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Commentary: pulmonary responses to inhaled exogenous agents

a source of aeroallergen associated with symptoms ofbronchial asthma. The recognition that the same allergenic material can generate HP/ EAA in certain susceptible individuals is an interesting observation but one which is well recognised in routine clinical practice in relation to Aspergillus fumigatus. The diagnosis of this type of hypersensitivity reaction hinges on the recognition of exposure to a source of organic materials with a particulate size within the respirable range that is, below 20 ztm and which is associated with the development of a symptom complex of fever, breathlessness and irritable cough, together with symptomatic upset which occurs some 4-6 hours after contact. In classical cases, interstitial changes are seen on the chest radiograph and a "ground glass" appearance is seen over the lung fields. These changes tend to regress quickly as recovery from the acute state occurs. When soluble antigen is involved as in the case of avian related alveolitis for example, pigeon fancier's lung radiological abnormalities are not common and frequently the chest radiograph is unhelpful in assisting with diagnosis. Immunological evidence of hypersensitivity and the presence of circulating antibody to the offending antigen allows confirmation of the diagnosis and Yoshida and his colleagues have outlined the basic procedures which can be used to clarify the immunological reaction and the presence of appropriate antibody. It is necessary in HP/EAA to identify evidence of appropriate circulating antibody. The simple gel diffusion test remains the easiest and the most convenient way of identifying circulating antibody but it is basically qualitative and, in current clinical thinking, the use ofa fluorescent antibody technique allows for some quantification and an ELISA system offers a positive and straightforward way ofquantifying the antibody response. Bronchoalveolar lavage (BAL) also permits the identification of the cellular pattern associated with the presence ofan active HP/EAA response to the lung with the presence of a high proportion of lymphocytes and pulmonary alveolar macrophages in the lavage fluid in the active phase of the reaction. In routine clinical practice, however, BAL is not readily available and the requirement to perform this test at the appropriate time following exposure to antigen in the development of the clinical reaction makes it less useful as a diagnostic tool where commonly occurring antigens are involved. In the diagnosis of HP/ EAA the importance of a carefully taken history cannot be overemphasised, and the presence of circulating specific antibody associated with hypergammaglobulinaemia on routine biochemical screening offers positive serological confirmation of an active hypersensitivity reaction in a case where crepitations are audible on auscultation over the lung field, whether or not radiological or pulmonary function abnormalities are present. The use of intradermal skin tests in the diagnosis ofHP/EAA is not an approach which is helpful in routine practice. Not only is it difficult to prepare sterile endotoxin-free buffered and standardised skin test material, but the responses can be variable. It is interesting that immediate reactions develop to intradermal injections which equate quantitatively with the level of circulating IgG antibody in addition to the occurrence of a delayed Arthus type of reaction which, in classical descriptions of the condition, is the recognised feature of an IgG mediated hypersensitivity response. l Although in scientific terms inhalation challenge tests remain one of the gold standards of diagnosis, they frequently pose major logisitic difficulties in normal clinical practice. They have a positive value in occupationally related HP/EAA where appropriate clinical observations and objective measurements can be conducted at the relevant time interval some 4-8 hours following the initial antigenic stimulus. Any investigations of this nature must be related in time to the period of antigen exposure. Thus, in many circumstances, patients who are referred to an outpatient clinic for assessment will attend well after the acute phase of the reaction has settled and, often, no positive findings are available by that stage to allow confirmation ofthe clinically suspected diagnosis. Serological evidence persists for much longer and the advantage of using a quantitative measurement system such as an ELISA allows the change in the level of antibody with time to be monitored. When a sensitised individual with HP/EAA is removed from the source of antigen or when the level of inhaled antigen is reduced by the use of an appropriate respirator system, the level of circulating specific IgG antibody declines and, if this is not seen in certain individuals, the likelihood is that compliance has been poor and/or the respirator system used has been inappropriate. The repeated measurement of IgG antibody following diagnosis is an important method ofmonitoring the effectiveness of treatment and the clinical management.2 Hussain and his colleagues (pp 652-3) have described a case of severe lipoid pneumonia which resulted from what must be an extreme Commentary: pulmonary responses to inhaled exogenous agents