What are the examination methods for melanoma

Melanoma has become a skin disease that many friends will talk about at gatherings. It can be seen that melanoma has become a disease that the public is concerned about. The key to the prevention and treatment of melanoma lies in treatment. Melanoma is not incurable. We mainly focus on preventing melanoma. People with melanoma should insist on using scientific methods to treat melanoma and not blindly treat it.

1. General inspection:

Some patients may have anemia and decreased hemoglobin. The most common cause of anemia is hypoproliferative anemia associated with chronic inflammation. It may also be secondary to iron deficiency anemia or megaloblastic anemia due to gastrointestinal involvement leading to impaired absorption of iron, folic acid or vitamin B12. Microangiopathic hemolytic anemia is often related to kidney involvement and is caused by fibrin present in the renal arterioles. Patients may have increased blood eosinophils and elevated platelets. When the kidneys are involved, proteinuria, hematuria, leukocyturia and various casts may occur, blood creatinine and urea nitrogen may increase, and creatinine clearance may decrease. Urinary 17-hydroxy and 17-ketocortisol measurements are low.

Patients may have an increased erythrocyte sedimentation rate, but C-reactive protein is generally normal. Serum albumin is decreased, globulin is increased, and there may be polyclonal gamma globulinemia, increased IgG, IgA, and IgM, and increased cryoglobulin. The fibrinogen content in the blood is increased. The patient's skin sensation time value measurement of the affected or unaffected skin is significantly longer than normal, up to 5 to 12 times the normal value.

2. Immunological examination:

Human laryngeal carcinoma cells (Hep-2) are used as substrates to detect antinuclear antibodies. The fluorescent nuclear type can be spot-type, nucleolar type and anticentromere type. Among them, the spot-type and nucleolar type are more meaningful for the diagnosis of scleroderma, especially diffuse scleroderma. Anti-nucleolar antibodies are relatively specific for the diagnosis of scleroderma and can be seen in patients. It has been confirmed that the anti-nucleolar antibodies related to scleroderma are anti-RNA polymerase I, II, and III antibodies, which can be seen in diffuse scleroderma of , and the incidence of heart and kidney involvement in patients is high. Anti-centromere antibodies can be seen in CREST syndrome, patients with localized scleroderma and diffuse scleroderma, and occasionally patients with Raynaud's phenomenon, but are rarely seen in other connective tissue diseases. Anti-centromere antibodies are considered to be the marker antibodies of CREST syndrome. Patients who are positive for this antibody are prone to skin capillary dilation and subcutaneous calcification, and have fewer lung diseases than those who are negative for this antibody. Its titer does not change with time or the course of the disease, which is helpful for the early diagnosis of CREST syndrome and the classification of scleroderma.

The antinuclear antibody with high specificity for the diagnosis of scleroderma is anti-topoisomerase I antibody, originally called Scl-70 antibody (70kD), which recognizes the nuclear enzyme DNA topoisomerase I. It appears in patients with diffuse scleroderma and is called the marker antibody of scleroderma. This antibody is related to diffuse skin involvement, interstitial lung lesions and other visceral organ involvement. It is rarely seen in other diseases and does not appear at the same time as anti-centromere antibodies.

Anti-ThRNP (ribonucleoprotein) antibodies may appear in localized scleroderma. Anti-PM-Sel antibodies, formerly known as anti-PM-1 antibodies, can be seen in patients with overlapping features of localized scleroderma and polymyositis. Anti-U3RNP, or anti-fibrillarin antibodies, are also very specific for the diagnosis of scleroderma and are associated with skeletal muscle, intestinal involvement, and pulmonary hypertension. Anti-U1RNP can be seen in patients with scleroderma and mixed connective tissue disease with features of scleroderma, and anti-SSA and/or anti-SSB antibodies are present in patients with overlapping scleroderma and Sjögren's syndrome. Anti-Sm antibodies and anti-dsDNA antibodies are negative, and anti-cardiolipin antibodies are IgG-negative or IgM-positive at low titers. Rheumatoid factor may be positive, but the titer is low, and lupus cells may appear in 7%.

50% of patients may have increased circulating immune complexes and decreased complement C3 and C4. Immunomodulatory T cell detection found that the number of helper T cells (Th, CD4) increased and the number of inhibitory T cells (Ts, CD8) decreased. In vitro tests showed a decrease in lymphocyte transformation rate.

3. Skin capillaroscopy and blood rheology examination:

In the nail root folds of patients with systemic sclerosis, most capillary loops are blurred, the number of vascular loops is significantly reduced, and the number of abnormal vascular loops increases, accompanied by edema and exudation, obvious expansion and bending of vascular branches, slow blood flow, and some with bleeding spots. It has been reported that the changes in the nail fold microcirculation of systemic sclerosis are consistent with the severity of visceral organ involvement, and therefore can indirectly reflect the involvement of visceral organs.

Patients with systemic sclerosis have abnormal blood rheology tests, manifested as increased whole blood viscosity, plasma viscosity and whole blood reduced viscosity, and prolonged red blood cell electrophoresis time.

Blood flow examination showed that the blood flow velocity in the extremities was slow, the blood volume was reduced, and the vascular elasticity was poor.

4. Histopathological examination:

Fibrosis and microvascular occlusion are characteristic pathological changes in all affected tissues and organs of patients with systemic sclerosis.

(1) Skin pathological examination: In the early stage, there is edema in the dermis, swelling of collagen fiber bundles, and lymphocyte infiltration between collagen fibers and around small blood vessels in the dermis, mainly T cells. In the late stage, collagen fibers in the dermis and subcutaneous tissue proliferate, the dermis thickens significantly, collagen swelling and fibrosis, elastic fiber destruction, vascular wall thickening, lumen narrowing, and even occlusion. Later, the epidermis, skin appendages and sebaceous glands atrophy, sweat glands decrease, and calcium salts are deposited in the deep dermis and subcutaneous tissue.

(2) Kidney pathology examination: Under the microscope, characteristic small arcuate arteries and interlobular arteries are affected, with thickening of the intima and proliferation of endothelial cells, presenting an "onion skin"-like change. In severe cases, the vascular lumen may be partially or completely blocked. The glomeruli often show ischemic changes, with atrophy of the capillary lumen, thickening and wrinkling of the vascular wall, and even necrosis. Tubular atrophy and renal interstitial fibrosis

Immunofluorescence examination revealed the presence of fibrinogen, immunoglobulins (mainly IgM), and complement C3 deposition in the vascular wall.

Electron microscopy showed mild mesangial proliferation and fusion of epithelial cell foot processes in the glomeruli, granular precipitation under the endothelium of the arterioles, splitting, thickening and wrinkling of the glomerular basement membrane, and fibrinogen deposition in the intima of the interlobular arteries.

5. X-ray examination:

The texture of both lungs is enhanced, or there are small cystic changes, and reticular-nodular changes may also appear in the lower lobe. The motility of the esophagus and gastrointestinal tract is weakened or absent, the lower end is narrow, the proximal side is widened, the small intestine motility is also reduced, the proximal small intestine is dilated, and the colon bag may change to a spherical shape. The bone of the fingertips is absorbed, and calcium salts are deposited in the soft tissue.