Evaluation of an Internet-based decision-support system for applying the ATS/CDC guidelines for tuberculosis preventive therapy.

Preventive therapy for patients infected with tuberculosis (TB) remains an important component of TB control. To guide physicians in applying preventive therapy, the American Thoracic Society and Centers for Disease Control (ATS/CDC) developed guidelines based on PPD reactivity and on pretest probability of infection. The guidelines have become complex, and many clinicians find them challenging to apply. The authors developed a computerized decision-support system to assist clinicians in applying the ATS/CDC guidelines. This tool, published on the World Wide Web using hypertext markup language, delivers patient-specific recommendations based on physician-delivered patient-specific information. Four local TB experts derived eight TB infection scenarios and validated the web-based tool, which was tested for effectiveness using general internal medicine residents, randomly divided into two groups. Group A (n = 12) used the web-based tool and group B (n = 17) used pre-existing understanding of the guidelines and/or written resources to determine the need for preventive therapy in the case scenarios. Group A correctly used therapy in 92/96 possible cases (95.8%), group B in only 77/136 (56.6%) (p < 0.001). Group A required a mean of three mouse-clicks and 1.5 minutes per scenario to reach their choices, and they rated the web-based tool both intuitive and effective. These data demonstrate that a computer-based decision-support system for applying TB treatment guidelines can be delivered over the Internet and provide an efficient and effective resource for clinicians.

Asthma guidelines: an assessment of physician understanding and practice.

In 1997 the NHLBI updated guidelines for the diagnosis and management of asthma. We hypothesized that not all components of the updated guidelines are well understood by the physicians who care for asthmatics. To develop appropriate educational interventions that address areas of physician misunderstanding, it is important to identify these components. Based upon NHLBI guidelines, we developed a multiple-choice test of asthma knowledge that was distributed to physicians at the University of Iowa; 108 physicians completed the test, including 20 asthma specialists, 11 asthma specialty fellows, 11 General Medicine faculty, five Family Medicine faculty, 51 Internal Medicine residents, and five Family Medicine residents. The mean correct total score for all physicians was 60 +/- 2% (mean +/- SEM). Asthma specialists scored higher in total score and in pharmacology and prevention. However, no group performed well on estimating disease severity. We further identified deficits in the use of spirometry and anti-inflammatory agents in caring for asthmatic patients. Thus, deficits exist in physician understanding and implementation of the NHLBI guidelines for the diagnosis and management of asthma. By identifying specific areas of misunderstanding, we can design better educational interventions. Clearly, educational programs should emphasize new models for estimating chronic disease severity.

Evaluation of internet-based clinical decision support systems.

BACKGROUND: Scientifically based clinical guidelines have become increasingly used to educate physicians and improve quality of care. While individual guidelines are potentially useful, repeated studies have shown that guidelines are ineffective in changing physician behavior. The Internet has evolved as a potentially useful tool for guideline education, dissemination, and implementation because of its open standards and its ability to provide concise, relevant clinical information at the location and time of need. OBJECTIVE: Our objective was to develop and test decision support systems (DSS) based on clinical guidelines which could be delivered over the Internet for two disease models: asthma and tuberculosis (TB) preventive therapy. METHODS: Using open standards of HTML and CGI, we developed an acute asthma severity assessment DSS and a preventative tuberculosis treatment DSS based on content from national guidelines that are recognized as standards of care. Both DSS's are published on the Internet and operate through a decision algorithm developed from the parent guidelines with clinical information provided by the user at the point of clinical care. We tested the effectiveness of each DSS in influencing physician decisions using clinical scenario testing. RESULTS: We first validated the asthma algorithm by comparing asthma experts' decisions with the decisions reached by nonpulmonary nurses using the computerized DSS. Using the DSS, nurses scored the same as experts (89% vs. 88%; p = NS). Using the same scenario test instrument, we next compared internal medicine residents using the DSS with residents using a printed version of the National Asthma Education Program-2 guidelines. Residents using the computerized DSS scored significantly better than residents using the paper-based guidelines (92% vs. 84%; p <0.002). We similarly compared residents using the computerized TB DSS to residents using a printed reference card; the residents using the computerized DSS scored significantly better (95.8% vs. 56.6% correct; p<0.001). CONCLUSIONS: Previous work has shown that guidelines disseminated through traditional educational interventions have minimal impact on physician behavior. Although computerized DSS have been effective in altering physician behavior, many of these systems are not widely available. We have developed two clinical DSS's based on national guidelines and published them on the Internet. Both systems improved physician compliance with national guidelines when tested in clinical scenarios. By providing information that is coupled to relevant activity, we expect that these widely available DSS's will serve as effective educational tools to positively impact physician behavior.

