Hypophosphatasia is a group of metabolic bone diseases characterized by low blood phosphorus, high urinary phosphorus, low (1,25) dihydroxyvitamin D3 levels, and impaired bone mineralization. The clinical manifestations are skeletal pain, deformity, limitation of movement, height shortening, and muscle weakness that progressively worsen with the disease course. The main biochemical examination features: low blood phosphorus, high urinary phosphorus, elevated blood alkaline phosphatase, decreased (1,25) dihydroxyvitamin D3 level, bone radiographs show a general decrease in bone density and blurred bone trabecular shadow. Adefovir was marketed in China in April 2005 for anti-hepatitis B virus treatment, and is widely used clinically because of the large base of hepatitis B patients in China. At present, there are several cases of hypophosphatasia osteochondrosis reported at home and abroad, and our hospital has also admitted several patients who developed hypophosphatasia osteochondrosis after taking adefovir treatment, as follows: Case 1, a middle-aged male, had been taking adefovir for 6 years and felt back pain 2 years ago, which gradually developed into generalized pain and even inability to walk, and was found to have positive urine sugar and urine protein, increased urine phosphorus excretion, and blood phosphorus The diagnosis of adefovir-associated hypophosphatasia was made definitively after several measurements (0.5-0.6 mmol/L). Case 2, an elderly male who had been taking adefovir for about 3 years, presented with bilateral knee pain, which gradually worsened and required walking with the aid of a wheelchair on admission. The post-admission examination suggested that the patient had significant hypophosphatemia, with blood phosphorus fluctuating from 0.59-0.67 mmol/L and increased urinary phosphorus excretion, and was diagnosed with adefovir-associated hypophosphatosis osteochondrosis. Adefovir, an oral adenosine monophosphate nucleotide analogue, was found to cause proximal renal tubular damage, decreased reabsorption, and increased urinary phosphorus excretion after prolonged treatment with adefovir 10 mg/d, leading to hypophosphatemia, decreased calcium and phosphorus product, affecting bone mineralization, and intracellular phosphorus deficiency resulting in decreased 1-a hydroxylase activity, resulting in intrarenal (1,25) dihydroxyvitamin D3 synthesis In addition, the renal tubular reabsorption of calcium is inhibited in acidosis. All of these factors lead to poor bone mineralization and hypophosphatemia. In summary of previous case reports, such conditions occur more often in Asian male populations. In addition, it has been found that adefovir causes a dose- and time-dependent impairment of renal tubular function, with the higher the dose and the longer the duration of application, the greater the chance of impairment of renal tubular function and impairment of calcium and phosphorus metabolism leading to hypophosphatasia. In conclusion, it is not uncommon to see hypophosphatasia after the application of adefovir. Currently, it is recommended that patients with hepatitis B should undergo regular tests such as blood potassium, blood phosphorus and blood calcium levels during adefovir treatment, regardless of the dose, to monitor whether renal tubular function and calcium and phosphorus metabolism are affected, so that hypophosphatasia can be detected early and treated accordingly to reduce patients’ pain and To improve the quality of life. If you or your friends or relatives are taking adefovir, especially if you have been taking it for more than 2 years or in higher doses, or if you have a combination of bone and joint pain, please be alert to hypophosphatasia and go to the Department of Endocrinology of Zhongshan Hospital as soon as possible for screening, early detection and early treatment.