Background: The development of Castleman's disease in the pulmonary hilum is extremely rare. Alth... more Background: The development of Castleman's disease in the pulmonary hilum is extremely rare. Although resection of only the lesion is sufficient because of its benign nature, lobectomy or more extensive procedures performed for the pulmonary hilar tumor have been reported. Case presentation: The patient was a 15-year-old male with a tumor in the right pulmonary hilum. Endobronchial ultrasound-guided transbronchial needle aspiration was performed but no specific findings were obtained from the cytological and histological evaluation. 18F-fluorodeoxyglucose positron emission tomography showed moderate accumulation in the tumor, which suggested potential malignancy. Intraoperative frozen section diagnosis did not show any malignant findings. Thus, we performed only tumor enucleation without any lung resection. The pathological diagnosis was hyaline vascular type Castleman's disease. No recurrence has been observed for seven years. Conclusion: Because hyaline vascular type Castleman's disease in solitary pulmonary hilar tumor is one of the benign diseases common in young people, intraoperative frozen section diagnosis is recommended to avoid unnecessary lung resection.
A 65-year-old man presented with cough and hoarseness for 3 months and was admitted to our hospit... more A 65-year-old man presented with cough and hoarseness for 3 months and was admitted to our hospital. Chest computed tomography revealed tumor around the aortic arch. Fluorodeoxyglucose positron emission tomography showed an accumulation in the same area of maximum standardized uptake value of 10.8 (Figs. 1, 2). Although endobronchial ultrasound-guided transbronchial needle aspiration failed to obtain a histological diagnosis, mediastinal type lung cancer with aortic invasion was strongly suspected. Therefore, videoassisted thoracoscopic surgery was conducted. Because of lung adhesions, both the aortic arch and left main pulmonary artery were difficult to identify. Therefore, to avoid aortic injury, biopsy sites were restricted. We obtained two puncture biopsies, but could not obtain a histological diagnosis. Moreover, we could not obtain a diagnosis by permanent specimen. However, polymerase chain reaction using a biopsy specimen revealed the presence of Mycobacterium intracellulare deoxyribonucleic acid. Mycobacterial culture also showed the same result. Thus, we started to treat the patient for nontuberculous mycobacteria (NTM) with clarithromycin 800 mg, rifampicin 450 mg, and
American Journal of Respiratory Cell and Molecular Biology, 2013
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator that activates many antioxi... more Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator that activates many antioxidant enzymes. Oxidative stress, which accumulates in diseased lungs associated with pulmonary hypertension (PH), is thought to be responsible for the progression of cardiopulmonary changes. To test whether Nrf2 activation would exert therapeutic efficacy against cardiopulmonary changes in a hypoxiainduced PH model, wild-type (WT) and Nrf2-deficient mice as well as Kelch-like ECH associating protein 1 (Keap1) (negative regulator of Nrf2) knockdown mutant mice were exposed to hypobaric hypoxia for 3 weeks. This chronic hypoxia exacerbated right ventricular systolic pressure, right ventricular hypertrophy (RVH), and pulmonary vascular remodeling in the WT mice. These pathological changes were associated with aberrant accumulation of Tenascin-C, a disease-indicative extracellular glycoprotein. Simultaneous administration of oltipraz, a potent Nrf2 activator, significantly attenuated RVH and pulmonary vascular remodeling and concomitantly ameliorated Tenascin-C accumulation in the hypoxic mice. Hypoxia-exposed Nrf2deficient mice developed more pronounced RVH than WT mice, whereas hypoxia-exposed Keap1-knockdown mice showed less RVH and pulmonary vascular remodeling than WT mice, underscoring the beneficial potency of Nrf2 activity against PH. We also demonstrated that expression of the Nrf2-regulated antioxidant enzymes was decreased in a patient with chronic obstructive pulmonary disease associated with PH. The decreased antioxidant enzymes may underlie the pathogenesis of cardiopulmonary changes in the patient with chronic obstructive pulmonary disease and PH. The pharmacologically or genetically induced Nrf2 activity clearly decreased RVH and pulmonary vascular remodeling in the hypoxic PH model. The efficacy of oltipraz highlights a promising therapeutic potency of Nrf2 activators for the prevention of PH in patients with hypoxemic lung disease.
