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Biomedical subjects

J Bernardo

Publications and source records attributed to J Bernardo.

42 records · Page 3Linked to original sources
PubMed1979

Acute hypersensitivity pneumonitis: serial changes in lung lymphocyte subopulations after exposure to antigen.

The earliest lesion in hypersensitivity penumonitis is an acute inflammatory alveolitis characterized by parenchymal hemorrhage and accumulations of polymorphonuclear leukocytes within the lung. In many instances, this initial lesion is replaced by a more chronic alveolitis, with development of mononuclear cell interstitial infiltrate, granuloma formation, and interstitial fibrosis. To help define the mechanisms by which the early polymorphonuclear leukocyte alveolitis of acute hypersensitivity pneumonitis evolves into a chronic mononuclear-cell process, an animal model of the disease was developed using guinea pigs sensitized by footpad injeection with either ovalbumin (OVA) in complete Freund's adjuvant (CFA), CFA alone, or phosphate-buffered saline. Ten days after sensitization, the animals were challenged by intratracheal injection of either particulate OVA, particulate human serum albumin, or phosphate-buffered saline alone, and their lungs were evaluated sequentially for changes in histologic appearance and lymphocyte subpopulations. After challenge, only animals sensitized with CFA plus OVA and challenged with particulate OVA developed pulmonary lesions consistent with acute hypersensitivity pneumonitis. Within 4 h after challenge, these animals developed an acute hemorrhagic alveolitis that persisted for more than 24 h. By 48 to 96 h, the alveolitis evolved into a predominantly mononuclear-cell infiltrate. This change in the histologic appearance of the lungs in these animals was preceded by a rapid increase in the proportions of T-lymphocytes within the lungs, noted by 24 h after intratracheal challenge with specific antigen. Before intratracheal challenge with antigen, lung lymphocytes from only the group of animals immunized with CFA plus OVA were capable of proliferating on exposure to OVA in vitro. In the same group, lymphocytes recovered from the lung after intratracheal particulate OVA demonstrated blast transformation in vivo, a phenomenon not found in any other group. These studies suggest that the alveolitis of acute hypersensitivity pneumonitis is rapidly associated with changes in populations of immune effector cells before development of the mononuclear cell alveolitis characteristic of the chronic disease.

Alveolitis, Extrinsic Allergic↗
PubMedDate not supplied

Noninvasive testing of asymptomatic bilateral hilar adenopathy.

The diagnostic strategy for asymptomatic patients with persistent bilateral bilar adenopathy often involves invasive procedures. The authors used Bayesian analysis to: 1) estimate the relative prevalences of diseases causing bilateral bilar adenopathy; 2) assess changes in the prevalence of disease by race, the presence of other clinical symptoms, and geography; and 3) determine the value of relevant noninvasive tests, including the angiotensin-converting enzyme (ACE) assay, gallium scan, and purified protein derivative (PPD), in order to assess when a strategy of watchful waiting is appropriate. The analysis indicated that the ACE assay, particularly when paired with the PPD, can identify many patients who might safely be managed without immediate invasive biopsy. Patients who are ACE+ and PPD- have an estimated probability of sarcoidosis of 0.95 or greater; patients who are ACE- and PPD+ have a probability of tuberculosis of 0.86 if black, 0.79 if white. In contrast, gallium scanning has no diagnostic role in this clinical situation. Bronchoscopic or mediastinoscopic biopsy has a limited role for patients who are ACE+ PPD- or ACE- PPD+ because of limited sensitivity. Patients who are both ACE- and PPD-, particularly if white, may have a high enough risk of lymphoma to consider invasive biopsy.

Bayes Theorem↗
PubMedDate not supplied

Tuberculosis screening in Boston's homeless shelters.

From February 1984, through March 1985, a total of 26 cases of tuberculosis (TB) were verified in homeless persons in Boston. Fifteen cases were resistant to isoniazid (INH) and streptomycin (SM) and were most likely the result of a common source exposure to one or possibly two highly infectious persons. Five cases without multiple drug resistant organisms occurred in persons with previous positive tuberculin tests who had not received adequate therapy for prophylaxis of infection or treatment of disease. The remaining cases were in persons with a previous negative skin test or no history of ever receiving a skin test. A screening program using chest roentgenograms (CXR), skin tests, and sputum smears led to the identification of several cases. CXR, the most readily accepted test, was the mechanism by which all cases detected through screening were identified. Detection and therapy of TB in the homeless, a group at particular risk for disease, required intensive intervention and outreach efforts.

Adult↗