Possible Dual Immunoreactivity for Laminin-332 and Type VII Collagen in a Case with Vancomycin-Induced Linear Iga Bullous Dermatosis Manifesting as Erythroderma

Abstract

SummaryWe report a unique case of vancomycin-induced linear IgA bullous dermatosis (LABD) presenting as erythroderma. Direct immunofluorescence showed a linear IgA deposition at the dermal side of the basement membrane zone (BMZ), and double immunostaining using patients' skin as a substrate revealed that the in vivo IgA signal co-localized with laminin-332 and type VII collagen. Our case is the first documentation of vancomycin-induced LABD, in which the pathogenic IgA deposit would concomitantly recognize the two distinct antigens at the dermal BMZ.

Sublamina densa-type linear IgA bullous dermatosis with IgA autoantibodies specific for type VII collagen: a case report and clinicopathological review of 32 cases

“…Overall clinical details suggest no gender/age predilection and no particular drug usage for developing anti-COL7 IgA antibodies in the disease. Interestingly, of the 32 COL7-reactive IgA sera, five (15.6%) had an immunoreactivity with other dermal antigen(s), [2,7]. Of these 5 sera, two had IgA antibodies to laminin-332 or BP180 in each; the latter case may be the reactivity in close proximity to the COOH terminus of BP180, the antigen mostly localized in the lamina densa [2,7].…”

“…LABD appears in a variety of clinical settings, particularly hematological malignancies, infections, autoimmune disease, and drugs. In addition to the heterogeneous disease backgrounds, the clinicopathology of LABD is highly variable and almost indistinguishable among the distinct causative origins, albeit vancomycin can be the most incriminated drug (40-42% of all the drug-induced cases), [4,7].…”

“…), and consisted of 20 studies comprising 76 cases [2,4,5,[7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23], including ours' . Of these, 32 cases had serum autoantibodies directed against COL7, as conducted by the eligibility criteria, including positive IgA at the dermal side of 1M NaCl split-skin and any combination of the following findings; i) positive bands for monomeric and/or dimeric COL7 on immunoblotting using human dermal substrates [2, 4, 5, 8-10, 13, 14, 22, 23], ii) immunodeposits specific for anchoring fibrils on immunoelectron microscopy [9, 13, 22], iii) negative indirect IF on recessive dystrophic Dermatology Online Journal || Case Report epidermolysis bullosa skin (a COL7-knockout human skin), [11,12], iv) in vivo bound IgA signal overlying with COL7 on FOAM-LSCM, like our present case [7,10], or v) positive COL7-specific ELISA [12]. Considering the serum antibodies below the detection sensitivity on indirect immunofluorescence, the 2 studies using FOAM-LSCM on the patient's skin were allowed to be included in our review [7].…”

“…Among 32 cases with anti-COL7 IgA autoantibodies, their ages ranged from 1.5 to 82.0 years old (median; 58.2 ± 27.5) and the male to female ratio was 3: 2. In addition, there were only four cases associated with drugs (12.5%); two cases were caused by penicillin and one case by vancomycin [2,4,5,[7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. Overall clinical details suggest no gender/age predilection and no particular drug usage for developing anti-COL7 IgA antibodies in the disease.…”

“…Interestingly, of the 32 COL7-reactive IgA sera, five (15.6%) had an immunoreactivity with other dermal antigen(s), [2,7]. Of these 5 sera, two had IgA antibodies to laminin-332 or BP180 in each; the latter case may be the reactivity in close proximity to the COOH terminus of BP180, the antigen mostly localized in the lamina densa [2,7]. The remaining 3 sera did not identify the IgA reactivity to the exact dermal antigen(s), and may harbor the immunoreactivity to laminin-332 and/ or laminin gamma 1, or their native conformational epitopes.…”