Efficacy of microsurgery in Reinke's oedema evaluated by traditional voice assessment integrated with the Vocal Extent Measure (VEM).

SUMMARY: There are few data analysing to what specific extent phonomicrosurgery improves vocal function in patients suffering from Reinke's oedema (RE). The recently introduced parameter vocal extent measure (VEM) seems to be suitable to objectively quantify vocal performance. The purpose of this clinical prospective study was to investigate the outcomes of phonomicrosurgery in 60 RE patients (6 male, 54 female; 56 ± 8 years ([mean ± SD]) by analysing its effect on subjective and objective vocal parameters with particular regard to VEM. Treatment efficacy was evaluated at three months after surgery by comparing pre- and postoperative videolaryngostroboscopy (VLS), auditory-perceptual assessment (RBH-status), voice range profile (VRP), acoustic-aerodynamic analysis and patient's self-assessment using the voice handicap index (VHI-9i). Phonomicrosurgically, all RE were carefully ablated. VLS revealed removal or substantial reduction of oedema with restored periodic vocal fold vibration. All subjective and most objective acoustic and aerodynamic parameters significantly improved. The VEM increased on average from 64 ± 37 to 88 ± 25 (p #x003C; 0.001) and the dysphonia severity index (DSI) from 0.5 ± 3.4 to 2.9 ± 1.9. Both parameters correlated significantly with each other (rs = 0.70). RBH-status revealed less roughness, breathiness and overall grade of hoarseness (2.0 ± 0.7 vs 1.3 ± 0.7). The VHI-9i-score decreased from 18 ± 8 to 12 ± 9 points. The average total vocal range enlarged by 4 ± 7 semitones, and the mean speaking pitch rose by 2 ± 4 semitones. These results confirm that: (1) the use of VEM in RE patients objectifies and quantifies their vocal capacity as documented in the VRP, and (2) phonomicrosurgery is an effective, objectively and subjectively satisfactory therapy to improve voice in RE patients.

The protective effect of hormone-replacement therapy on fracture risk is modulated by estrogen receptor alpha genotype in early postmenopausal women.

Genetic factors regulate bone mineral density (BMD) and possibly development of osteoporosis. It has been suggested that estrogen receptor alpha (ERalpha) genotype is associated with BMD, but the association between ERalpha genotype, fracture risk, and postmenopausal hormone replacement therapy (HRT) has not been studied. Therefore, we evaluated whether ERalpha polymorphism is associated with fracture risk in a 5-year trial with HRT in a population-based, randomized group of 331 early postmenopausal women. The participants consisted of two treatment groups: the HRT group (n = 151) received a sequential combination of 2 mg of estradiol valerate (E2Val) and 1 mg of cyproterone acetate with or without vitamin D3, 100-300 IU + 93 mg calcium as lactate per day; and the non-HRT group (n = 180) received 93 mg of calcium alone or in combination with vitamin D3, 100-300 IU/day. All new symptomatic, radiographically defined fractures were recorded. Pvu II restriction fragment length polymorphism of the ERalpha was determined using polymerase chain reaction (PCR). In all, 28 women sustained 33 fractures during the approximately 5.1-year follow-up. In the HRT group, the ERalpha genotype (PP, Pp, and pp) was not significantly associated with fracture risk (p = 0.138; Cox proportional hazards model). When the genotype was dichotomized (PP + Pp vs. pp), the incidence of new fractures in the HRT group was significantly reduced in women with the P allele (p = 0.046) with the relative risk (HR) of 0.25 (95% CI, 0.07-0.98), in comparison with the non-P allele group. After adjustment for time since menopause and previous fracture, the association between the dichotomous genotype and fracture risk persisted with HR of 0.24 (95% CI, 0.06-0.95;p = 0.042). In the non-HRT group, the ERalpha genotype was not significantly associated with fracture risk. During HRT, women with the pp genotype have a greater fracture risk than those with the P allele. The results suggest that the pp genotype is a relatively hormone-insensitive genotype, and it appears that women with the P allele may benefit more from the protective effect of HRT on fracture risk than women with the pp genotype.

Early postmenopausal bone loss is associated with PvuII estrogen receptor gene polymorphism in Finnish women: effect of hormone replacement therapy.

Genetic factors regulate bone mineral density (BMD) and possibly the development of osteoporosis. An association between estrogen receptor (ER) polymorphism, BMD, and postmenopausal hormone replacement therapy (HRT) has not been established. Therefore, we studied the influence of the ER genotype on BMD before and after a 5-year HRT in a placebo-controlled, population-based, randomized group of 322 early postmenopausal women. The participants were randomized into two treatment groups: the HRT group (n = 145) received a sequential combination of 2 mg estradiol valerate and 1 mg CPA with or without vitamin D3, 100-300 IU + 500 mg calcium lactate/day (equal to 93 mg Ca2+), and the non-HRT group (n = 177) received calcium lactate, 500 mg alone or in combination with vitamin D3, 100-300 IU/day. PvuII restriction fragment length polymorphism (RFLP) of the ERalpha was determined using polymerase chain reaction (PCR). BMDs of the lumbar spine (L2-4) and proximal femur were measured by using dual-energy X-ray absorptiometry (DXA). At the baseline, there were no significant differences in the lumbar or femoral neck BMDs between the three ER PvuII genotype groups (PP, Pp, pp). After 5 years, the BMD of the femoral neck remained unaltered and that of the lumbar spine increased by 1.7% in the HRT group, whereas both BMDs were decreased by 4-5% in the non-HRT group. The ER genotype did not modulate the femoral neck BMD change during the follow-up. In contrast, in the non-HRT-group the lumbar spine BMD decreased more in subjects with the ER genotypes PP (6.4%) and Pp (5.2%) than in subjects with the pp genotype (2.9%) (p = 0.002). In the HRT group, the relative changes of the lumbar spine BMD were similar in all three ER genotype groups. Thus without HRT, the pp genotype was associated with a smaller decrease in the lumbar spine BMD than the Pp and PP genotypes. Long-term HRT seemed to eliminate the ER genotype-related differences in the BMD. We conclude that subjects with the ER PvuII genotypes PP and Pp may have a greater risk of relatively fast bone loss after menopause than those with the pp genotype and that they may preferentially derive benefit from HRT.