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PubMed1986

[Extrinsic allergic alveolitis (extrinsic allergic broncho- alveolitis, pneumopathies with precipitins, hypersensitivity pneumopathies)].

The author does a general survey on this subject. Having evoked the EAA history, he describes the clinical syndrome with 3 forms (sharp to chronic). He relates in a first part, the main forms linked with rural occupation, from farmer's lung disease, the most frequent, to illnesses dues to cereals, woods exposition, then the one in touch with industry as coffee workers disease, and breeders of silkworms. At last, the ones in connection with urban activities as air-conditioner disease. These descriptions ended with EAA caused by a drug. Having evoked the complementary investigations necessary for diagnosis, he insists on the alveolitis washing and biochemicals studies. In conclusion, the author insists on the interest of steroids treatment in attacks.

Alveolitis, Extrinsic Allergic↗

PubMed2006

Extrinsic allergic alveolitis.

Extrinsic allergic alveolitis (also known as hypersensitivity pneumonitis) is caused by repeated inhalation of mainly organic antigens by sensitized subjects. This induces a hypersensitivity response in the distal bronchioles and alveoli and subjects may present clinically with a variety of symptoms. The aims of this review are to describe the current concepts of the immunological response, the diverse clinical presentation of this disease, the relevant investigations and management, and areas for future studies.

Alveolitis, Extrinsic Allergic↗

PubMed1999

[Extrinsic allergic alveolitis].

Extrinsic allergic alveolitis (EEA) is a lung disease mediated by immunologic mechanisms and induced by repeated exposure to organic dusts. EAA in children are mostly observed around 10 years of age. Subacute clinical presentation is the most frequent. Diagnosis is based on simultaneous presence of most of the following arguments: exposure to a known risk factor, spontaneous improvement after cessation of the exposure, identification of specific precipitins, demonstrative aspects on X-ray and tomodensitometry, and CD8+ lymphocytosis in bronchoalveolar lavage. Lung biopsy and specific provocation test are rarely necessary for diagnosis. Treatment is based on total eviction from inhaled antigen and on oral corticosteroids in acute and subacute forms.

Adrenal Cortex Hormones↗

PubMedDate not supplied

[Effect of pregnancy and the puerperium on the development of extrinsic allergic alveolitis].

Extrinsic Allergic Alveolitis (EAA) is a disease characterized by an exaggerated immune response to inhaled organic dusts that can result in alveolar, and occasionally bronchiolar, damage. This damage can disappear completely with the elimination of the antigen and/or treatment with anti-inflammatory agents. Nonetheless, an important group of these patients do not improve; the inflammatory reaction persists. With time, this results in the deposit of abnormal connective, tissue with respect to its quantity and quality, in the pulmonary interstitium destroying the normal parenchymal architecture and making gas exchange impossible. The most common cause of this disease is inhalation of pigeon antigen with a 5:1 predominance in women. Pregnancy has been considered as a case of allotransplantation that produces in the mother a relative hyporeactive condition. In modifying the immune response to the fetus, it is also modified to other foreign antigens. In this work, we studied 80 cases of EAA, 67 females and 13 males. Of the 67 women, 11 (17.1%) presented with the disease after delivery. Symptoms began from 5 days to 7 months after delivery. Eight of the 11 women had been in contact with the antigen before the beginning of the pregnancy without showing symptoms until after delivery. In 4 cases, there had been contact with the antigen in other pregnancies, without symptoms. EAA is a disease involving the immune system in which changes can be seen in its development during pregnancy, as is also seen in other immune diseases, such as Lupus Erythematosus, Rheumatoid Arthritis and other connective tissue diseases. During pregnancy, the mother becomes tolerant. There is a decrease in non-self recognition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1973

Extrinsic allergic alveolitis.

Extrinsic allergic alveolitis is caused by the inhalation of small organic allergen particles by non-atopic subjects which provoke an allergic reaction, thought to be chiefly due to a type III mechanism, in the peripheral respiratory tissues. The clinical features are determined by the nature of exposure, the immunopathological mechanism(s) involved and the site of reaction in the lung. When the exposure is intermittent and intensive, febrile episodes with respiratory symptoms beginning after four to six hours are prominent, but when it is more continuous and less intensive they are not and the features are those of a chronic fibrosing lung disease. The diagnosis is important to make because management by the avoidance of exposure is followed by improvement. It is made by recognizing the clinical presentation, by identifying the source of allergen exposure and by obtaining supportive evidence from precipitin and skin tests, or from allergen inhalation tests or lung biopsy.

