RESUMO
Data sourcesSeveral electronic databases were searched such as Cochrane Oral Health's Trials, Cochrane Library, Medline Ovid, CINAHL EBSCO and AMED Ovid and ongoing registered clinical trials in clinicaltrials.gov and in the World Health Organization International Clinical Trials Registry Platform. No restriction was placed on language and date of publication.Study selectionThe authors included randomised clinical trials (RCTs) and cross-over trials comparing any pharmacological intervention or any non-pharmacological agent with a control intervention.Data extraction and synthesisTwo pairs of review authors independently and in duplicate assessed the quality of trials and extracted data.ResultsThe review included ten trials (581 participants). Nine were included in the quantitative analysis. Three trials were assessed as having a low risk of bias, four at high risk of boas and three were assessed as unclear risk of bias. The studies included in the review were studies evaluating patients with taste disorders either idiopathic or resulting from zinc deficiency or chronic renal failure.Nine trials compared zinc supplements to placebo for patients with taste disorders. The participants in two trials were children and adolescents with respective mean ages of ten and 11.2 years and the other seven trials had adult participants. Out of these nine, two trials of very low quality assessed the patient-reported outcome for improvement in taste acuity using zinc supplements (risk ratio (RR) 1.40, 95% confidence interval (CI) 0.94 to 2.09.The meta-analyses of three trials classified as very low-quality evidence for taste acuity improvement in idiopathic and zinc-deficient taste disorder patients resulted in a standardised mean difference (SMD) = 0.44, (95% CI 0.23 to 0.65); 366 participants.One cross-over trial using the first half of the results for taste detection (mean difference (MD) 2.50, 95% CI 0.93 to 4.07; 14 participants, very low-quality evidence), and taste recognition (MD 3.00, 95% CI 0.66 to 5.34; 14 participants, very low-quality evidence). The authors performed a meta-analysis for taste acuity improvement using objective outcome (dichotomous data) in idiopathic and zinc-deficient taste disorder patients (RR 1.42, 95% CI 1.09 to 1.84; 292 participants, two trials, very low-quality evidence). Out of the nine trials using zinc supplementation, four reported adverse events like eczema, nausea, abdominal pain, diarrhoea, constipation, decrease in blood iron, increase in blood alkaline phosphatase and minor increase in blood triglycerides.One trial tested taste discrimination using acupuncture (MD 2.80, 95% CI -1.18 to 6.78; 37 participants, very low-quality evidence).No adverse events were reported in the acupuncture trial.ConclusionsThe authors found very low-quality evidence that was insufficient to conclude on the role of zinc supplements to improve taste acuity reported by patients and very low-quality evidence that zinc supplements improve taste acuity in patients with zinc deficiency/idiopathic taste disorders. They could not find any evidence to conclude the role of zinc supplements for improving taste discrimination, or any evidence addressing health-related quality of life due to taste disorders.Very low-quality evidence was found that is not sufficient to conclude on the role of acupuncture for improving taste discrimination in cases of idiopathic dysgeusia (distortion of taste) and hypogeusia (reduced ability to taste).The authors were unable to draw any conclusions regarding the superiority of zinc supplements or acupuncture as none of the trials compared these interventions.
Assuntos
Disgeusia , Paladar , Adolescente , Adulto , Criança , Humanos , Qualidade de Vida , Distúrbios do Paladar , Resultado do TratamentoRESUMO
PURPOSE: Structural and compositional heterogeneity within drusen comprising lipids, carbohydrates, and proteins have been previously described. We sought to detect and define phenotypic patterns of drusen heterogeneity in the form of optical coherence tomography-reflective drusen substructures (ODS) and examine their associations with age-related macular degeneration (AMD)-related features and AMD progression. DESIGN: Retrospective analysis in a prospective study. PARTICIPANTS: Patients with intermediate AMD (n = 349) enrolled in the multicenter Age-Related Eye Disease Study 2 (AREDS2) ancillary spectral-domain optical coherence tomography (SD OCT) study. METHODS: Baseline SD OCT scans of 1 eye per patient were analyzed for the presence of ODS. Cross-sectional and longitudinal associations of ODS presence with AMD-related features visible on SD OCT and color photographs, including drusen volume, geographic atrophy (GA), and preatrophic features, were evaluated for the entire macular region. Similar associations were also made locally within a 0.5-mm-diameter region around individual ODS and corresponding control region without ODS in the same eye. MAIN OUTCOME MEASURES: Preatrophy SD OCT changes and GA, central GA, and choroidal neovascularization (CNV) from color photographs. RESULTS: Four phenotypic subtypes of ODS were defined: low reflective cores, high reflective cores, conical debris, and split drusen. Among the 349 participants, there were 307 eligible eyes and 74 (24%) had at least 1 ODS. The ODS at baseline were associated with (1) greater macular drusen volume at baseline (P < 0.001), (2) development of preatrophic changes at year 2 (P = 0.001-0.01), and (3) development of macular GA (P = 0.005) and preatrophic changes at year 3 (P = 0.002-0.008), but not development of CNV. The ODS at baseline in a local region were associated with (1) presence of preatrophy changes at baseline (P = 0.02-0.03) and (2) development of preatrophy changes at years 2 and 3 within the region (P = 0.008-0.05). CONCLUSIONS: Optical coherence tomography-reflective drusen substructures are optical coherence tomography-based biomarkers of progression to GA, but not to CNV, in eyes with intermediate AMD. Optical coherence tomography-reflective drusen substructures may be a clinical entity helpful in monitoring AMD progression and informing mechanisms in GA pathogenesis.