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In the course of chronic respiratory insufficiency, acute episodes often require the use of mechanical ventilation. Failure of weaning, or worsening of alveolar hypoventilation, results in long term ventilatory assistance with the need of overall care of the patient. The pneumologist has a key role in the choice of indications, devices and mode of home mechanical ventilation. Thanks to the non-invasive ventilation with a facial or nasal mask, tracheostomy is less often needed. Respiratory failure due to lung restriction is the best indication of mechanical ventilation. The results in COPD are questionable. Whatever to the technique of ventilation and the underlying disease, the pneumologist has to ascertain the steady state of the medical condition, patient and family education, and social situation, all factors to be taken into account before the patient can be discharged. Knowing the specific needs in these patients'care, the pneumologist plays a key role at each stage of home return and follow-up. He co-ordinates the different aspects of pneumological care, like rehabilitation and acute episodes treatment. The overall care of the patients should be improved by the development of health networks in the field of chronic respiratory insufficiency.

Ulcerative colitis and sarcoidosis are seldom associated. A 33-year-old diabetic man developed simultaneously a rectitis and a non-productive cough leading to the diagnosis of ulcerative colitis and sarcoidosis. These diagnoses are discussed because of the possible gastrointestinal lesions from sarcoidosis or the respiratory disorders due to ulcerative colitis. Some pathophysiological evidence can be found in this case in favor of a non-fortuitous association.

The hepatopulmonary syndrome (HPS) consists of a triad of liver dysfunction, increased alveolar-arterial oxygen gradient and intrapulmonary vascular dilations. The mechanisms of impaired arterial oxygenation are still debated but the multiple inert gases elimination technique and more recently contrast echocardiography, greatly facilitated the investigation of such mechanisms. Subsequently the cause of hypoxemia can be attributed to several mechanisms such as ventilation-perfusion mismatch, right-to-left intrapulmonary shunts and alveolar-to-capillary diffusion defect, variously implicated in the severity of the disease. SHP may result from intrapulmonary vascular dilations and angiogenesis but the pathogenesis of such abnormalities is not completely explained. The hypothesis of an imbalance in vasoactive mediators and angiogenic factors has been put forward. Increasing data support the theory that the increase in synthesis and release of nitric oxide (NO) is the key factor modulating vascular tone. If this hypothesis is true, the use of compettive inhibitors of NO synthesis should restore pulmonary vascular tone, reversing the hemodynamic changes and gas exchange impairment of HPS.