Pulmonary function in patients presenting with Raynaud's phenomenon without an underlying connective tissue disease. A prospective, longitudinal study.

Forty-two patients presenting with Raynaud's phenomenon (RP) were prospectively evaluated for pulmonary function changes over a 6-year followup period. Fifteen patients had secondary RP at presentation, 27 patients had nonsecondary RP. In the latter group, decreased pulmonary diffusing capacity (Tlco) was observed in only 2 patients (7%) whereas 9 patients with secondary RP (60%) had decreased Tlco. In the group of patients with nonsecondary RP exhibiting one or more autoantibodies, Tlco values were lower than in the group without autoantibodies (p less than 0.01). In patients with nonsecondary RP the duration of disease was correlated with the level of Tlco (r = 0.55), probably explained by a higher prevalence of truly primary RP in patients with longstanding nonsecondary RP. During followup no significant changes in pulmonary function were observed in the group with nonsecondary RP. We conclude that pulmonary function testing in patients presenting with nonsecondary RP without autoantibodies does not appear of clinical value.

The effects of oral slow-release terbutaline on the circadian variation in spirometry and arterial blood gas levels in patients with chronic airflow obstruction.

The circadian variation of spirometry and blood gases was studied in eight male, normoxemic, patients with chronic air flow obstruction and complaints of early morning dyspnea. The patients were selected for a high amplitude in circadian variation of PEFR. They were treated for eight days with placebo and slow-release terbutaline tablets (5 mg at 8 am and 10 mg at 8 pm). Thereafter, arterial blood gas levels were measured at four-hour intervals over 24 hours. Just after blood sampling, FEV1 measurements were performed. The results on placebo therapy were compared with results in eight healthy volunteers matched for age, sex, and smoking habits. The circadian rhythms of FEV1, PaO2, and SaO2 in these patients showed a higher amplitude than in normal subjects. The decrease of FEV1 in the patient group at 8 am coincided with the decrease in PaO2 and SaO2. In normal subjects no significant nocturnal fall in FEV1, PaO2, or SaO2 occurred. Administration of slow-release terbutaline tablets for eight days, providing comparable diurnal and nocturnal serum levels, prevented the nocturnal decrease of FEV1, PaO2, and SaO2. The increase of the FEV1 at all hours of observation showed a significant correlation with the increase of the PaO2.

Local immune complexes and inflammatory response in patients with chronic interstitial pulmonary disorders associated with collagen vascular diseases.

Evidence is accumulating that the lung injury in collagen vascular diseases (CVD) is triggered by immune complexes (IC). These reactions are neutrophil- and complement-dependent. The direct, in vivo phagocytosis of IC by bronchoalveolar lavage polymorphonuclear leucocytes (BAL-PMN), was studied in 15 patients with CVD and chronic interstitial pulmonary disorders. A control group (NC) consisted of nine healthy, non-smoking volunteers. Concentrations of soluble IC were measured using a solid phase Clq ELISA assay, and an indirect, in vitro phagocytosis assay performed using healthy donor PMN. Local Ig and C3 concentrations were determined using laser nephelometry and Mancini techniques, respectively. In the patient group the total cell counts/ml recovered lavage fluid and the proportions of BAL-PMN were significantly increased (P less than 0.05 and P less than 0.001, respectively). The influxed PMN showed high scores of direct IC phagocytosis. Soluble IC concentrations were significantly increased compared with controls (all comparisons P less than 0.01), and in the BAL relatively higher than in the serum of the same patients. Concomitantly high local IgG concentrations were observed. Corticosteroid treatment gave rise to significantly decreased total cell counts (P less than 0.05), and proportions of BAL-PMN (P less than 0.001), a decrease in the in vivo IC phagocytosis (P less than 0.05), in the indirect, in vitro IC phagocytosis, in the Clq ELISA and in the local IgG concentrations (all comparisons P less than 0.001). We concluded that locally formed IC may induce an inflammatory response in the lungs of patients with CVD.