Airway wall thickening and emphysema make independent contributions to airflow obstruction in COPD. These phenotypes show independent aggregation within families of individuals with COPD, suggesting that different genetic factors influence these disease processes.

Although familial clustering has been described, few studies have quantified the risk of airflow obstruction in siblings of patients with chronic obstructive pulmonary disease (COPD). One hundred fifty-two subjects with airflow obstruction and a low gas transfer factor (but without PiZ alpha(1)-antitrypsin deficiency) were identified and 150 were enrolled in the study. Complete data were obtained from 173 of 221 siblings of these subjects. Forty-four of 126 current or ex-smoking siblings had airflow obstruction (FEV(1)/FVC < 0.7) and 36 also had a FEV(1) < 80% predicted, in keeping with COPD. One hundred eleven current or ex-smoking siblings were matched for age, sex, and smoking history with 419 subjects, without a known family history of COPD, from the European Prospective Investigation of Cancer (EPIC)-Norfolk cohort. The prevalence of COPD was much lower in the EPIC group (9.3%) when compared with the siblings (31.5%; odds ratio, 4.70; 95% confidence interval, 2.63 to 8.41). The odds ratio for COPD in siblings with less than a 30 pack-year smoking history was 5.39 (95% confidence interval, 2.49 to 11.67) when compared with matched control subjects. Taken together these results demonstrate a significant familial risk of airflow obstruction in smoking siblings of patients with severe COPD.

Background: Several antioxidant nutrients have been reported to be inversely associated with asthma. A study was undertaken to assess the independent associations of these nutrients with asthma in adults. Methods: A nested case-control study was performed in 515 adults with physician diagnosed asthma and 515 matched controls using dietary data obtained from 7 day food diaries. The main outcome measures were physician diagnosed asthma and current symptomatic asthma (diagnosed asthma and self-reported wheeze within the previous 12 months). Results: Cases were similar to controls in age, sex, social class, and daily energy intake but had a lower median intake of fruit (132.1 v 149.1 g/day, p(0.05). 51.5% of the population reported zero consumption of citrus fruit; relative to these individuals, people who consumed .46.3 g/day had a reduced risk of diagnosed and symptomatic asthma (OR adjusted for potential confounders 0.59 (95% CI 0.43 to 0.82) and 0.51 (95% CI 0.33 to 0.79), respectively). In nutrient analysis, dietary vitamin C and manganese were inversely and independently associated with symptomatic asthma (adjusted OR per quintile increase 0.88 (95% CI 0.77 to 1.00) for vitamin C and 0.85 (95% CI 0.74 to 0.98) for manganese), but only manganese was independently associated with diagnosed asthma (OR 0.86 (95% CI 0.77 to 0.95)). Adjusted plasma levels of vitamin C were significantly lower in symptomatic cases than in controls (54.3 v 58.2 mmol/l, p = 0.003). Conclusions: Symptomatic asthma in adults is associated with a low dietary intake of fruit, the antioxidant nutrients vitamin C and manganese, and low plasma vitamin C levels. These findings suggest that diet may be a potentially modifiable risk factor for the development of asthma.

Background: Cigarette smoking causes accelerated facial wrinkling and predisposes to chronic obstructive pulmonary disease (COPD). However, it has long been recognised that there is a subgroup of susceptible smokers who are at increased risk of developing airflow obstruction. We have tested the hypothesis that there is a common susceptibility for the development of COPD and facial wrinkling in cigarette smokers. Methods: One hundred and forty nine current and ex-smokers were recruited from a family based study of COPD genetics, 68 (45.6%) of whom fulfilled the definition of COPD. 124 (83.2%) had no or minor facial wrinkling (Daniell ,IV) and 25 (16.8%) were wrinkled (Daniell score >IV). Generalised estimating equations were used to adjust for familial correlations between related individuals and the potential confounding effects of age and pack years smoked. Results: Forced expiratory volume in 1 second (FEV 1 ) was significantly lower in those with wrinkles than in those without (mean difference in FEV 1 % predicted 213.7%, 95% CI 227.5 to 0.0, p = 0.05) and facial wrinkling was associated with a substantially increased risk of COPD (adjusted OR 5.0, 95% CI 1.3 to 18.5, p,0.02). The Daniell score correlated with the extent of emphysema on the CT scan (p,0.05) and facial wrinkling was also associated with a greater risk of more extensive emphysema (adjusted OR 3.0, 95% CI 1.0 to 9.3, p = 0.05). Conclusion: Facial wrinkling is associated with COPD in smokers, and both disease processes may share a common susceptibility. Facial wrinkling in smokers may therefore be a biomarker of susceptibility to COPD.

