Melanoma, also known as malignant melanoma, is a type of malignant tumor that originates from melanocytes and is commonly found in the skin, as well as in the mucous membranes and the choroid of the eye. Melanoma is the most malignant type of skin tumor and is prone to distant metastasis. Early diagnosis and treatment are therefore particularly important. How to examine melanoma? 1. General examination Some patients may have anemia and decreased hemoglobin. The most common cause of anemia is hypoproliferative anemia related to chronic inflammation, or iron deficiency anemia or megaloblastic anemia secondary to impaired absorption of iron, folic acid or vitamin B12 due to gastrointestinal tract involvement. Microangiopathic hemolytic anemia is often associated with renal involvement and is caused by fibrin, which is present in the small renal arteries. Patients may have increased blood eosinophilia and elevated platelets. Proteinuria, hematuria, leukocyturia and various tubular patterns, elevated blood creatinine and urea nitrogen, and decreased creatinine clearance are seen in the presence of renal involvement. Urinary 17 hydroxyl and 17 ketone cortisol measurements are low. Patients may have increased blood sedimentation, but C-reactive protein is generally normal. Serum albumin is decreased, globulin is increased, and polyclonal engramma may be present; globulinemia, IgG, IgA, IgM are elevated, and cold globulin is elevated. Fibrinogen levels in the blood are increased. Patients involved or uninvolved skin sensory time value measurement are significantly prolonged compared to normal, can reach 5 to 12 times normal. 2.Immunological examination Using human laryngeal cancer cells (Hep-2) as substrate to detect anti-nuclear antibody, about 95% of patients can be positive. The fluorescent karyotype can be speckle type, nucleolus type and anticentromere type. The speckled and nucleolus types are more relevant for the diagnosis of scleroderma, especially diffuse scleroderma. Anti-nucleolus antibodies are relatively specific for the diagnosis of scleroderma and can be found in 20% to 30% of patients. Anti-nucleolus antibodies that have been confirmed to be associated with scleroderma are anti-RNA polymorphase I, II and III antibodies, which can be found in 5% to 40% of diffuse scleroderma, with a high rate of cardiac and renal involvement. Anti-adherent antibodies are seen in 50% to 90% of CREST syndrome, 60% to 80% of limited scleroderma and 10% of diffuse scleroderma patients, occasionally in patients with Raynaud’s phenomenon, and rarely in other connective tissue diseases. Anti-adhesion antibodies are considered to be the marker antibody for CREST syndrome. Patients positive for this antibody are more likely to have skin capillary dilation and subcutaneous calcium deposits and less likely to have pulmonary disorders than those negative for this antibody, and its titer does not vary with time and disease duration, which is useful for early diagnosis of CREST syndrome and classification of scleroderma. An antinuclear antibody that is highly specific for the diagnosis of scleroderma is the anti-topoisomerase I antibody, initially called Scl-70 antibody (70kD), which recognizes the nuclease DNA topoisomerase I. Occurring in 20% to 40% of patients with diffuse scleroderma, it is known as the marker antibody for scleroderma and is associated with diffuse skin involvement, interstitial lung lesions, and other visceral organ involvement. It is rarely seen in other diseases and does not occur in conjunction with anti-synovial antibodies. Anti-Th RNP (ribonucleoprotein) antibodies are seen in 14% of limited scleroderma. Anti-PM-Sel antibodies, formerly known as anti-PM-1 antibodies, are seen in 25% of patients with overlapping features of limited scleroderma and polymyositis. Anti-U3 RNP, or anti-fibrillarin, antibodies are also specific for the diagnosis of scleroderma and have been associated with skeletal muscle and intestinal involvement as well as pulmonary hypertension. Anti-U1 RNP is seen in 5% to 10% of patients with scleroderma and in 95% to 100% of patients with mixed connective tissue disease with scleroderma features. Anti-SSA and/or anti-SSB antibodies are present in patients with overlapping scleroderma and Schegren’s syndrome. Anti-Sm and anti-dsDNA antibodies are negative, and anticardiolipin antibodies are negative for IgG type or positive for IgM type in low titers. 30% may be positive for rheumatoid factor but with low potency, and 7% may have lupus cells. Circulating immune complexes may be elevated and complement C3 and C4 may be decreased in 50% of patients. Immunomodulatory T-cell assays reveal increased numbers of helper T cells (Th, CD4 ) and decreased numbers of suppressor T cells (Ts, CD8 ). Lymphocyte conversion rate was decreased in the in vitro test. 3.Dermal capillaroscopy and blood rheology examination In the nail root folds of patients with systemic sclerosis, most capillary collaterals were blurred, the number of vascular collaterals was significantly reduced, while the number of abnormal vascular collaterals increased, accompanied by edema and exudation, vascular branches were obviously dilated and curved, blood flow was retarded, and some were accompanied by bleeding spots. It has been reported that changes in nail fold microcirculation in systemic sclerosis are consistent with the severity of visceral organ involvement, and thus can indirectly reflect visceral organ involvement. Patients with systemic sclerosis have abnormal blood rheology tests, which show increased whole blood specific viscosity, plasma specific viscosity and whole blood reducing viscosity, and prolonged red blood cell electrophoresis time. Hemogram examination shows slowed blood flow velocity at the extremities, reduced blood flow, and poor vascular elasticity. 4.Histopathological examination Fibrosis and microvascular occlusion are the characteristic pathological changes of all involved tissues and organs in patients with systemic sclerosis. (1) Skin pathological examination: In the early stage, dermal interstitial edema, swelling of collagen fiber bundles, and lymphocyte infiltration between collagen fibers and around small vessels in the dermis, with T cells predominant. In the late stage, the dermis and subcutaneous tissue collagen fibers proliferate, the dermis is significantly thickened, collagen is swollen and fibrotic, elastic fibers are destroyed, the vessel wall is thickened, the lumen is narrowed, or even occluded. Later, atrophy of epidermis, skin appendages and sebaceous glands, reduction of sweat glands, and calcium salt deposits in deep dermis and subcutaneous tissues appear. (2) Renal pathological examination: light microscopy reveals characteristic small arcuate artery and interlobular artery involvement, showing intimal thickening with endothelial cell hyperplasia, ldquo;onion skin rdquo;-like changes, which can partially or completely block the vascular lumen in severe cases. The glomerulus often shows ischemic changes, with capillary lumen atrophy, vessel wall thickening, wrinkling, and even necrosis. Renal tubular atrophy and interstitial fibrosis were observed. Immunofluorescence examination revealed the presence of fibrinogen in the vessel wall, with immunoglobulins, mainly IgM, and complement C3 deposition. Electron microscopy showed mild glomerular thylakoid hyperplasia and epithelial cell pedicle fusion, subendothelial granular deposits in the small arteries, splitting, thickening, and wrinkling of the glomerular basement membrane, and fibrinogen deposition in the interlobular arterial lining. 5.X-ray examination Both lungs have enhanced texture or small cystic changes, or reticular-nodular changes may appear in the lower lobes. The peristalsis of the esophagus and gastrointestinal tract is reduced or absent, the lower end is narrowed and the proximal side is widened, the peristalsis of the small intestine is also reduced, the proximal small intestine is dilated, and the colonic pouch may show spherical changes. There is bone resorption at the fingertips and calcium salt deposits in the soft tissues.