The main symptom of brown yellows arthritis is that the skin, sclera, cornea pigmentation is brownish-yellow, the ear, nose and cartilage can become blue, the edge of the tympanic membrane is grayish-black, and the hearing is often reduced. Brownish yellow disease is due to the lack of uronic acid oxidase, so that phenylalanine, tyrosine intermediate metabolites (uronic acid) can not be further oxidation decomposition, accumulation in the body. The skin, sclera, and cartilage become darker, while urea causes hyperpigmentation of cartilage and other connective tissues and degenerative arthritis of the spine and peripheral large joints. On the other hand, urinary black acid is excreted in urine, where it is alkalized and oxidized to make the urine darker, so it is also called black aciduria. This disease is a rare genetic disease and is rare. The prevalence is reported abroad as 3 to 5 cases per million population. Because uric black acid is easily deposited in cartilage, it degenerates joints. The disease is often seen clinically as arthrosis, so it is called brown yellows disease arthropathy. What can cause this symptom? Fucoidosis is a rare genetic disorder of amino acid metabolism. Usually there is a family history of the disease and the incidence varies between men and women, approximately 2:1, while xanthomatous arthritis is caused by pigmentation of the intervertebral discs or cartilage, resulting in degenerative disc degeneration and arthropathy, i.e. xanthomatous pigmentation. Deposition in the structural tissues of the joints causes xanthomatous arthritis. The main symptoms of this disease are brownish-yellow pigmentation of the skin, sclera and cornea, blue coloration of the ears, nose and cartilage, grayish-black rim of the tympanic membrane, and hearing loss. If uric acid is deposited on the aortic and mitral valves, the valves become stiff and murmurs appear. In men, the disease is often combined with black prostate stones. Bone and joint changes usually erode the spine first, followed by the knee, shoulder and hip. The incidence of spondylitis is 10% to 15%, more in men than in women. The patient complains of lumbar pain and examines the lumbar plate, with loss of anterior convexity, mild hunchback deformity, and posture similar to that of ankylosing spondylitis. In terms of differential diagnosis, other causes of darkening of urine, such as hematoporphyria, myoglobulinuria, bilirubinuria, and hematuria, should be excluded. Based on the clinical features of these diseases and relevant laboratory tests, it is not difficult to differentiate them from brownish yellow disease. Long-term use of miparin (Adiponectin) can cause fucoidosis-like pigmentation, and clinical care should be taken not to confuse this medically induced pigmentation with fucoidosis. Multiple applications of phenol (carbolic acid) for skin ulcers can also cause yellow pigmentation, and care should be taken to differentiate them. There is no effective therapy for this disease, and it is unrealistic to restrict dietary phenylalanine and tyrosine intake to reduce uveitis. Long-term administration of vitamin C may inhibit the oxidation and polymerization of uronic acid and may have some significance in relieving clinical joint symptoms. For the treatment of joint lesions, appropriate rest and physical therapy are the mainstays, and pain medication is given when necessary. In cases where joint deformity has occurred, surgical orthopedics may be indicated as appropriate.