No abstract

Cavernous sinuses are paired interconnected venous plexuses situated in the floor of the middle cranial fossa on either side of the sella turcica and sphenoid sinus. They are lined by dura mater and consist of multiple venous channels within. The cavernous sinuses are intimately related to the internal carotid artery and its associated sympathetic plexus, the oculomotor nerve, the trochlear nerve, the abducens nerve, and the ophthalmic nerve. Cavernous sinuses are connected to the orbit, the pterygopalatine fossa, the infratemporal fossa, the nasopharynx, and the posterior cranial fossa by various foramina, fissures, and canals in the skull base. A multitude of structures in close relation to the cavernous sinus give rise to a myriad of possible pathologic conditions that can be broadly classified into (a) neoplastic, (b) vascular, (c) infective or inflammatory, or (d) miscellaneous lesions. These pathologic conditions can have overlapping clinical manifestations. Hence, imaging plays a crucial role in identifying the disease, assessing its extent, providing a pertinent differential diagnosis to guide further management, and suggesting a site or route for biopsy. MRI is the modality of choice to depict the cavernous sinuses, with CT and digital subtraction angiography playing supplementary roles in certain situations. In this article, the cavernous sinus lesions encountered in our institution during a 10-year period are reviewed. The purpose of the article is to (a) describe the anatomy of the cavernous sinus; (b) demonstrate the multimodality imaging spectrum of a wide variety of pathologic conditions involving the cavernous sinus, correlating with the histopathologic findings; (c) highlight important imaging clues for differential diagnosis; and (d) help the reader overcome potential pitfalls in interpretation.

Objective: To assess whether starting to smoke in childhood increases the risk of obstructive airways disease (OAD) in adult life. Methods: A retrospective cohort analysis was undertaken of 12 504 current and ex-smokers in the EPICNorfolk cohort. The main exposure was starting to smoke during childhood (age ,16 years). Three definitions of OAD were used: doctor diagnosed asthma, doctor diagnosed bronchitis/emphysema, and ''any OAD'' (doctor diagnosed asthma or bronchitis/emphysema, or taking medication used in the treatment of OAD). Results: Childhood smokers had significantly more pack years of exposure and poorer lung function than subjects who started to smoke in adulthood (>16 years). Compared with starting in adulthood, starting to smoke in childhood was associated with a greater risk of bronchitis/emphysema in female smokers (OR 1.79, 95% CI 1.25 to 2.56) and ex-smokers of both sexes (OR 1.29, 95% CI 1.07 to 1.55 in men and OR 1.40, 95% CI 1.05 to 1.85 in women), and of ''any OAD'' in female smokers (OR 1.72, 95% CI 1.24 to 2.38) and male and female ex-smokers (OR 1.20, 95% CI 1.03 to 1.40 in men and 1.34, 95% CI 1.07 to 1.57 in women). After adjustment for pack years, childhood smoking was associated with poorer lung function (FEV 1 92.3% predicted in adult smokers and 89.5% in childhood smokers, p = 0.03) and a greater risk of bronchitis/emphysema (adjusted OR 1.55, 95% CI 1.08 to 2.24) and for ''any OAD'' (OR 1.54, 95% CI 1.10 to 2.13) in female smokers but not in male and female ex-smokers. Conclusion: Starting to smoke in childhood is associated with an increased risk of airways disease because of the extra pack years smoked. In women, childhood smoking is itself an independent risk factor for the development of airways disease. O ver the past 25 years the prevalence of smoking has remained stable in English children aged 11-15 years at a time when smoking rates have fallen in adults.

Changes in blood gas tensions occurring when 100% oxygen or air was used as the driving gas for nebulised salbutamol were studied in 23 patients with severe airways obstruction.