Scleroderma, a common chronic autoimmune disease, is characterized clinically by inflammation, degeneration, thickening and fibrosis of the skin leading to sclerosis and atrophy. Focal or diffuse fibrosis, sclerosis and finally atrophy can occur in multiple systems throughout the body, such as the lungs, kidneys, gastrointestinal tract and heart, causing organ dysfunction. Its etiology and pathogenesis are not clear. According to the degree of skin thickening and the location of lesions, scleroderma is usually clinically classified into two categories: focal scleroderma and systemic scleroderma. (1) Focal scleroderma: The typical lesions are characterized by limited subcutaneous tissue atrophy, usually without involvement of internal organs and other systems. These include: (1) scleroderma: patchy scleroderma, drippy scleroderma; (2) linear scleroderma; (3) saber wound scleroderma: a special type of strip scleroderma, mainly involving the frontal face. (2) Systemic scleroderma: that is, systemic sclerosis (SSc). According to the presence or absence of visceral involvement, it is divided into: â‘ limited cutaneous disease (lcSSc): it starts with Raynaud’s phenomenon, and then gradually develops into sclerosis of the skin at the ends of the limbs. Visceral damage may occur in the later stages of the disease. The prognosis is relatively good because of the positive anti-synovial antibodies. Diffuse cutaneous disease (dcSSc): In addition to the distal extremities, the skin of the proximal extremities and even the trunk and face is also accumulated. The disease progresses rapidly. Most of the disease is associated with internal organs such as lung, heart, gastrointestinal tract and kidney damage. Anti-Scl-70 antibodies are mostly positive, while mitotic antibodies are mostly negative. The prognosis is poor. Focal scleroderma can be linguistically confused with limited cutaneous scleroderma, which are separate diseases. The following pages will only cover systemic sclerosis (SSc). The common first symptom of scleroderma is Raynaud’s phenomenon, which can precede other symptoms by months or even years. Raynaud’s phenomenon is a spasm of the small blood vessels in the hands after cold stimulation, resulting in a 3-stage change in finger color: whitening, purple, and redness. Raynaud’s phenomenon is also likely to occur during emotional stress. Clinical signs of scleroderma: The starting symptoms are often nonspecific and include Raynaud’s phenomenon, weakness, and musculoskeletal pain, which persist for weeks or months before other symptoms appear. Typical early clinical manifestations of SSc are swollen and thickened skin, beginning in the fingers and hands, followed by a variety of manifestations, mainly in the skin, lungs, heart, gastrointestinal tract, and kidneys. Skin lesions: symmetrical, first seen in the fingers and face, then spreading to the trunk. Initially, the fingers swell like salami, and the swelling on the back of the hand gradually spreads to the forearm. After a few weeks to months, the skin of the fingers, back of the hand and forearm becomes thickened and hardened like leather, wax-like and shiny, and adheres to deeper tissues. After 5 to 10 years, the skin enters the atrophic stage, when the skin is purple, swelling is no longer obvious, smooth and thin, close to the subcutaneous bone surface, the skin pattern disappears, and the hair is lost. Joint lesions: 60% to 80% of patients have painful joints due to fibrosis of the tendons, fascia and skin around the joints, but they are mostly mild non-erosive arthritis. The thickening of the skin and the tightness of the skin against the joints can lead to joint contractures and functional limitations. Cardiac lesions: irregular myocardial fibrosis and local ischemic damage, manifested as conduction abnormalities, arrhythmias, pericarditis, heart failure, etc. Gastrointestinal lesions: Dysfunction of the lower esophagus with damage to the sphincter muscle, manifested by choking sensation after swallowing food, as well as acid reflux, heartburn, and burning sensation behind the sternum. Damage to the anal sphincter can cause urinary and fecal incontinence and rectal prolapse. Pulmonary lesions: have become the leading cause of death in SSc patients. The most common severe pulmonary lesions are interstitial pulmonary fibrosis and pulmonary hypertension. Chest radiographs, CT, pulmonary function tests, and echocardiography help in the diagnosis. Renal damage: manifests as hypertension, proteinuria, and azotemia. In severe cases, it can be malignant hypertension and acute renal failure. Treatment: early diagnosis, early treatment, there is a lack of specific drugs, the purpose of treatment is: to control disease progression. The main methods are vasodilation, anti-fibrosis, immunosuppression, immunomodulation and symptomatic treatment.