Allergens↗

PubMed1993

Plasma lactate dehydrogenase: a marker of disease activity in cryptogenic fibrosing alveolitis and extrinsic allergic alveolitis?

Total plasma lactate dehydrogenase (LDH) activity may be elevated in cryptogenic fibrosing alveolitis (CFA) and extrinsic allergic alveolitis (EAA), and may be a useful monitor of disease progress. In a retrospective, primary referral centre study, we compared LDH at presentation, prior to bronchoalveolar lavage BAL, and after treatment and follow-up with changes in pulmonary function, in patients with CFA, EAA and pulmonary sarcoidosis. Plasma levels of LDH at presentation in CFA (n = 47) and EAA (n = 10) were significantly higher than in patients with sarcoidosis (n = 36). LDH activity decreased in patients with improving lung function (EAA, p = 0.008; CFA, p = 0.02), whereas it increased in CFA patients with deteriorating lung function (p = 0.015). Total plasma LDH is a simple, though nonspecific test, which appears to reflect changes of disease activity in patients with CFA and EAA.

Adult↗

PubMed1978

[Physiopathology of extrinsic allergic alveolitis].

The extrinsic allergic alveolites classically represent the immunological reaction of type III of the lower respiratory tract. In fact, all immunological mechanisms and several non specific factors are involved in these affections. If delayed hypersensitivity (type I) is today considered as part of the disease, the mechanisms involving reagins (type I) are also probably part of it but it is not so evident for type II reactions. Non specific factors are numerous, often hypothetical, because they are still experimental and not all enumerated. The activation of alveolar macrophages, the triggering of the complement system by another way, the enzymes found in dust or the irritation produced by inhaled products are all important factors.

Allergens↗

PubMed2002

Takes your breath away--the immunology of allergic alveolitis.

Extrinsic allergic alveolitis (synonym: hypersensitivity pneumonitis) is caused by inhaling antigenic aerosols which induce hypersensitivity responses in susceptible individuals. It is an interstitial inflammatory disease affecting the distal, gas-exchanging parts of the lung, in contrast to allergic asthma where the inflammation is more proximal, affecting the conducting airways. The aims of this review are to describe current concepts of the immunology of this model of lung inflammation, to describe some of the constitutional and environmental characteristics which affect disease susceptibility and development, and to describe topics for prospective study.

Alveolitis, Extrinsic Allergic↗

PubMed1997

Lung and blood T-cell receptor repertoire in extrinsic allergic alveolitis.

Patients with extrinsic allergic alveolitis (EAA) have accumulations of T-lymphocytes in their lungs. CD8+ lung T-cells, in particular, have been implicated in the pathogenesis of EAA. The objective of the present study was to analyse the T-cell receptor (TCR) V alpha and V beta gene usage of CD4+ and CD8+ lung and peripheral blood lymphocytes (PBLs) before and after treatment. Twelve patients with clinical signs of extrinsic allergic alveolitis were studied at disease onset, and nine of the 12 were also studied after treatment and clinical recovery. Lung cells, obtained by bronchoalveolar lavage (BAL), and paired PBL samples were analysed by flow cytometry using a panel of anti-TCR V monoclonal antibodies. The changes in TCR V gene usage were most pronounced in BAL CD8+ cells, as compared to the BAL CD4+, PBL CD8+ and PBL CD4+ subsets. At disease onset, 10 of the 12 patients had lung restricted expansions of CD8+ T-cells using a particular V alpha or V beta gene segment, and 8 of the 12 patients had CD8+ T-cell expansions in PBL. For the patients in whom a follow-up was possible, a majority of the expansions in the lungs were normalized, whereas most of the expansions in PBL remained. An over-representation of human leucocyte antigen (HLA)-DR2 (15) was detected, particularly among patients with farmer's lung. An increased selected T-cell receptor V gene usage may follow specific interactions between T-cells and antigens. In extrinsic allergic alveolitis, we determined that such expansions occur most frequently in the lung CD8+ T-cells. Since most expansions of lung CD8+ T-cells normalized with clinical improvement, these are further implicated in the pathogenesis of extrinsic allergic alveolitis.

