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Scleroderma is a clinically with limitations or diffuse fibrosis is characterized by thickening of the skin and can affect the heart, lungs, kidneys, and digestive tract and other organs of connective tissue disease. If both lesions involving the skin, but also invades internal organs, known as systemic scleroderma; if lesions confined to the skin without damage to internal organs, then known as localized scleroderma.

Skin lesions

The degree of systemic scleroderma skin lesions vary widely, the light only local skin sclerosis and calcification, there may be serious systemic sclerosis extensive skin thickening. The typical skin lesions usually go through three distinct periods:

1, edema period: mainly for the symmetry of the non-depressed, painless edema, skin thickening tension, wrinkles disappear, pale skin was smooth sausage-like fingers. Starting from the onset of the extremities, gradually spreading to the forearm, shoulder; often by the onset of the trunk to the surrounding expansion. After a few weeks or a few months later, the skin gradually thickening into the hardening period.

2, hardening period: hardening of the skin was waxy shiny, skin elasticity to reduce or disappear, can not be picked by hand. If lesions occur on the face, there may mask faces: look dull, eyelid activity limitation; difficulty in opening mouth, lips thin, small mouth fission, radial contraction of the skin around the mouth; try to measure the distance between the upper lip and lower lips than the normal maximum mouth people significantly reduced. If lesions occur in the fingers, finger flexion can be limited. If lesions occur in the chest, chest physio flu can occur. All the affected area of ​​skin pigmentation may occur or depigmentation, sparse hair, skin itching or a foreign body sensation.

    3, atrophy of: thinning of the skin, such as kraft paper, subcutaneous tissue and muscle atrophy close to the bone, as hard as wood. The affected hairs and hair loss can occur. Fingers and joints prone intractable ulcer or ischemic necrosis.

Gastrointestinal symptoms

The most common (about 90%) for esophageal dysfunction, gastrointestinal symptoms, manifestations of dysphagia, chest pain when swallowing, or swelling sense of nausea after drinking ice water and the symptoms are more prominent (esophagus Raynaud's phenomenon). If there is inflammation of the esophagus, burning sensation can occur after sternum. To late disease, due to esophageal stenosis, swallowing more difficult, and often accompanied by vomiting.

Little stomach in the digestive system are violated, but the gut often involved. Often appear to be involved after intestinal bloating, abdominal pain, diarrhea or constipation alternating with diarrhea. Due to expansion and movement of the duodenum and jejunum bad conducive to microbial growth, increasing bile salt decomposition, prone steatorrhea. Small number of patients, such as colic or intestinal manifestations of acute abdomen

Heart Disease

Systemic scleroderma often accompanied by varying degrees of heart attack, an autopsy found that the majority of patients with interstitial myocardial fibrosis plaque. Depends on the severity of heart attack myocardial fibrosis and pulmonary arterial inflammation caused by the extent of pulmonary hypertension. Severe myocardial fibrosis and pulmonary hypertension, can cause pulmonary second sound Kang strong gallop and systolic cardiac arrhythmia, and ultimately heart failure. Approximately 15% to 30% of patients with pericarditis can occur, but rarely cause cardiac tamponade. Near there are more than a moderate amount of pericardial effusion in patients. There are very few patients endocarditis can occur, leading to aortic valve regurgitation.

Kidney disease

Systemic scleroderma kidney damage occurs is a sign of poor light. Kidney damage can be divided into acute and chronic types. Rapidly progressive kidney damage often sudden severe hypertension with acute renal failure, this "renal crisis phase" is the main cause of death in systemic sclerosis; much in the pathogenesis of chronic kidney damage 3 to 5 years after the emergence begins as continue proteinuria, and gradually developed into persistent proteinuria, hematuria, hypertension and azotemia.

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