Biomedical subjects

Laurent Plantier

Publications and source records attributed to Laurent Plantier.

4 recordsLinked to original sources

PubMed2006

Hemoptysis in lung transplant recipients: a series of 15 cases.

STUDY OBJECTIVES: Respiratory complications are frequent after lung transplantation (LTx), and many of these complications have the potential to cause hemoptysis. However, surprisingly, only a few isolated cases of hemoptysis have been reported in LTx recipients. Here, we describe a series of patients who underwent LTx at our center who developed hemoptysis during their postoperative course. SETTING: A tertiary care university hospital. RESULTS: Of 197 LTx recipients, hemoptysis developed in 15 over a 16-year period. The pulmonary circulation as well as the systemic circulation were involved in the mechanism of hemoptysis. Six patients had moderate or minimal hemoptysis, while nine patients had life-threatening hemoptysis, which occurred during the first year after LTx in all cases. Active necrotizing ischemic airway injury was present in five of the nine patients with life-threatening hemoptysis. Eight of those nine patients died as a result of hemoptysis. Overall, hemoptysis was the cause of death in 4.5% of patients who underwent LTx at our institution. CONCLUSION: In our series of transplant patients, hemoptysis was not rare and was associated with a high rate of mortality.

Adult↗

PubMed2005

Keratinocyte growth factor expression by fibroblasts in pulmonary fibrosis: poor response to interleukin-1beta.

Keratinocyte growth factor (KGF) is secreted by fibroblasts and protects from pulmonary fibrosis in animal models. Interleukin (IL)-1beta is the most potent inducer of KGF in fibroblasts, acting through the c-Jun pathway. We evaluated in vitro KGF production by human lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF, n = 10) and from control subjects (n = 7) at baseline and after IL-1beta stimulation. Basal KGF secretion by IPF fibroblasts was similar to controls. In fibroblasts from control subjects, IL-1beta increased c-Jun expression, c-Jun activation, and KGF secretion. SP600125, a specific c-Jun N-terminal kinase (JNK) inhibitor, inhibited the effect of IL-1beta. By contrast, in IPF fibroblasts, IL-1beta did not increase c-Jun expression and c-Jun activation, and weakly increased KGF secretion, whereas SP600125 had no effect. IL-1beta similarly increased JunB expression in fibroblasts from patients with IPF and control subjects. Total JNK content was not different in either unstimulated or IL-1beta-stimulated IPF and control fibroblasts. IL-1beta increased phosphorylated JNK in control and IPF fibroblasts, but this increase was weaker and heterogeneous in IPF. Altogether, our results demonstrate a dysregulation of KGF secretion by IPF fibroblasts. The weak response to IL-1beta is associated with a defect of c-Jun expression and activation and a defect of JNK activation.

Adult↗

PubMed2004

Defect of hepatocyte growth factor production by fibroblasts in human pulmonary emphysema.

Pulmonary emphysema results from an excessive degradation of lung parenchyma associated with a failure of alveolar repair. Secretion by pulmonary fibroblasts of hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) is crucial to an effective epithelial repair after lung injury. We hypothesized that abnormal HGF or KGF secretion by pulmonary fibroblasts could play a role in the development of emphysema. We measured in vitro production of HGF and KGF by human fibroblasts cultured from emphysematous and normal lung samples. HGF and KGF production was quantified at basal state and after stimulation. Intracellular content of HGF was lower in emphysema (1.52 pg/mug, range of 0.15-7.40 pg/mug) than in control fibroblasts (14.16 pg/mug, range of 2.50-47.62 pg/mug; P = 0.047). HGF production by emphysema fibroblasts (19.3 pg/mug protein, range of 10.4-39.2 pg/mug) was lower than that of controls at baseline (57.5 pg/mug, range of 20.4-116 pg/mug; P = 0.019) and after stimulation with interleukin-1beta or prostaglandin E(2). Neither retinoic acids (all-trans and 9-cis) nor N-acetylcysteine could reverse this abnormality. KGF production by emphysema fibroblasts (5.3 pg/mug, range of 2.2-9.3 pg/mug) was similar to that of controls at baseline (2.6 pg/mug, range of 1-6.1 pg/mug; P = 0.14) but could not be stimulated with interleukin-1beta. A decreased secretion of HGF by pulmonary fibroblasts could contribute to the insufficient alveolar repair in pulmonary emphysema.

Acetylcysteine↗

PubMed2003

[Hemoptysis].

Hemoptysis is a common respiratory symptom that always requires investigation. Its severity varies from bloodstained sputum to life-threatening hemoptysis. Blood originates most often from bronchial circulation. The most common causes of hemoptysis are tuberculosis, lung carcinoma, bronchiectasis but idiopathic forms are frequent. The diagnostic investigation is based mainly on history, chest radiograph, fibroscopy and CT scan of the thorax. The goal is to determine the cause as well as the site of bleeding. The management of life-threatening hemoptysis is mainly based on either surgical approach or bronchial artery embolization. The majority of centers favor this latter approach.

Bronchial Arteries↗