Decreased tobacco-glycoprotein-induced lymphocyte proliferation in vitro in pulmonary eosinophilic granuloma.

Youkeles, Lisa H.; Grizzanti, Joseph N.; Liao, Zenghua; Chang, Chao-Yu; Rosenstreich, David L.

doi:10.1164/ajrccm.151.1.7812544

Cited by 56 publications

(20 citation statements)

References 23 publications

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“…An immune response to a component of tobacco smoke has been suggested, but, surprisingly, proliferation of blood lymphocytes from patients with PLCH in response to tobacco glycoprotein was found to be decreased compared with controls [147]. More recently, the effects of nicotine on DC function were evaluated and both stimulatory and inhibitory effects were reported [148,149].…”

Section: Smoking and Plchmentioning

confidence: 99%

Adult pulmonary Langerhans’ cell histiocytosis

Tazi¹

2006

Eur Respir J

283

297

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Adult pulmonary Langerhans' cell histiocytosis is a rare disorder of unknown aetiology that occurs predominantly in young smokers, with an incidence peak at 20-40 yrs of age. In adults, pulmonary involvement with Langerhans' cell histiocytosis usually occurs as a single-system disease and is characterised by focal Langerhans' cell granulomas infiltrating and destroying distal bronchioles.High-resolution computed tomography (HRCT) of the chest is essential to the diagnosis, typically showing a combination of nodules, cavitated nodules, and thick-and thin-walled cysts. A high macrophage count in bronchoalveolar lavage (BAL) fluid is a common but nonspecific finding that merely reflects exposure to tobacco smoke. BAL is useful for eliminating infections and the other infiltrating lung disorders that can be seen in young adults. Langerhans' cells can be identified in BAL fluid, but, in contrast to what was initially hoped, this test shows a very low sensitivity and is rarely useful in the diagnosis of the disease.The definite diagnosis of pulmonary Langerhans' cell histiocytosis requires identification of Langerhans' cell granulomas, which is usually achieved by surgical lung biopsy at a site selected by chest HRCT. In practice, however, lung biopsy is performed on a case-by-case basis.No effective treatment is available to date, and improved understanding of the mechanisms involved in the pathogenesis of pulmonary Langerhans' cell histiocytosis is urgently needed, and should help in the development of specific therapeutic strategies for patients with this orphan disease.

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Section: Smoking and Plchmentioning

confidence: 99%

Adult pulmonary Langerhans’ cell histiocytosis

Tazi¹

2006

Eur Respir J

283

297

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“…It has been shown that tobacco glycoprotein is a potent stimulator of macrophages, inducing the production of interleukin-1 and interleukin-6 cytokines. 17 Another hypothesis is that the development of hyperplastic or dysplastic bronchiolar lesions may be involved in both the accumulation and the activation of Langerhans cells in bronchioles. 6 This would explain the bronchiole- , x400), C. Cytoplasmic S100 positivity in the histiocytic cells (S100, x400).…”

Section: Discussionmentioning

confidence: 99%

Primary pulmonary Langerhans cell histiocytosis associated with smoking in an adolescent boy

Çıtak

Sağcan

et al. 2017

Turk J Pediatr

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Pulmonary Langerhans cell histiocytosis (PLCH) is a well known entity in adults but is exceedingly rare in children. It is better described in adults than in children. Smoking is a major etiological factor in adulthood. We report a case of a previously healthy 16-year-old male with a history of cigarette smoking, who presented with cough with sputum, breathlessness, easy fatigability and loss of appetite for two weeks. He was first diagnosed with bronchiectasis according to the cystic pulmonary changes demonstrated by computed tomography. After appropriate treatment, there was no sign of clinical improvement. A lung biopsy confirmed Langerhans cell histiocytosis (LCH). The definitive diagnosis was isolated pulmonary LCH. PLCH should be considered in the etiology of cystic lung diseases. Isolated pulmonary LCH is rare so such cases are needed to be reported and followed-up to understand the treatment response and course of this illness.

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“…6 PLHH patogenezi bilinmemektedir, ancak sigaranın tetikleyici bir faktör olduğu dü-şünülmektedir. 7 Yayınlarda hastaların % 90-100'ü sigara içme öyküsü vermektedir. 8,9,10,11 PLHH, 20-40 yaşlarında pik yapar ve erkeklerde biraz daha sık görülür.…”

Section: Discussionunclassified

Pulmonary Langerhans' Cell Histiocytosis and Diabetes Insipidus: On the occasion of two cases

Sezgı¹,

Abakay²,

Tanrıkulu³

et al. 2012

Solunum

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ÖZETPulmoner langerhans hücreli histiyositozis (PLHH), etyolojisi bilinmeyen ve sigara içenlerde görülen, nadir bir interstisyel akciğer hastalığıdır. Hastalıkta genellikle izole akciğer tutulumu vardır ve santral sinir sistemi tutulumu nadirdir. Bu olgu sunumunda, birinde takip, diğerinde ise tanı sırasında santral diabetes insipidus (Dİ) saptanan iki olgu sunulmaktadır. Olgular, yaşları sıra-sıyla 24 ve 39 olan, sigara içme öyküsü olan erkek hastalardı. İki olgunun da yüksek rezolüsyonlu bilgisayarlı tomografilerinde (YRBT) yaygın kistik lezyonlar izlenmiş olup, video-yardımlı torakoskopik cerrahiyle (VATS) alınan biyopsilerinde PLHH saptandı. Takipte solunum fonksiyonlarının bozulmuş olduğu görülen birinci olguya 0,5 mg/kg metil prednisolon başlandı. Bir ay sonra yapılan kontrolde PLHH için kısmi düzelme gözlenmesi üzerine tedavi 6 aya uzatıldı, tedavi bitiminde tam remisyon saptanarak steroid tedavisi kesildi. İki hastaya da Dİ için oral 0,1 mg/gün desmopressin başlandı, bir ay sonra tam klinik düzelme gözlendi.Anah tar kelimeler: Histiyositozis X, pulmoner Langerhan hücreli histiyositozis, diabetes insipidus ABST RACTPulmonary Langerhans' cell histiocytosis (PLCH) is an uncommon interstitial lung disease with an unknown etiology in smokers. Disease is usually seen with isolated lung involvement and central nervous system involvement is rare.Two PLCH cases, with central diabetes insipidus (DI) determined at diagnosis in one of the cases and during follow-up in the other, is being presented in this report. The patients' ages were 39 and 24, respectively and they were both male patients with a history of smoking. Widely cystic lesions were viewed at high-resolution computed tomography scans (HRCT) and PLCH was detected at the biopsies obtained by video-assisted thoracoscopic surgery (VATS), in both two cases. Therapy was started with 0.5 mg/kg methyl prednisolone for latter case, because of impairment in pulmonary function tests during follow up. On control, after one month therapy, partial improvement was seen for PLCH and the therapy was continued up to 6 months. At the end of the therapy complete remission was seen and corticotherapy was stopped. Desmopressin was started for both cases at 0.1 mg/day, orally. After one month of treatment clinical improvement was observed during control.

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Decreased tobacco-glycoprotein-induced lymphocyte proliferation in vitro in pulmonary eosinophilic granuloma.

Cited by 56 publications

References 23 publications

Adult pulmonary Langerhans’ cell histiocytosis

Adult pulmonary Langerhans’ cell histiocytosis

Primary pulmonary Langerhans cell histiocytosis associated with smoking in an adolescent boy

Pulmonary Langerhans' Cell Histiocytosis and Diabetes Insipidus: On the occasion of two cases

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