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1 Cardiovascular and airways response to two non-cardioselective beta- adrenoceptor blocking drugs, propranolol and pindolol (with partial agonist activity) and two cardioselective beta-adrenoceptor blocking drugs, acebutolol (with partial agonist activity) and atenolol, were compared in twelve patients with asthma. 2 All four drugs produced a significant reduction in resting pulse rate and prevented the increase in heart rate following inhaled isoprenaline (1,500 microgram). 3 Seven patients in clinical remission showed no significant bronchoconstrictor response to any of the drugs. In the remaining five patients, bronchoconstriction was greatest following propranolol (mean reduction in FEV1 26.6%) and least following atenolol (mean reduction in FEV1 6.5%). 4 The bronchodilator response to inhaled isoprenaline was blocked by propranolol and pindolol but not by acebutolol and atenolol. 5 Partial agonist activity did not appear to be clinically useful. [ABSTRACT FROM AUTHOR]

To understand more fully the nature of events leading to asthmatic death, we conducted a confidential enquiry prospectively throughout 1994-96 among the surviving relatives and respective general practitioners of subjects whose deaths could be attributed to asthma, whether wholly or partly. We also reviewed relevant hospital records and autopsy reports, and we submitted all the gathered information to an enquiry panel for evaluation. The subjects were identified from death certificates issued in five districts of the Northern Health Region of England (population 1 million) on which asthma was recorded as the primary cause of death. The enquiry panel agreed that asthma had been a critical factor in causing death in only 33 of the 79 certified cases for which there were sufficient data. The level of concordance was substantially greater for subjects aged < 65 years (76%) than for those who were older (17%). In 16 of the 33 cases asthma alone appeared to be responsible for death, but in 17 cases a wide variety of additional, co-morbid, disorders appeared to have contributed. They included, during the 24 h preceding death, gastric aspiration, septicaemia, a single dose of a beta-blocker, the abuse of organic solvents or illicit drugs and possibly, an inadvertent exposure to horse allergen. More chronic causes of co-morbidity included ischaemic heart disease, chronic obstructive pulmonary disease (COPD), thoracic cage deformity and alcohol abuse. There were possible errors of judgement in two cases by the supervising physician (6%) and in three cases by the patient (9%). Poor compliance and psychosocial disruption probably exerted an additional adverse influence in nine cases (27%). We conclude: (1) that asthma death certification in subjects aged 65 years or more is very unreliable, (2) that for approximately half of the deaths in which asthma exerted a critical role there were critical co-morbid disorders and (3) that errors of judgement, poor compliance, or psychosocial disruption are likely to have exerted an additional adverse influence in an important minority of cases.

Although the death rate from asthma in England and Wales is reported to be about 2000 a year, clinical experience suggests that it is much rarer. Doctors in West Cumbria health district could recall only seven cases in 14 years. Examination of case notes of patients officially recorded as dying of asthma showed that many were aged over 60 and cigarette smokers. An alternative cause of death was evident in over half the patients. If the picture is representative of that in the whole of Britain the reported mortality from asthma may be much too high.

Sixteen patients with bird-fancier's lung were screened for evidence of coeliac disease by assessing their clinical features, red-bloodcell or serum folate levels, and serum for reticulin antibodies. Five of nine patients selected for jejunal biopsy showed villous atrophy, and in some this seemed to be a true gluten-sensitive enteropathy.

To assess its value as a screen for avian antibodies, indirect immunofluorescence against avian intestinal tissue has been to test sera from thirty-nine patients with documented bird-fancier's lung disease, thirty-eight asymptomatic bird-fanciers and 257 controls without known avian contact. Immunofluorescent antibodies occurred more frequently than precipitins among patients with BFL and asymptomatic bird-fanicers. Globular fluorescence within the mucus occurred only in patients with avian contact, although other fluorescent antibodies were seen with control patients. No particular pattern was confined to patients with the lung disease. When included in an autoantibody profile, indirect immunofluorescence provides a sensitive and convenient alternative to precipitin methods in screening for avian antibodies.