Tyrosinemia is divided into three types depending on the site of enzyme deficiency. Tyrosinemia type I, also known as hepatorenal tyrosinemia, is characterized clinically by the development of progressive liver and kidney damage and eventually cirrhosis and Fanconi syndrome. Clinical examination: The acute type presents with symptoms of hepatic insufficiency, hypoglycemia, hemorrhagic tendency and ascites about one month after birth, along with acidosis and hypophosphatemia renal proximal tubular damage with rickets; the chronic type has the same symptoms as the acute type, except that the disease progresses more slowly, with the onset of rickets and hepatomegaly at about 1 year of age, and the onset of rickets at school age has also been reported. Tyrosinemia type II is characterized by ocular symptoms such as lacrimation, photophobia and conjunctival congestion in the first few months of life, followed by corneal ulceration and clouding, nystagmus, etc., as well as blisters, ulcers and hyperkeratosis on the palms of the hands and soles of the feet, and intellectual and developmental impairment after 1 year of age. Children with tyrosinemia type III are generally asymptomatic, but may also have mild mental retardation, spasticity, and ataxia. In addition to the above symptoms to examine tyrosinemia, the urinary tyrosine and metabolites (4HPL, 4HPP, 4HPA) components resulting from tyrosine accumulation are significantly increased. In addition, the examination may include hyperamino acidemia, such as tyrosine, proline, threonine and phenylalanine, abnormal liver function, hypoglycemia, low serum protein and bleeding tendency.