TY - JOUR
T1 - Dialysis-related spinal canal stenosis
T2 - A clinicopathological study on amyloid deposition and its AGE modification
AU - Nokura, Kazuya
AU - Koga, Hiroshi
AU - Yamamoto, Hiroko
AU - Kimura, Akihiro
AU - Tamai, Hirofumi
AU - Yazaki, Susumu
AU - Suzuki, Nobuo
AU - Miyazaki, Shigeru
AU - Niwa, Toshimitsu
PY - 2000/9/15
Y1 - 2000/9/15
N2 - Three cases operated for spinal canal stenosis induced by dialysis- related amyloidosis (DRA) were investigated clinicopathologically. Cases were all-male, and had undergone hemodialysis around 20 years. In two cases, cervical plain X-rays showed only minor spondylotic changes. However, magnetic resonance imaging (MRI), myelography, and computed tomography (CT) showed extradural thickness with compression on the cervical spinal cord and cauda equina. In one case cervical X-rays showed typical destructive spondyloarthropathy (DSA), and MRI showed compression myelopathy. Surgical treatment on both cervical and lumbar spine in two cases and on cervical spine only in one case successfully reduced the symptoms. Extradural thickened tissue and ligament flavum obtained during surgery were studied histopathologically and immunostained by using anti-CD68, anti-β2- microglobulin (β2m), and anti-advanced glycation end product (AGE) antibody. Congo red stain showed diffuse or nodular amyloid deposition, and immunostaining with anti-β2m and anti-AGE antibodies also demonstrated the same distribution pattern. Thus, β2m-positive amyloid tissue in the extradural thickness (extradural amyloid deposition) was immunohistochemically demonstrated to be modified with AGE. Inflammatory reaction with histiocytic and giant cell infiltration was also shown around the amyloid tissues. There were CD68-positive cells, and some cells were positive for AGE and β2m. These findings suggest that β2m accumulation and inflammatory reaction finally promote destruction of connective tissues. MRI, CT and/or myelography are necessary for diagnosing spinal canal stenosis accompanied by DRA. In conclusion, we propose a more comprehensive concept of dialysis-related spinal canal stenosis, which includes both DSA and myeloradiculopathy induced by extradural thickness. (C) 2000 Elsevier Science B.V.
AB - Three cases operated for spinal canal stenosis induced by dialysis- related amyloidosis (DRA) were investigated clinicopathologically. Cases were all-male, and had undergone hemodialysis around 20 years. In two cases, cervical plain X-rays showed only minor spondylotic changes. However, magnetic resonance imaging (MRI), myelography, and computed tomography (CT) showed extradural thickness with compression on the cervical spinal cord and cauda equina. In one case cervical X-rays showed typical destructive spondyloarthropathy (DSA), and MRI showed compression myelopathy. Surgical treatment on both cervical and lumbar spine in two cases and on cervical spine only in one case successfully reduced the symptoms. Extradural thickened tissue and ligament flavum obtained during surgery were studied histopathologically and immunostained by using anti-CD68, anti-β2- microglobulin (β2m), and anti-advanced glycation end product (AGE) antibody. Congo red stain showed diffuse or nodular amyloid deposition, and immunostaining with anti-β2m and anti-AGE antibodies also demonstrated the same distribution pattern. Thus, β2m-positive amyloid tissue in the extradural thickness (extradural amyloid deposition) was immunohistochemically demonstrated to be modified with AGE. Inflammatory reaction with histiocytic and giant cell infiltration was also shown around the amyloid tissues. There were CD68-positive cells, and some cells were positive for AGE and β2m. These findings suggest that β2m accumulation and inflammatory reaction finally promote destruction of connective tissues. MRI, CT and/or myelography are necessary for diagnosing spinal canal stenosis accompanied by DRA. In conclusion, we propose a more comprehensive concept of dialysis-related spinal canal stenosis, which includes both DSA and myeloradiculopathy induced by extradural thickness. (C) 2000 Elsevier Science B.V.
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U2 - 10.1016/S0022-510X(00)00377-4
DO - 10.1016/S0022-510X(00)00377-4
M3 - Article
C2 - 11018703
AN - SCOPUS:0034665032
VL - 178
SP - 114
EP - 123
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
SN - 0022-510X
IS - 2
ER -