We present a case of secondary corneal amyloidosis whose etiological mechanism was investigated by immunohistochemistry and electron microscopy. A 48-year-old woman had suffered from trichiasis in the right eye for 35 years, and developed secondary corneal amyloidosis, a phenomenon previously described but whose etiological mechanism has not been explained. Slitlamp examination of the cornea revealed a white excrescence with a diameter of 2 mm. The lesion was excised and examined by light and electron microscopy. Large deposits of an amorphous eosinophilic material were observed beneath the atrophic epithelium. Amyloid was detected in these deposits using Congo red stain, polarized light, and electron microscopy. Neither vascularization nor infiltration of inflammatory cells was observed. Immunohistochemical tests for protein AL, protein AA, prealbumin, beta 2-microglobulin and cytokeratin in paraffin sections were all negative. Characteristic findings were observed in the border zone between the basal cells and the deposits. Numerous digitiform cell processes and membrane-bound globular fragments of basal cells were seen in the superficial region of the deposits. The cell membrane of some globules was interrupted and the contents appeared to have been discharged into the stroma. These findings suggest that basal cells of the corneal epithelium provide an amyloid precursor on the stroma.
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J Fr Ophtalmol
January 2025
Department of Ophthalmology, Guangxi University of Chinese Medicine, Nanning, China; Department of Ophthalmology, Jingliang Eye Hospital, Guangxi Medical University, Nanning, China. Electronic address:
Acta Haematol
October 2024
Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Introduction: Treatment for relapsed/refractory AL amyloidosis (AL) is an unmet need. The safety and efficacy of belantamab mafodotin (BLM) in multiple myeloma are known, whereas in AL data are limited.
Methods: We report a multi-center cohort of AL patients receiving BLM, and review all previous data on BLM therapy in AL.
Neurol Sci
January 2025
Department of Neurology, Peking University First Hospital, 8 Xishiku Street, Xicheng District, Beijing, 100034, China.
Background: Hereditary transthyretin amyloidosis (ATTR) is an autosomal dominant disease characterized by amyloid fibril deposition. The TTR c.148G > T mutation (V30L) in ATTR is rarely reported, and its biochemical properties are unknown.
View Article and Find Full Text PDFCornea
November 2024
Department of Ophthalmology, Saarland University Medical Center, Homburg/Saar, Germany.
Purpose: To present ocular clinical, histological, systemic, and genetic findings of a patient with familial lecithin-cholesterol acyltransferase (LCAT) deficiency caused by a novel genetic variant of the LCAT gene associated with secondary corneal amyloidosis.
Methods: Case report.
Results: A 74-year-old woman presented with decreased visual acuity (VA), sensitivity to light, and progressive whitening of both corneas for approximately 20 years.
Can J Ophthalmol
August 2024
Bascom Palmer Eye Institute, University of Miami School of Medicine, Miami, FL. Electronic address:
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