PMC10204759_01
Histopathology (H&E) of skin. (A) A biopsy of the back lesions before using secukinumab describes features of psoriasis, including epidermal hyperkeratosis and acanthosis with elongation of the rete ridges. (B) Skin biopsy pathology of the groin after 8 months of secukinumab treatment illustrates epidermal hyperkeratosis, spongiosis, and a little eosinophil.
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The patient had a biopsy of the back lesions before using secukinumab and was diagnosed with psoriasis (Figure 1A). The skin tissues of the groin were embedded in paraffin for hematoxylin-eosin (H&E) staining. The biopsy specimens showed: (i) epidermal hyperkeratosis with mild focal parakeratosis; (ii) acanthosis with spongiosis; (iii) lymphocytes and little eosinophils infiltrating around the small vessels (Figure 1B).
Skin lesions change during tofacitinib treatment. (A1-D1) Before tofacitinib treatment. (A2-D2) After one week's treatment. (A3-D3) After six weeks of treatment. (A4-D4) In 3 months of follow-up after discontinuation of tofacitinib.
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One week later, the lesions became smaller, lighter, and pruritus-free (Figure 2A2-D2). After six weeks, the patient's lesions remained only hyperpigmented, without new lesions (Figure 2A3-D3). In 3 months of follow-up after discontinuation of tofacitinib, we observed no adverse effects or recurrence of PsoD (Figure 2A4-D4).
Timeline of the pathological/skin lesion diagram, diagnosis, and their management during the treatment.
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After six weeks, the patient's lesions remained only hyperpigmented, without new lesions (Figure 2A3-D3). In 3 months of follow-up after discontinuation of tofacitinib, we observed no adverse effects or recurrence of PsoD (Figure 2A4-D4). The timeline of this case report is shown in Figure 3.
Potential mechanism of tofacitinib for the treatment of PsoD caused by secukinumab. JAKs phosphorylate tyrosine residues on the cytokine receptors, leading to the recruitment and phosphorylation of STATs. Phosphorylated STATs dimerize and translocate to the nucleus, where they promote gene transcription. Tofacitinib binds to JAK, prevents downstream gene transcription, and differentially reduces cytokines production to regulate the differentiation of Th0 to Th cells to varying degrees. In this case, Tofacitinib restores the Th1-Th2 balance by inhibiting T cell differentiation and suppressing Th2 more than Th1 in the treatment of Th2-dominant PsoD. In this process, different Th cell subsets interacted with each other.
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In 3 months of follow-up after discontinuation of tofacitinib, we observed no adverse effects or recurrence of PsoD (Figure 2A4-D4).