Acute-phase markers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), have been studied in inflammatory and malignant disorders. We examined the diagnostic value of these markers for the differentiation among parapneumonic, tuberculous and malignant effusions. We studied 124 patients with pleural effusions, classified as exudates [total (n=97), parapneumonic (n=15), tuberculous (n=25), malignant (n=57)] and transudates due to congestive heart failure (n=27). CRP, IL-6 and TNF-alpha were measured in pleural fluid and serum. Pleural fluid CRP was higher in parapneumonic compared to tuberculous and malignant effusions, providing 100% sensitivity for a cut-off point of 5.3mg/dL. IL-6 was higher in both parapneumonic and tuberculous compared to malignant effusions. TNF-alpha was higher in tuberculous compared to malignant effusions, providing 96.0% sensitivity, and 93.0% specificity for a cut-off point of 88.1 pg/mL. Pleural fluid CRP levels were lower than serum in all groups, probably reflecting systemic inflammation, whereas IL-6 and TNF-alpha were higher in pleural fluid indicating local production. Our data suggest that these markers may provide useful information for the differentiation of infectious and malignant effusions in clinical practice. However, further studies are needed for the validation of these findings in usual clinical circumstances.

Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis which has multiple effects in lung development and physiology. VEGF is expressed in several parts of the lung and the pleura while it has been shown that changes in its expression play a significant role in the pathophysiology of some of the most common respiratory disorders, such as acute lung injury, asthma, chronic obstructive pulmonary disease, obstructive sleep apnea, idiopathic pulmonary fibrosis, pulmonary hypertension, pleural disease, and lung cancer. However, the exact role of VEGF in the lung is not clear yet, as there is contradictory evidence that suggests either a protective or a harmful role. VEGF seems to interfere in a different manner, depending on its amount, the location, and the underlying pathologic process in lung tissue. The lack of VEGF in some disease entities may provide implications for its substitution, whereas its overexpression in other lung disorders has led to interventions for the attenuation of its action. Many efforts have been made in order to regulate the expression of VEGF and anti-VEGF antibodies are already in use for the management of lung cancer. Further research is still needed for the complete understanding of the exact role of VEGF in health and disease, in order to take advantage of its benefits and avoid its adverse effects. The scope of the present review is to summarize from a clinical point of view the changes in VEGF expression in several disorders of the respiratory system and focus on its diagnostic and therapeutic implications.

Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 +/- 1.6 ml kg(-1) min(-1); mean +/-s.e.m.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O(2) saturation (S(a,O(2))): 92 +/- 1%) and one hyperoxic (F(I,O(2)): 0.5% O(2); S(a,O(2)) : 97 +/- 1%) 5 min exercise test at intensities equal to 80 +/- 3 and 90 +/- 3% of maximal work rate (WR(max)), respectively, producing the same tidal volume (V(T)) and breathing frequency (f) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P(di,tw)) during recovery. Hyperoxic exercise at 90% WR(max) induced significantly (P= 0.022) greater post-exercise reduction in P(di,tw) (15 +/- 2%) than did normoxic exercise at 80% WR(max) (9 +/- 2%), despite the similar mean ventilation (123 +/- 8 and 119 +/- 8 l min(-1), respectively), breathing pattern (V(T): 2.53 +/- 0.05 and 2.61 +/- 0.05 l, f: 49 +/- 2 and 46 +/- 2 breaths min(-1), respectively), mean changes in P(di) during exercise (37.1 +/- 2.4 and 38.2 +/- 2.8 cmH(2)O, respectively) and end-exercise arterial lactate (12.1 +/- 1.4 and 10.8 +/- 1.1 mmol l(-1), respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S(a,O(2)) tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.

We have examined the role of age on the continuous positive airway pressure (CPAP) levels required to treat two groups of elderly (n=70) and young (n=70) sleep apneic patients, matched for disease severity (apnea/hypopnea index), body mass index and neck circumference. Elderly patients required lower CPAP levels compared to young [mean (sd): 6.9(1.9)cm H(2)O and 9.4(3.5)cm H(2)O, respectively; P<0.0001]. To investigate this finding, we studied the effects of CPAP and its components (inspiratory and expiratory positive airway pressure) on lung volume and upper airway resistance in two groups of elderly [n=9, age 71.7(3.3) years] and young [n=9, age 36.7(4.4)] patients with sleep apnea during wakefulness. CPAP produced a greater decrease in airway resistance (P=0.009) and a greater increase in lung volume (P=0.008) in the elderly compared to young patients. We conclude that both the greater lung inflation and the greater direct splinting of the upper airway contributed to the lower CPAP level required by the elderly. Ageing may be an important determinant of therapeutic CPAP levels in clinical practice, especially in older sleep apneic patients.

