Complement activation in sudden deafness.

OBJECTIVE: To test whether complement activation is associated with sudden deafness. DESIGN: Plasma samples obtained from patients in the acute phase of sudden deafness were analyzed for complement activation measured by C3bc levels and terminal complement complex. Comparisons were made with plasma samples from healthy controls. PATIENTS: Twenty-five adult patients with unilateral sudden deafness. The criteria for inclusion were symptoms of hearing loss for not longer than 14 days and a hearing loss of 35 dB or more measured at entry. RESULTS: Levels of C3bc were higher in patients compared with controls (P<.001). There were no differences in the formation of terminal complement complex in patients and controls. CONCLUSIONS: The elevated levels of C3bc in patients with sudden deafness indicate an activation of the first part of the complement cascade and therefore suspected inflammatory causes. Measurements of C3bc levels might identify patients with sudden deafness who would benefit from treatment with anti-inflammatory drugs.

Glutamate is the afferent neurotransmitter in the human cochlea.

Glutamate, the most important afferent neurotransmitter in the auditory system, is thought to be the afferent transmitter between the cochlear inner hair cells and afferent neurons, hitherto visualized only in the cochlea of animal species. It has been identified for the first time in sections from the human inner ear. L-glutamate, NMDAR2B and the enzyme glutamine synthetase were identified by using monoclonal antibodies. The distribution pattern of the transmitter L-glutamate in the human cochlea is similar to that observed in other mammals. L-glutamate was identified adjacent to outer and inner hair cells and in the spiral ganglion. Similar distributions were found for glutamine synthetase and the ionotropic NMDA receptor subunit NMDAR2. The identification of neurotransmitters and their receptors in the human cochlea has implications for the pharmacotherapy of inner ear diseases.

Exercise-induced dyspnea is a problem among the general adolescent population.

RATIONALE: Respiratory symptoms during exercise are common and might limit adolescents' ability to take part in physical activity. OBJECTIVE: To estimate the prevalence, determinants and consequences of exercise-induced dyspnea (EID) on daily life in a general population of 12-13 year old adolescents. METHODS: A letter was sent to the parents of all 12-13 year old adolescents in the city of Uppsala (n = 3838). Parents were asked to complete a questionnaire together with their child on EID, asthma and allergy, consequences for daily life (wheeze, day time- and nocturnal dyspnea) and physical activity. The response rate was 60% (n = 2309). RESULTS: Fourteen percent (n = 330) reported EID, i.e. had experienced an attack of shortness of breath that occurred after strenuous activity within the last 12 months. Female gender, ever-asthma and rhinitis were independently associated with an increased risk of EID. Ever-asthma was reported by 14.6% (n = 338), and 5.4% (n = 128) had both EID and ever-asthma. Sixty-one percent (n = 202) of the participants with EID did not have a diagnosis of asthma. In addition to rhinitis, participants with EID reported current wheeze and day-time as well as nocturnal dyspnea more often than the group without EID. No difference was found in the level of physical activity between participants with and without EID. CONCLUSION: Adolescents with undiagnosed exercise-induced dyspnea have respiratory symptoms and are affected in daily life but have the same level of physical activity as adolescents without exercise-induced respiratory symptoms.

Phenotype standardization of angioedema in the head and neck region caused by agents acting on the angiotensin system.

Angioedema is a potentially life-threatening adverse reaction to angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. To study the genetic etiology of this rare adverse event, international consortia and multicenter recruitment of patients are needed. To reduce patient heterogeneity, we have standardized the phenotype. In brief, it comprises swelling in the head and neck region that first occurs during treatment. It should not coincide with urticaria or have another likely cause such as hereditary angioedema.

Hearing loss in relation to round window membrane morphology in experimental chronic otitis media.

The present study was performed to test the effect of single and repeated Pseudomonas aeruginosa exotoxin A (PaExoA) instillations in the middle ear of the rat. The hearing level was examined by the ABR technique, round window membrane (RWM) thickness was measured and morphology was studied by light microscopy. The results showed both reversible and permanent hearing loss (HL). In animals that received a single dose of PaExoA, the RWM thickness doubled initially and remained thickened during the observation period. When PaExoA was instilled on several occasions, RWM thickness doubled, before decreasing to near-control levels. This study confirms the toxicity of PaExoA and the partially reversible HL occurring after a single application of the toxin. The diminished effect of repeated toxin instillations--despite the decreasing thickness of the RWM--is discussed.