case_images: PMC3420776_01
case_images: Chest radiograph revealed bilateral ground-glass infiltrates and reticular shadows.
case_images: CRIM.RHEUMATOLOGY2011-185657.001.jpg
case_images: PMC3420776_01_CRIM.RHEUMATOLOGY2011-185657.001.jpg
case_images: fig1
case_images: Serum beta-D-glucan was found to be positive, and sputum polymerase chain reaction (PCR) was positive for pneumocystis (Figure 1).
case_images: Time course of serum cytokines concentrations from baseline to 8 days. (a) TNF-alpha was not detectable in baseline samples. One day after the start of etanercept therapy TNF-alpha was measurable by ELISA. TNF-alpha levels became steady within 2 days of etanercept therapy. TNFR-II concentrations became elevated after the start of etanercept therapy. Within the first week of etanercept therapy, TNFR-II reached levels ranging from 160 ng/mL to 190 ng/mL. (b) Serum IL-6, IL-1 beta, and CRP concentrations were decreased just after the initiation of treatment.
case_images: CRIM.RHEUMATOLOGY2011-185657.002.jpg
case_images: PMC3420776_01_CRIM.RHEUMATOLOGY2011-185657.002.jpg
case_images: fig2
case_images: CRP value and high clinical disease activity. Conversely, the serum level of TNF-alpha was nondetectable (<0.2 pg/mL); the sTNFR-I, -II, and IL-1 beta values were not found to be significantly elevated (Figure 2).
case_images: Time course of serum cytokines concentrations. (a) TNF-alpha concentration increased between weeks 1 and 2 after the initiation of etanercept therapy then remained steady ranging from 100 pg/mL to 170 pg/mL. At 12 weeks, the patient developed PCP and the TNF-alpha value increased steeply (arrow). With cessation of etanercept, the TNF-alpha concentration immediately returned to pretreatment levels. Four weeks after the initiation of therapy, the TNFR-II concentration became steady, ranging from 300 ng/mL to 700 ng/mL. With cessation of etanercept due to the PCP, TNFR-II concentration returned to pretreatment levels. (b) On the other hand, at week 12, the levels of IL-6, CRP, and TNF-alpha showed an acute peak (arrow), which tapered downward over the following 3 weeks with the institution of an appropriate antifungal regimen.
case_images: CRIM.RHEUMATOLOGY2011-185657.003.jpg
case_images: PMC3420776_01_CRIM.RHEUMATOLOGY2011-185657.003.jpg
case_images: fig3
case_images: At week 12, concurrent to the patient developing clinical symptoms of PCP, the levels of IL-6, CRP, and TNF-alpha showed an acute peak, which tapered downward over the following 3 weeks with the institution of an appropriate antifungal regimen (Figures 3 and 4).
case_images: (a) Computed tomography scans on the day patient diagnosed as PCP showed infiltrates and reticular shadows. (b) The shadows disappeared after treatment with antifungal agents.
case_images: CRIM.RHEUMATOLOGY2011-185657.004.jpg
case_images: PMC3420776_01_CRIM.RHEUMATOLOGY2011-185657.004.jpg
case_images: fig4
case_images: At week 12, concurrent to the patient developing clinical symptoms of PCP, the levels of IL-6, CRP, and TNF-alpha showed an acute peak, which tapered downward over the following 3 weeks with the institution of an appropriate antifungal regimen (Figures 3 and 4).