JPRAS open · 2026
Serum tryptase and IgE before and after explantation in women with breast implant illness.
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Azahaf Siham, Hoff Jinske, Spit Karlinde A, de Blok Christel J M, Rustemeyer Thomas, Nanayakkara Prabath W B
Аннотация
BACKGROUND: Breast Implant Illness (BII) is characterized by systemic and local symptoms in a subset of women with silicone breast implants, but its pathophysiology remains unclear. Mast cell activation has been proposed as an underlying mechanism, yet systemic mast cell-related biomarkers have not been systematically evaluated in this context. This study aimed to assess whether explantation is associated with changes in serum tryptase and total IgE in women with BII.
METHODS: Seventy-one women with BII at a tertiary outpatient clinic provided paired blood samples before and after explantation (median interval, 8 months). Serum tryptase was measured by enzyme-linked fluorescence assay and total immunoglobulin E (IgE) by ImmunoCAP/EliA. Paired changes were analyzed in the overall cohort and in baseline-defined subgroups, including allergy status and pre-explantation IgE >100 kU/L.
RESULTS: In the full cohort, neither serum tryptase nor total IgE changed significantly after explantation (median differences: +0.09 ng/mL and -1.2 kU/L, respectively; both p > 0.1). Among 13 women with high baseline IgE (>100 kU/L), nine showed declines (median -118 kU/L), whereas tryptase levels remained unchanged and within normal limits. Of five women with elevated baseline tryptase (>11.4 ng/mL), three showed decreases after explantation, but only one normalized.
CONCLUSIONS: These findings show no evidence of explantation-associated changes in serum tryptase in women with Breast Implant Illness. Total IgE levels showed no consistent change overall, although heterogeneous post-explantation IgE changes were observed in a small subgroup with elevated baseline IgE. Mast cell involvement in BII cannot be excluded, as local mast cell activity and other mast-cell-derived mediators were not assessed.
METHODS: Seventy-one women with BII at a tertiary outpatient clinic provided paired blood samples before and after explantation (median interval, 8 months). Serum tryptase was measured by enzyme-linked fluorescence assay and total immunoglobulin E (IgE) by ImmunoCAP/EliA. Paired changes were analyzed in the overall cohort and in baseline-defined subgroups, including allergy status and pre-explantation IgE >100 kU/L.
RESULTS: In the full cohort, neither serum tryptase nor total IgE changed significantly after explantation (median differences: +0.09 ng/mL and -1.2 kU/L, respectively; both p > 0.1). Among 13 women with high baseline IgE (>100 kU/L), nine showed declines (median -118 kU/L), whereas tryptase levels remained unchanged and within normal limits. Of five women with elevated baseline tryptase (>11.4 ng/mL), three showed decreases after explantation, but only one normalized.
CONCLUSIONS: These findings show no evidence of explantation-associated changes in serum tryptase in women with Breast Implant Illness. Total IgE levels showed no consistent change overall, although heterogeneous post-explantation IgE changes were observed in a small subgroup with elevated baseline IgE. Mast cell involvement in BII cannot be excluded, as local mast cell activity and other mast-cell-derived mediators were not assessed.