Patients with an abnormal chest radiograph and latent tuberculosis.

Patients with latent tuberculosis characterized by a positive tuberculin (purified protein derivative) skin test and radiographic evidence of fibronodular changes or silicosis are at increased risk for the development of active tuberculosis. Before preventive therapy is initiated, the radiographic abnormalities must be differentiated from those representing active disease. According to recommendations from the American Thoracic Society and the Centers for Disease Control and Prevention, patients with latent tuberculosis who exhibit fibronodular changes or silicosis on chest radiographs should be given either isoniazid alone for one year or the combination of isoniazid and rifampin for four months, preferably with pyrazinamide for the first two months. Patients with similar radiographic findings and sputum or culture evidence of active tuberculosis require full multidrug therapy.

Low-dose methotrexate may cause air trapping in patients with rheumatoid arthritis.

Both rheumatoid arthritis (RA) and methotrexate (MTX) are reported to be associated with the development of pulmonary disease. To determine whether MTX enhanced the risk of developing abnormalities in pulmonary function in patients with RA, we prospectively studied 31 subjects (12 male, 19 female) with the diagnosis of classic RA for an average period of 4.4 yr (range, 1 to 5 yr). Each subject was placed on low-dose weekly MTX (mean 17 mg, range 2.5 to 40) for control of RA symptoms. Other medications included non-steroidal anti-inflammatory agents and prednisone if required for control of arthritis symptoms. No other immunosuppressive therapy was used. Each subject was evaluated by pulmonary function tests (PFT) and chest X-ray initially, and at 1, 2, 3.5, and 5 yr. Chest X-rays obtained initially and at the end of the study period were found to be normal. The percent predicted values for initial PFTs in the study group were within the normal range. From the beginning to the end of the observation period, the following mean changes in lung function were observed: 1.9% increase in TLC, 5.1% increase in residual volume (RV), 1.8% increase in FVC, 0.71% decrease in FEV1, 14.7% improvement in alveolar-arterial oxygen (A-aO2) difference, and a 12.7% increase in single-breath diffusing capacity (DLCO). To determine whether MTX (average dose, weekly dose, or cumulative dose) was significantly related to changes in pulmonary function, we used multivariate techniques to control for the initial measure of lung function while assessing the relationship between MTX and the subsequent measures of lung function.(ABSTRACT TRUNCATED AT 250 WORDS)

Longitudinal changes in lung function among asbestos-exposed workers.

To prospectively identify the determinants of persistent or accelerated loss of lung function among workers occupationally exposed to asbestos and assess the relative contribution of cigarette smoking, asbestos-induced pleural fibrosis, and specific findings from bronchoalveolar lavage and high resolution CT scans, we examined the determinants of lung function changes in 117 subjects occupationally exposed to asbestos for at least 1 yr in a high exposure setting. A minimum of 20 yr was required between the first exposure to asbestos and entry into the study. Baseline studies included an independent assessment of dyspnea, lung volumes, diffusing capacity of carbon monoxide (DLCO), a chest radiograph, a high resolution CT (HRCT) scan, and bronchoalveolar lavage (BAL). Subjects were observed for an average of 2 yr (range, 0.5 to 4.0 yr), and lung function was measured on at least two separate occasions (mean, 4.1 separate tests). During the period of observation, there was an average 1.5% decrease in the TLC and a 2.5% decrease in the DLCO. In this longitudinal data set, after controlling for age, height, pack-years of cigarette smoking, and follow-up time, persistently lower measures of TLC were independently related to moderate to severe dyspnea (p = 0.005), diffuse pleural thickening (p = 0.007), and higher concentrations of fibronectin in BAL fluid (p = 0.01). Interstitial lung disease either on the chest radiograph or HRCT scan was not independently associated with persistently lower measures of TLC during the period of observation. However, none of the clinical variables we examined were associated with an accelerated decline in TLC.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of progression in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive form of lung disease with a median survival of less than 5 yr. To address the progressive nature of this disease process, we investigated the determinants of decrements in lung function in patients with IPF. We prospectively evaluated 39 subjects with IPF. Our study subjects were followed for an average of 2 yr (range, 49 to 1,883 days) and lung function was measured on at least two separate occasions (mean = 9.1 separate tests) during the follow-up period. Since IPF is characterized by reduced lung volume and abnormal gas exchange, our analysis focused on the determinants of total lung capacity (TLC) and diffusing capacity of carbon monoxide (DLCO) during the period of observation. Although, on average, there was a 5.3% increase in the TLC and a 9.8% increase in DLCO between the first and last measure of lung function, 25% of the study population experienced a decline in the TLC and 28% of the study population experienced a decline in the DLCO. Decrements in TLC were independently associated with severe dyspnea (p = 0.01) and treatment with cyclophosphamide (p = 0.03). Decrements in DLCO were significantly and independently associated with more pack-years of cigarette smoking (p = 0.02), moderate (p = 0.03) or severe (p = 0.02) dyspnea, and treatment with cyclophosphamide (p = 0.0002). These findings indicate that several clinical characteristics are independently associated with subsequent declines in TLC and DLCO in patients with IPF.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of survival in idiopathic pulmonary fibrosis.

