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Ankylosing spondylitis (AS) has been shown to produce exercise limitation and breathlessness. The purpose of this study was to investigate factors which may be responsible for limiting aerobic capacity in patients with AS. Twenty patients with no other cardio-respiratory disease performed integrative cardiopulmonary exercise testing (CPET). The results were compared to 20 age and gender matched healthy controls. Variables that might influence exercise tolerance, including pulmonary function tests (body plethysmography), respiratory muscle strength (MIP, MEP) and endurance (Tlim), AS severity assessment including chest expansion (CE), thoracolumber movement (TL), wall tragus distance and peripheral muscle strength assessed by maximum voluntary contraction of the knee extensors (Qds), hand grip strength and lean body mass (LBM), were measured in the patients with AS and used as explanatory variables against the peak VO2 achieved during CPET. As subjects achieved a lower peak VO2 than controls (25.2 +/- 1.4 vs. 33.1 +/- 1.6 ml kg-1min-1, mean +/- SEM, P = 0.001). When compared with controls, ventilatory response (VE/VCO2) in AS was elevated (P = 0.01); however gas exchange indices, transcutaneous blood gases and breathing reserve were similar to controls. AS subjects developed a higher HR/VO2 response (P < 0.01) on exertion but without associated abnormalities in ECG, blood pressure response or anaerobic threshold. The AS group experienced a greater degree of leg fatigue (P < 0.01) than controls at peak exercise. Although the breathlessness scores (BS) were comparable to controls at peak exercise, the slopes of the relationship between BS and work rate (WR) [AS 0.054 (0.1), Controls 0.043 (0.06); P < 0.05] and BS and % predicted oxygen uptake [AS 0.084 (0.18), Controls 0.045 (0.06); P < 0.01] were steeper in the AS subjects. There was weak association between peak VO2 and vital capacity (r2% 12.0), MIP (11.8) but no association between Tlim, CE, Wall tragus distance or TL movement. The strongest association with aerobic capacity was between measurements of peripheral muscle strength (Qds; r = 0.75; hand grip; r = 0.47) accounting for 53% (P < 0.001) and 23.5% (P < 0.01) of the total variance in peak VO2, respectively. The addition of LBM to Qds in the regression model significantly improved the explained variance to 78.3% (P < 0.001). This study shows that peripheral muscle function is the most important determinant of exercise intolerance in AS patients suggesting that deconditioning is the main factor in the production of the reduced aerobic capacity.

Objective: To assess the additive value of pleural fluid carcinoembryonic antigen (CEA.PF) level in the diagnosis of malignant pleural effusion. Methods: Thoracentesis and closed pleural biopsy were performed in consecutive patients with pleural effusions. CEA.PF, cell analysis, and biochemical, cytopathologic and microbiologic studies were carried out. Further diagnostic interventions were undertaken if initial tests were inconclusive. Results: A total of 176 patients were evaluated. The effusions proved malignant in 78 patients (44%). Benign etiologies were diagnosed in 89 cases, comprising 51 tuberculous pleurisies, 12 empyemas, 26 others. The cause was unknown in 9 patients. Median (range) in ng/ml of CEA.PF were 233 (1–12,500) in malignant vs. 2.5 (0.3–9) in tuberculosis, 1.4 (0.1–2) in transudates, 19.4 (0.6–312) in empyemas, p < 0.001. Receiver operating characteristic curve identified 10 ng/ml as the best cut-off for CEA.PF, yielding a sensitivity of 0.77, a specificity of 0.94, a positive and negative predictive value of 0.92 and 0.82, respectively. Among the 78 patients with malignant effusions, CEA.PF was elevated but initial cytopathologic study was nondiagnostic in 14 patients (18%). Prompted by the raised CEA.PF, further diagnostic interventions were undertaken and secured the diagnosis of malignancy in all of these 14 patients. Conclusions: CEA.PF level adds limited value on cytopathologic study in the diagnosis of malignant pleural effusions. It potentially identifies 18% of patients with malignant effusions who require further investigations despite negative initial cytopathologic study.

Chylothorax may rarely occur in osteolysis. A fatal case of bilateral chylothorax complicating massive osteolysis is described and the pathogenesis and management are discussed. (Thorax 1996;51:1277-1278 Keywords: chylothorax, massive osteolysis, Gorham's syndrome. His respiratory compromise necessitated repeated aspirations and, subsequently, bilateral intercostal tube drainage. Gastrointestinal rest and total parenteral hyperalimentation were promptly instituted. Lymphangiography showed normal lymph channels in the inguinal and lumbar areas, but areas ofminimal contrast leakage were noted in the upper and lower part of the left thoracic cavity; however, the thoracic duct was not visualised on the 24 and 48 hour films. Subsequent chest radiographs showed progressive resorption of the left first to third ribs, left transverse processes of the first to third thoracic vertebrae, part of the body of the seventh cervical vertebra, spinous process of the left scapula, and the right first and second ribs ( figure). Division of MedicineDespite maximal nutritional support his condition deteriorated. Chest tube drainage persisted at a rate of approximately 1500 ml/day. By the third week a diagnosis of massive osteolysis was considered and open thoracotomy with a view to thoracic duct ligation was planned. However, the patient rapidly de- teriorated and died the following day. Necroscopic examination of the affected ribs showed enlargement of the marrow spaces which were completely replaced by numerous lymphatic vessels.