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Radiology · Chest Radiology

Nonspecific interstitial pneumonia

Pneumonia interstitialis non-specifica

Nonspecific interstitial pneumonia (NSIP) is a form of interstitial lung disease characterized on HRCT by bilateral "ground-glass opacity" with prominent sparing of the subpleural regions. It is often considered in the differential diagnosis of other pathologies, such as respiratory bronchiolitis and desquamative interstitial pneumonia, requiring careful analysis of radiological patterns.

Key sign of NSIPFocal bilateral ground-glass opacities on tomograms
Distribution specificsSparing of subpleural regions (subpleural sparing) with uniform involvement
Risk factor for RB-ILDSmoking association: identified predominantly in heavy smokers
Low sensitivityConventional chest radiography may be normal in 20–25% of patients with RB-ILD and DIP
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Tomographic presentation of nonspecific interstitial pneumonia (NSIP)

High-resolution computed tomography (HRCT) serves as the primary tool for detecting nonspecific interstitial pneumonia. The radiological picture has several distinct patterns that allow differentiating this condition from other pulmonary parenchymal lesions.

  • Dominant sign: presence of bilateral focal ground-glass opacities of the lung tissue (ground-glass opacification).
  • Distribution of changes: the pathological process spreads uniformly throughout the lung volume. At the same time, a predominantly peribronchovascular localization is noted.
  • Specific feature: the most important diagnostic criterion is the pronounced sparing, i.e., absolute preservation, of the subpleural regions of the lungs (subpleural sparing).

In addition to the main pattern, concomitant changes may be visualized on tomograms. These include mild reticular changes (mild reticulation) and the formation of mild traction bronchiectasis (traction bronchiectasis). The absence of severe deformation distinguishes this form from more severe fibrosing processes.

Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD)

Respiratory bronchiolitis-associated interstitial lung disease (Respiratory Bronchiolitis–Interstitial Lung Disease, RB-ILD) is closely associated with tobacco smoke exposure and is diagnosed predominantly in heavy smokers. The disease manifests insidiously, with the gradual onset of cough and progressive dyspnea (dyspnoea).

Classic chest radiography in this pathology has low diagnostic value. In almost 20% of patients, the radiograph remains completely normal.

HRCT reveals the following characteristic changes:

  1. Distribution: the pathological process is localized predominantly in the upper lobes of the lungs.
  2. Main pattern: focal ground-glass opacities, which are pathomorphologically caused by massive accumulation of macrophages in the lumens of alveoli and alveolar ducts.
  3. Focal opacities: ill-defined centrilobular nodules of decreased density are formed. They have a typical "fluffy" (fluffy) appearance.

As additional signs, areas of "air trapping" (air trapping) indicating a bronchiolitic component of the lesion, and limited centrilobular emphysema of the upper lobes may be visualized. Scattered interlobular septal thickening and mild signs of interstitial fibrosis occur, but never act as the dominant pattern.

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Desquamative interstitial pneumonia (DIP)

Desquamative interstitial pneumonia (Desquamative Interstitial Pneumonia, DIP) represents another variant of pulmonary parenchymal involvement. As with RB-ILD, standard chest radiography is often uninformative: up to 25% of patients have a normal radiological picture.

HRCT findings in DIP have their distinctive features:

  • Leading symptom: extensive ground-glass opacity of the lung tissue.
  • Localization: unlike RB-ILD, changes are typically concentrated in the lower zones of the lungs and have a peripheral distribution.
  • Form of involvement: the pattern can be focal or form extensive "geographic" zones.

In a certain proportion of patients, signs of pulmonary fibrosis develop. This is manifested by disruption of normal lung architecture and dilatation (expansion) of some bronchi, although the extent of these changes usually remains limited.

General aspects of RB-ILD and DIP course

Respiratory bronchiolitis-ILD and desquamative interstitial pneumonia share a number of common clinical characteristics. First of all, both nosological forms can coexist in the same patient to varying degrees of severity, indicating the commonality of their pathogenetic mechanisms related to the pulmonary tissue reaction.

Most patients with a verified diagnosis of DIP or RB-ILD are characterized by a relatively stable clinical course without rapid deterioration of respiratory function. The most important, decisive role in the management of such patients is played by non-specific therapy—complete and unconditional smoking cessation (smoking cessation), which stops the progression of interstitial changes.

Briefly: answers to topical questions

What histological variants of nonspecific interstitial pneumonia are distinguished?

Two histological variants of nonspecific interstitial pneumonia are distinguished: cellular and fibrotic.

  • Cellular type — characterized by a predominance of lymphocytes in the infiltrate and a bronchiolocentric distribution (found as an isolated pattern or in typical hypersensitivity pneumonitis).
  • Fibrotic type (fibrotic NSIP) — is the most frequent pattern of lung involvement (e.g., in systemic sclerosis).

What groups of drugs are used for the medical treatment of nonspecific interstitial pneumonia?

Corticosteroids and immunosuppressive therapy are used for the medical treatment of NSIP, particularly in polymyositis or dermatomyositis. NSIP in polymyositis or dermatomyositis usually responds well to corticosteroids and immunosuppression.

With which interstitial lung diseases should NSIP be differentiated, in addition to RB-ILD and DIP?

NSIP must be differentiated from usual interstitial pneumonia and other interstitial lung diseases, including hypersensitivity pneumonitis, eosinophilic pneumonia, sarcoidosis, cryptogenic organizing pneumonia, and lymphocytic interstitial pneumonia. In NSIP, fibrosis is generally uniform temporally; fibroblastic foci and "honeycombing" are absent or sparsely represented. According to BAL data, neutrophils are more numerous in IPF than in hypersensitivity pneumonitis, NSIP, and eosinophilic pneumonia; eosinophils are fewer than in eosinophilic pneumonia; lymphocytes are fewer than in NSIP, sarcoidosis, cryptogenic organizing pneumonia, and lymphocytic interstitial pneumonia; the CD4/CD8 ratio is lower than in sarcoidosis and higher than in NSIP.

How to memorize

For NSIP, it is easy to remember the rule: "NSIP — Non-affected SubPleural zone" (subpleural sparing).

Class and exam questions

What is the dominant HRCT sign in nonspecific interstitial pneumonia?

The dominant sign is bilateral focal ground-glass opacities with mild reticular changes.

In which parts of the lungs are changes predominantly localized in RB-ILD and DIP?

In RB-ILD, the upper lobes are predominantly affected, whereas DIP is typically characterized by lower zone involvement and peripheral distribution.

Are changes on conventional chest radiography always visible in interstitial lung diseases?

No, conventional chest radiography has low sensitivity. Up to 20% of patients with RB-ILD and up to 25% with DIP have a normal radiograph.

What conservative measure is the main one in the treatment of patients with RB-ILD and DIP?

The most important role in the management of patients with these diseases is played by complete smoking cessation (smoking cessation).

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What else to study on this topic

  • Pathomorphological substrate of the "ground-glass" sign during macrophage accumulation.
  • Differential diagnosis of the "air trapping" pattern on HRCT.
  • Mechanism of centrilobular emphysema formation in heavy smokers.
  • Traction bronchiectasis: causes of formation in interstitial fibrosis.

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