Acute Disease↗

PubMed1992

Enhancement of the antigen-presenting function of monocytes by cholesterol: possible relevance to inflammatory mechanisms in extrinsic allergic alveolitis and atherosclerosis.

Extrinsic allergic alveolitis (EAA) (synonym: hypersensitivity pneumonitis) is a hypersensitivity lung disease characterized by lymphocytic infiltrates in the pulmonary interstitial tissues. We have previously reported that the numbers of lymphocytes in bronchoalveolar lavage (BAL) samples in this disease correlate with levels of cholesterol and neutral lipid-laden 'foamy' macrophages. We have also reported that the macrophages express an increased density of MHC class II antigens (in particular HLA-DQ) which are known to be essential for antigen recognition by T lymphocytes. The aim of the present study was to explore whether cholesterol is capable of enhancing the antigen-presenting function of mononuclear phagocytes by modulating the expression of HLA-D region products. Incubation of purified monocytes from healthy volunteers with cholesterol in serum-free medium induced a significant increase in both the percentages of monocytes expressing HLA-DQ (P less than 0.02) and in the intensity of expression of the three HLA-D sub-region products, HLA-DQ, -DP and -DR (P less than 0.02, less than 0.01, less than 0.05, respectively). The cholesterol pre-incubated monocytes also exhibited enhanced antigen-presenting function (P less than 0.05), compared with controls pre-incubated without cholesterol. These findings indicate that increases in cholesterol in the extracellular milieu may augment antigen presentation by modulating the expression of HLA-D region products on antigen-presenting cells. Apart from EAA, this observation may also have relevance to inflammatory mechanisms in atherosclerosis, where 'foamy' macrophages also occur in association with hypercholesterolaemia.

Alveolitis, Extrinsic Allergic↗

PubMed1991

High-resolution computed tomography in extrinsic allergic alveolitis.

Seventeen patients with extrinsic allergic alveolitis were examined with high-resolution computed tomography (CT). Increased attenuation of the lung parenchyma was present in eleven cases; the corresponding abnormality on chest radiography of ground-glass opacification was found in only five cases. The apparent upper zone sparing on chest radiography was not confirmed on CT which demonstrated a global increase in lung density. Several other abnormalities identified on CT in the subacute phase of extrinsic allergic alveolitis are described and correlated with chest radiographs. Whilst there is no single pathognomonic CT feature of extrinsic allergic alveolitis, there is a characteristic constellation of abnormalities which provide support for an otherwise uncertain clinical diagnosis.

Adult↗

PubMed2005

Involvement of eicosanoids and surfactant protein D in extrinsic allergic alveolitis.

The pathophysiology of extrinsic allergic alveolitis (EAA) involves oxidative lung damage as well as interstitial and alveolar inflammation. Macrophages and mast cells are inflammatory components of EAA that produce both leukotrienes (LTs) and prostaglandin D2 (PGD2). In addition, PGD2 is also produced by the free-radical-catalysed peroxidation of arachidonic acid during oxidative stress. Urinary 8-iso prostaglandin F2alpha (8-isoPGF2alpha) and serum surfactant protein D (SP-D) are considered appropriate biomarkers of oxidative stress and interstitial lung disease activity, respectively. The present study aimed to assess the association of these biomarkers with the pathophysiology of EAA. Two cases of acute EAA caused by the inhalation of fungi spores were reported. Eight asthmatic patients and six healthy control subjects were also enrolled in the current study. The serum SP-D and urinary eicosanoid (LTE4, PGD2 metabolite (9alpha,11betaPGF2), 8-isoPGF2alpha) concentrations markedly increased during the acute exacerbation phase. These concentrations decreased following corticosteroid therapy in the EAA patients. There was a significant correlation between serum SP-D and urinary 9alpha,11betaPGF2 concentrations in the EAA patients. In conclusion, although the present study proposes that serum surfactant protein-D and urinary eicosanoids are new biomarkers involved in the various immunological responses in extrinsic allergic alveolitis, further large-scale studies are needed to investigate the role of these compounds, not just as biomarkers, but also as biological potentiators of extrinsic allergic alveolitis.

