Patterns of lung disease in a "normal" smoking population: are emphysema and airflow obstruction found together?

STUDY OBJECTIVES: We determined whether emphysema demonstrated on high-resolution CT (HRCT) scanning in apparently well smokers is associated with airflow obstruction. INTERVENTIONS: Lung function testing and limited HRCT scanning. DESIGN: Lung function measurements and scans were analyzed independently of each other. We used analysis of covariance to compare FEV(1) and maximum expiratory flow at 50% of vital capacity (MEF(50)) values after suitable corrections, between subjects with and without parenchymal damage (emphysema and/or reduced carbon monoxide transfer coefficient [KCO]), and to compare indexes of parenchymal damage between subjects with and without airflow obstruction. SETTING: Radiology and lung function departments of a district general hospital. PARTICIPANTS: Eighty current cigarette smokers and 20 lifetime nonsmoking control subjects (aged 35 to 65 years) who volunteered following publicity in local media. In all subjects, FEV(1) was > 1.5 L; no subjects were known to have lung disease. MEASUREMENTS AND RESULTS: FEV(1) and MEF(50) were measured spirometrically; static lung volumes were measured by helium dilution and body plethysmography; KCO was measured by a single-breath technique. HRCT scans were analyzed for emphysema by two radiologists. Of smokers, 25% had HRCT emphysema, generally mild; 16.3% and 25% had reduced FEV(1) and MEF(50), respectively; 12.5% had reduced KCO. Smokers with airflow obstruction were not more likely to have parenchymal damage. Smokers with parenchymal damage did not have reduced airway function. Nonsmokers generally had normal airways and parenchyma. CONCLUSIONS: "Normal" smokers with lung damage had either airflow obstruction or parenchymal damage, but not generally both.

Cigarette smoke inhalation and lung damage in smoking volunteers.

Cigarette smoking is the dominant risk factor for chronic obstructive pulmonary disease (COPD) but only 10-15% of smokers develop the condition. Risk does not relate closely to cumulative cigarette consumption, perhaps because smokers vary in the degree and depth of smoke inhalation. This study examined the role of smoke inhalation in the development of COPD. Eighty current smokers and 20 lifetime nonsmoking volunteers (aged 35-65 yrs) were recruited. Lung function variables were measured and high-resolution computed tomography (HRCT) scans performed. Smoke inhalation was assessed by CO boost (the increment of expired carbon monoxide 5 min after smoking a cigarette) and serum cotinine. Mean CO boost was 6.3 parts per million (ppm) in smokers with low CO transfer coefficients (KCO) and 2.9 ppm in those with normal KCO (p=0.006); 7.2 ppm in smokers with both HRCT-defined emphysema and a low KCO and 2.6 ppm in those with neither abnormality (p=0.002); 4.5 ppm in smokers with HRCT-defined emphysema alone and 2.8 ppm in those without (p=0.08). Mean serum cotinine was 328 ng x mL(-1) in smokers with chronic productive cough and 243 ng x mL(-1) in those without (p=0.005). Lifetime nonsmokers had normal HRCT scans, lung function and serum cotinine. Emphysema is associated with high alveolar smoke exposure as measured by CO boost. Productive coughing is associated with high nicotine uptake, probably from airway smoke particle deposition.

Management of non-palpable breast lesions detected mammographically.

A total of 212 consecutive fine-wire localization breast biopsies in 202 patients were performed on impalpable mammographically suspicious lesions. Preoperative fine-needle aspiration cytology was performed on 159 lesions and was valuable in planning the extent of the fine-wire localization biopsy. All 212 target lesions were accurately biopsied during the initial surgery. Overall, 134 lesions were malignant and 78 benign (benign:malignant ratio 1:1.72), with fewer biopsies for benign lesions performed in screened patients (benign:malignant ratio 1:2.43) than in those with symptoms (ratio 1:1). Breast conservation was achieved in 72 patients (80 per cent) with screen-detected in situ or invasive carcinoma and in 19 of 37 presenting via a symptomatic clinic. In 160 of 202 patients (79 per cent) the initial fine-wire localization biopsy was diagnostic and therapeutic.

Ultrasonography, HIDA scintigraphy or both in the diagnosis of acute cholecystitis?

The benefit of early surgery for patients with acute cholecystitis is now accepted but rapid accurate pre-operative diagnosis is important and the single best investigation has not yet been clearly established. All 47 patients with suspected acute cholecystitis admitted to a district general hospital during a 6 month period underwent ultrasonic examination and scintigraphy with HIDA within 48 h of admission. In 23 patients acute cholecystitis was proven. Ultrasound correctly diagnosed this in 21 patients but in 2, changes attributed to chronic cholecystitis only were detected. Two false positive ultrasound results also occurred, one in a patient with adenomyomatosis and acute pancreatitis, the other in a case of duodenitis. HIDA scan was diagnostic in 19 patients but in the remaining 4 the presence of abnormal liver function tests accounted for non-visualization of the biliary tree (a non-diagnostic result). In the absence of jaundice a HIDA scan is the more specific test for confirming acute cholecystitis.