Wegener's granulomatosis and subglottic stenosis: management of the airway.

Wegener's granulomatosis is a multisystemic disease characterized by foci of necrotizing vasculitis and granuloma formation. Subglottic stenosis may occur either as a presenting feature or a late-stage manifestation of the disease, but will occur in approximately 10-20 per cent of cases. We present a series of seven cases of Wegener's granulomatosis with subglottic stenosis and discuss our management of this condition. Where there is active disease, tracheostomy is the first-line surgical treatment of respiratory obstruction, as an adjunct to full medical therapy. More aggressive or elaborate surgical treatments should be reserved for non-active cases in which patients have not required medical treatment for one year.

Frequent 3p allele loss and epigenetic inactivation of the RASSF1A tumour suppressor gene from region 3p21.3 in head and neck squamous cell carcinoma.

Studies of allelic imbalance and suppression of tumourigenicity have consistently suggested that the short arm of chromosome three (3p) harbours tumour suppressor genes (TSGs) whose inactivation leads to the development of various types of neoplasia including head and neck squamous cell carcinoma (HNSCC). Previously, we defined a critical minimal region of 120kb at 3p21.3 that contains overlapping homozygous deletions in lung and breast tumour lines and isolated eight genes from the minimal region. Mutation analysis in a large panel of lung and breast cancers revealed only rare mutations, but the majority of lung tumour lines showed loss of expression for one of the eight genes (RASSF1A) due to hypermethylation of a CpG island in the promoter region of RASSF1A. We found RASSF1A to be methylated in the majority of lung tumours, but to a lesser extent in breast and ovarian tumours. In order to define the role of 3p TSGs, in particular RASSF1A in HNSCC, we (a) analysed 43 primary HNSCC for allelic loss in regions proposed to contain 3p TSGs (3p25-26, 3p24, 3p21-22, 3p14 and 3p12), (b) analysed 24 HNSCC for evidence of RASSF1A methylation and (c) undertook mutation analysis of RASSF1A in HNSCC. We found that 81% of HNSCC showed allele loss at one or more 3p markers, 66% demonstrated loss for 3p21.3 markers and 56% showed allelic losses at 3p12 loci. Thus, 3p loss is common in HNSCC and extensive 3p loss occurs even in early stage tumours. RASSF1A promoter region hypermethylation was found in 17% (4/24) of the sporadic HNSCC, but RASSF1A mutations were not identified. Furthermore, we found RASSF1A methylation to be significantly higher in poorly differentiated then in moderate to well differentiated HNSCC (P=0.0048). Three of the four tumours showing RASSF1A methylation also underwent 3p21.3 allelic loss, hence RASSF1A behaves as a classical TSG (two hits, methylation and loss). One tumour with RASSF1A methylation had retention of markers at 3p providing further evidence of specific inactivation of RASSF1A as a critical step in some HNSCC. Although the frequency of 3p21.3 allele loss was substantially higher than that of RASSF1A methylation this does not necessarily suggest that other genes from 3p21.3 are also implicated in HNSCC, as 3p21.3 LOH was invariably found with LOH at other 3p loci. Thus, the presence of 3p21.3 allele loss without RASSF1A methylation might reflect a propensity for 3p21.3 loss to occur as a secondary consequence of large 3p deletions targeted at other 3p TSG regions. Furthermore, in the presence of homozygous inactivation of other 3p TSGs, RASSF1A haploinsufficiency might be sufficient to promote tumourigenesis in many HNSCC.

Parotid duct carcinoma arising in bilateral chronic sialadenitis.

It is well recognized that, in general, chronic inflammation can predispose to malignant change. There is however, to our knowledge, no previously reported association between chronic obstructive sialadenitis and salivary gland epithelial malignancy. We describe here the first reported example in the English literature of a salivary duct carcinoma arising in a parotid gland with a long history of chronic obstructive sialadenitis. It is possible that a causal relationship exists between the two conditions. If this were the case then non-surgically treated chronic obstructive sialadenitis patients may well warrant careful clinical follow-up.

Invasion of the recurrent laryngeal nerve by adenoid cystic carcinoma. An unusual cause of true vocal fold paralysis.

True vocal fold paralysis and goitre are both common problems encountered in ENT practice. Their co-existence, however, should arouse suspicion of the presence of malignant thyroid disease. A rare case of true vocal fold paralysis caused by a clinically occult subglottic adenoid cystic carcinoma, in a 72-year-old, is described. The existence of multinodular goitre in this patient was co-incidental and confounded the diagnostic process.

Admission rates, early readmission rates and patient acceptability of 142 cases of day case septoplasty.

Day case surgery should be confined to those procedures where less than 3% of patients require admission. The aim of this study was to establish the admission rates, early readmission rates and patient acceptability of 142 consecutive cases of day case septoplasty. Data acquisition was by retrospective postal questionnaire. One hundred and fifty-three patients were studied and data was acquired on 142. Ninety per cent (128/142) of patients had operations on afternoon lists. Admissions were 7/142 (5%), the early readmission rate (within 24 h) was 0% and 25/142 (17%) of patients felt they would rather have stayed in hospital for the first night after surgery. The conclusion of this work is that day case septoplasty is an acceptable practice in appropriately selected patients who are operated upon in the morning and when the technique described here is applied. An acceptably small proportion of planned day cases may require admission.

Idiopathic CSF rhinorrhoea presenting with tension pneumocephalus and hemiparesis.

A case of non-traumatic/non-iatrogenic CSF rhinorrhoea, presenting with tension pneumocephalus and hemiparesis is described. The possible pathological processes involved in this rare case are discussed. Cases in the literature of idiopathic CSF rhinorrhoea and also those of spontaneous pneumocephalus are reviewed.