatients (mean +/- SE duration of diabetes 11.4 +/- 0.4 yr) and 38 control subjects were screened for taste disorders with electrogustometry and chemical gustometry. Both groups were comparable for all subject characteristics except body mass index, which was higher in the diabetic group (P less than .05). A taste impairment was found in the diabetic group relative to the control group with electrogustometry (mean threshold 184.3 +/- 15.8 vs. 58.7 +/- 9.2 microA; P less than .001) and chemical gustometry (mean score 13.2 +/- 0.7 vs. 17.1 +/- 0.8; P less than .001). Hypogeusia was found among 73% of the diabetic patients versus 16% of the control subjects (P less than .001). The four primary tastes were involved in taste impairment. With multivariate analysis, taste disorders were related to diabetic status and tobacco and alcohol consumption. In the diabetic group, taste impairment was significantly associated with complications and duration of disease. With multivariate analysis, peripheral neuropathy had the strongest association with taste disorders. These results suggest that taste is impaired during the course of type I diabetes mellitus and that taste impairment could be a complication of the disease. A mechanism of the neuropathic type could be involved.
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