# Immune profiling-informed immunomodulation associated with gestational extension in early-onset preeclampsia with monochorionic twins: a case report

## TL;DR

A pregnant woman with severe preeclampsia showed improved symptoms after an immunomodulatory treatment, suggesting immune profiling could guide treatment.

## Contribution

This case report explores immunomodulation in early-onset preeclampsia and its potential to extend gestation.

## Key findings

- Immunomodulatory treatment was associated with reduced proteinuria and improved blood pressure in a severe preeclampsia case.
- Gestation extended by 3–4 weeks following treatment initiation, allowing for fetal compromise management.
- Placental pathology showed infarctions and fibrinoid deposition, consistent with preeclampsia features.

## Abstract

Early-onset preeclampsia (EOPE) is associated with placental malperfusion and systemic endothelial dysfunction. Maternal immune dysregulation has been implicated in EOPE, but immune findings obtained during severe disease are descriptive and do not define a validated EOPE subtype.

A 22-year-old woman (G2P0) with a monochorionic diamniotic twin pregnancy developed gestational hypertension at 25+5 weeks and met criteria for EOPE at 30–31 weeks. Because of refractory progression under standard management, immune testing obtained at 31+1 weeks showed elevated TNF-α, low complement C4, weak ANA positivity, and T/B-cell imbalance (descriptive findings in this single case). After multidisciplinary discussion and informed consent for off-label therapy in pregnancy, an immunomodulatory regimen was started at 31+1 weeks (prednisone 10 mg/day, hydroxychloroquine 200 mg bid, and a single 200 mg SC dose of certolizumab pegol). Over the subsequent week, proteinuria decreased by >50% (10.78 to 4.99 g/24 h), blood pressure improved to 100–120/60–80 mmHg, and edema regressed. Gestation continued until 35+0 weeks, when cesarean delivery was performed for fetal compromise (Type II sFGR with umbilical-artery AEDF). Placental pathology showed multifocal infarctions and basal-plate fibrinoid deposition.

EOPE likely involves heterogeneous pathways in which inflammatory mediators, complement dysregulation, and cytokine excess have been reported. This case is hypothesis-generating and highlights the need for validated immune/angiogenic stratification and prospective evaluation of any adjunctive immunomodulatory approach in severe EOPE.

In this single MCDA twin pregnancy complicated by severe EOPE and concurrent immune-activation markers, initiation of a pregnancy-compatible immunomodulatory regimen was temporally associated with maternal clinical stabilization and a 3–4-week interval to delivery for fetal indications. Controlled studies with validated phenotyping, serial biomarkers (including sFlt-1/PlGF), standardized endpoints, and detailed safety follow-up are needed before attributing benefit or recommending this approach.