Belimumab use during pregnancy: a summary of birth defects and pregnancy loss from belimumab clinical trials, a pregnancy registry and postmarketing reports

Comment on:Belimumab use during pregnancy: a summary of birth defects and pregnancy loss from belimumab clinical trials, a pregnancy registry and postmarketing reports“.
Petri M, et al. Ann Rheum Dis 2022;0:1–9. doi:10.1136/annrheumdis-2022-222505

Commented by: Angela Tincani, Rheumatology and Clinical Immunology, ASST-Spedali Civili and University of Brescia, Italy

Pregnancy is a hot problem in women affected by SLE because they are usually young and therefore often expecting to have a family but also because pregnancy can have an unsuccessful outcome and can be linked to disease flares. For these reasons, drugs to be used to control the disease without affecting the fetus development are today certainly an unmet need.

Belimumab is one of the few new drugs introduced in the SLE treatment and data on its use in pregnancy generate a great expectance.

The paper collects information on 319 belimumab exposed pregnancies: 110 from clinical trials (with additional 16 exposed to placebo), 56 from the Belimumab Pregnancy Registry (BPR), 137 from spontaneous post marketing reports. Birth defects were reported among livebirths and pregnancy losses data excluded the elective terminations.

Among the pregnancy occurring in clinical trials, malformations were reported in 4/72 (5.6%) Belimumab exposed and 0/9 placebo exposed women; pregnancy losses were 35/110 (31.8%) in the Belimumab arm and 7/16 (43.8%) in the placebo arm.

The BPR reported prospective and retrospective data in 48 and 8 pregnancies respectively. The malformation rate was 21.7% and 4.2% in the 2 categories, while the occurring pregnancy losses were 4.2% and 50.0%.

Among the 137 spontaneously reported pregnancies, malformations were reported in 1/92 (1.1%) and losses in 43/137 (31.4%).

Unfortunately, the lack of a comparable disease control group, the presence of concurrent medications, the different exposure time and the often-insufficient data on birth defects do not allow to draw conclusions on the eventual Belimumab responsibility in their occurrence. In addition, the list of described birth defects include one case of congenital heart block that is known to be linked to maternal anti Ro/SS-A and /or anti La /SS-B antibodies. Finally, a consistent pattern of birth defects could not be identified.

On the other hand, it is well known that SLE itself carries many risk factors for pregnancy loss. Among them the presence of antiphospholipid antibodies and disease activity (that also could require an effective treatment such as Belimumab) are the most frequent.   But the clinical data necessary to verify the disease related risk factors were not systematically collected in the exposed cases. Consequently, the paper cannot say if Belimumab administration per se is linked to an increase rate of pregnancy losses.

In conclusion, analyzing different available sources, the paper collects all the published pregnancies exposed to Belimumab up to 8 March 2020. Even if the scarcity and heterogeneity of data do not allow to draw recommendations about the use of the drug in pregnancy, at least this publication shows that several physicians decided to administer or to maintain Belimumab during pregnancy certainly considering the risk/benefit balance. This supports the need of proper studies designed to collect clinical data and pregnancy outcome of SLE patients exposed to drugs particularly if relatively new.

A high burden of SLE risk genes is associated with persistent activation of the interferon system in patients with lupus.

Comment on: Single-cell RNA-seq reveals a persistent interferon signature in immune cells from  systemic lupus erythematosus patients with high versus low polygenic risk scores despite antimalarial  treatment. J Autoimmun. 2026 May 12:161:103575. doi: 10.1016.  Commented by: Lars Rönnblom, Department of Medical Sciences, Uppsala University, Sweden.    Genome-wide association studies have identified more than 300 loci associated to increased risk for  SLE. For the majority of the gene variants in these loci the functional consequences in the SLE disease  process are unknown. However, a large proportion of identified risk genes are connected to the  interferon signaling pathway and contribute to the interferon signature in SLE. Calculating a polygenic  risk score (PRS) is a method to quantify the cumulative genetic burden in a single patient and studies  have shown that patients with a high PRS have a more severe disease phenotype with increased  organ damage and reduced survival, compared to individuals with a low PRS.   Antimalarial therapy is a well-established treatment of SLE and have shown efficacy in a large  proportion of patients. The therapeutic effect is partly mediated by down regulation of the activated  interferon system, which is connected to clinical response. However, despite therapeutic  concentrations of hydroxychloroquine, many patients still have flares and accumulation of organ  damage. The main objective of the present study was therefore to clarify if antimalarial treatment has  different effects in patients with a high or a low PRS.  SLE patients in remission with a high or a low PRS were compared in gene expression profile at single  cell level on peripheral blood mononuclear cells. A total of 6 healthy controls and 16 matched  patients treated with similar antimalarial doses, but no corticosteroids, were investigated. On  average, 9636 cells were analyzed from each donor and 2724 genes detected per cell. Despite similar  clinical picture, patients with a high PRS had a prominent interferon signature across multiple  immune cell types, compared to patients with a low PRS who had a weak expression of interferon  stimulated genes only in monocytes. Pathway analysis revealed that the interferon signaling pathway 

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