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean +/- SE: age, 25 +/- 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P < 0.001) and a significant decrease in R-R interval at 3 s (P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 +/- 3 to 104 +/- 3 mmHg; O, 86 +/- 3 to 105 +/- 3 mmHg; P = 0.99. R-R interval: C, 1.12 +/- 0.03 to 0.89 +/- 0.04 s; O, 1.11 +/- 0.02 to 0.87 +/- 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P < 0.001); this increase was not different between the two conditions (C: 4.40 +/- 0.29 to 6.76 +/- 0.61 l/min, O: 4.35 +/- 0.34 to 7.65 +/- 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.

A case of a 30-year-old male with a fever, dry cough and associated abnormal findings in imaging modalities (bilateral hilar lymphadenopathy and nodular parenchymal opacities) is described. After a further and scrutinized work-up, the diagnosis of GLUS syndrome was made. Clinical, etiological, pathological and therapeutical aspects of the disease are discussed, demonstrating the paramount importance of the use of the immunohistochemical methods in the diagnosis of this disorder.

Inhaled prostaglandin (PG)E2 has been found to cause bronchodilation in asthmatics, although it does not have bronchodilative effects in normal subjects. The aim of this study was to investigate the levels of PGE2 in the expired breath condensate of patients with asthma, the possible contribution of smoking habit to its levels and the possible relationship between PGE2 and the degree of bronchial hyperresponsiveness, as assessed by the provocation dose of histamine causing a 20% fall in forced expiratory volume in one second (FEV1) (PD20). A total of 30 mild asthmatics (15 smokers, all steroid-naive, FEV1 88+/-6 (%+/-SD)) and 20 healthy control subjects (10 smokers) were studied. Histamine challenge testing was performed in all subjects and the PD20 was determined. The results showed that asthmatic smokers had significantly higher values of PGE2 compared to asthmatic nonsmokers and control subjects (40+/-21 versus 14.5+/-4.5 versus 11.7+/-3 pg x mL(-1), respectively). Further analysis showed that PGE2 levels were significantly higher in asthmatic smokers compared to smoker and nonsmoker controls (40+/-21 versus 11.6+/-2 versus 11.7+/-4 pg x mL(-1), respectively). No significant difference was observed between asthmatic nonsmokers and both control smokers and control nonsmokers. No significant correlation was found between PGE2 levels and PD20 in all groups of asthmatics, irrespective of smoking habit. In conclusion, the elevation of prostaglandin E2 in the expired breath condensate of patients with asthma is mainly attributed to smoking habit and prostaglandin E2 levels do not predict the degree of bronchial hyperresponsiveness.

BACKGROUND: Cardiac tamponade as the initial manifestation of metastatic cancer is a rare clinical entity. Furthermore, a thoraco-biliary fistula is another rare complication of echinococcosis due to rupture of hydatid cysts located at the upper surface of the liver to the pleural or pericardial cavity. We report a case of non-small cell lung cancer with a coexisting hepatic hydatid cyst presenting as a bilious pericardial effusion. CASE REPORT: A 66-year-old patient presented with cardiac tamponade of unknown origin. Chest CT-scan demonstrated a left central lung tumor, a smaller peripheral one, bilateral pleural effusions and a hydatid cyst on the dome of the liver in close contact to the diaphragm and pericardium. Pericardiotomy with drainage was performed, followed by bleomycin pleurodesis. The possible mechanism for the bilious pericardial effusion might be the presence of a pericardio-biliary fistula created by the hepatic hydatid cyst. CONCLUSIONS: This is the first case of a bilious pericardial effusion at initial presentation in a patient with lung cancer with coexisting hepatic hydatid cyst.

Endogenous airway acidification, as assessed by pH in expired breath condensate, has been implicated in asthma pathophysiology. We measured pH in breath condensate of patients with inflammatory airway diseases in stable condition and examined its relationship with the inflammatory process (as assessed by differential cell counts in induced sputum), oxidative stress (as assessed by H(2)O(2) and 8-isoprostane), and nitric oxide metabolism (as assessed by total nitrate/nitrite). We studied 40 patients with bronchial asthma (20 with moderate disease, forced expiratory volume in 1 second 60 [10]% SD predicted), 20 patients with bronchiectasis, 20 patients with chronic obstructive pulmonary disease (COPD), and 10 normal subjects. Mean (95% confidence intervals) pH values were significantly lower in patients with COPD and bronchiectasis compared with patients with asthma and control subjects (7.16, 7.09-7.23 and 7.11, 7.04-7.19 versus 7.43, 7.35-7.52 and 7.57, 7.51-7.64, respectively, p < 0.0001). Patients with moderate asthma had significantly lower values compared with mild and control subjects. In patients with COPD and bronchiectasis, the values of pH were significantly correlated with both sputum neutrophilia and oxidative stress. Respectively, in patients with moderate asthma, a significant correlation was observed between pH and sputum eosinophilia, total nitrate/nitrite, and oxidative stress. The pH of the expired breath condensate might be a simple, noninvasive, inexpensive, and easily repeatable procedure for the evaluation of the inflammatory process in airway diseases.