ALVEOLITIS ALERGICA EXTRINSECA PDF

Hypersensitivity pneumonitis HP , also known as extrinsic allergic alveolitis EAA , represents a group of pulmonary disorders mediated by an inflammatory reaction to inhalation of an allergen that can lead to lung fibrosis. Its diagnosis relies on a constellation of findings: exposure to an offending antigen, characteristic signs and symptoms, abnormal chest findings on physical examination, and abnormalities on pulmonary function tests and radiographic evaluation. Most cases of hypersensitivity pneumonitis develop only after many years of continuous or intermittent inhalation of the inciting agent e. In the acute hypersensitivity pneumonitis , presentation symptoms may include fevers, rigors, myalgia, coughing, chest tightness, dyspnea, and leukocytosis 3. In the chronic hypersensitivity pneumonitis , the disease usually manifests as a gradual onset of exertional dyspnea, fatigue, coughing, sputum production, and weight loss.

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Hypersensitivity pneumonitis HP , or extrinsic allergic alveolitis, is an immunologically mediated disease resulting from the inhalation of organic substances that trigger an inflammatory response in the alveolar wall, bronchioles, and interstitium in susceptible individuals.

Although HP is predominantly an occupational disease, seen in adulthood, cases in children have been described. The diagnosis of HP requires a high degree of suspicion. The treatment consists in avoiding contact with the antigen, and, in some cases, systemic corticosteroids might be necessary in order to prevent its progression to pulmonary fibrosis.

We report the clinical cases of three children with a history of contact with birds and a family history of HP.

All three patients presented with cough and dyspnea on exertion. Early diagnosis is crucial in order to prevent HP from progressing to pulmonary fibrosis. Hereditary factors seem to influence the onset of the disease. Hypersensitivity pneumonitis HP , or extrinsic allergic alveolitis, is an immunologically mediated disease caused by the inhalation of organic substances that, in susceptible individuals, trigger an inflammatory response in the alveolar wall, bronchioles, and interstitium.

HP can be classified on the basis of symptoms as acute, subacute, or chronic or on the basis of the dynamic nature of the disease as acute progressive, acute intermittent non-progressive, or recurrent non-acute disease. There is no pathognomonic diagnostic test, and a presumptive diagnosis is made on the basis of a high index of suspicion, clinical history, physical examination, laboratory test results, pulmonary function testing PFT , and imaging study results.

In the chronic phase, it is possible to find an obstructive pattern, and DLCO is usually decreased. The treatment consists in avoiding contact with the antigen, which can be the sole treatment in acute forms. Systemic corticosteroids are the treatment of choice in subacute and chronic forms. The degree of pulmonary fibrosis at diagnosis is the major prognostic factor. We report the case of a year-old boy with a history of asthma and a family history of HP. Living in a rural area, the boy had contact with pigeons and canaries, which aggravated the symptoms.

He presented to the emergency room with a 2-day history of productive cough and fever, accompanied by anorexia and weight loss. A chest X-ray showed a bilateral perihilar infiltrate, and the patient was discharged after being treated with clarithromycin, which was replaced by a combination of amoxicillin and clavulanic acid 5 days later because of persistence of symptoms.

The patient received oral corticosteroids for a year, which resulted in complete resolution of the symptoms and complete resolution of the lesions seen on HRCT of the chest, as well as in improvement in PFT results by the end of a three-year follow-up period.

A year-old girl who lived in a rural area and had birds at home presented with a family history of HP. The patient had been healthy until November of , when she sought emergency room treatment due to fever and cough.

Physical examination revealed crackles and respiratory distress. A chest X-ray showed an interstitial infiltrate. The patient was discharged on clarithromycin and prednisolone. She returned to the outpatient clinic one week later, reporting dyspnea on minimal exertion. The patient was maintained on inhaled corticosteroids for 2 years, which resulted in progressive clinical improvement. A 7-year-old boy, whose father and paternal grandmother were under investigation for suspected HP, presented with a personal history of situs inversus totalis and recurrent respiratory infection.

The boy was admitted to the emergency room with a 5-month history of productive cough, accompanied by progressively worsening dyspnea on exertion, with no improvement with bronchodilators and inhaled corticosteroids.

It was reported that there had been a parakeet at home since the onset of the symptoms, and that the home also had a henhouse and a cooperage.