To identify the determinants of survival in patients with idiopathic pulmonary fibrosis (IPF), we performed a survival analysis on 74 subjects with IPF. The study subjects were on average 64 yr of age (range, 25 to 83 yr), 62% were male, and 29% were never smokers. A tissue diagnosis was made in 67 (91%) of our study subjects. These subjects were followed for a mean period of 4 yr (range, 1.4 to 118.8 months) after the onset of pulmonary symptoms. During the period of observation, 41 subjects died (median survival = 28.2 months) and 33 continue to survive (median follow-up period = 60.9 months). A univariate analysis demonstrated that diminished survival was significantly associated with male gender (hazard ratio = 1.98; 95% confidence interval [CI] = 1.01-3.85), a higher FEV1/FVC ratio (hazard ratio = 1.82 [per 10% increase in the FEV1/FVC ratio]; 95% CI = 1.21-2.73), a lower percent predicted FVC (hazard ratio = 0.74; 95% CI = 0.60-0.91), a lower percent predicted total lung capacity (TLC) (hazard ratio = 0.75; 95% CI = 0.60-0.94), a lower percent predicted diffusing capacity of carbon monoxide (DLCO) (hazard ratio = 0.69; 95% CI = 0.53-0.89), a higher ILO profusion category on chest radiograph (hazard ratio = 3.52; 95% CI = 1.58-7.87), and an enhanced release of prostaglandin E2 (PGE2) by cultured alveolar macrophages (hazard ratio = 1.32 [per 10 pm/ml of PGE2]; 95% CI = 1.07-1.62).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical relevance of cellular mediators of inflammation in workers exposed to asbestos.

To identify the clinical relevance of cellular mediators of inflammation in workers exposed to asbestos, we investigated the relationship between inflammatory products primarily released by alveolar macrophages and the clinical expression of asbestos-induced interstitial fibrosis. Our study population consisted of 93 white men who had been occupationally exposed to asbestos and were on average 60 yr of age. Pulmonary function tests, chest radiographs, high-resolution CT scans, and bronchoalveolar lavage (BAL) were performed on almost all study subjects; 11 (11.8%) had restrictive lung function, 22 (23.7%) had abnormal gas exchange, 30 (32.3%) had interstitial fibrosis on chest x-ray, and 24 (25.8%) had interstitial changes on high-resolution CT scan. The cellular markers of parenchymal inflammation that we examined included fibronectin in BAL fluid and alveolar macrophage release of prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta), and tumor necrosis factor (TNF-alpha) under unstimulated and endotoxin (LPS)-stimulated culture conditions. Significantly higher concentrations of fibronectin in BAL fluid were observed among those with restrictive lung function. In addition, higher concentrations of PGE2, released from cultured but otherwise unstimulated alveolar macrophages, were associated with restrictive lung function. However, the inverse relationship with PGE2 was observed among subjects with abnormal gas exchange. Interestingly, no consistent changes in these inflammatory mediators were observed in those with interstitial changes identified on either the chest radiograph or the high-resolution CT scan.(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship between alveolar macrophage TNF, IL-1, and PGE2 release, alveolitis, and disease severity in sarcoidosis.