Adult↗

PubMed1977

[Extrinsic allergic alveolitis of drug origin].

Extrinsic allergic alveolitis of drug origin is now a better known branch of respiratory pathology. The symptoms and course of these cases resemble in many ways those of extrinsic allergic alveolitis in general with a few differences. The list of drugs responsible is longer every day, and it is important to be aware of it. The diagnosis of these diseases is not always easy, as there are certain similarities between them and other long diseases either iatrogenic or not, but not immuno-allergic. Our physiopathological knowledge is based on already known data concerning allergic alveolitis, but includes many theories which still have to be verified. It is important for the clinician to be aware of this new type of respiratory disease as the treatment includes withdrawal of the responsible drug as soon as possible, failing which irreversible pulmonary fibrosis develops.

Alveolitis, Extrinsic Allergic↗

PubMed1981

[The effect of steroid therapy on cytological and histopathological changes during experimental extrinsic allergic alveolitis (hypersensitivity pneumonitis)].

Acute extrinsic allergic alveolitis was experimentally induced in rabbits using horseradish peroxidase (HRP) as antigen. Broncho-alveolar lavage was performed on the excised lungs and total and differential cellular yields determined, and correlated with the histopathological changes in the lungs as well as the total and differential white blood cell counts. After a single parenteral immunization with HRP without adjuvants, and weekly aerosol challenges with nebulized HRP solution for 3 consecutive weeks, a 3-fold increase in the total cell count as well as a very pronounced rise in the percentage of lymphocytes was noticed. Histopathologically, the bronchi-associated lymphoid tissue (BALT) became more prominent, an increase in the number of foreign body giant cells was noticed and a focal interstitial and intra-alveolar accumulation of lymphocytes, granulocytes and macrophages could be demonstrated, as well as a mild hyperplasia of type 2 alveolar epithelial cells. Intramuscular injections of methylprednisolone acetate (Depo-Medrol) every 72 hours induced a pronounced peripheral lymphopenia, thymic involution and an almost complete disappearance of the BALT in both the control and HRP-challenged rabbits. Similarly, a marked decrease in the total cell count and percentage of lymphocytes was noticed in the broncho-alveolar fluid of the animals with hypersensitivity pneumonitis. No signs of interstitial or intra-alveolar reactions were seen in the lungs of the experimental animals after 3 weeks of aerosol antigen challenge when treated with steroids. Collectively, these data suggest that the development of hypersensitivity pneumonitis was, at least in part, due to a cell-mediated immunological reaction in the lung. This animal model in which steroid suppression of experimental allergic alveolitis has been demonstrated, may be employed to elucidate the cellular pathogenesis of this disease process.

Alveolitis, Extrinsic Allergic↗

PubMed1996

[Subacute extrinsic allergic alveolitis with lesion edema].

BACKGROUND: Extrinsic allergic alveolitis may have a chronic, subacute or acute course. Its fulminant form with interstitial edema is unusual. CASE REPORT: An 11-year-old girl was referred to our intensive care unit because she suffered from high fever. Chest X-rays showed bilateral alveolitis. History revealed home exposure to several birds for many years, and episodes of dyspnea and fever for a few months. Diagnosis of extrinsic allergic alveolitis was confirmed by strongly positive results of precipitins to avian antigens. In addition, a paramyxovirus influenzae was recovered from broncho-alveolar lavage. Treatment, including high dose steroids, hydroxychloroquine, and suppression of antigenic exposure allowed weaning from mechanical ventilation after 50 days. Severe pulmonary restriction was disclosed by lung function testing following weaning and slow improvement occurred 5 months later, despite persistent interstitial lesions on chest X-rays. CONCLUSION: Extrinsic allergic alveolitis may mimic an acute respiratory distress syndrome. Documenting bird exposure in such a case helps to achieve appropriate diagnosis which requires early administration of steroids in order to improve vital and functional prognosis.

