Pneumocystis carinii pneumonia in HIV-infected patients: effect of steroid therapy on surfactant level

Abstract

Previous studies have suggested alterations in pulmonary surfactant lipid in the setting of Pneumocystis carinii pneumonia in HIV-infected patients. Because pulmonary surfactant lipid is composed of a variety of lipid products and because other phospholipids might be present in bronchoalveolar lavage (BAL) lipid determinations, a single molecular species of phospholipid which comprises a substantial portion of the surfactant lipid fraction, dipalmitoyl phosphatidylcholine (DPPC), was measured by capillary column gas chromatography in BAL samples taken at the time of the diagnosis of P. carinii pneumonia, and 10 days after treatment for P. carinii pneumonia. DPPC was measured at day 0 and day 10 in seven patients who had been randomized to receive methylprednisolone adjuvant therapy for P. carinii pneumonia and in six patients who had been randomized to not receive methylprednisolone therapy. The level of DPPC in BAL from all patients at day 0 was 0.49 +/- 0.06 microgram ml-1 BAL. This level is significantly lower that the level of DPPC determined in BAL from five normal volunteers 2.48 +/- 0.40 micrograms ml-1. At day 0, the BAL level of DPPC in patients treated with methylprednisolone was not different from the BAL level of DPPC in patients not treated with methylprednisolone. By day 10 of therapy for P. carinii pneumonia, BAL levels of DPPC in all patients had increased to 1.05 +/- 0.19 micrograms ml-1 BAL. At day 10 DPPC levels in the methylprednisolone treated group were not different from the group not treated with methylprednisolone. We conclude that in HIV-infected patients, lung surfactant lipid is reduced in the setting of P. carinii pneumonia. The lipid levels return toward normal levels with treatment. Adjuvant therapy with corticosteroids does not alter the rate of recovery of surfactant lipid levels at least after 10 days of therapy.

Sensitized Splenocytes Result in Deleterious Cytokine Cascade and Hyperinflammatory Response in Rats withPneumocystisPneumonia despite the Presence of Corticosteroids

“…The beneficial effects of CS in HIV ϩ patients with Pneumocystis pneumonia who are receiving anti-Pneumocystis drugs were thought to be due either to their anti-inflammatory properties or to their effects on the surfactant system (36). Steroids reduce cytokine production in peripheral blood, but their effects on inflammatory mediators and surfactant components in BALF have not been consistent (8,12,15,18).…”

Clinical manifestation and initial treatment on infectious respiratory illnesses in HIV-infected patient: a case report

“…The chest radiograph of PCP typically demonstrates diffuse, bilateral, symmetrical "ground-glass" interstitial infiltrates emanating from the hila; however, in patients with early disease, a chest radiograph may be normal. 5,7 Individuals with bacterial pneumonia characteristically exhibit unilateral, focal, segmental, or lobar consolidation on chest radiograph. The frequency of these typical radiographic findings, however, may depend on the underlying bacterial pathogen.…”

“…13 The administration of the antibiotic cotrimoxazole which is a trimethoprim-sulfamethoxazole (TMP-SMX) antibiotic in this case was based on first line prophylaxis and treatment of choice for PCP. 1,5,7,10,13,14 For mild to moderate PCP, the dose of TMP-SMX is TMP 15 -20 mg/kg/day and SMX 75 -100 mg/kg/day orally, divided into 3 doses. For most patient, oral doses are 2 doublestrength (DS) tablets three times daily.…”

XVI. The Pneumocystis carinii major surface glycoprotein (MSG): its potential involvement in the pathophysiology of pneumocystosis

“…Patients with HIV infection who develop P. carinii pneumonia have decreased levels of bronchoalveolar lavage (BAL) phospholipids compared to HIV infected patients without P. carinii pneumonia [37]. The reduced levels of surfactant lipid returned to normal levels with treatment [38]. In vitro isolated alveolar type II pneumocytes from rats with P. carinii pneumonia incorporate less radiolabeled choline into secreted phosphatidylcholine than do type II cells from rats without P. carinii pneumonia [39].…”