A mononuclear cell alveolitis, comprised in part of activated macrophages, is thought to precede granuloma formation and fibrosis in pulmonary sarcoidosis. Tumor necrosis factor-alpha (TNF), interleukin 1-beta (IL-1), and prostaglandin E2 (PGE2) are potent mediators released by activated alveolar macrophages. To determine if alveolar macrophage TNF, IL-1, and PGE2 release was associated with clinically progressive pulmonary sarcoidosis, we obtained alveolar macrophages from bronchoalveolar lavage of 68 patients with biopsy specimen-confirmed sarcoidosis, cultured the macrophages in the presence and absence of lipopolysaccharide (10 mg/L) for 24 h, and measured TNF (enzyme-linked immunosorbent assay), IL-1 (enzyme-linked immunosorbent assay), and PGE2 (radioimmunoassay) release. Alveolar macrophages from most patients with sarcoidosis spontaneously released TNF, IL-1, and PGE2. The amounts of these mediators released (either spontaneously or following lipopolysaccharide stimulation) did not positively correlate with the numbers of any of the cells in bronchoalveolar lavage fluid, the clinical status of disease (stable vs deterioration), steroid usage, or cigarette smoking. The relative release of each of the individual mediators, however, was highly correlated with the release of the other mediators. The studies suggest that these markers of alveolar macrophage activation from a single bronchoalveolar lavage are poor indicators of clinically progressive disease.

Outcome of subjects with idiopathic pulmonary fibrosis who fail corticosteroid therapy. Implications for further studies.

To evaluate the outcome of subjects with idiopathic pulmonary fibrosis (IPF) whose conditions clinically deteriorate while receiving corticosteroid therapy, we studied 12 of these subjects (7 male, 5 female) who received subsequent therapy with intravenous (IV) pulse cyclophosphamide (CPX). Seven of the 12 study subjects died during the course of therapy. Six of these subjects died of respiratory failure, and one died of cholecystitis. Among those who died, the mean age at diagnosis was 63 years compared with 57 years in those who have continued to survive (p = 0.29). Smoking status and pack-years of cigarette smoking were similar between those subjects who died and those who continue to survive. However, subjects who died received CPX for a mean of 6 months, while subjects still living have received CPX for a mean of 16 months (p = 0.01). Subjects who died were given a CPX a mean of 64 months after the onset of symptoms, compared with a mean of 50 months for subjects who are still alive (p = 0.57). Interestingly, there were no significant differences in measures of pulmonary function between living and dead subjects. In fact, measures of lung function and gas exchange remained stable in both groups throughout the period of observation. These data suggest that (1) measures of lung function may not be a reliable indicator of patient mortality in end-stage IPF, and (2) while not statistically significant, these data raise the possibility that duration of symptomatic disease may play a role in the outcome of IPF patients receiving alternative therapeutic agents after failure of corticosteroid therapy. In future intervention trails, controlling entry criteria for duration of disease may prove helpful in determining the effects of these agents on the disease process. These data do not permit a determination of the effect of CPX in patients with IPF.

Bronchoalveolar lavage cellularity. The distribution in normal volunteers.

Bronchoalveolar lavage (BAL) is used to obtain inflammatory cells from the lung. For clinical research, parametric statistics are frequently used to compare cells present in BAL of patients with lung disease with cells present in BAL of normal subjects. To determine if these populations can be compared in this manner we performed BAL on 111 never-smoking, normal volunteers and determined: (1) the mean, median, standard deviation, and range of the cells in BAL; (2) whether the data are normally distributed and satisfy the criteria for use of parametric statistical analysis. The BAL cellularity was expressed as a percentage of total cells, cells per milliliter return, and total cells per lavage. Regardless of the means of expression, no measure of BAL cellularity (total cells, macrophages, lymphocytes, neutrophils, or eosinophils) conformed to the normal (bell-shaped) distribution when tested for goodness of fit with the G statistic (all p < 0.001). The lack of fit to the normal distribution was not substantially altered by either the method of expressing the data (i.e., cells per milliliter, total cells, or percent of cells) or log transformation of the data. The poor fit in all cases resulted from clumping of the data about the mean and large tails. The percent of cells were, therefore, tested for goodness of fit to the Poisson distribution, a distribution of discrete variables. The neutrophil and eosinophil percentages resulted in an excellent fit to the Poisson distribution, but macrophage and lymphocyte percentages did not.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease.

