It is generally accepted that pregnancy does not alter the long-term prognosis of SLE, but the disease may worsen during early pregnancy and the puerperium. The overall rate of disease activity during pregnancy and puerperium in patients with SLE is described in the literature as 50% to 70%, with approximately 2/3 of SLE pregnancies worsening. The main factors that may influence the activity or aggravation of SLE during pregnancy and postpartum are: (1) Pregnancy increases the burden on the already involved heart and kidneys, triggering SLE activity. (ii) The increased glucocorticoid during pregnancy decreases rapidly after delivery, and rebound changes in the disease occur. (iii) The sex hormone changes during pregnancy and the enhanced immune response of the body. Most of the literature suggests that the exacerbation of SLE during pregnancy mainly involves the skin and joints, with a small proportion having renal, hematological and neurological involvement. Risk factors for exacerbation of SLE include: active disease in the first 3-6 months of pregnancy or with renal pathology, mild SLE rarely exacerbates during pregnancy, increased incidence of pre-eclampsia and hypertension during pregnancy in SLE, about 20% of SLE attacks may occur during pregnancy, so young women with unexplained rash, arthritis, hair loss, proteinuria, psychiatric symptoms, chorea There is no definite conclusion as to where SLE is likely to occur during pregnancy, so close monitoring of the patient’s condition is needed throughout pregnancy and the postpartum period. The majority of scholars now believe that pregnancy is possible in women with SLE, but the indications for pregnancy should be well established. Julkunen reported that when LN patients have been stable for at least 3 months, with serum creatinine values less than 140 μmol/L, urinary protein less than 3 g/24h, and blood pressure under control, pregnancy outcomes are usually good, but the risk of fetal loss is 2-3 times higher than normal. The risk of fetal loss is two to three times higher than normal. Although the conditions for allowing pregnancy in patients with SLE vary and it is difficult to establish uniform criteria, the following points can be summarized for reference ① SLE is in remission for at least 6 months after regular treatment and the maintenance dose of prednisone is ≤10 mg/d; ② no important internal organs such as kidney and central nervous system lesions caused by SLE; ③ no use of immunosuppressive drugs or discontinuation of immunosuppressive drugs for at least 6 months before pregnancy ④No serious side effects caused by glucocorticoids; ⑤Pregnancy can be considered if the blood creatinine value is less than 140μmol/L, urine protein is less than 3g/24h, and there is no hypertension if the patient has SLE nephropathy. If SLE is active and the dose of prednisone is >15mg/d and there is significant organ involvement, pregnancy should not be an option at this time. However, in case of contraceptive failure, care must be taken not to terminate the pregnancy arbitrarily, because termination of pregnancy will not change the SLE disease, but may contribute to its aggravation. When SLE patients have endocarditis, myocarditis, cardiac failure, progressive glomerulonephritis, renal failure, nephrotic syndrome, pregnancy should be terminated and timely therapeutic abortion should be performed in early pregnancy; after 33 weeks of gestation, when the estimated fetal weight is about 2 kg, planned interventional termination of pregnancy and preterm delivery is better than just waiting for natural delivery.