Bronchoscopy in North America. The ACCP survey.
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Biomedical subjects
Publications and source records attributed to G T Anders.
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BACKGROUND: Serum angiotensin-converting enzyme (ACE) level is elevated in a number of disease states and medical conditions. Based on review of the medical literature, we postulated that serum ACE level elevation may occur during infection with the human immunodeficiency virus (HIV). METHODS: In a prospective, controlled study, serum ACE levels of HIV-positive patients were compared with those of an HIV-negative control population. RESULTS: Serum ACE levels were significantly elevated in patients with the acquired immunodeficiency syndrome (55.4 +/- 11.4 U/L) and in patients with an intermediate stage of HIV infection (57.2 +/- 25.3 U/L) when compared with levels in controls (31.9 +/- 14.0 U/L). CONCLUSIONS: Elevated serum ACE levels occur in HIV infection and may be an important marker for this disease.
This study prospectively evaluated the alveolar content of transbronchial biopsy specimens based on whether or not they floated in formalin. One hundred biopsy specimens were obtained from 18 patients. Specimens with any alveoli were significantly more likely to float (45 of 61, 74%) than those with no alveolar tissue (15 of 39, 39%; p less than 0.001). The majority of diagnostic specimens were obtained in eight patients with sarcoidosis, where 47 biopsies were obtained. Fourteen of 19 specimens (74%) with noncaseating granulomas floated, whereas only 11 of 28 (39%; p less than 0.05) nondiagnostic specimens floated. The results of this study suggest that this simple bedside observation may serve to determine the adequacy of transbronchial biopsy specimens, particularly in sarcoidosis.
To confirm the presence of cardiac dysfunction in a group of patients seropositive for the human immunodeficiency virus with either dyspnea on exertion or a reduced anaerobic threshold, 9 patients with no history of opportunistic infection underwent exercise right-sided heart catheterization. When compared with 13 control patients previously exercised in the same manner, the patients showed elevated exercise pulmonary capillary wedge pressure (14.6 +/- 3.3 mm of mercury versus 9.9 +/- 3.3 mm of mercury; P less than .005) and right atrial pressure (10.1 +/- 2.1 mm of mercury versus 4.7 +/- 3.2 mm of mercury; P less than .001) at a similar exercise oxygen consumption and cardiac index. Of the 9 patients, 8 had at least 1 catheterization value outside the 95% confidence limits for the control group and 4 patients had multiple abnormalities. Values for blood CD4 lymphocytes were 0.2 x 10(9) per liter or more for 7 of the 9. One patient underwent endomyocardial biopsy with findings consistent with a cardiomyopathy. We conclude that cardiac disease may occur at any immunologic stage of human immunodeficiency virus infection. These observations suggest an effect of this disease on the heart.
Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) are potent immunomodulatory cytokines which are produced principally by cells of the macrophage-monocyte lineage. We conducted an investigation to assess the secretion of these cytokines by bronchoalveolar macrophages from patients with progressive stages of human immunodeficiency virus (HIV-1) infection. The mean level of TNF-alpha produced by macrophages from 9 patients with AIDS was significantly reduced compared with the responses of macrophages from 6 healthy HIV-1-seronegative persons, 6 patients with either asymptomatic HIV-1 infection or persistent generalized lymphadenopathy, and 6 patients with AIDS-related complex (ARC). The four study groups did not differ in their mean IL-1 beta responses. However, within the HIV-1-infected patient population, macrophages from 4 patients, 3 of whom had AIDS and 1 with ARC, failed to secrete detectable levels of IL-1 beta. All 4 patients were also nonresponsive in assays for TNF-alpha. These data establish that advanced HIV-1 infection may result in a pronounced dysfunction in the cytokine responses of alveolar macrophages.
The use of gallium scanning in the treatment of patients with AIDS has been well described. In this study, 27 HIV-infected patients (Walter Reed Staging Classification I-V) with normal chest roentgenograms were evaluated to determine the occurrence of thoracic gallium abnormalities in early HIV infection. SPECT was used for gallium scanning. Patients received gallium injection on day 1 and bronchoalveolar lavage on day 2, and scanning was performed on day 3. Twenty-eight scans in 27 patients were performed. Mean nodal SPECT activity was compared with corresponding values for lung parenchyma, bronchoalveolar lavage cell counts, and peripheral blood T4 lymphocyte counts. No relationship between nodal and parenchymal activity and cell counts was observed. Although visual scan interpretation was unaffected, gallium activity was significantly increased in the region of bronchoalveolar lavage compared with uptake in other lung regions. It is concluded that SPECT gallium scanning demonstrates significant gallium avidity in recently lavaged lung areas, although no impact on visual scan interpretation was seen. Further, no correlation was seen between the degree of nodal uptake and the immunologic status of these patients with early HIV infection.
To confirm the presence of exercise dysfunction in patients seropositive for the human immunodeficiency virus (HIV), 32 such patients without AIDS were evaluated with cardiopulmonary exercise testing, pulmonary function testing, bronchoalveolar lavage, chest roentgenography, and gallium scanning. No evidence of pulmonary opportunistic infection was found. When compared to an otherwise similar group of HIV-seronegative controls, the patients exercised to a significantly lower workload (195 +/- 30 versus 227 +/- 31 W, p less than 0.001). The ventilatory anaerobic threshold (VAT) values were also significantly lower for the patients (49.2 +/- 13.0 versus 61.9 +/- 9.1% of maximum predicted VO2, p less than 0.001). Nine of the patients had VAT values less than the 95% confidence interval for the controls. This subgroup exercised to a significantly lower maximum VO2 (69.9 +/- 11.2 versus 95.9 +/- 17.5% of maximum predicted VO2, p less than 0.001) and workload (165 +/- 21 versus 227 +/- 31 W) when compared to the control group. These patients demonstrated a mild tachypnea throughout exercise relative to the controls and had a significant increase in the slope of the heart rate to VO2 relationship. These findings are most consistent with a limitation of oxygen delivery to exercising muscles, which may represent occult cardiac disease in this group.
To evaluate bronchoalveolar lavage (BAL) findings in patients infected with human immunodeficiency virus (HIV), 39 patients seropositive for the virus but with no history of opportunistic infection were studied. Opportunistic organisms such as Pneumocystis carinii were not found in any of the 35 BAL fluids sent for special stains and cultures. Three of 16 (18 percent) BAL fluids sent for HIV culture were positive compared with a 60.9 percent blood HIV culture positivity in the same group. To evaluate cellular recovery, the patients were divided into Walter Reed (WR) groups 1 and 2 (blood CD4 greater than or equal to 400/cu mm) and WR3 to WR5 (blood CD4 less than 400/cu mm). Compared with ten nonsmoking healthy controls, the WR1 and WR2 group had a greater overall cellular recovery but this was not statistically significant when the smokers were excluded. There was no difference in macrophage or lymphocyte percentages in either patient group compared with controls. T-cell subset analysis of a small group of WR1 to WR5 patient BAL fluids revealed no difference in CD4 numbers or the CD4/CD8 rate between WR1 and WR2 and WR3 to WR5 patients. We conclude that opportunistic pulmonary infection is unlikely in HIV-seropositive patients with normal chest roentgenograms despite symptoms of dyspnea on exertion. Also, HIV can be isolated from BAL fluid from these patients although not as often as from blood. Finally, there appears to be no distinct progression in BAL cellular findings before the onset of acquired immunodeficiency syndrome.
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