Clinical case 4

A 27-year-old woman is referred by her rheumatologist following a new diagnosis of mild-to-moderate systemic lupus erythematosus (SLE) with early renal involvement. The rheumatologist plans to initiate first-line therapy with corticosteroids and hydroxychloroquine, reserving immunosuppressants if renal disease progresses. Cyclophosphamide is not indicated at this stage. Because of her age and desire for future pregnancy (not short-term), the patient is referred to a fertility preservation specialist before starting systemic therapy.

Fertility assessment: At consultation, menstrual cycles are regular and painless, and there are no menopausal symptoms. Baseline reproductive testing at early follicular phase shows FSH 6.5 IU/L, LH 5.8 IU/L, estradiol 90
pg/mL, and AMH 2.8 ng/mL; ultrasound confirms an antral follicle count (AFC) of 16, consistent with normal ovarian reserve.

The specialist explains that women with SLE face two distinct reproductive risks:

• Therapy-related gonadotoxicity, particularly from alkylating agents such ascyclophosphamide, which can induce irreversible premature ovarian insufficiency.
• Disease-related ovarian autoimmunity, in which chronic inflammation and anti-ovarian antibodies may trigger autoimmune oophoritis, leading to premature ovarian insufficiency.

Counseling and management:

The patient receives comprehensive counseling on reproductive health in SLE. She is informed that her current regimen (steroids and hydroxychloroquine) poses minimal gonadotoxic risk, but that fertility preservation should be reconsidered promptly if treatment escalation is required.

Open questions for discussion:

1. Should fertility preservation be offered immediately and which technique would be most appropriate given the potential risk of autoimmune oophoritis, or should it be reserved for when gonadotoxic treatments such as cyclophosphamide are required?
2. If fertility preservation is not performed at diagnosis, when should it be reconsidered — after therapy changes, ovarian reserve decline, or menstrual alterations?
3. Is there a valid follow-up with available tools like FSH, AMH or AFC to predict the risk of premature ovarian insufficiency?