Diagnosis of amyloidosis is made on surgical path. It requires the demonstration of the amyloid protein by polarised light and Congo Red staining. Most cases of amyloidosis are AL type, secondary to a plasma cell dyscrasia and a paraprotein is normally demonstrable using serum immuno-electrophoresis or fixation. A monoclonal B-cell population is supportive evidence for this but cannot be considered as prima facie evidence for the diagnosis of amyloidosis. The AA and familial type do not have a monoclonal B cell population. The monoclonal B-cell in question is additionally plasmacytoid in nature. The immunotype you describe is CD38 dim / 19+ and not really the classical phenotype for a plasma cell. I think you need to pass the buck back to your clinician and ask him for further details to enable you to write a meaningful report. Te Chih Liu, MD National University Hospital Singapore -----Original Message----- From: Andrea Illingworth [mailto:dcdsflow@mint.net] Sent: Thursday, 25 April 2002 2:45 To: cyto-inbox Subject: monoclonal B-cells due to amyloidosis Dear group, once again I need your help! We recently had a case (left cervical lymph node) which showed a mixture of 55% T-cells (predominance of CD4) and 45% B-cells. The B-cells were CD19+, CD20+, CD22+, CD10-, CD5-, CD56-, CD38 weak+ with 15% expressing kappa and 32% expressing bimodal lambda (abnormal cells appear brighter positive for lambda). The patient had similar flow findings (reported as suspicious for LPD/B) about a year with no evidence of lymphoma by surgical pathology. It was sent out to a consultant who interpreted the reversed kappa/lambda findings as due to amyloidosis. I have done some "light" reading on this subject and am still not quite sure how to report the flow findings. If I understand it correctly, in primary amyloidosis (the only one associated with plasma cell dyscrasias) the amyloid is derived from all or a part of a monoclonal Ig light chain. 20% of patients with amyloidosis have multiple myeloma, the remaining patients have increased clonal plasma cells but they don't reach 10% in the bone marrow which is required for a dx of MM. My questions are: 1. What exactly does the reversed kappa lambda ratio mean in our case? That there are monoclonal B-cells somewhere in this patient's body (?MM), producing the amyloid but since these abnormal cells are not seen in this particular tissue, we can't call it a LPD/B? In other words, if we find a monoclonal B-cell population, do we need to check for amyloid first? 2. Can you see a reversed kappa/lambda ratio in cases other than primary amyloidosis (secondary and familial)? I know some people might challenge me on the ratio still being within the normal range but looking at the histograms, it looks restricted (bimodal expression). 3. How do we report this out? Your help is much appreciated Andrea Illingworth, MS, H(ASCP) Dahl-Chase Flow Cytometry 333 State Street Bangor, Maine 04401
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