The patient received inhaled corticosteroids for 2 years, which resulted in progressive clinical and radiological improvement. The patients described had a family history of HP accompanied by a clinical profile that corresponded to the subacute form of HP, with an obstructive pattern and symptoms such as cough, dyspnea on exertion, weight loss, and sometimes fever, the onset of which occurred within weeks to months of exposure to an antigen.

A high index of suspicion was essential for the diagnosis, as were analytical and laboratory criteria. Among the major criteria, defined by Schuyler et al. Chief among the minor criteria are crackles at the lung bases and arterial hypoxemia. In only one of the patients was there a decrease in DLCO. In none of the cases was it possible to detect precipitating antibodies to the antigen. Although they are objective markers of exposure, negative results do not absolutely exclude the diagnosis.

The need for lung biopsy should be weighed in terms of its cost-benefit ratio, and it should be considered in rare cases in which there is diagnostic uncertainty or in which the clinical course or treatment response is unclear. HP is an uncommon disease in children and has nonspecific symptoms. For the diagnosis of HP, it is important that clinical evaluation be performed and allergen exposure be investigated. In all three cases described above, the patients had a family history of HP, although they were not screened for the presence of HLA.

These facts lead us to believe that, although allergens are the major triggering factor for this disease, heredity is also an important cofactor. Early diagnosis of HP is crucial in order to prevent severe and irreversible complications, such as pulmonary fibrosis. Financial support: None. A paciente recebeu alta, sendo medicada com claritromicina e prednisolona. Apoio financeiro: Nenhum. National Center for Biotechnology Information , U.

Journal List J Bras Pneumol v. J Bras Pneumol. Author information Article notes Copyright and License information Disclaimer. Received Dec 5; Accepted May Copyright notice. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Abstract Hypersensitivity pneumonitis HP , or extrinsic allergic alveolitis, is an immunologically mediated disease resulting from the inhalation of organic substances that trigger an inflammatory response in the alveolar wall, bronchioles, and interstitium in susceptible individuals. Keywords: Alveolitis, extrinsic allergic; Bronchoalveolar lavage; Glucocorticoids.

Introduction Hypersensitivity pneumonitis HP , or extrinsic allergic alveolitis, is an immunologically mediated disease caused by the inhalation of organic substances that, in susceptible individuals, trigger an inflammatory response in the alveolar wall, bronchioles, and interstitium.

Case reports Case 1 We report the case of a year-old boy with a history of asthma and a family history of HP. Open in a separate window. Figure 1. Chest X-ray showing bilateral perihilar and basilar reticulonodular infiltrate.

Case 2 A year-old girl who lived in a rural area and had birds at home presented with a family history of HP. Figure 2. HRCT scan of the chest showing mild, slightly heterogeneously distributed parenchymal thickening in both lungs; small nodules with ill-defined borders; and ground-glass changes.

Case 3 A 7-year-old boy, whose father and paternal grandmother were under investigation for suspected HP, presented with a personal history of situs inversus totalis and recurrent respiratory infection.

Figure 3. HRCT scan of the chest showing pronounced ground-glass changes in both lung fields, consistent with extrinsic allergic alveolitis. Discussion The patients described had a family history of HP accompanied by a clinical profile that corresponded to the subacute form of HP, with an obstructive pattern and symptoms such as cough, dyspnea on exertion, weight loss, and sometimes fever, the onset of which occurred within weeks to months of exposure to an antigen. References 1. An Esp Pediatr.

Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Hypersensitivity pneumonitis. Hypersensitivity pneumonitis: spectrum of high-resolution CT and pathologic findings.

Hypersensitivity pneumonitis: current concepts. Eur Respir J Suppl. Schuyler M, Cormier Y. The diagnosis of hypersensitivity pneumonitis. Pneumonite de hipersensibilidade. Author information Copyright and License information Disclaimer. Figura 1. Figura 2. Figura 3. Support Center Support Center. External link. Please review our privacy policy.

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CT-semiotics and clinical aspects of extrinsic allergic alveolitis. Extrinsic allergic alveolitis can be a difficult diagnostic problem. The comparison of the results of CT research with the clinical immunological and morphological data allowed to define the forms and diagnose the characteristic symptoms of the disease. 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.

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