Background: The development of Castleman's disease in the pulmonary hilum is extremely rare. Alth... more Background: The development of Castleman's disease in the pulmonary hilum is extremely rare. Although resection of only the lesion is sufficient because of its benign nature, lobectomy or more extensive procedures performed for the pulmonary hilar tumor have been reported. Case presentation: The patient was a 15-year-old male with a tumor in the right pulmonary hilum. Endobronchial ultrasound-guided transbronchial needle aspiration was performed but no specific findings were obtained from the cytological and histological evaluation. 18F-fluorodeoxyglucose positron emission tomography showed moderate accumulation in the tumor, which suggested potential malignancy. Intraoperative frozen section diagnosis did not show any malignant findings. Thus, we performed only tumor enucleation without any lung resection. The pathological diagnosis was hyaline vascular type Castleman's disease. No recurrence has been observed for seven years. Conclusion: Because hyaline vascular type Castleman's disease in solitary pulmonary hilar tumor is one of the benign diseases common in young people, intraoperative frozen section diagnosis is recommended to avoid unnecessary lung resection.
A 65-year-old man presented with cough and hoarseness for 3 months and was admitted to our hospit... more A 65-year-old man presented with cough and hoarseness for 3 months and was admitted to our hospital. Chest computed tomography revealed tumor around the aortic arch. Fluorodeoxyglucose positron emission tomography showed an accumulation in the same area of maximum standardized uptake value of 10.8 (Figs. 1, 2). Although endobronchial ultrasound-guided transbronchial needle aspiration failed to obtain a histological diagnosis, mediastinal type lung cancer with aortic invasion was strongly suspected. Therefore, videoassisted thoracoscopic surgery was conducted. Because of lung adhesions, both the aortic arch and left main pulmonary artery were difficult to identify. Therefore, to avoid aortic injury, biopsy sites were restricted. We obtained two puncture biopsies, but could not obtain a histological diagnosis. Moreover, we could not obtain a diagnosis by permanent specimen. However, polymerase chain reaction using a biopsy specimen revealed the presence of Mycobacterium intracellulare deoxyribonucleic acid. Mycobacterial culture also showed the same result. Thus, we started to treat the patient for nontuberculous mycobacteria (NTM) with clarithromycin 800 mg, rifampicin 450 mg, and
American Journal of Respiratory Cell and Molecular Biology, 2013
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator that activates many antioxi... more Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator that activates many antioxidant enzymes. Oxidative stress, which accumulates in diseased lungs associated with pulmonary hypertension (PH), is thought to be responsible for the progression of cardiopulmonary changes. To test whether Nrf2 activation would exert therapeutic efficacy against cardiopulmonary changes in a hypoxiainduced PH model, wild-type (WT) and Nrf2-deficient mice as well as Kelch-like ECH associating protein 1 (Keap1) (negative regulator of Nrf2) knockdown mutant mice were exposed to hypobaric hypoxia for 3 weeks. This chronic hypoxia exacerbated right ventricular systolic pressure, right ventricular hypertrophy (RVH), and pulmonary vascular remodeling in the WT mice. These pathological changes were associated with aberrant accumulation of Tenascin-C, a disease-indicative extracellular glycoprotein. Simultaneous administration of oltipraz, a potent Nrf2 activator, significantly attenuated RVH and pulmonary vascular remodeling and concomitantly ameliorated Tenascin-C accumulation in the hypoxic mice. Hypoxia-exposed Nrf2deficient mice developed more pronounced RVH than WT mice, whereas hypoxia-exposed Keap1-knockdown mice showed less RVH and pulmonary vascular remodeling than WT mice, underscoring the beneficial potency of Nrf2 activity against PH. We also demonstrated that expression of the Nrf2-regulated antioxidant enzymes was decreased in a patient with chronic obstructive pulmonary disease associated with PH. The decreased antioxidant enzymes may underlie the pathogenesis of cardiopulmonary changes in the patient with chronic obstructive pulmonary disease and PH. The pharmacologically or genetically induced Nrf2 activity clearly decreased RVH and pulmonary vascular remodeling in the hypoxic PH model. The efficacy of oltipraz highlights a promising therapeutic potency of Nrf2 activators for the prevention of PH in patients with hypoxemic lung disease.
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Papers by Yui Watanabe