Desquamative interstitial pneumonia

Liebow, Averill A.; Steer, Arthur; Billingsley, James G.

doi:10.1016/0002-9343(65)90206-8

Cited by 423 publications

(200 citation statements)

References 36 publications

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“…' Section of Pathology (Meeting 9 November 1976) Lastly (5) there is a group of cases in which the cause is unknown. Cryptogenic fibrosing alveolitis is the commonest condition and is called UIP (usual interstitial pneumonia) in America (Liebow 1975) to distinguish it from the variants DIP (desquamative interstitial pneumonia) (Liebow et al 1965), LIP (lymphoid interstitial pneumonia, which when localized is also called pseudolymphoma) (Liebow & Carrington 1973), GIP (giant-cell interstitial pneumonia, which is very uncommon) and BIP (interstitial pneumonia with bronchiolitis). The usual (or mural) and desquamative variants also affect the lower zones predominantly and the pathogenesis is probably the same as with diffuse alveolar damage, but the process is slower.…”

Section: Interstitial Lung Diseaselmentioning

confidence: 99%

Interstitial Lung Disease

2010

Handbook of Disease Burdens and Quality of Life Measures

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Section: Interstitial Lung Diseaselmentioning

confidence: 99%

Interstitial Lung Disease

2010

Handbook of Disease Burdens and Quality of Life Measures

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“…At the same time, RB-ILD has been distinguished from the more exaggerated panlobular diffuse mild-to-moderate interstitial fibrosis and massive accumulation of macrophages in the alveoli described in DIP [33]. Both of these uncommon conditions have significant clinical and histopathologic overlap [34] and were suggested to be synonymous [7,11,35].…”

Section: Etiology and Pathogenesismentioning

confidence: 99%

Respiratory Bronchiolitis with Interstitial Lung Disease

Galanski¹

2010

Thoracic Imaging

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Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) is a rare, mild inflammatory pulmonary disorder that occurs almost exclusively in current or former heavy smokers, usually between the third and sixth decades, most likely with no gender predilection. The onset is usually insidious with exertional dyspnea and persistent cough, which may be non-productive, developing over a course of weeks or months. RB-ILD may also be diagnosed in asymptomatic patients with functional impairment and chest radiograph or high-resolution computed tomography (HRCT) abnormalities. Histologically, RB-ILD is characterized by the accumulation of yellow-brown pigmented macrophages within the lumens of respiratory bronchioles and alveolar ducts, associated with a patchy submucosal and peribronchiolar chronic inflammation. Common findings also include mild bronchiolar and peribronchiolar alveolar fibrosis that expands contiguous alveolar septa and leads to architectural distortion as well as centrilobular emphysema. Chest radiographs in patients with RB-ILD typically show fine reticulonodular interstitial opacities, while on HRCT central and peripheral bronchial wall thickening, centrilobular nodules, and ground-glass opacities associated with upper lobe centrilobular emphysema are most frequently reported. Pulmonary function testing may be normal but usually demonstrates mixed, predominantly obstructive abnormalities, often combined with hyperinflation and usually associated with a mild to moderate reduction in carbon monoxide diffusion capacity (DLco). The course of RB-ILD is heterogeneous. Some patients respond favorably to corticosteroids and/or smoking cessation, but often there is no functional improvement and the disease progresses despite smoking cessation and treatment.

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“…DISCUSSION DIP is one of the seven different clinico-pathological entities included in the group of the idiopathic interstitial pneumonias (IIPs), according to the recent consensus classification, and affects primarily cigarette smokers in their fourth and fifth decades of life [1]. It was first described by LIEBOW et al [2] in 1965 as a distinct entity and was included in his first classification of the IIPs in 1975 [3]. It soon appeared that patients with DIP had a better prognosis [4], and, therefore, DIP has erroneously been considered to be an early stage of the fibrotic usual interstitial pneumonia.…”

Section: Diagnosis: Desquamative Interstitial Pneumonia (Dip)mentioning

confidence: 99%

“…It soon appeared that patients with DIP had a better prognosis [4], and, therefore, DIP has erroneously been considered to be an early stage of the fibrotic usual interstitial pneumonia. The histological hallmark of DIP is an abnormal accumulation of pigmented macrophages (''smoker's pigment'') evenly dispersed within the distal air spaces [2,3,5]. The inflammatory process affects the lung almost uniformly, the presence of fibrosis is minimal or absent, and the alveolar architecture is usually well preserved [1][2][3]5].…”

