Hypersensitivity pneumonitis is a pulmonary disease with symptoms of cough and dyspnea resulting from the inhalation of an antigen to which the subject has been previously sensitized,such as microbes,animal or plant proteins and certain chemicals that form haptens.The radiologic findings include diffuse ground-glass opacification,small centrilobular nodules,air trapping,fibrosis and emphysema.Bronchoalveolar lavage fluid reveals a lymphocyte alveolitis with CD4/CD8 decrease.The histopathologic process consists of chronic inflammation of the bronchi and peribronchiolar tissue,often with poorly defined granulomas.The diagnosis usually rests on a variable combination of findings from history,clinical manifestation,radiography,serology,bronchoalveolar lavage fluid and lung biopsy.Treatment includes avoiding the allergen and systemic corticosteroids.The long-term prognosis is usually good.

Key words: 
Hypersensitivity pneumonitis; Etiology; Clinical presentation; Diagnosis; Treatment

Hypersensitivity pneumonitis

Summary
This study was undertaken to confirm the high incidence of the ‘late’ bronchial reaction after house dust inhalation and to assess whether symptoms and signs of these ‘late’ reactions were comparable with the clinical features of the classic Type III (Gell and Coombs) allergic reactions in the lung as shown by extrinsic allergic alveolitis.

Although the time sequence of this late reaction is in agreement with the classic Type Ml reaction (Arthus phenomenon), other features of alveolitis are absent. There were no crepitations on physical examination, no fever, no leucocytes, no decrease of the PaO2, and no abnormal radiological findings. These results were related to the protective effects of some drugs. The protective effect of disodium cromoglycate and prednisolone is probably the same in both types of late reactions. The protective effect of antihistamine drugs, which is found in this late obstructive reaction, is, according to the literature, absent in the classical Type III reaction. There seem to be no valid arguments to ascribe the ‘late’ bronchial obstructive reaction to the toxic complex syndrome.

Theoretical and practical implications of the late obstructive bronchial reaction are mentioned.

Late bronchial obstructive reaction to experimental inhalation of house dust extract.

The validity of inhalation tests in the investigation of extrinsic allergic alveolitis was assessed from the results of 144 antigen and control tests in 31 subjects. A definitive pattern of positive late responses was observed. Reactions to nebulised bird serum and droppings in subjects with bird fancier's lung were identical to reactions after "natural" exposures in aviaries or lofts, and to reactions after "occupational" challenges in subjects with farmer's lung and mushroom worker's lung. In general, positive tests were easily recognised subjectively from symptoms and signs appropriate to an influenza-like illness and undue respiratory effort on exercise. They were associated with significant changes in six readily available objective monitoring measurements--exercise minute ventilation (greater than or equal to +15%), body temperature (> 37.2 degrees C), circulating neutrophils (greater than or equal to +2500/mm3), exercise respiratory frequency (greater than or equal to +25%), circulating lymphocytes (greater than ore equal to -500/mm3 with lymphopenia), and forced vital capacity (greater than or equal to -15%). These confirmatory monitoring tests had specificities of approximately 95% and sensitivities of 85-48%. Measurement of diffusing capacity, lung volume subdivisions, or resting minute ventilation/respiratory frequency proved to be too insensitive to be useful, as did auscultation and chest radiography. We conclude that responses that do provoke significant changes in these less sensitive tests are unnecessarily distressing and, presumable, unnecessarily hazardous.

https://thorax.bmj.com/content/thoraxjnl/35/6/415.full.pdf

Positive "alveolar" responses to antigen inhalation provocation tests: their validity and recognition.

Grain-induced asthma is a frequent occupational allergic disease mainly caused by inhalation of cereal flour or powder. The main professions affected are bakers, confectioners, pastry factory workers, millers, farmers, and cereal handlers. This disorder is usually due to an IgE-mediated allergic response to inhalation of cereal flour proteins. The major causative allergens of grain-related asthma are proteins derived from wheat, rye and barley flour, although baking additives, such as fungal α-amylase are also important. This review deals with the current diagnosis and treatment of grain-induced asthma, emphasizing the role of cereal allergens as molecular tools to enhance diagnosis and management of this disorder. Asthma-like symptoms caused by endotoxin exposure among grain workers are beyond the scope of this review. Progress is being made in the characterization of grain and bakery allergens, particularly cereal-derived allergens, as well as in the standardization of allergy tests. Salt-soluble proteins (albumins plus globulins), particularly members of the α-amylase/trypsin inhibitor family, thioredoxins, peroxidase, lipid transfer protein and other soluble enzymes show the strongest IgE reactivities in wheat flour. In addition, prolamins (not extractable by salt solutions) have also been claimed as potential allergens. However, the large variability of IgE-binding patterns of cereal proteins among patients with grain-induced asthma, together with the great differences in the concentrations of potential allergens observed in commercial cereal extracts used for diagnosis, highlight the necessity to standardize and improve the diagnostic tools. Removal from exposure to the offending agents is the cornerstone of the management of grain-induced asthma. The availability of purified allergens should be very helpful for a more refined diagnosis, and new immunomodulatory treatments, including allergen immunotherapy and biological drugs, should aid in the management of patients with this disorder.

/pdf/diagnosis-and-management-of-grain-induced-asthma-jyzfegrlku.pdf

Diagnosis and Management of Grain-Induced Asthma

In pulmonary allergic aspergillosis the fungus grows in secretions of the respiratory tract. Its pathogenesis results from two types of hypersensitivity to aspergillus immediate, due to re...

Pulmonary allergic aspergillosis.

A case of inhalant allergy to the grain weevil is described. Provocation inhalations of the weevil protein produced immediate responses shown by falls of as much as 25% in the F.E.V. 1·0 . These changes were reversed by a bronchodilator. Arthus-type reactions also occurred approximately three hours after the inhalation of protein. In these the transfer factor was reduced by 25% and was not affected by a bronchodilator. Antihistamines were found to inhibit the immediate response but to have no effect on the Arthus reaction. Coincident with the fall in transfer factor there were rises in the temperature and pulse rate. An Arthus-type as well as an immediate skin response was demonstrated. Precipitating antibodies were detected in the serum. The similarity of these reactions to those seen in farmer9s lung and to reactions to avian protein is discussed, together with the possibility of the wider implications of sensitivity to the grain weevil.

https://oem.bmj.com/content/oemed/24/2/158.full.pdf

D. T. D. Hughes

Papers

Pulmonary Hypersensitivity to the Grain Weevil

Pulmonary Hypersensitivity to the Grain Weevil