Background/Purpose: Pneumonia is an important cause of death in patients with SLE. In general population, recommendations encourage the use of procalcitonin for management of pneumonia, however, evidence in patients with SLE is scant. The aim is to investigate the diagnostic and prognostic utility of procalcitonin and selected chemokines/cytokines in patients with SLE and pneumonia.

Methods: Cases: We studied 46 constitutive SLE patients (SLICC 2012 criteria) with pneumonia (respiratory symptoms + compatible image study) in a single tertiary care center, from Dec 2014 – Dec 2015. Patients were prospectively evaluated and samples for cultures and respifinder-22 (PCR for 18 viral + 4 bacterial pathogens) were obtained. Follow-up: 30 days after discharge. Basal procalcitonin determination on admission and in 42 (91%) patients a second sample 48-72 hrs later.

Control groups: We included 27 active SLE and 24 inactive SLE patients (SLEDAI 2-K), without evidence of infection and a single procalcitonin measurement.

In 58 unselected patients (17 pneumonia, 23 active, and 18 inactive) we obtained serum for cytokines/chemokines determination by luminometry (IFNg, IL-10, IL-12, IL-17, IL-1β, IL-2, IL-21, IL-23, IL-5, IL-6, IL-8, TNFα, BAFF, IP-10, and CXCL-9).

Statistics analysis: Student-T test, Mann-Whitney U, Wilcoxon signed-rank test, Chi-squared test, Fisher exact test or Kruskal-Wallis test were used as appropriate.

Results:

We included 97 patients, 83 women (86%). SLEDAI 2k: 1 ± 1.2 inactive vs 8.8 ± 4.5 active vs 8.2 ± 5.7 pneumonia. Patients with pneumonia had a shorter time from diagnosis (pneumonia 6 ± 8 years; p<0.001; active 9 ± 6 years; inactive 14 ± 7 years).

Thirteen (28%) patients with pneumonia had a negative outcome (mechanical ventilation, shock or death). In 25 (54%) patients, a causal germ was identified. Patients with pneumonia had higher procalcitonin levels vs control groups (p<0.001) whereas no differences were seen between active vs inactive patents. Thirty two patients (70%) with pneumonia had positive basal procalcitonin (>0.5 µg/L) vs 0.0 µg/L in control groups (p<0.001); sensitivity 70% (95% CI: 54 – 82%), specificity 100% (95% CI: 93 – 100%). Twelve (38%) patients with positive basal procalcitonin had negative outcome vs one (7%) with procalcitonin ≤0.5 µg/L (p=0.072). Procalcitonin levels diminished in the second determination: median 0.95 (IQR 0.25 – 6.98) vs 0.36 (0.11 – 1.7), p<0.001. In this determination, 16 patients had procalcitonin <0.25 µg/L; two of them (12%) had negative outcome; 11 of 26 patients with procalcitonin >0.25 µg/L had a negative outcome (42%); p=0.084.

Among the cytokines/chemokines evaluated, only CXCL9 was significantly higher in pneumonia vs control groups: median 1614 (IQR 905 – 2527) vs 641 (247 – 1096) active SLE and 313 (179 – 522) inactive SLE (p<0.001).

Conclusion: Patients with SLE have a high rate of complications secondary to pneumonia. Procalcitonin is useful for diagnosis of pneumonia with a high specificity, even when comparing vs active SLE patients. CXLC9 is a potential biomarker for pneumonia in patients with SLE.

ACR Meeting Abstracts - https://acrabstracts.org/abstract/procalcitonin-and-cxcl9-as-potential-biomarkers-for-pneumonia-in-patients-with-systemic-lupus-erythematosus/