Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-beta1 and alpha1-AT may reflect differences between the diseases.

These results suggest it may be prudent to test patients with chronic urticaria, prurigo chronica multiformis, pruritus cutaneus, and eczema nummulare for H. pylori infection and to eradicate the infection in those whose test is positive.

Matrix metalloproteinase (MMP)-9 and tissue inhibitors of metalloproteinase (TIMP)-1 concentrations are increased in the sputum of asthma and chronic bronchitis patients, and are thought to be related to airflow obstruction. However, serum concentrations of these enzymes have not been clearly evaluated in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to examine the serum concentrations of these enzymes in COPD and asthmatic patients in order to determine their relationship with airway obstruction.Serum samples were obtained from 72 patients with COPD: 66 control subjects and 26 patients with asthma. Smoking histories of control subjects were matched with those of COPD patients. Serum concentrations of TIMP-1 and MMP-9 were determined by ELISA.The circulating TIMP-1 concentration was significantly higher in stable COPD patients than in control and asthmatic subjects, and was significantly negatively correlated with forced expiratory volume in one second/forced vital capacity in COPD patients. The molar ratio between MMP-9 and TIMP-1 was significantly lower in COPD patients than in control subjects. In patients with COPD, the serum TIMP-1 concentration was significantly increased during disease exacerbation.In conclusion, the current findings suggest that serum tissue inhibitors of metalloproteinase-1 concentration can be used as a serum marker of airway obstruction and exacerbation in chronic obstructive pulmonary disease patients.KEYWORDS: Bronchial asthma, chronic obstructive pulmonary disease, exacerbation, metalloproteinases, serum markers, tissue inhibitors of matrix metalloproteinases P ulmonary emphysema, the major contributor to morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), is characterised by progressive destruction of the extracellular matrix (ECM) of the lung [1-4]. The most widely accepted theory of the pathogenesis of pulmonary emphysema is a proteinase-antiproteinase imbalance. Although a number of studies have demonstrated the important role of increased elastolytic activity derived from neutrophils in emphysema [4,5], recent studies have shown that matrix metalloproteinases (MMPs) play key roles in tissue remodelling of the airways in COPD and asthma patients [2,[6][7][8]. MMPs are a family of structurally related enzymes that are capable of degrading all components of the ECM [9]. Members of the MMP family are selectively inhibited by tissue inhibitors of metalloproteinases (TIMPs). TIMP-1 has been shown to bind to both the active and precursor form of MMP-9, in a 1:1 proportion, and to inhibit its enzymatic activity. Sputum concentrations of MMP-9 and TIMP-1 are increased in patients with COPD and asthma [2,10]. RUSSELL et al. [11] showed that alveolar macrophages from patients with COPD release larger amounts of MMP-9 with greater enzymatic activity than those from healthy smokers. Two recent studies found that the MMP-9/TIMP-1 ratio was correlated with the degree of airway obstruction. BOSSE et al. [12]...

It has recently been demonstrated that nitric oxide (NO) is highly concentrated in the gastric lumen and plays an important role in defending against pathogenic microorganisms in the stomach. NO in the gastric lumen is mainly delivered by extrinsic sources from saliva. We studied whether Helicobacter pylori infection affected intraluminal NO levels in humans. H. pylori infection was diagnosed on the basis of histology and culture or (13C)-urea breath test. Air and gastric juice in the gastric lumen were collected endoscopically. The concentration of intraluminal NO was measured by a chemiluminescence system, using an NO analyzer. The concentration of nitrite in gastric juice was measured by the Griess reaction. The intraluminal concentration of NO in H. pylori-positive patients (198.2 +/- 41 parts per billion [ppb] mean +/- SE; n = 70) was significantly lower than that in H. pylori-negative patients (353.0 +/-57.9ppb; n = 43; P < 0.05). In contrast, the concentration of nitrite in gastric juice in H. pylori-positive patients (57.7 +/- 12.3 RM; n = 70) was significantly higher than that in H. pylori-negative patients (25.9 +/- 6.4 microM; n = 43, P < 0.01). The intraluminal concentration of NO in H. pylori-positive patients was markedly increased and the concentration of nitrite in H. pylori-positive patients was markedly decreased following the completion of eradication therapy. Based on these results, we propose that a decrease in NO and excess nitrite production in the gastric lumen are associated with H. pylori infection and may play an important role in the pathogenesis of H. pylori-related abnormalities.