Although USS-guided core provides more satisfactory specimens than freehand FNA, in our centre it does not provide increased accuracy.

Alcohol remains second only to cigarette smoking as a risk factor for head and neck cancer worldwide. The increase in incidence in head and neck cancer in a number of countries appears linked at least in part to contemporaneous rises in alcohol consumption. The relative increase in risk in women may also relate to increasing alcohol consumption. Women may be particularly sensitive to alcohol‐induced tumours in the oral/oropharyngeal sites. The risk is dose related, but with a non‐linear increase for heavy drinkers (>100 g i.e. 12 units/day). The type of alcoholic beverage consumed seems less important. Potential mechanisms include local toxic cellular proliferation; carcinogenic action of metabolites e.g. acetaldehyde or impurities; induction of enzymes which activate procarcinogens; reduction of the protective retinoic acid; genetic polymorphism may play a part in certain geographic locations. Alcohol is also linked to stage at presentation, risk of second primary and the occurrence of comorbidity. Public awareness of the risks of alcohol remains disappointingly low. Those in identifiable high‐risk groups should perhaps be targeted specifically for counselling.

MUC5B secretion is significantly up-regulated in CRS compared with control subjects (p = 0.04). Correlation between viscosity and mucin content was lost in CRS. This is likely to have important implications for future therapies in CRS.

No abstract