Section: Diagnosis: Desquamative Interstitial Pneumonia (Dip)mentioning

confidence: 99%

“…The histological hallmark of DIP is an abnormal accumulation of pigmented macrophages (''smoker's pigment'') evenly dispersed within the distal air spaces [2,3,5]. The inflammatory process affects the lung almost uniformly, the presence of fibrosis is minimal or absent, and the alveolar architecture is usually well preserved [1][2][3]5]. This clinico-pathological entity might be better described by the term ''alveolar macrophage pneumonia'', since its characteristic inflammatory infiltrate does not represent desquamation of alveolar epithelial cells, but a true abnormal accumulation of macrophages.…”

Section: Diagnosis: Desquamative Interstitial Pneumonia (Dip)mentioning

confidence: 99%

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Dry cough and dyspnoea rapidly increasing to respiratory failure in a male smoker

Sigala

Kalomenidis²,

Malagari³

et al. 2005

European Respiratory Journal

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A 65-yr-old male, current smoker of .30 cigarettes?day -1 (total smoking history 150 pack-yrs), who was working as a bus driver, presented at the Evangelismos Hospital (Athens, Greece) complaining of increasing breathlessness on exertion and dry cough during the past 2 months. He had no animal exposure and he hadn't travelled abroad during the last few years. His medical history showed arterial hypertension, for which he was receiving treatment with an angiotension-converting enzymeinhibitor (ramipril) plus hydrochlorothiazide, as well as asymptomatic cholelithiasis and prostate hypertrophy for which he was receiving tamsulosin hydrochloride. He did not mention suffering from fever in the last few months.On admission, the patient was mildly tachypnoeic (22 breaths? min -1 ), but apparently in discrete health, with a body temperature of 36.8˚C, pulse rate 85 beats?min -1 and blood pressure 130/70 mmHg. On chest auscultation, rare fine inspiratory rales were audible over both hemithoraces. He had no clubbing. The tuberculin test was negative. The routine blood analysis and chemistry was normal. Arterial blood gas analysis while breathing room air gave results as follows: arterial oxygen tension (Pa,O 2 ) 7.95 kPa; carbon dioxide arterial tension (Pa,CO 2 ) 3.94 kPa; pH: 7.45. Chest radiography on admission is shown in figure 1. Spirometry 2 days later was compatible with a moderate restrictive pattern (forced vital capacity (FVC): 1.52 L (48% predicted); forced expiratory volume in one second (FEV1): 1.28 L?sec -1 (53.6% pred); FEV1/FVC6100 ratio: 84%). Lung volumes and diffusing capacity could not be assessed because the patient was unable to cooperate. A bronchoscopy was performed on the 4th day of hospitalisation and no endobronchial abnormalities were found. Bronchoalveolar lavage (BAL) was performed during bronchoscopy and the total cell count was 26.6610, with a differential of 82% macrophages, 12% lymphocytes and 6% neutrophils. No infective agents were detected in sputum or in bronchial secretions. Serology for HIV infection was negative, as was the urinary test for Legionella pneumophila and Streptococcus pneumoniae. Serology for common virus, and mycoplasma, ricketsiae and chlamydiae were pending. No underlying immunosuppressive condition was evident.During the 2-3 days following bronchoscopy, the patient's respiratory condition rapidly deteriorated. Respiratory rate was 34 breaths?min -1 and pulse rate 130 beats?min -1 . Arterial blood gases on supplemental oxygen and fractional concentration of oxygen in inspired gas 60% were: Pa,O 2 9.24 kPa; Pa,CO 2 4.2 kPa; pH 7.44. However, he remained afebrile and the new haematology and biochemical laboratory studies, including total and differential white cell blood count, were within the normal range.Another chest radiograph obtained on the 7th day of his hospital stay, is shown in figure 2, and the chest computed tomography (CT) obtained at the same time point is shown in figure 3. During the next few hours, the patient was admitted to the intensive care unit ...

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Desquamative interstitial pneumonia

Cited by 423 publications

References 36 publications

Interstitial Lung Disease

Interstitial Lung Disease

Respiratory Bronchiolitis with Interstitial Lung Disease

Dry cough and dyspnoea rapidly increasing to respiratory failure in a male smoker

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