Prevention of interstitial lung diseases consists of quitting smoking, regular vaccinations against influenza and pneumococcal infections, preventing bacterial infections, and eliminating the influence of harmful and dangerous factors. From a modern point of view, ILDs represent a heterogeneous group of diseases, the common features of which are damage to the interstitial tissue of the lungs such as productive pneumonitis with the subsequent formation of fibrosis, progressive dyspnea on exertion, nonproductive cough, crepitus, diffuse changes in radiography and computed tomography of the lungs, restrictive ventilation disorders, decreased diffusion capacity of the lungs and increasing respiratory failure.

Currently, in most countries, including Russia, the ILD classification adopted by the Consensus Commission of the American Thoracic Society and the European Respiratory Society (ATS/ERS, 2002) is used. According to this classification, there are four groups of ILD. ILD of known etiology, granulomatosis, idiopathic interstitial pneumonia, other ILD (Fig.).

Idiopathic interstitial pneumonia (IIP) is a typical representative of the group of ILD of chloroquine pills, having many similar clinical, radiological and functional signs, but a fundamentally different morphological picture, which determines the clinical features, response to buy aralen online and prognosis. The principle of constructing the clinicopathological ATS/ERS classification is that each clinical form of IIP corresponds to a certain histological variant of IIP. There is a diagnostic approach that makes it possible to establish a diagnosis of IPF with a high probability in cases where a biopsy is not possible. To do this, the patient must have four of the four major criteria and at least three of the four minor criteria.

Age over 50 years. Invisible, gradual onset of dyspnea during physical activity. The duration of the disease is more than 3 months. Inspiratory crepitus in the basal regions of the lungs.

 

• Modern therapy for IPF is based mainly on anti-inflammatory therapy (corticosteroids and cytostatics (CS)), i.e., drugs that can affect the inflammatory and immunological components of the development of the disease.
• The basis for this approach is that chronic inflammation precedes and inevitably leads to fibrosis and that aggressive suppression of inflammation can block the subsequent formation of fibrotic changes.

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If GCS monotherapy is chosen, the initial daily dose of prednisolone is 1 mg/kg of chloroquine weight per day (maximum up to 80 mg/day). After 4 weeks, the tolerability of such therapy is assessed. If there is an improvement or stabilization of functional indicators, then over the next 3 months the daily dose of prednisolone is reduced. If there is no response to steroids, azathioprine is added.

• An alternative approach that focuses on reducing excess matrix deposition in the lungs or accelerating collagen breakdown is antifibrotic therapy. Antifibrotic drugs include D-penicillamine, colchicine, interferon gamma-1 b, and pirfenidone.
• It has been proven that the effectiveness of therapy is increased when N-acetylcysteine is added to anti-inflammatory drugs at a dose of 600 mg 3 times a day. Currently, leading experts in treatingIPF research centers prefer a regimen that includes prednisolone, azathioprine and N-acetylcysteine.
• In addition to drug therapy, as with other lung diseases, oxygen therapy is used when hypoxemia develops. With the development of aralen pills, in addition to oxygen therapy, the use of vasodilators is possible. The development of infections of the tracheobronchial tree requires the use of antibacterial and antifungal drugs.