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April Hendryx D.O.MUSC
June 12, 2010Case # 2
51st ANNUAL AANPDIAGNOSTIC SLIDE SESSION
Case # 2
68 year old male
Pain in the mid-thorax radiating to the right; ataxic gait
Past medical history: Ulnar neuropathy, tendonitis, degenerative joint disease, gout.
Case # 2
Neuro Exam: T6 sensory level deficit, spastic paraparesis
Thoracic MRI: Erosive extradural lesion involving the right 6th rib and vertebra; Compression of the spinal cord
Thoracic laminectomy and spinal decompression
Frozen section analysis: CPPD crystalline disease vs. hydroxyapatite deposition
Decompression was completed without further mass removal to preserve neurological function. Postoperative improvement in gait and balance
Case # 2
1.5 years later: Return of symptoms
MRI: Progression of the bony involvement. New epidural component
Encasing and compressing the spinal cord
Extending into the right paraspinal tissues
Radical excision of the entire process
Sagittal T1
Mass in dorsal longitudinal ligament
Coronal T1: Spinal cord compression and extension of the mass
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Hematoxylin-eosin
Cortical bone and amorphous eosinophilic deposits admixed with multinucleated giant cells, histiocytes, lymphocytes, and plasma cells
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Hematoxylin-eosin
20x
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Hematoxylin-eosin
Polarization
Differential Diagnosis
Gout (Monosodium urate)
Pseudogout (Ca ²pyrophosphate) ⁺
Hydroxyapatite crystal disease
Amyloid deposition
GOUT
l
CPPD
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Congo red stain
Highlights the amorphous material
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Polarization
Apple-green birefringence
Diagnosis: Primary Solitary Amyloidoma
Rare subset of amyloidosis
Deposition is focal and idiopathic
Deposition not secondary to a systemic process or plasma cell dyscrasia
Benign lesions
No associated risk of plasmacytoma related diseases
Primary Solitary Amyloidoma
Reported in multiple sites
Extremely rare in the vertebral column
Predilection for the thoracic region
2:1 Male predominance
Primary Solitary Amyloidoma
Tumor like appearance and behavior make it difficult to diagnose on imaging
The lesions grow slowly and can produce significant local destruction
Bony destruction and can mimic crystalline deposition diseases
Etiology
Product of local immunoglobulin production and amyloid formation within a “burned out” neoplasm
Usually AL fibrils from immunoglobulin light chains (primary)
AA fibrils secondary to inflammatory conditions and β-2 microglobulin in dialysis patients has also been described
Treatment and Prognosis
Surgical excision and spinal stabilization
Complete removal of the mass:
Relieve local compression
Stops the production of amyloid and associated infiltrative neuropathy
Low recurrence rate and cure with complete excision
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6/15/10
Comments by Dr. Brian Summers
6/15/10
EQUINE SKIN MASS 2010-2
CR CR
Polarized light