To investigate the influence of cigarette smoking on bronchoalveolar lavage (BAL) cellularity in asbestos-induced lung disease, we compared BAL cells in asbestos-exposed, nondiseased subjects (n = 20) with those with either asbestosis (n = 25) or asbestos-induced pleural fibrosis (n = 28). Patients with asbestosis (ILO greater than or equal to 1/0) had higher concentrations of BAL macrophages (p = 0.04), neutrophils (p = 0.003), and eosinophils (p = 0.01), while patients with asbestos-induced pleural fibrosis (circumscribed plaques and diffuse pleural thickening) had higher concentrations of BAL lymphocytes (p = 0.02). Within our study population, however, cigarette smoking (smoking status or pack-years of smoking) was strongly associated with BAL macrophages, neutrophils, and eosinophils but was not associated with the concentration of BAL lymphocytes. Using multivariate analysis, we found that although asbestosis remained associated with higher concentrations of BAL macrophages, neutrophils, and eosinophils, cigarette smoking had a far greater contribution to the concentrations of BAL macrophages and eosinophils than did asbestosis. Although cigarette smoking accounted for 17 to 18% of the variance of BAL macrophages and eosinophils, asbestosis was associated with approximately 6% of the variance associated with these cells. In contrast, the concentration of BAL neutrophils remained associated with asbestosis and was not influenced by smoking behavior. We conclude that cigarette smoking strongly influences BAL cellularity (macrophages and eosinophils) in our patients with asbestosis but does not appear to affect the type or concentration of BAL cells in patients with asbestos-induced pleural fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of bronchoalveolar lavage cellularity in idiopathic pulmonary fibrosis.

To investigate factors that determine bronchoalveolar lavage (BAL) cellularity in patients with idiopathic pulmonary fibrosis (IPF), we compared BAL cells in patients with IPF (n = 83) to both nonsmoking (n = 111) and smoking (n = 19) normal volunteers. Patients with IPF had higher concentrations of BAL total cells and alveolar macrophages than nonsmoking volunteers and more BAL neutrophils and eosinophils than normal volunteers regardless of smoking status. Among patients with IPF, the numbers of alveolar macrophages, neutrophils, or eosinophils were strongly associated with either smoking status or pack-years of cigarette smoking. In fact, after accounting for cigarette smoking, using multivariate analysis, the only additional factors that were found to be associated with BAL cellularity were age (macrophages and eosinophils) and the percent predicted forced expired volume in 1 s (neutrophils). Additional multivariate models failed to identify a significant relationship between BAL cellularity and either the type of immunosuppressive therapy or other physiological measures of lung function. We conclude that cigarette smoking strongly influences BAL cellularity in patients with IPF. These findings suggest that cigarette smoking may have a role in the pathogenesis of IPF or may adversely affect the prognosis in patients with IPF.

The clinical utility and reliability of asbestos bodies in bronchoalveolar fluid.

Although asbestos bodies are easily identified in bronchoalveolar lavage (BAL) fluid and are thought to be strongly associated with the asbestos body burden in the lung parenchyma, the clinical utility and reliability of this biologic measure of exposure has not been sufficiently studied. To assess the clinical relevance of BAL asbestos bodies we compared this bioassay of exposure to other measures of exposure and also indices of lung disease in asbestos-exposed workers (n = 71). The median concentration of asbestos bodies was 0.8 bodies per ml of BAL fluid (range 0 to 34.3). Seven workers or 9.9% had zero asbestos bodies identified in the BAL fluid. The concentration of BAL asbestos bodies was not associated with the duration of exposure (r = -0.02), the time from first exposure to asbestos (r = 0.12), or the time since last exposure to asbestos (r = 0.05). Moreover, radiographic and physiologic measures of asbestos-induced lung disease were not found to be associated with the concentration of BAL asbestos bodies. In fact, of the seven study subjects with zero BAL asbestos bodies, the mean duration of exposure was 32 yr, and six of these subjects had radiographic evidence of asbestos-induced lung disease. To assess the reliability of measuring BAL asbestos bodies, we performed a second bronchoscopy on 54 subjects and directly compared the concentration of BAL asbestos bodies from both the first and second BAL samples. Within these 54 subjects, the concentration of BAL asbestos bodies was found to be a very reliable measure (r = 0.76; p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of cigarette smoking on lung function in patients with idiopathic pulmonary fibrosis.

