Interstitial lung disease is the most common pulmonary complication in patients with inflammatory myopathy, with a high case fatality rate, unknown pathogenesis, and complex clinical manifestations, and the treatment is difficult. Early and timely treatment can improve the patient’s clinical symptoms and inhibit the development of the disease. The present treatment protocols can be mainly summarized as the commonly used drugs (corticosteroids, azathioprine, cyclophosphamide, mycophenolate mofetil, and intravenous immunoglobulin) and new drugs (cyclosporin A, tacrolimus, biological agents, and anti-fibrosis drug), etc. In this paper, the treatment progress of inflammatory myopathy-related interstitial lung disease and different myositis antibody-related interstitial lung disease in recent years at home and abroad is reviewed, so as to provide a basis for clinical treatment.
Melanoma differentiation associated gene 5 (MDA5) antibody is a kind of myositis-specific autoantibodies, which can be used as a biological marker for dermatomyositis (DM) patients. It has been shown that this antibody is closely related to the occurrence of interstilung disease (ILD) in DM patients, which may lead to rapidly progressive interstitial lung disease in DM patients with MDA5 antibody positive, leading to a higher mortality rate. Therefore, the early detection, diagnosis and treatment of this disease have attracted the attention of clinical workers. In this paper, the progress of diagnosis and treatment of MDA5 antibody-positive DM with ILD is reviewed.
After pirfenidone and nintedanib showed efficacy, drug treatment for idiopathic pulmonary fibrosis began to focused on anti-fibrosis. Current research on idiopathic pulmonary fibrosis mainly focus on the pathogenesis and therapeutic targets, and more targeted drugs are gradually entering clinical trials. This article summarizes the results of recent studies on the treatment of idiopathic pulmonary fibrosis with pirfenidone and nintedanib alone or in combination by searching the literature, and reviews the mechanism and test results of the new target anti-fibrosis drugs based on molecular biology that are currently undergoing clinical research in various phases, and aims to provide a basis for how to choose drugs to treat idiopathic pulmonary fibrosis.
Extrinsic allergic alveolitis is a general term for type Ⅲ or Ⅳ allergic pneumonia caused by repeated inhalation of various antigenic organic dusts and low molecular weight chemicals in susceptible people. The lesions involve alveolar, pulmonary interstitial, and airway. The main clinical manifestations are cough, expectoration, and dyspnea. Clinically, extrinsic allergic alveolitis is classified into acute, subacute, and chronic forms. Extrinsic allergic alveolitis has a great impact on the pulmonary function of patients. Timely treatment will improve clinical symptoms and inhibit the development of disease. The current treatment plan is mainly avoiding exposure to antigen, glucocorticoid therapy, immunosuppressive therapy, anti-fibrotic therapy, and lung transplantation.