Oral ethanol potentiates the loss of outer hair cells in cisplatin-exposed rats.

OBJECTIVE: The aim of this study was to examine the effect of oral ethanol on cisplatin ototoxicity. STUDY DESIGN AND SETTING: Twenty-seven-week-old, female Fisher 344 rats were divided into 4 experimental groups. The animals were administered per os (PO) saline (group 1), PO ethanol (group 2), PO saline with intraperitoneal (IP) cisplatin (group 3), or PO ethanol with IP cisplatin (group 4). After 3 days, scanning electron microscopy and counts of outer auditory hair cells were performed. RESULTS: A 2-fold increase in outer hair cell loss was obtained in the basal cochlear turn of rats receiving concomitant cisplatin and ethanol compared with animals receiving cisplatin and saline. No hair cell loss was observed in the middle cochlear turn of any experimental group. CONCLUSION: Our findings support potentiation of ototoxicity when cisplatin is combined with oral ethanol. SIGNIFICANCE: Contraindications for alcohol use in cancer patients receiving cisplatin are implicated.

Jugular foramen fibromatosis in a 3-month-old male.

A 3-month-old male with a chief complaint of episodic choking with feeds and a hoarse cry is presented. Left eye ptosis and asymmetric soft palate elevation were detected on physical examination. Fiberoptic examination showed a left vocal fold paresis and pooling of secretions in the pyriform sinuses. MRI demonstrated an ill-defined lesion at the left jugular foramen extending into the left carotid sheath. A fine needle biopsy revealed spindle shaped cells consistent with fibromatosis. The histopathology of fibromatosis and the differential diagnosis of jugular foramen masses in children will be described. To our knowledge, this represents the earliest reported case of fibromatosis in the jugular foramen.

Factors that predict the need for intubation in patients with smoke inhalation injury.

Early identification of smoke inhalation patients who will require intubation is crucial. We conducted a retrospective chart review to identify predictors of respiratory distress in patients who present with smoke inhalation injury. Our study involved 41 patients who had been treated in the emergency room at a regional burn center. Eight of these patients required intubation. Intubation was positively correlated with physical examination findings of soot in the oral cavity (p < 0.001), facial burns (p = 0.025), and body burns (p = 0.025). The need for intubation was also predicted by fiberoptic laryngoscopic findings of edema of either the true vocal folds (p < 0.001) or the false vocal folds (p < 0.01). No statistically significant correlation was found between intubation and any of the classic symptoms of smoke inhalation: stridor, hoarseness, drooling, and dysphagia (all p = 1.0). Also, multivariate analysis revealed that facial burns correlated significantly with edema of the true vocal folds (p = 0.01) and body burns correlated significantly with edema of both the true (p = 0.047) and false (p = 0.003) vocal folds. We conclude that patients with soot in the oral cavity, facial burns, and/or body burns should be monitored closely because these findings indicate a higher likelihood of laryngeal edema and the need for intubation.

Left cervical chyloma following right thyroidectomy.

Cervical chylomas are rare entities, as only four cases have been previously reported. All of these previous cases involved the left side, all were related to the thoracic duct, and all occurred following trauma or surgery. We report a new case of a left-sided chyloma that was unusual because it arose following a right-sided subtotal thyroidectomy. The chyloma arose as a left supraclavicular mass within 3 months of the thyroidectomy, and it slowly enlarged over a period of 9 years. Following evaluation by computed tomography, the mass was excised, and the patient recovered uneventfully. We also review what is known about the diagnosis and treatment of cervical chylomas.

Arrest of apoptosis in auditory neurons: implications for sensorineural preservation in cochlear implantation.

HYPOTHESIS: The JNK/c-Jun cell death pathway is a major pathway responsible for the loss of oxidative stress-damaged auditory neurons. BACKGROUND: Implantation of patients with residual hearing accentuates the need to preserve functioning sensorineural elements. Although some auditory function may survive electrode insertion, the probability of initiating an ongoing loss of auditory neurons and hair cells is unknown. Cochlear implantation can potentially generate oxidative stress, which can initiate the cell death of both auditory neurons and hair cells. METHODS: Dissociated cell cultures of P4 rat auditory neurons identified the apoptotic pathway initiated by oxidative stress insults (e.g., loss of trophic factor support) and characterized this pathway by arresting translation of pathway-specific mRNA with antisense oligonucleotide treatment and with the use of pathway specific inhibitors. The presence or absence of apoptosis-specific protein and changes in the level of neuronal survival measured the efficacy of these interventional strategies. RESULTS: These in vitro studies identified the JNK/c-Jun cascade as a major initiator of apoptosis of auditory neurons in response to oxidative stress. Neurons pretreated with c-jun antisense oligonucleotide and exposed to high levels of oxidative stress were rescued from apoptosis, whereas neurons in treatment control cultures died. Treatment of oxidative-stressed cultures with either curcumin, a MAPKKK pathway inhibitor, or PD-098059, a MEK1 inhibitor, blocked loss of neurons via the JNK/c-Jun apoptotic pathway. CONCLUSION: Blocking the JNK/c-Jun cell death pathway is a feasible approach to treating oxidative stress-induced apoptosis within the cochlea and may have application as an otoprotective strategy during cochlear implantation.