恩瑞格的治疗效果怎样呢？

The chemical name is 4-[3,5-bis(2-hydroxyphenyl)-1,2,4-triazol-1-yl]benzoic acid. Enrig is an iron chelator product developed by the Swiss pharmaceutical company Novartis. Enrig is the first oral iron anthelmintic approved by the US FDA for routine use. Enrig is approved for use in patients with iron accumulation caused by long-term blood transfusions (such as thalassemia or other rare anemias). , suitable for children over two years old and adults.

In order to ensure the efficacy of Enrig, scientific and rational use of drugs is undoubtedly very important. Therefore, for patients, it is recommended that Enrig be used under the guidance of a doctor. It is recommended for patients with iron accumulation, such as those who require long-term blood transfusion (transfusion volume up to 100ml/kg) and whose serum ferritin exceeds 1000ug/liter; Depending on the body weight, it is initially recommended to take 20 mg/kg of Enrig every day. Depending on the improvement of serum ferritin indicators, patients may need to adjust or increase the dosage of Enrig. Generally, the dose will be increased in units of 5 mg/kg or 10 mg/kg, but the total dose should not exceed 30 mg/kg per day. Taking Enriga may cause a rash. Generally, the rash will disappear automatically without the need to adjust the dose or stop the medication. If the condition is severe or persistent, the medication should be stopped.

Study the iron-removing efficacy and safety of Enrig in patients with aplastic anemia (AA) associated with iron overload. Methods: The iron-removing efficacy of 64 AA patients with iron overload after 12 months of treatment with Enrige was analyzed, and the safety was evaluated. Results The starting dose of Enriga in all patients was 20.0 mg·kg-1·d-1, and the average dose was (18.6±3.60) mg·kg-1·d-1. After 12 months of treatment, the median serum ferritin (SF) level dropped from the baseline of 4 924 (2 718 to 6 765) μg/L (64 cases) to 3 036 (1 474 to 5 551) μg/L (23 cases), a decrease of 38%, and the median SF reduction was 651 (126 to 2 125) μg/L; the median SF level of 23 patients who completed 12 months of treatment dropped from the baseline of 5 271 (3 420 ~ 8 278) μg/L to 3 036 (1 474 ~ 5 551) μg/L, a decrease of 42%, and the median SF reduction was 1 167 (580 ~ 4 806) μg/L. Increased serum creatinine (40.98%) and gastrointestinal discomfort (40.98%) were the main adverse events during treatment with Enriga, followed by increased liver aminotransferases (ALT: 21.31%; AST: 13.11%) and proteinuria (24.59%). The increase in serum creatinine was reversible and non-progressive.

For the 38 patients who were concurrently taking cyclosporine, 12 patients (31.8%) had creatinine values >the upper limit of normal (ULN) for 2 consecutive times, 10 patients (26.3%) had creatinine values >1.33 baseline value for 2 consecutive times, and only 1 patient (2.6%) had serum creatinine that increased beyond the 1.33 baseline value and exceeded the ULN. For AST and ALT, no patient throughout the study had two post-baseline values ​​>5×ULN or >10×ULN. For patients with baseline PLT levels below 50 × 109/L, median PLT did not decrease during treatment with Enriga. Conclusion: Treatment of AA patients with iron overload can achieve good iron removal efficacy, the drug is well tolerated, and there are no clinically uncontrollable serious adverse events.