Faculty Bibliography

We investigated the source of elevated serum lactate dehydrogenase (LDH) levels in seven patients with Pneumocystis carinii pneumonia (PCP) by analyzing blood and bronchoalveolar lavage (BAL) albumin (ALB) and LDH, with isoenzyme fractionation. Four patients with non-PCP lung disease served as control subjects. In PCP patients, BAL LDH was sixfold higher, and BAL ALB, fourfold higher than in the non-PCP patients. The increased LDH/ALB in BAL as compared to serum, in addition to a BAL isoenzyme pattern characteristic of lung, suggest that BAL LDH arises from a pulmonary source. We postulate that the high correlation observed between BAL and serum LDH (r = 0.93, p less than 0.001) reflects backflow of pulmonary-derived LDH into the blood through an alveolocapillary membrane (ACM) compromised by PCP. Furthermore, a comparison of BAL LDH/ALB for each isoenzyme with the same serum ratio showed less backflow for the cationic isoenzymes. The ACM appears to sieve proteins on an electrical basis which may account for the LDH isomorphic pattern observed in the serum of PCP patients

We reviewed 18 cases of histoplasmosis in patients at risk for the acquired immunodeficiency syndrome seen at two New York City hospitals in the past 3 1/2 years. Seventeen patients were Hispanic, including 13 born in Puerto Rico and three in South America. Clinical presentation was subacute, with high fever, weight loss, and mild respiratory symptoms with well-maintained gas exchange. Five patients had normal chest roentgenograms. The most common chest roentgenographic abnormality was diffuse small nodules. A rapid diagnosis was established histologically in 72 percent of patients, most commonly by transbronchial lung biopsy; cultures were positive in 94 percent of patients while serology was positive in five of six patients. Mycobacterium tuberculosis was a concurrent, often unrecognized, pathogen in six cases. Most patients responded to amphotericin therapy. Histoplasmosis may represent an early sign of altered host immunity in the acquired immunodeficiency syndrome.

We correlated bronchoalveolar lavage (BAL) cell populations with clinical course and outcome in 19 patients with Pneumocystis carinii pneumonia and acquired immunodeficiency syndrome. Twelve patients demonstrated an elevated (greater than or equal to 5 percent) BAL combined neutrophil and eosinophil count, which correlated with the magnitude of the alveolar-arterial PO2 gradient. Patients with elevated BAL granulocytes also had significantly higher serum lactate dehydrogenase levels. Three of the four patients who died had the highest percentage of neutrophil counts observed in lavage fluid. Although no patient was thought to have a concurrent bacterial infection, potential pathogens were cultured from the sputum of patients with the most elevated neutrophil counts. Whether BAL granulocytes reflect an inflammatory process analogous to the adult respiratory distress syndrome or signify concomitant bacterial infection remains to be determined. We conclude that BAL granulocytes are associated with more severe respiratory compromise in patients with Pneumocystis carinii pneumonia