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Giulio Rossi - One of the best experts on this subject based on the ideXlab platform.

  • diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia dipnech syndrome and carcinoid tumors with without nech a clinicopathologic radiologic and immunomolecular comparison study
    The American Journal of Surgical Pathology, 2018
    Co-Authors: Mc Mengoli, Em Silini, Giulio Rossi, Alberto Cavazza, Renato Franco, Federica Zito Marino, Mario Migaldi, Letizia Gnetti, Luca Ampollini, Marcello Tiseo
    Abstract:

    The diagnostic criteria of diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia (DIPNECH) are not well defined, and DIPNECH can be mistaken for carcinoids associated with neuroendocrine Cell Hyperplasia (NECH). In this study, we compared clinical, radiologic, histologic, immunohistochemical,

  • Diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia syndrome
    European Respiratory Journal, 2016
    Co-Authors: Giulio Rossi, Alberto Cavazza, Paolo Spagnolo, Nicola Sverzellati, Lucia Longo, Agita Jukna, Gloria Montanari, Cristiano Carbonelli, Giada Vincenzi, Giuseppe Bogina
    Abstract:

    The term diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia (DIPNECH) may be used to describe a clinico-pathological syndrome, as well as an incidental finding on histological examination, although there are obvious differences between these two scenarios. According to the World Health Organization, the definition of DIPNECH is purely histological. However, DIPNECH encompasses symptomatic patients with airway disease, as well as asymptomatic patients with neuroendocrine Cell Hyperplasia associated with multiple tumourlets/carcinoid tumours. DIPNECH is also considered a pre-neoplastic lesion in the spectrum of pulmonary neuroendocrine tumours, because it is commonly found in patients with peripheral carcinoid tumours. In this review, we summarise clinical, physiological, radiological and histological features of DIPNECH and critically discuss recently proposed diagnostic criteria. In addition, we propose that the term "DIPNECH syndrome" be used to indicate a sufficiently distinct patient subgroup characterised by respiratory symptoms, airflow obstruction, mosaic attenuation with air trapping on chest imaging and constrictive obliterative bronchiolitis, often with nodular proliferation of neuroendocrine Cells with/without tumourlets/carcinoid tumours on histology. Surgical lung biopsy is the diagnostic gold standard. However, in the appropriate clinical and radiological setting, transbronchial lung biopsy may also allow a confident diagnosis of DIPNECH syndrome.

Alberto Cavazza - One of the best experts on this subject based on the ideXlab platform.

  • diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia dipnech syndrome and carcinoid tumors with without nech a clinicopathologic radiologic and immunomolecular comparison study
    The American Journal of Surgical Pathology, 2018
    Co-Authors: Mc Mengoli, Em Silini, Giulio Rossi, Alberto Cavazza, Renato Franco, Federica Zito Marino, Mario Migaldi, Letizia Gnetti, Luca Ampollini, Marcello Tiseo
    Abstract:

    The diagnostic criteria of diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia (DIPNECH) are not well defined, and DIPNECH can be mistaken for carcinoids associated with neuroendocrine Cell Hyperplasia (NECH). In this study, we compared clinical, radiologic, histologic, immunohistochemical,

  • Diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia syndrome
    European Respiratory Journal, 2016
    Co-Authors: Giulio Rossi, Alberto Cavazza, Paolo Spagnolo, Nicola Sverzellati, Lucia Longo, Agita Jukna, Gloria Montanari, Cristiano Carbonelli, Giada Vincenzi, Giuseppe Bogina
    Abstract:

    The term diffuse idiopathic pulmonary neuroendocrine Cell Hyperplasia (DIPNECH) may be used to describe a clinico-pathological syndrome, as well as an incidental finding on histological examination, although there are obvious differences between these two scenarios. According to the World Health Organization, the definition of DIPNECH is purely histological. However, DIPNECH encompasses symptomatic patients with airway disease, as well as asymptomatic patients with neuroendocrine Cell Hyperplasia associated with multiple tumourlets/carcinoid tumours. DIPNECH is also considered a pre-neoplastic lesion in the spectrum of pulmonary neuroendocrine tumours, because it is commonly found in patients with peripheral carcinoid tumours. In this review, we summarise clinical, physiological, radiological and histological features of DIPNECH and critically discuss recently proposed diagnostic criteria. In addition, we propose that the term "DIPNECH syndrome" be used to indicate a sufficiently distinct patient subgroup characterised by respiratory symptoms, airflow obstruction, mosaic attenuation with air trapping on chest imaging and constrictive obliterative bronchiolitis, often with nodular proliferation of neuroendocrine Cells with/without tumourlets/carcinoid tumours on histology. Surgical lung biopsy is the diagnostic gold standard. However, in the appropriate clinical and radiological setting, transbronchial lung biopsy may also allow a confident diagnosis of DIPNECH syndrome.

Koichiro Matsumoto - One of the best experts on this subject based on the ideXlab platform.

  • differential regulation by glucocorticoid of interleukin 13 induced eosinophilia hyperresponsiveness and goblet Cell Hyperplasia in mouse airways
    American Journal of Respiratory and Critical Care Medicine, 2003
    Co-Authors: Atsuko Kibe, Hiromasa Inoue, Satoru Fukuyama, Kentaro Machida, Koichiro Matsumoto
    Abstract:

    Interleukin (IL)-13 induces important features of bronchial asthma such as eosinophilic infiltration, airway hyperresponsiveness (AHR), and mucus hypersecretion. Although glucocorticoids suppress airway inflammation and remain the most effective therapy for asthma, the effects of glucocorticoids on the IL-13–dependent features are unknown. We studied the effects of dexamethasone on eotaxin production, eosinophil accumulation, goblet Cell Hyperplasia, and AHR after IL-13 administration into the airways of mice in vivo. MUC5AC gene expression, a marker of goblet Cell Hyperplasia, was also analyzed. IL-13 alone dose dependently induced AHR. Treatment with dexamethasone inhibited eotaxin expression and completely abolished eosinophil accumulation, but it did not affect AHR, MUC5AC overexpression, or goblet Cell Hyperplasia induced by IL-13. The effects of tumor necrosis factor-α on IL-13–induced AHR were also examined. Tumor necrosis factor-α did not affect AHR despite marked enhancement of eosinophil infiltr...

Marcello Tiseo - One of the best experts on this subject based on the ideXlab platform.

Scott Akers - One of the best experts on this subject based on the ideXlab platform.