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Behcet's disease (BD) is an autoimmune vasculitis of unknown aetiology that is characterised by relapsing episodes of oral aphthous ulcers, genital ulcers, ocular lesions, skin lesions, and other manifestations, including vascular, gastrointestinal and neurological involvement. Behcet's disease exists worldwide, although there are significant regional differences, with the highest number of incidences in the Mediterranean, Middle East, and Far East. Behcet's disease occurs mainly between 18 and 40 years of age, and the male-to-female ratio is 7:1. The cause of Behcet's disease is unknown. It is believed to be due to an autoimmune process triggered by an infectious or environmental agent (possibly local to a geographic region) in a genetically predisposed individual. T cell homeostasis perturbation, especially Th1 and Th17 expansions and decrease regulation by Tregs are now supposed to be the cornerstone of BD pathogenesis. Inflammatory cytokine such as IL21 plays a critical role in pathogenesis of BD. Inner ear involvement in Behcet's disease was first reported by Alajouanine in 1961. Thereafter, many cases of inner ear involvement were described by other authors. The otological features of Behcet's disease can be divided into hearing loss and disequilibrium. The incidence of hearing loss in Behcet's disease has been reported to be 12 to 80% in several studies in the literature. Recently, some authors observed a significant percentage (59.2%) of hearing loss associated with Behcet's disease. According to other studies, hearing loss can be the fourth or even the third most common manifestation of the disease. The treatment of inner ear lesions remains unsatisfactory and is based on immunosuppressive agents and will not be reviewed here. This review focuses on the etiophatogenesis and otological manifestations of Behcet's disease and specifies the role of the otorhinolaryngologist as an integral member of the multidisciplinary team for clinical management of these patients.

In this study, we review our current knowledge of the autoimmune etiopathogenesis of chronic rhinosinusitis with nasal polyps including bacterial infections, viral infections and immunomediated mechanisms and to discuss pathogenesis with relevance for pharmacotherapy. Relevant publications on the etiopathogenesis and treatment of chronic rhinosinusitis with nasal polyps (CRSwNP) from 1977 to 2013 were analyzed. The characteristic signs and symptoms include appearance of relapsing nasal polyps, with typical symptoms such as nasal obstruction, nasal discharge and, usually, loss of the sense of smell. The etiology and pathogenesis remain unknown. Proposed theories of causation include bacterial or viral infections and immunomediated mechanisms. The autoimmune aetiology of of unknown origin or failure to respond to classic pharmacological treatments with nasal and oral steroids is now suspected. At present, the nature of the antigen trigger, the exact role played by B/T cells and anti-dsDNA autoantibodies in the pathogenesis of nasal polyposis remains unclear. Corticosteroids and surgery are the first line of treatment in CRSwNP. In the case of corticosteroid treatment failure, other drugs can be used such as rituximab, belimumab or omalizumab which have demonstrated clinical efficacy in the treatment of nasal polyposis with comorbid asthma. Immunosuppressive drugs such as methotrexate, and cyclophosphamide have also been used with varying degrees of success.

Clin. Otolaryngol. 2012, 37, 376–381 Objectives: To determine the prevalence of radiation-induced carotid stenosis, in patients who were treated for head and neck malignancies, using colour-flow duplex scanning. Design: Prospective controlled study at a single medical centre. Participants: We enrolled two groups of patients. The first (radiotherapy group) consisted of patients who received surgical treatment and adjuvant radiotherapy of the neck. The control group consisted of patients with head and neck malignancies who received only surgical treatment. Main outcome measures: All patients were evaluated with carotid artery ecoDoppler imaging 1 week before and 36 months after the surgical procedure. Intima-media thickness was measured bilaterally at the internal carotid artery and at the bifurcation. Carotid obstruction was classified as low (0–30%), moderate (31–49%) or severe (≥50%). Results: The preoperative stenosis grade did not differ between groups. In 15/25 patients (60%) in the radiotherapy group, mild stenosis evolved to moderate stenosis, while only 6/37 (16%) of the controls did (P = 0.004). Additionally, 9/39 (23%) patients in the radiotherapy group progressed to severe stenosis compared with only 3/54 (6%) controls (P = 0.029). The overall evolution showed that stenosis worsened in 24/32 (62%) patients in the radiotherapy group and 9/54 (17%) patients in the control groups (P

