Different authors have showed the epidermal origin of amiloyd in lichen amyloidosis (LA) and macular amyloidosis (MA).1 We examined eight consecutive patients suffering from LA, MA, or biphasic amyloidosis (BA) in a clinicopathologic study characterizing amyloid deposits with several monoclonal antikeratin antibodies and establishing immunohistochemical differences among the three disorders.
Patients, Materials, and Methods.
Biopsy specimens were taken from all patients and divided into two portions. Half of the specimen was formalin-fixed, paraffin-embedded, and processed for hematoxylin-eosin, Congored, and thioflavine T staining. Samples were scored as positive or negative for the presence of amyloid deposits in the epidermis; papillar, middle, or deep dermis; and perivascular or periadnexial area. The other half was snap frozen in liquid nitrogen and processed for immunohistochemistry (avidin-biotin complex technique, Table).
Patients 1 and 2 had MA, patients 2 through 6 had LA, and patients 7 and 8 had BA. Their mean age was
Ortiz-Romero PL, Ballestin-Carcavilla C, Lopez-Estebaranz JL, Iglesias-Diez L. Clinicopathologic and Immunohistochemical Studies on Lichen Amyloidosis and Macular Amyloidosis. Arch Dermatol. 1994;130(12):1559-1560. doi:10.1001/archderm.1994.01690120103018