Case Reports in Pathology / 2018 / Article / Tab 1

Case Report

Cerebral Amyloidoma Resulting from Central Nervous System Lymphoplasmacytic Lymphoma: A Case Report and Literature Review

Table 1

(a) Presentation, treatment, and outcome of primary CNS mature B-cell lymphomas presented as an amyloidomas published in literature

ReferenceAge/sexSymptoms at presentationDuration of symptomssiteClinical diagnosisTreatmentFollow-upDiagnosis rendered

(1) Lehman et al. [1]63FFocal sensory seizure- trigeminal neuralgia and mild right sided hearing loss3 yearsDural, frontal lobeMeningiomaSurgical resection of the largest mass, radiation therapy8 months- alive with disease, imaging showed no change in the size of the amyloid massPrimary CNS Marginal zone lymphoma

(2) Pace et al. [2]46FSeizuresAcute onsetLeft frontal lobeOligodendroglioma or metastasisSurgical resection only24 months- no evidence of diseasePrimary CNS lymphoplasmacytic lymphoma

(3) Tu et al. [3]49 MSeizuresNRDural, left frontalNRMethotrexate, recurrence treated with fludarabine7.6 years- Recurrence at 4 months, No evidence of disease after treatment with fludarabinePrimary CNS Marginal zone lymphoma

(4) Tu et al. [3]62FAtaxiaNRDural, left occipitalNRRadiation25 months- No evidence of diseasePrimary CNS Marginal zone lymphoma

(5) Our case87FLeft sided weakness6 monthsRight frontal lobeLymphoma, vasculitis, or sarcoidosisRituximab, status post 1st cycle2 months- patient developed hemorrhagic strokeLow grade B-cell lymphoma with plasmacytic differentiation

NR: not reported; ND: not done.
(b) Diagnostic testing performed on the primary CNS mature B-cell lymphomas presented as an amyloidomas published in literature

ReferenceImagingHistopathologyLight chain restrictionBone marrowSystemic amyloidosisLab testsMolecular testing

(1) Lehman et al. [1]MRI- isointense on T1 and hyperintense on T2Intracerebral and vascular amyloid deposition, CD 20+ B cells and plasmacytoid cell infiltrates, CD138+ plasma cellsKappaNormalNRSPEP and UPEP- normal,
CBC- normal
ND

(2) Pace et al. [2]MRI- isointense on T1, hypointense on T2Intracerebral and vascular amyloid deposition, CD 20+ B cells and plasmacytoid cell infiltrates, CD138+ plasma cellsKappaNormalRuled out by serum amyloid P component scanSPEP- normal, normal serum free kappa, free lambda and kappa: lambda ratioND

(3) Tu et al. [3]NRAmyloid deposition, CD20 + B cell infiltratesKappaNRNRNRTrisomy 3 positive, Negative for MALT1 and IgH translocation

(4) Tu et al. [3]NRAmyloid deposition, cyclin D1-, CD20 + B-cell infiltratesKappaNRNRNRTrisomy 3 positive, Negative for MALT1 and IgH translocation

(5) Our caseMRI-T2 hyperintenseIntraparenchymal and perivascular amyloid deposition (AL subtype). CD20+, CD3-, CD5-, BCL1-, CD23- plasmacytoid lymphocytes and CD138+ plasma cellsLambdaNormalRuled out by abdominal fat biopsyNormal serum free kappa, free lambda and kappa: lambda ratioMYD88 L265P mutation analysis was negative

NR: not reported; ND: not done.