Background: Both the immediate beneficial physiological changes in a laboratory setting and the long-term clinical outcomes of heat and moisture exchanger (HME) use are well described. So far, there has not been any research published that provides detailed insight in the pattern of changes in both respiratory function and patients’ experiences with HMEs in the first weeks of use. Methods: A multicenter time-series study design with a 2-week double baseline period. All patients used the XtraHME for 12 weeks afterward. Data were collected 2 weeks, 6 weeks, and 12 weeks after the start of HME use. Results: Data of 30 patients were analyzed. Pulmonary symptoms decreased significantly during the 12 weeks of HME use. After 2 weeks, a significant decrease in daily coughs and daily forced expectorations was seen. The general quality of life showed a significant increase throughout the study. More general physical complaints also significantly decreased with HME use. Patient satisfaction with the HME was high. Conclusions: This study shows that there is a significant influence of the XtraHME on pulmonary status that can already be observed after 2 weeks of using the XtraHME and continues to improve further after 6 weeks of XtraHME use.

Background Squamous cell carcinoma (SCC) is the most common oral cavity malignant tumor. Surgery, radiotherapy, and chemotherapy have been the major options for its treatment. Electrochemotherapy (ECT) is a novel local treatment successfully used in secondary or primary skin or subcutaneous tumors. This new cancer treatment is a modality in which a locally applied electrical field enhances cell membrane permeability, thereby allowing greater intracellular accumulation of a chemotherapeutic agent. Methods We report a case of a man affected by an ulcerated SCC. The man was treated with ECT with good results. Results In our case, ECT was successful in the management of extensive metastasis of SCC in clinical conditions, whereas other approaches were rejected. Conclusion This case shows good clinical results; however, other studies are necessary to show that ECT should be considered as a promising treatment option. © 2014 The Authors. Head & Neck Published by Wiley Periodicals, Inc. Head Neck 36: E86–E90, 2014

Objectives. To review the current knowledge of the aetiology of vestibular neuritis including viral infections, vascular occlusion, and immunomediated mechanisms and to discuss the pathogenesis with relevance to pharmacotherapy.Systematic Review Methodology. Relevant publications on the aetiology and treatment of vestibular neuritis from 1909 to 2013 were analysed.Results and Conclusions. Vestibular neuritis is the second most common cause of peripheral vestibular vertigo and is due to a sudden unilateral loss of vestibular function. Vestibular neuronitis is a disorder thought to represent the vestibular-nerve equivalent of sudden sensorineural hearing loss. Histopathological studies of patients who died from unrelated clinical problems have demonstrated degeneration of the superior vestibular nerve. The characteristic signs and symptoms include sudden and prolonged vertigo, the absence of auditory symptoms, and the absence of other neurological symptoms. The aetiology and pathogenesis of the condition remain unknown. Proposed theories of causation include viral infections, vascular occlusion, and immunomediated mechanisms. The management of vestibular neuritis involves symptomatic treatment with antivertiginous drugs, causal treatment with corticosteroids, and physical therapy. Antiviral agents did not improve the outcomes.

Objectives The objectives of this study are to review our current knowledge of the aetiopathogenesis of Vogt–Koyanagi–Harada syndrome, including viral infection, genetic factors and immunomediated mechanisms, and to discuss pathogenesis and its relevance to pharmacotherapy. Systematic review methodology Relevant publications from 1965 to 2012 on the aetiopathogenesis and pharmacotherapy of VKHS were analysed. Results and conclusion Vogt–Koyanagi–Harada syndrome (VKHS) is a rare multisystemic autoimmune disease that affects tissues containing melanin, including the eye, inner ear, meninges, and skin. The disease is characterised by bilateral uveitis associated with a varying constellation of auditory, neurological and cutaneous manifestations. The disease occurs more frequently among people with darker skin pigmentation. Asians, Native Americans, and Hispanics are most frequently affected. It predominates in patients aged between 20 and 50 years, and females are affected more frequently, with a female:male ratio of 2:1. The classic clinical course is characterised by bilateral panuveitis, hypoacusis, and meningitis, in addition to cutaneous involvement with poliosis, vitiligo, and alopecia. Although the exact cause of VKH disease remains unknown, it is thought to be a T-cell-mediated autoimmune process directed against melanocytes. VKHS classically begins with vague systemic symptoms suggestive of a viral infection, although a clear association between a specific viral agent and the disease has not been established. Genetic factors may play an important role in the loss of self-tolerance in VKHS. The HLA-DRB1*0405 allele is the main susceptibility allele for VKHS. Early and aggressive systemic corticosteroids are still the primary initial therapy for VKHS. Ocular complications may require an intravitreous injection of corticosteroids. Despite proper treatment with steroids, a number of patients experience recurrent attacks or steroid-associated complications. Thus, non steroid immunomodulatory therapy (IMT) has become necessary for the treatment of VKHS.

