Health-related quality of life after polypectomy with and without additional surgery

OBJECTIVE: The objective of this study was to compare the health-related quality of life of patients undergoing simple polypectomy with that of patients undergoing polypectomy with additional surgery. STUDY DESIGN: This was a prospective, multicenter cohort study of adults undergoing sinonasal surgery. METHODS: Eight hundred forty-four patients received simple polypectomy and 1,004 patients received polypectomy with additional surgery. Health-related quality of life was compared at 12 and 36 months after surgery using the Sino-Nasal Outcome Test (SNOT-22). Total SNOT-22 scores may range from zero to 110 with lower scores representing better outcomes. We used linear regression to adjust postoperative SNOT-22 scores for baseline characteristics. When comparing the difference between the two surgical techniques, positive SNOT-22 scores represent a better outcome for those undergoing additional surgery. RESULTS: There were only small differences between the two groups at 12 months (difference in SNOT-22 -0.5; 95% confidence interval [CI]=-2.3-1.3; P=.58) and 36 months after surgery (difference -2.1; 95% CI=-4.4-0.2; P=.08). The additional surgery group had a slightly higher risk of excessive perioperative bleeding (8.6% vs. 6.0%; P=.04) but a slightly lower risk of revision surgery within 36 months (10.4% vs. 13.3%; P=.12). CONCLUSIONS: Nasal polypectomy with additional surgery seems to have no benefit over simple polypectomy in terms of health-related quality of life improvement for patients with nasal polyposis.     

Variations in IBD (ACAD8) in children with elevated C4-carnitine detected by tandem mass spectrometry newborn screening

The isobutyryl-CoA dehydrogenase (IBD) enzyme is involved in the degradation of valine. IBD deficiency was first reported in 1998 and subsequent genetic investigations identified acyl-CoA dehydrogenase (ACAD) 8, now IBD, as the gene responsible for IBD deficiency. Only three individuals homozygous or compound heterozygous for variations in the IBD gene have been reported. We present IBD deficiency in an additional four newborns with elevated C(4)-carnitine identified by tandem mass spectrometry (MS/MS) screening in Denmark and the United States. Three showed urinary excretions of isobutyryl-glycine, and in vitro probe analysis of fibroblasts from two newborns indicated enzymatic IBD defect. Molecular genetic analysis revealed seven new rare variations in the IBD gene (c.348C>A, c.400G>T, c.409G>A, c.455T>C, c.958G>A, c.1000C>T and c.1154G>A). Furthermore, sequence analysis of the short-chain acyl-CoA dehydrogenase (SCAD) gene revealed heterozygosity for the prevalent c.625G>A susceptibility variation in all newborns and in the first reported IBD patient. Functional studies in isolated mitochondria demonstrated that the IBD variations present in the Danish newborn (c.409G>A and c.958G>A) together with a previously published IBD variation (c.905G>A) disturbed protein folding and reduced the levels of correctly folded IBD tetramers. Accordingly, low/no IBD residual enzyme activity was detectable when the variant IBD proteins were overexpressed in Chang cells.     

Comment la douleur temporomandibulaire affecte l’activité des muscles masticateurs

From many years, treatment of temporomandibular pain and other related disorders has been based on the “vicious cycle theory”, which postulates that chronic pain enhances muscular activity, which in return maintains the pain. Clinical and experimental evidence do not support this model and rather suggest that pain reduces maximum voluntary contraction by reducing agonist muscle activity, while increasing antagonist muscle activity. The pain-adaptation model, which takes these findings into account, suggests that therapeutic approaches should be revised accordingly.     

The fungal debate: where do we stand today?

Chronic rhinosinusitis (CRS) is an inflammatory disorder affecting the nose and paranasal sinuses. Although bacteria have long been implicated as pathogens in most forms of CRS, it has been recognized that fungi may be responsible for some forms of CRS. Recent studies have shown that under optimal conditions, fungi can be identified within the nose and paranasal sinuses of nearly every individual. Considerable controversy exists concerning the proper diagnosis of and potential overlap between 'allergic fungal rhinosinusitis' and 'chronic rhinosinusitis'. Although the disease name 'allergic fungal rhinosinusitis' is suggestive of an immunoglobulin E (IgE) mediated reaction to fungi, recent studies demonstrate the presence of elevated serum IgE levels to one fungus while another fungus is present in CRS mucin of the same individual, questioning the role of type I hypersensitivity. Several mechanisms explaining the role of fungi in the pathogenesis of CRS, all requiring additional investigations with adequate controls, have been suggested and will be reviewed. Although preliminary trials suggest a beneficial effect of topical and oral antifungal agents in the treatment of CRS patients, several double-blind placebo controlled trials do not. Presently, in the absence of convincing immunological data and evidence of clinical improvement of CRS upon therapy with antifungal agents, the case against the fungus remains unproven.     

Does erythropoietin augment noise induced hearing loss?

Noise-induced hearing loss may result from excessive release of glutamate, nitrogen oxide and reactive oxygen species. The effects of these factors on the inner ear may potentially be prevented or reduced by erythropoietin (EPO), as indicated by previously demonstrated neuro-protective effects of EPO upon damage to the central nervous system and the retina. This paper reports three separate trials, conducted to investigate the hypothesis that noise-induced hearing loss is prevented or reduced by erythropoietin. The trials employed three different modes of drug application, different administration time windows and different rodent species. In trial 1, guinea pigs were exposed to 110dB SPL, 4-20kHz wide band noise (WBN) for 8h. EPO was administered to the round window membrane 24h after noise exposure, either sustained by pump for a week or by single dose middle ear instillation. In trial 2, rats were exposed to 105dB SPL, 4-20kHz WBN for 8h. EPO was administered by single dose middle ear instillation 1 or 14h after noise exposure. In trial 3, rats were exposed to 105dB SPL, 4-20kHz WBN for 8 or 3x8h. EPO was injected intraperitoneally 1h before noise exposure. Oto-acoustic emissions and auditory brainstem responses (at 16kHz) were recorded before and after noise exposure in all trials. The noise exposure induced a hearing loss in all animals. In trial 1, no recovery and no improvement of hearing occurred in any treatment group. In trial 2 and 3, a partial hearing recovery was seen. However, the hearing loss of the EPO treated animals was significantly worse than controls in trial 2. In trial 3, the hearing of the EPO treated animals exposed for 3x8h was significantly worse than controls. Thus, surprisingly, the results from 2 of the 3 present trials indicate that erythropoietin may in fact augment noise-induced hearing loss. This is contradictory to the beneficial effect of EPO reported by the vast majority of studies on stressed neural tissues. EPO administration may alter the blood flow dynamics of the cochlear vascular bed during or after noise exposure, by a potential induction of vasoconstriction. This may be the cause of the surprising findings.