Type 2 diabetes was associated with prevalent, but not incident hearing loss in this older population. Accelerated hearing loss progression over 5 years was more than doubled in persons newly diagnosed with diabetes. These data explore further reported links between Type 2 diabetes and age-related hearing loss.

Combined metformin and repaglinide therapy resulted in superior glycemic control compared with repaglinide or metformin monotherapy in patients with type 2 diabetes whose glycemia had not been well controlled on metformin alone. Repaglinide monotherapy was as effective as metformin monotherapy.

There have been few studies investigating the mechanism and nature of the hearing loss that occurs in the mitochondrial disorders. We studied 18 patients with the MELAS A3243G point mutation from four different kindreds. Pure tone audiometry, speech discrimination testing, acoustic reflexes, tympanometry, and brain stem auditory evoked responses were performed to localize the site of pathology in the auditory pathways. In 12 patients, we performed electrocochleography and otoacoustic emissions to assess cochlear involvement. Neuroimaging and promontory nerve stimulation were performed to exclude retrocochlear pathology. Audiological testing confirmed sensorineural hearing loss in 14 of the 18 patients studied; hearing loss was usually gradual in onset, was symmetrical, and initially affected the higher frequencies. In some patients, there were features that distinguished the hearing loss from presbyacusis, including a young age at onset, asymmetrical involvement, stepwise progression, and partial recovery. We treated one patient who had profound bilateral hearing loss with cochlear implantation; this restored good functional hearing. Hearing loss in MELAS syndrome appears to be due to dysfunction of the cochlea, probably resulting from metabolic failure of the stria vascularis and outer hair cells. Cochlear implantation is a therapeutic option worth considering in those patients who become deaf.

Iodine is an essential nutrient for human growth and development. The thyroid gland is dependent upon iodine for production of thyroid hormone. It is a common perception that iodine deficiency is not a major public health concern in mainland Australia, with sporadic studies carried out about a decade ago showing average urinary iodine excretion levels of around 200 microg/day. Recent evidence, however, has shown that the consumption of iodine is declining in Australia. A similar situation has occurred in the USA. The present study was designed to evaluate the urinary iodine excretion (UIE), as the indicator of iodine nutrition, in samples obtained from various demographic groups in the Sydney metropolitian area, namely: schoolchildren, healthy adult volunteers. pregnant women and patients with diabetes. Urinary iodine in spot urine sample was measured in a Technicon II autoanalyser using an in-house, semiautomated method. The results in this communication show that all four study groups had the median UIE below 100 microg/L. the criteria set by the World Health Organization for iodine repletion, and confirm what has been described previously, that iodine deficiency has reemerged in Sydney, Australia. One of the major causes of the reduced iodine intake is the reduction of iodine in milk since the dairy industry replaced iodine-rich cleaning solutions with other sanitisers. Secondly, less than 10% of the population are currently using iodised salt. A national survey into the iodine nutrition status in Australia is urgently required as part of the establishment of a systematic surveillance and legislation is required to iodise all edible salt.