IgE Above 60 IU/mL Predicts Deeper Ustekinumab Clearance in Psoriasis

Psoriasis patients whose baseline total IgE exceeded 60 IU/mL reached deeper skin clearance on ustekinumab — at every measured threshold where it counted — than patients below that line. That's the sharpest finding from a retrospective single-center study of 42 biologic-naive Chinese patients with plaque psoriasis, published in BMC Genomic Data. The genetic marker HLA-C*06:02 mattered too, but mainly for speed, not final outcome.

Every patient in the cohort received ustekinumab at weeks 0, 4, 16 and 28. The researchers ran genome-wide microarray analysis on all 42 participants and tracked improvement with the standard PASI 50, PASI 75 and PASI 90 thresholds — reductions in disease severity of 50, 75 and 90 percent. Lead author Bai and colleagues at the Chinese center framed the work explicitly as exploratory. They state the findings require validation.

What did HLA-C*06:02 actually change?

The allele shaped the timeline, not the destination. Patients positive for HLA-C*06:02 hit significantly higher PASI 50 response rates at week 4 and higher PASI 75 rates at week 16 than allele-negative patients. All reported differences reached statistical significance. But by week 28, the gap closed completely: every patient in both groups had reached PASI 75, meaning at least three-quarters of their disease severity had cleared.

At the deepest threshold, PASI 90 at week 28, the allele-positive group posted a numerically higher rate. The difference did not reach statistical significance. A multivariate binary logistic regression confirmed the pattern: HLA-C*06:02 positivity associated with achieving PASI 75 at week 16. The takeaway in plain words: the allele marks faster responders, not better end results.

Why is IgE the stronger signal?

Baseline IgE above 60 IU/mL outperformed the genetic marker at the time points that matter most. Those patients showed superior PASI 75 response rates at weeks 4 and 16, plus higher PASI 90 rates at weeks 16 and 28 — all statistically significant. That's the key contrast. The IgE signal held at the deepest clearance threshold both mid-study and at the final visit, while the genetic signal faded there. In this cohort, IgE was the stronger of the two associations at week 28.

The clinical appeal is obvious. A routine blood draw already measures total IgE, while HLA-C*06:02 requires genotyping. A cheap lab value that tracks both the pace and the depth of clearance on an interleukin-12/23 inhibitor would be useful — if it survives prospective testing. It hasn't yet.

How solid is the evidence?

The authors are direct about the limits, and those limits are real:

• Retrospective, single-center design cannot show either marker causes better response.
• Just 42 patients means imprecise estimates.
• All participants were biologic-naive Chinese patients, so results may not transfer to patients already exposed to other biologics, or to populations with different genetic backgrounds.
• No validated prospective cohort has confirmed either association.

Neither HLA-C*06:02 status nor baseline IgE should guide treatment decisions outside a research setting today. The study establishes something narrower: both markers were measurable before treatment and correlated with the pace and depth of clearance across 28 weeks of ustekinumab therapy in this specific cohort.

What comes next?

The path forward is well marked. Larger, prospective, multi-center studies in diverse populations would need to confirm the associations before either marker could enter routine practice as a predictor of biologic response in plaque psoriasis. If those trials replicate what this 42-patient cohort observed, clinicians could eventually pair one genotype and one standard blood value to anticipate who will clear fastest on ustekinumab — turning an exploratory pharmacogenomic observation into a practical tool for selecting biologic therapy.