case_images: PMC9755325_01
case_images: Clinical and histopathological features of the patient during the first visit. (a) Clinical features on the back. (b) Dermoscopic features.
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case_images: PMC9755325_01_fmed-09-1047870-g0001.jpg
case_images: F1
case_images: During his first visit, a physical examination revealed extensive exudative erythema and slight pigmentation in a reticulated pattern on the back (Figure 1a). A dermoscopy of the pigmented area showed a brownish-brown pigment network (Figure 1b).
case_images: The results of histopathology and IF tests. (a,b) Histopathological features [H&E staining; magnifications: (a) x100; (b) x200]. (c) The results of indirect IF of a normal human skin section. (d) The results of indirect IF of 1M NaCl split skin section. IF, immunofluorescence.
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case_images: PMC9755325_01_fmed-09-1047870-g0002.jpg
case_images: F2
case_images: Histopathology of the biopsy taken from the blistering skin lesion revealed blister formation with eosinophil infiltration in the epidermis (Figures 2a,b). Indirect IF of normal human skin sections was negative for both IgG and IgA antibodies (Figure 2c), whereas indirect IF of 1M NaCl-split normal human skin sections showed very weak IgG reactivity on both the epidermal and dermal sides of the split, but no IgA reactivity was detected (Figure 2d).
case_images: The results of immunoblotting analyses. (a) Immunoblotting of the RPs of BP180 NC16a domain showing IgG reactivity with the RPs. (b) Immunoblotting of concentrated culture supernatant of HaCaT cells showing IgG reactivity with the 120 kDa LAD-1. (c) Immunoblotting of RPs of laminin 332 showing IgG reactivity with the 165 kDa laminin alpha3. RP, recombinant protein; BP, bullous pemphigoid; LAD-1, linear IgA disease antigen 1; Ig, immunoglobulin.
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case_images: F3
case_images: IgG, but not IgA, antibodies reacted with the recombinant protein (RP) of the BP180 NC16a domain (Figure 3a); IgG, but not IgA, antibodies reacted with the 120 kDa linear IgA disease antigen 1 (LAD-1) in the concentrated culture supernatant of HaCaT cells (Figure 3b); and IgG antibodies reacted with the 165 kDa laminin alpha3 subunit of laminin 332 RPs (Figure 3c). Immunoblotting analyses using normal human epidermal and dermal extracts and BP180 C-terminal domain RP showed no positive results for either IgG or IgA antibodies.
case_images: Clinical features during the disease course. (a) The skin lesions improved with the first treatment with PIH. (b) The recurrence of the skin lesions after the tapering of prednisolone. (c) The clearance of erythematous lesions with reticular pigmentation following the second treatment. PIH, post-inflammatory hyperpigmentation.
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case_images: F4
case_images: Then, the skin lesions were almost cleared with post-inflammatory hyperpigmentation (PIH) with slight erythema (Figure 4a). When the prednisolone dose was reduced to 10 mg/day, multiple new erythema and blisters recurred on the back with PIH (Figure 4b). While the prednisolone was tapered off, erythematous lesions disappeared, leaving reticulated pigmentation (Figure 4c).