Exposure to endotoxin and to its purified derivative lipopolysaccharide (LPS) is related to several occupational pulmonary diseases and to severe domestic asthma. An inhalation of a given dose of pure LPS produces both a systemic and a bronchial inflammatory response. Information on the dose-response relationship to inhaled LPS in normal subjects is a prerequisite to define the safety threshold of exposure. In the present study, the clinical and inflammatory responses to rising doses of inhaled LPS was evaluated. Nine normal volunteers were challenged weekly by inhalation with saline, 0.5, 5, and 50 microg LPS (Escherichia coli). The response determinators are the clinical symptoms, fever, FEV1, blood polymorphonuclear neutrophils (PMNs) with their level of activation (measured by luminol enhanced-chemiluminescence), and both the blood and the urine concentrations of the C-reactive protein (CRP). To assess the bronchial inflammatory response, an induced sputum was obtained 6 h after each dose of LPS, and the total and differential cell counts as well as the MPO, ECP, and TNF-alpha concentrations were measured. Compared with the saline, an inhalation of 0.5 microg LPS induces a significant decrease in the PMN luminol-enhanced chemiluminescence (p < 0.01), which could reflect a process of margination and/or extravascular sequestration of activated PMN. Inhalation of 5 microg LPS is associated with a significant rise in blood CRP (p < 0.01) and PMNs (p < 0.001) and in sputum PMNs (p < 0.05), monocytes (p < 0.05), and MPO (p < 0.05). Inhalation of 50 microg LPS was characterized by a significant increase in temperature (p < 0.01), blood PMNs (p < 0.001), blood and urine CRP (p < 0.01 and < 0.01), and sputum PMNs (p < 0.001), monocytes (p < 0.05), lymphocytes (p < 0.05), MPO (p < 0.01), TNF-alpha (p < 0.01), and ECP (p < 0.01) while five subjects develop symptoms. In normal subjects, the response to inhaled LPS is dose-related, the most sensitive markers of LPS-induced inflammation being the blood PMNs count with their level of activation, the blood CRP concentration, and the sputum PMNs count. The no-response threshold to an acute inhalation of LPS is less than 0.5 microg.

Pulmonary lymphangitic carcinomatosis (PLC) is a well-known form of tumour metastasis to the pulmonary lymphatic system or to the adjacent interstitial tissue resulting in thickening of the bronchovascular bundle and septa. Another type of tumour metastasis to the lung involves the pulmonary vascular system and is known as pulmonary tumour thrombotic microangiopathy (PTTM). In this article, we will describe the unusual case of a young Chinese woman with gastric adenocarcinoma revealed by atypical radiographic lesions consistent with both PLC and PTTM. We will discuss the existing evidence and hypotheses about the pathophysiology of both conditions.

A 67-year-old female patient was evaluated at the Hepatogastroenterology Department for the management of a chronic tracheoesophageal fistula. She had previously undergone a right lobectomy for congenital bronchiectasis, an aortic valve replacement, and a laparoscopic Heller myotomy with Toupet fundoplication for achalasia. In the past, she had also been admitted to the intensive care unit several times because of respiratory tract infections that required mechanical ventilation. An upper endoscopy showed a 6-mm fistulous orifice in the upper third of the esophagus. Argon plasma coagulation was applied and the tract was closed using EZ clips (Olympus Medical Corp., Tokyo, Japan) and Endoloops (Olympus). Her symptoms persisted and a second treatment was attempted. A fully covered metal stent was first placed in the airway. The borders of the fistular opening were then dissected in order to create a submucosal virtual space and a mucosal flap without tension (• " Video 1). The incision was started using a FlexKnife (Olympus), and then an IT-Knife (Olympus) was employed to continue the dissection with circular movements (• " Fig. 1) and retroflexion. A two-channel gastroscope was used to place two round pieces of 25-mm biological mesh (Surgisis; Cook Medical, Dublin, Ireland) into the previously created space. This maneuver was performed using grasping forceps (• " Fig. 2). The mesh was fixed using EZ clips 90°and four 20-mm Endoloops (• " Fig. 3), under the mucosal flap. The patient successfully restarted oral food intake and was discharged. Upper endoscopy and bronchoscopy confirmed the closure of the orifice during the subsequent 8 months. There are currently multiple endoscopic options available for the treatment of tracheoesophageal fistulas, with an overall success rate of 84 % [1]. Only one case report has described the use of mucosal resection [2]. Biosynthetic mesh is frequently used in the surgical repair of multiple defects. However, endoscopic placement of mesh for tracheoesophageal fistula has only been described once, where it was deployed from the respiratory tract and achieved a complete closure of the orifice [3]. The case reported here describes a new endoscopic approach to tracheoesophageal fistulas that should be considered as an alternative in the management of these challenging cases.

No abstract

Abstractold man who developed a pericardial effusion. Chest radiography showed pleural thickening and calcification. Pericardiotomy was performed and revealed nonspecific inflammatory lesions. Occupational exposure to asbestos and exclusion of other causes led to the diagnosis of benign asbestos pericardial effusion.