Is Interstitial Lung Disease Contagious?
Is Interstitial Lung Disease Contagious?
The usual interstitial pneumonitis (idiopathic pulmonary fibrosis) is not contagious. A lesion is produced in the alveolus that stimulates fibrosis. The cause is unknown, but it is not due to an infectious cause, therefore: it does not spread and become contagious.
Diffuse interstitial lung diseases (DILD) constitute a very heterogeneous group of conditions that have clinical, radiological and functional manifestations, in the which the main anatomopathological alterations affect alveolointerstitial structures, that means that they affect the epithelium, the alveolar walls, the capillary endothelium and the connective tissue (perilymphatic and perivascular) comprised between the septa and located in the peribronchiolar tissue.
More than 150 entities are known, although it is only possible to identify the causal agent in about a third of the cases. Three groups are distinguished. The first group is constituted by idiopathic interstitials pneumonia, which is of unknown cause. The second group includes those entities of a known cause or associated with other diseases, including those associated with collagen diseases, caused by drugs, organic dust (extrinsic allergic alveolitis), inorganic dust (pneumoconiosis) and those associated with hereditary diseases. The third group consists of a set of entities that, despite being idiopathic, have well-defined clinical and histological features.
Most of these entities have a similar pathogenesis. Theories accepted in the past held that, as a consequence of the action of a causative agent (known or not), lesions occur at the level of the alveolar epithelium, activating the inflammatory cells (macrophages, neutrophils, eosinophils, mast cells, lymphocytes) and parenchymal cells (fibroblasts, epithelial cells) that secrete cellular mediators (cytokines, free radicals...) that act in an autocrine and/or paracrine way, giving rise to chronic alveolar inflammation (alveolitis) and the appearance of pulmonary fibrosis.
In the case of idiopathic pulmonary fibrosis, recent studies consider that inflammation is a secondary phenomenon. The new theories postulate that the main event in the development of this disease would be the cellular lesion of the alveolar epithelium, which would stimulate the proliferation of fibroblasts and the development of fibrosis. This would explain in a certain way the ineffectiveness of anti-inflammatory treatments based on the use of corticosteroids.
Not all DILD lead to pulmonary fibrosis, there are certain factors that modulate evolution from alveolitis to pulmonary fibrosis.
Among them, it is worth noting the nature of the etiological agent, the integrity of the basement membrane of the pulmonary interstitium, the genetic predisposition, and hereditary factors.
It usually occurs after 50 years, with an insidious onset, in the form of progressive dyspnea and dry cough. In the physical examination, doctors will find crepitant type velcro in 90% and acropachy in 20-50% of cases. There is a form of familial pulmonary fibrosis that affects two or more members of the same family, with similar characteristics but with earlier onset.
Radiological studies show infiltrates peripheral reticules more marked in bases associated with honeycombing and loss of volume of lower lobes and extensive architectural distortion.
Tobacco: Some entities occur with more frequency in smokers, such as desquamative interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease, and histiocytosis X. Smokers are less susceptible to presenting sarcoidosis or hypersensitivity pneumonitis.
A history of smoking can lead to the coexistence of chronic obstructive pulmonary disease.
Age and sex: Some DILD are more frequent between 20-40 years of age, as is the case of sarcoidosis and histiocytosis X. On the contrary, the majority of patients with idiopathic pulmonary fibrosis (IPF) are older than 55 years. Lymphangioleiomyomatosis occurs exclusively in women of childbearing age.
Occupation, hobbies, trips, environment: History of exposure, its duration and whether it carried out respiratory protection.
Family background: 5% of the IPF can be transmitted in a family. The alveolar microlithiasis, tuberous sclerosis, and neurofibromatosis are examples of DILD with a hereditary history.
Previous treatments: Chemotherapy, radiotherapy. There is a wide list of drugs capable of causing interstitial disease.
- Consumption of drugs.
- Symptoms of systemic diseases.
- Risk factors for HIV, due to possible opportunistic diseases.
There are three well-distinguished groups of interstitial lung diseases, most of them of unknown cause.
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