Correlation between Peripheral Blood T-cell Profiles and Clinical and Inflammatory Parameters in Stable COPD

Background: Recent studies suggest that Tcl/Tc2 imbalances are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). The purpose of this study was to clarify the relationship between peripheral blood T-cell profiles and pulmonary function or inflammatory parameters. Methods: Thirty-one patients with stable COPD (median age 70 years, 30 males, 15 current smokers and 16 ex-smokers) and 30 healthy control subjects were enrolled in this study. The subjects underwent blood tests, exhaled nitric oxide (eNO) measurement, pulmonary function tests, and sputum induction. Tc1/Tc2 and Th1/Th2 were determined by analyzing intracellular cytokine staining for IFN-γ and IL-4 in peripheral blood CD8+ and CD4+ T cells using flow cytometry after stimulation with phorbol 12-myristate 13-acetate and ionomycin. Results: There was a significantly increased proportion of IFN-γ-producing and IL-4-producing CD8+ T cells in patients with COPD compared with control subjects (median [IQR] 73.6% [63.9%-80.7%] vs 62.0% [45.6%-73.8%], p = 0.004; and 2.6% [1.1%-6.9%] vs 1.1% [0.6%-2.2%], p = 0.002, respectively). In addition, the proportion of IFN-γ-producing CD4+ T cells was significantly higher in patients with COPD compared with control subjects (25.7% [21.2%-38.0%] vs 22.8% [15.6%-29.2%], p = 0.027). The proportion of IFN-γ-producing CD8+ T cells was correlated negatively with single-breath carbon monoxide transfer coefficient (Kco) (ρ = −0.45, p = 0.033) and positively with eNO (ρ = 0.50, p = 0.012). The proportion of IL-4-producing CD8+ T cells was positively correlated with body mass index (ρ = 0.42, p = 0.023) and Kco (ρ = 0.47, p = 0.026). Conclusions: It is suggested that Tc1 cells have a detrimental role and that Tc2 cells have a protective role in disease progression

Development of non-steroidal anti-inflammatory drug intolerance over a 3 year period

We report the detailed clinical course of a 47-year-old woman with aspirin-induced asthma in which non-steroidal anti-inflammatory drug (NSAID) intolerance developed over a 3 year period. The patient had mild asthma and was admitted with a femoral fracture in August 1996. Although she was given NSAIDs, including rectal diclofenac and oral loxoprofen, there was no worsening of asthma. After discharge, she was followed as having NSAID-tolerant asthma. When she developed perennial rhinitis and anosmia subsequent to an upper respiratory tract infection, asthma control was well maintained. Later, she experienced three episodes of severe asthmatic attacks after intake of aspirin or ketoprofen. Thus, we investigated her NSAID tolerability in September 1999. Sodium tolmetin inhalation challenge demonstrated a positive reaction, leading to the diagnosis of aspirin-induced asthma. Open challenges with loxoprofen and diclofenac also provoked positive reactions. The present case illustrates the potential variability of aspirin-induced asthma. Aspirin or NSAIDs challenge tests should be performed when nasal symptoms, particularly anosmia, develop or worsen