Objectives The objective of our study was to review our current knowledge of the aetiopathogenesis of Cogan's syndrome, including viral infection and autoimmunity, and to discuss disease pathogenesis with relevance to pharmacotherapy. Systematic review methodology Relevant publications on the aetiopathogenesis and pharmacotherapy of Cogan's syndrome from 1945 to 2012 were analysed. Results and conclusions Cogan's syndrome is a rare autoimmune vasculitis, and its pathogenesis is unknown. Infection, but primarily autoimmunity, may play contributing roles in the pathogenesis of this disease. It is characterised by ocular and audiovestibular symptoms similar to those of Meniere's syndrome. Approximately 70% of patients have systemic disease, of which vasculitis is considered the pathological mechanism. The immunologic theory is based on the release of auto-antibodies against corneal, inner ear and endothelial antigens, and of anti-nuclear cytoplasmic auto-antibodies (ANCA). Corticosteroids are the first line of treatment, and multiple immunosuppressive drugs have been tried with varying degrees of success. Tumour necrosis factor (TNF)-alpha blockers are a category of immunosuppressive agents representing a recent novel therapeutic option in Cogan's syndrome.

Rheumatoid arthritis rarely involves the cricoarytenoid joint. The possible consequent symptom includes hoarseness, dysphagia, odynophagia, dysfunctional dysphonia, and acute dyspnea. Etiologic diagnosis is possible with high-resolution computed tomography, which can show spacing of the articular cartilage, density and volume alterations, and subluxation of the cartilage. However, these radiologic signs are not pathognomonic for rheumatoid arthritis, and they should be combined with anamnestic data.

Objectives To review our current knowledge of the pathogenesis of sudden sensorineural hearing loss, including viral infection, vascular occlusion and immune system-mediated mechanisms, and to discuss the pathogenesis as it relates to pharmacotherapy. Systematic review methodology Relevant publications on the pathogenesis of sudden sensorineural hearing loss from 1944 to 2010 were analysed. Results and conclusions Sudden sensorineural hearing loss is defined as hearing loss of 30 dB in three sequential frequencies over 3 days or less. It can be an isolated symptom or the presenting symptom of a systemic disease. The aetiology and pathogenesis remain unknown. Detailed investigation typically reveals a specific cause in about 10% of patients. Proposed theories of causation include viral infections, vascular occlusion and immune system-mediated mechanisms. A variety of therapies have been proposed based on the various proposed aetiologies.

E-Mail: antonio.grecoo@uniroma1.it Objective: The aim of our study was to evaluate prevalence of carotid stenosis in patients with head and neck malignant tumours treated with radiotherapy. Methods: In our study we included 137 patients with head and neck cancers treated during a period of about 5 years. The larynx was the most common affected site of primary tumour. Only 93 patients were alive at the moment of our observation. A group of 39 patients underwent neck radiation. A control group of 54 patients were not treated with radiotherapy. All patients undergoing radiotherapy received a local dose of 50-70 Gy for 6 weeks. An ecodoppler scan of the carotid arteries was performed in all patients with estimation of common and internal carotid artery Intimal Medial Thickness (IMT). Stenosis grading was divided into low (0-30%), moderate (31-49%) and severe (more than 50%). In addition, we considered hematochimic and flogistic parameters. Statistic evaluation was performed with Chi-square test. Results: We found that severe carotid stenosis was higher (41%) in patients who had undergone radiotherapy than in the control group (16.6 %) (P = 0.008). The ecodoppler examination demonstrated that the most commonly affected site was the internal carotid artery, just past the carotid fork.