subject: Pathogenesis of pulmonary eosinophilia [print this page] Pulmonary eosinophilia is a transient pulmonary infiltrate associated with an elevated blood eosinophil count. Acause can only be identified in some cases.The blood eosinophil count is elevated above its normalupper level of 400/mm3 and may in some circumstancesbe as high as 50000/mm3. The serum IgE level is usuallyelevated in those cases with an identifiable cause, especially the allergic mycoses. Asthma is almost always present incases of allergic bronchopulmonary aspergillosis, occurs inabout half the patients with cryptogenic pulmonary eosinophilia,and is unusual with helminth infections apart fromfilariasis.
Pathogenesis
The eosinophil has cytotoxic and anti-inflammatory properties.The cytotoxic properties act against parasites butmay also damage host tissues. The pathological response tothe various identifiable causes of pulmonary eosinophilia depends on the route by which they reach the lungs;if inhaled (e.g. allergic mycoses) the response is in the airways (bronchocentric), whereas if delivered to the lungvia the pulmonary circulation the response is in the blood vessels (angiocentric).
Allergic bronchopulmonary mycoses
By far the commonest cause in developed countries isallergic bronchopulmonary aspergillosis (ABPA). Thisis due to sensitivity to the ubiquitous fungus Aspergillusfumigatus. This fungus thrives in warm, wet conditions, andsymptoms therefore tend to occur in the autumn. Thebronchial tree provides an ideal environment for colonization.When the fungus is inhaled there is an immediatehypersensitivity reaction, with eosinophils being drawninto the area. There may be several responses there after
: A simple asthmatic reaction with an eosinophilia but noradiological change
; Pulmonary eosinophilic infiltrates with consolidationand chest X-ray shadowing;
Mucus impaction with distal collapse and progressiveairway damage due to the release of tissue-damagingfactors; this in time may lead to a characteristic proximalbronchiectasis and upper zone fibrosis ,sometimes making it difficult to differentiate ABPAfrom old tuberculosis.Clinically, ABPA presents, often in early adult life, asworsening asthma. The patient may complain of coughingup rubbery brown or green plugs, and exacerbations ofasthma are often accompanied by fever and fleetingpulmonary infiltrates. Almost all patients have a positiveimmediate-type hypersensitivity to Aspergillus fumigatuson skinprick testing, and about 90% have precipitatingantibody.
Treatment with oral prednisolone (30-40 mg/day)leads to rapid symptomatic and radiological improvement;whether or not it affects the long-term outcome is uncertain.Physiotherapy and occasionally bronchoscopy help toremove troublesome plugs, and the asthma responds toconventional treatment, usually including inhaled steroid.Many patients require a small maintenance dose of oralprednisolone to prevent relapse.
