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In distinguishing between infection and rejection after human lung transplantation clinical and radiological features were unhelpful, and even confusing. However, incipient rejection could be predicted and distinguished from infection by monitoring alterations in lymphocyte activity by the rosette inhibition test. Earlier prediction seems possible by detecting circulating lung-binding antibody. The ability to detect changes in the immunological status of a patient, even before clinical deterioration, has fundamental implications for the management of patients after transplantation. [ABSTRACT FROM PUBLISHER]

The transplantation of the right lung into a man aged 40 who was suffering from cryptogenic fibrosing alveolitis is described. Before transplantation he had been dependent on oxygen, even at rest, for 24 hours a day for almost two years. The donor was a boy of 16 years who had had a fatal cerebral haemorrhage. The transplanted lung functioned perfectly from the time of operation until the patient's sudden death two months later from an overwhelming haemoptysis apparently from a small peribronchial abscess rupturing into the pulmonary artery. By the third postoperative week the patient had been able to walk unaided and without distress outdoors. The problem of differentiating infection from incipient rejection is discussed. We conclude that clinically successful lung transplantation can be achieved, but only if the problems of lung function, infection, and immunosuppression can all be overcome. [ABSTRACT FROM PUBLISHER]

Of 72 patients with radiological evidence of pulmonary emphysema, emphysema occurred either alone or in association with bronchitis in 61, and 8 of these (13%) were found to have alpha(1)-antitrypsin deficiency. The main features of this condition are: exertional dyspnoea of relatively early onset (generally between 30 and 45 years of age), severely impaired FEV(1) and T(L)CO, and radiological emphysema predominantly affecting the lower zones of the lungs. It is probable that any patient with all the above abnormalities has alpha(1)-antitrypsin deficiency. There is evidence to suggest that cigarette smoking may hasten the onset of this type of emphysema.

In a study of 52 patients admitted into the coronary intensive care unit the incidence of deep-vein thrombosis was measured with the (125)I-fibrinogen test. Of these patients 31 were eventually confirmed to be suffering from acute myocardial infarction. This preliminary study showed that in patients with a confirmed infarct who were not treated with anticoagulants the incidence of deep-vein thrombosis was 38% and in those treated it was 5.5%. In patients who were "severely ill" from whatever the cause there was a high incidence of deep-vein thrombosis (68%).