What Are the Causes of Lung Nodules?

Pulmonary sarcoidosis (sarcoidosis) is a multi-system, multi-organ granulomatous disease of unknown etiology, which often invades the lungs, bilateral hilar lymph nodes, eyes, skin and other organs. Its chest invasion rate is as high as 80% to 90%. .

Pulmonary nodule

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Pulmonary sarcoidosis (sarcoidosis) is a multi-system, multi-organ granulomatous disease of unknown etiology, which often invades the lungs, bilateral hilar lymph nodes, eyes, skin and other organs. Its chest invasion rate is as high as 80% to 90%. .

Pulmonary nodules are distributed worldwide. The incidence is higher in Europe and the United States, and rare in the Eastern nations. They are more common in 20 to 40 years old, and slightly more women than men.

nickname

Pulmonary nodule

Visiting department

Respiratory Medicine

Common locations

chest

Disease code

ICD-9: 135-12ICD-10: D86.001

Disease classification

Respiratory diseases

Cause: Unclear. Observation of infectious factors (such as bacteria, viruses, mycoplasma, fungi, etc.) has not been concluded. Genetic factors have also been studied and cannot be confirmed. In recent years, some authors found that the positive rate of Mycobacterium tuberculosis DNA was 50% in patients with sarcoidosis by PCR. Therefore, sarcoidosis was the result of mycobacteria invading tissues, but many experiments did not confirm this argument.

At present, most people think that cellular immune function and humoral immune dysfunction are important pathogenesis of sarcoidosis. Stimulated by some (some) sarcoidosis antigens, macrophages (Am) and T4 cells in the alveoli are activated. Activated Am releases interleukin-1 (IL-1). IL-1 is a strong lymphokine, which can stimulate the release of IL-2 by lymphocytes, multiply T4 cells and play a role in lymphokine. Then, B lymphocytes are activated, immunoglobulins are released, and the function of autoantibodies is enhanced. Activated lymphocytes can release monocyte chemokines, leukocyte inhibitors, and macrophage migration inhibitors. Monocyte chemokines cause mononuclear cells in the surrounding blood to continuously accumulate toward the alveolar stroma. In sarcoidosis, the concentration in the alveoli is about 25 times that of blood. Under the action of many unknown antigens and mediators, T lymphocytes, monocytes, and macrophages infiltrate the alveoli, forming the early stage of sarcoidosis, the alveolitis stage. With the development of lesions, the cellular components of alveolitis continue to decrease, and macrophage-derived epithelial cells gradually increase. Under the action of their synthetic and secreted granuloma-inciting factors, they gradually become typical Granulomatosis of non-casey sarcoidosis. In the later period, fibronectin (Fn) released by macrophages can attract a large number of fibroblasts (Fb) and make them adhere to the extracellular matrix, plus fibroblast growth factor ( growth factor of fibroblasts (GFF), leading to an increase in the number of fibroblasts; at the same time, the surrounding inflammation and immune cells are further reduced to disappear, leading to extensive fibrosis of the lung.

Sarcoidosis is the result of a counterbalance between unknown antigens and cellular and humoral immune functions. Due to individual differences (age, gender, race, genetic factors, hormones, HLA) and the regulatory effect of antibody immune response, depending on the imbalance between the promoters and antagonists it produces, the development and regression of granulomas are determined, Showing different pathological conditions of sarcoidosis and the trend of natural remission.

Sarcoidosis granuloma can be seen as a cluster of skin-like cells on the tissue section, including multinucleated macrophages, lymphocytes around it, and no caseous lesions. Inclusion bodies can be seen in the macrophage vesicles, such as oval-shaped Schaumann bodies, birefringent crystals, and asteroid bodies. The primary lesions of pulmonary sarcoidosis include extensive monocytes, macrophages, and lymphocytic alveolitis, involving the alveolar wall and interstitial. Both alveolitis and granulomas may resolve on their own. However, in the chronic phase, fibroblasts are collagenized and vitreous, becoming non-specific fibrosis. Histomorphology of granulomas has no characteristics. It can be seen in mycobacterial and fungal infections, or is a foreign body or trauma tissue reaction. It can also be seen in beryllium disease, third stage syphilis, lymphoma and exogenous allergic alveolitis Etc. should be identified. However, the same tissue lesions are seen in multiple organs, and combined with clinical data, the disease can be diagnosed.

Symptoms and signs vary depending on how quickly the disease starts and how many organs are involved. Intrathoracic sarcoidosis is often without obvious symptoms and signs in the early stages. Sometimes cough, cough a little sputum, occasionally a small amount of hemoptysis; may have fatigue, fever, night sweats, loss of appetite, weight loss, and so on. When the lesions are extensive, chest tightness, shortness of breath, and even cyanosis can occur. Can be aggravated by co-infection, emphysema, bronchiectasis, and pulmonary heart disease. If sarcoidosis involves other organs at the same time, corresponding symptoms and signs can occur. If the skin is most commonly nodular erythema, it is more common in the face and neck, shoulders or limbs. There are also lupus pernio, spotted rash, pimples and so on. Subcutaneous nodules are sometimes found. Violations of the scalp can cause hair loss. Skin damage can occur in about 30% of patients. About 15% of the cases of eye damage may include iris ciliary body inflammation, acute uveitis, and corneal-conjunctivitis. Eye pain, blurred vision, and congestion of the ciliary body can occur. Some patients have enlarged liver and (or) spleen, showing a slight increase in bilirubin and elevated alkaline phosphatase, or liver damage. Mediastinal and superficial lymph nodes are often invaded and enlarged. If it involves joints, bones, muscles, etc., there may be multiple arthritis. X-ray examination shows multiple small cystic bone defects (bone cysts) in the short bones of the limbs, hands and feet. Muscle granulomas can cause local swelling and pain. About 50% of the cases involve the nervous system, and its symptoms vary widely. May have clinical manifestations of cerebral palsy, neuromuscular disease, space occupying lesions in the brain, and meningitis. When sarcoidosis affects the myocardium, there may be arrhythmias and even heart failure. About 5% of the cases involve the heart. Pericardial effusion may also occur. Sarcoidosis can interfere with calcium metabolism, leading to an increase in blood calcium and urine calcium, causing renal calcium salt deposition and kidney stones. Diabetes insipidus can be caused when the pituitary is involved, and excessive milk and serum prolactin can occur when the hypothalamus is involved. When the parotid glands, tonsils, larynx, thyroid, adrenal glands, pancreas, stomach, reproductive system are involved, it can cause related symptoms and signs, but it is rare. Sarcoidosis can involve one organ or invade multiple organs at the same time.

1 Medical examination

1.1

1 Principles of treatment

1.1 Because most patients can resolve on their own, stable and asymptomatic patients do not require treatment. Patients with obvious symptoms of stage and and thoracic sarcoidosis such as ocular sarcoidosis, invasion of sarcoidosis in the nervous system, skin,

Related to sarcoidosis. Acute onset patients have a better prognosis after treatment or remission on their own; chronic progression, invasion of multiple organs, causing functional impairment, extensive pulmonary fibrosis or acute infection have a poor prognosis. The cause of death is often caused by pulmonary heart disease or myocardial and brain invasion. It has been reported that during an average 5-year follow-up, 34% of the cases recovered completely, 30% improved, and 20% remained unchanged. Each condition deteriorated and death accounted for 8%. ^[1]