Acute Disease↗

PubMed2000

Extrinsic allergic alveolitis in domestic environments (Domestic allergic alveolitis) caused by mouldy tapestry

Extrinsic allergic alveolitis often occures as bird fancier's lung or is caused by occupational treatment with antigenic materials. In housing environments antigens of allergic alveolitis are also found, especially mould fungi. lf a source of antigens is absent in the anamnesis and the clinical picture as well as the clinical findings are ambiguous, the diagnosis of extrinsic allergic alveolits is delayed or unobtained. The following example shows that in spite of a detailed allergic anamnesis the source of antigens may remain occult and only an inspection of the dwelling rooms leads to an elucidation. - A sixty-one year old non-smoking women was twice admitted to hospital with a temperature of more than 39 degrees C, intense dyspnea on exertion and a strong dry cough under the persumed diagnosis pneumonia. The laboratory values showed nonspecific signs of inflammation, the blood gas analysis was changed to a heavy hypoxemia (pO subset2 49.2 mmHg) and in the chest x-ray there were seen miliary and partly reticular alterations. The chest computed tomography showed extensive densities in both upper and lower parts of the lungs and the pulmonary function test corresponded with a low-grade to middle-grade restriction (VC subsetin = 67%, TLC = 69%). A high dose of corticosteroids produced an improvement of the radiological findings and of the pulmonary function. Also the specialized diagnostic in a hospital for pulmonary diseases yielded no new knowledge, and an interstitial pneumonia was diagnosed. Only the new formation of an acute pneumonic clinical picture on the day of returning to the patients own habitation suggested a noxious substance in the domestic environment. The inspection of the rooms finally showed the source of antigen to be from a condensation water soaked, moulded tapestry on the embrasure of a small unopenable window in the bedroom just on the head of the bed. The nutritive mediums left in the rooms furnished evidence of the mould-species Penicillium, Cladosporium and Botrytis, in the bedroom however mostly Penicillium. The RAST of specific IgG proved a positive result of all three mould species (Penicillium sp. 1 : 100, Cladosporium sp. 1 : 200 and Botrytis sp. 1 : 200). The diagnosis of an extrinsic allergic alveolitis caused by mould was confirmed by a controlled re-exposure test, which promptly gave rise to a relapse and forced the patient to change habitation with the result of no further ailments. - Characteristic for the extrinsic allergic alveolitis in the described case is the inefficiency of antibiotic therapy, the immediate recovery by corticosteroids and furthermore the outbreak of relapses caused by re-exposure. If the source of antigens is unclear, the inspection of the habitation by an experienced allergologist may lead to success.

Journal Article↗

PubMed1986

Bronchoalveolar lavage in extrinsic allergic alveolitis.

The precise immunopathological mechanism of extrinsic allergic alveolitis explaining the clinical picture as well as the pathological findings is not known. Bronchoalveolar lavage can be a diagnostic help and a method to unravel the pathophysiology of this disease. In the acute stage of extrinsic allergic alveolitis or within 24 h after antigen exposure an increase in the number of neutrophils is seen. After the acute stage, the number of lymphocytes is even higher than in sarcoidosis. In extrinsic allergic alveolitis as well as in sarcoidosis these lymphocytes are mainly T lymphocytes. However, the distribution of OKT 4 and OKT 8 positive lymphocytes was clearly different in both diseases. In sarcoidosis OKT 4 lymphocytes predominate (OKT 4/8 = 7.8) while in extrinsic allergic alveolitis an increase of both OKT 4 and OKT 8 lymphocytes has been found (OKT 4/8 = 1.5). Whether a type III Arthus reaction or a type IV delayed hypersensitivity with an early component is involved, is discussed.

Acute Disease↗

PubMed1998

[Extrinsic allergic alveolitis: a review for the practitioner].

Extrinsic allergic alveolitis (EAA) or hypersensitivity pneumonitis (HP) is a clinical syndrome characterised by an inflammatory, partly granulomatous, immune disorder involving interstitial and alveolar spaces secondary to inhalation of organic substances. The disorder is mainly due to occupational exposure, farmer's lung being the best-known example. Acute, subacute or chronic forms can be clinically differentiated. Given the fact that chronic forms may present a pattern of irreversible pulmonary fibrosis, clinicians must be aware of the diagnosis of EAA in every situation where the history shows a potential antigenic exposure. Prevention should be reinforced by increasing individual protective measures and by improving techniques used at the workplace.

Alveolitis, Extrinsic Allergic↗