The purpose of this investigation was to quantify the effect of cigarette smoking on standard measures of lung function in patients with idiopathic pulmonary fibrosis (IPF). Our study population consisted of 73 patients in whom IPF had been clinically diagnosed; in 67% the diagnosis was confirmed by open lung biopsy. The average age was 63 yr; 62% were men, and 70% were either former or current cigarette smokers. Current cigarette smokers were found to have a greater percent predicted residual volume. Interestingly, in a univariate analysis, pack-years of cigarette smoking was found to be directly associated with increased measures of lung volumes (TLC, FRC, and RV) and diminished gas exchange (DLCO). Linear multivariate regression models demonstrated that current cigarette smokers have greater measures of RV and FRC and that increasing pack-years of cigarette smoking is associated with diminished gas exchange. Importantly, the FEV/FVC ratio was not significantly related to either smoking status or pack-years of cigarette smoking. Results from our study indicated that among patients with IPF, current cigarette smokers will tend to trap air (higher RV and FRC), and that cigarette smoking appears to adversely alter gas exchange. Moreover, IPF appears to reduce the likelihood of developing physiologic correlates of airflow obstruction among cigarette smokers. However, this does not imply that IPF prevents the development of cigarette-induced lung disease. In fact, the association between cigarette smoking and both increased lung volumes and diminished gas exchange suggests the presence of both emphysema and interstitial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of restrictive lung function in asbestos-induced pleural fibrosis.

We evaluated whether restrictive lung function among asbestos-exposed individuals with pleural fibrosis was caused by radiographically inapparent parenchymal inflammation and/or parenchymal fibrosis. All 24 study participants were sheet metal workers who were nonsmokers with normal parenchyma on posteroanterior chest radiograph. These subjects had either normal pleura (n = 7), circumscribed plaques (n = 9), or diffuse pleural thickening (n = 8). After controlling for age, years in the trade, and pack-years of smoking, we found that sheet metal workers with diffuse pleural thickening had a lower forced vital capacity (P less than 0.001), total lung capacity (P less than 0.01), and CO-diffusing capacity of the lung (P less than 0.05) than those with normal pleura. Similarly, sheet metal workers with circumscribed plaques were found to have a reduced forced vital capacity; however, because of the small number of study subjects, this difference (regression coefficient = -11.0) was only marginally significant (P = 0.06). Although circumscribed plaque and diffuse pleural thickening were both associated with a lymphocytic alveolitis and a higher prevalence of parenchymal fibrosis on high-resolution computerized tomography (HRCT) scan, neither a lymphocytic alveolitis nor the finding of parenchymal fibrosis on HRCT scan influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that pleural fibrosis is associated with restrictive lung function and abnormally low diffusion that appears to be independent of our measures of parenchymal injury (chest X-ray, bronchoalveolar lavage, and HRCT scan).(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchoalveolar lavage in interstitial lung disease: effect of volume of fluid infused.

To evaluate the effect of varying infusate volume on the results of bronchoalveolar lavage (BAL) in patients with interstitial lung disease, 55 patients underwent 58 BAL during which both a 100- and 250-ml lavage was performed in the same lobe of the lung. Although the percent of the fluid that was returned and the total numbers of cells were greater in the 250- vs. the 100-ml lavage, there were no significant differences in cell differentials or numbers of cells per milliliter between the 100- and 250-ml BAL. We conclude that infusate volume does not affect cell differentials or numbers of cells per milliliter of bronchoalveolar lavage fluid in patients with interstitial lung disease.

Nontuberculous mycobacterial lung disease. Substantiation of a less aggressive approach.

A nonsurgical, less aggressive, less toxic chemotherapeutic protocol for the management of nontuberculous mycobacterial (NTB) pulmonary infections has been uniformly applied to patients in our institution between 1972 and 1985. Forty-three nonimmunocompromised patients with active lung disease caused by Mycobacterium avium-intracellulare (MAI) (n = 26), M kansasii (n = 16), and M xenopi (n = 1) were identified retrospectively. Eighteen MAI patients were treated with three or four antituberculosis agents resulting in sputum conversion and clinical improvement in 12 (67 percent). Additionally, 11 out of 16 (69 percent) patients completing therapy or still undergoing therapy for persistent MAI disease, achieved sputum conversion and clinical improvement after prolonged therapy (3.6 +/- 0.5 years [SEM]). When M kansasii was identified as the etiologic agent, all patients were treated with four or fewer antituberculosis agents and 14 out of 16 patients (88 percent) achieved sputum conversion and clinical improvement throughout the follow-up period. We conclude that the use of three or four chemotherapeutic agents in the treatment of NTM lung disease provides an excellent probability of successful outcome even in MAI infections.

Pharmacist involvement in a tuberculosis outpatient clinic.

The role of a pharmacist in a rural tuberculosis outpatient clinic is described. The clinic functions primarily in a follow-up capacity, necessitating complete records of each patient's medical progress, including a summary of prior drug therapy and observed response. The pharmacist is responsible for maintenance of patient records, patient consultation, onsite drug preparation and dispensing, and teaching responsibilities. The pharmacist-physician interaction in this setting is discussed. This program was devised to help improve patient compliance with antituberculosis drug therapy.