Lymphocyte Subpopulations in Benign Monoclonal Gammopathy

2009 ◽  
Vol 31 (1) ◽  
pp. 78-84
Author(s):  
I. Silvian ◽  
A. Carter ◽  
I. Tatarsky ◽  
G. Spira
2009 ◽  
Vol 36 (1) ◽  
pp. 115-117 ◽  
Author(s):  
Paolo Gavarotti ◽  
Felice Fortina ◽  
Daniela Costa ◽  
Giuseppe Verzetti ◽  
Valter Redoglia ◽  
...  

1987 ◽  
Author(s):  
B S Coller ◽  
J Jesty

A 68 year old male hospitalized for cardiac disease was found to have an elevated prothrombin time (18.5/12.4 s) and aPTT (59.6/25.9s). He had no history of excessive bleeding or bruising. Subsequent evaluation revealed: thrombin time >500/34.1 s; fibrinogen 260 mg/dl functional and 522 mg/dl immunologic; reptilase 25.6/18.1 s; thrombin-induced platelet release of ATP (patient=0 and control=14.6 nmoles/109 platelets at 0.5 U/ml); AT-III 89% functional and 36.5 mg/dl immunologic; and prothrombin 167%. Mixing experiments showed the presence of an inhibitor of the thrombin time, and purification of IgG by protein A affinity chromatography showed the inhibitor of fibrin formation to reside in the IgG fraction. When coupled to Affi-gel 10, patient IgG (but not control IgG) removed purified thrombin from solution; the same gel did not remove prothrombin. The patient's IgG did not inhibit thrombin’s cleavage of a chromogenic substrate (Chromozym TH). Studies on the patient's serum revealed: IgG 2,360 mg/dl, IgA 371 mg/dl, and IgM 107 mg/dl. Serum protein electrophoresis and immunoelectrophoresis showed a monoclonal IgG lambda protein with probably normal amounts of normal IgG. Other parameters (hematocrit, albumin, calcium, bone marrow histology, bone X-rays) indicated that the patient has a benign monoclonal gammopathy, not multiple myeloma. We conclude that our patient is producing an IgG inhibitor that reacts with a neo-antigen produced by the cleavage of prothrombin to thrombin; the IgG can prevent the interaction of thrombin with fibrinogen and the thrombin receptor on platelets, but not small synthetic substrates. We suspect that his monoclonal IgG is the inhibitor and find it remarkable that he has no increase in bleeding.


1982 ◽  
Vol 51 (4) ◽  
pp. 531-539 ◽  
Author(s):  
E. Ösby ◽  
L. Noring ◽  
R. Hast ◽  
K. G. Kjellin ◽  
E. Knutsson ◽  
...  

Haematologica ◽  
2007 ◽  
Vol 92 (6) ◽  
pp. e74-e76 ◽  
Author(s):  
N. P Riksen ◽  
B. M Luken ◽  
I. S Klasen ◽  
J. Voorberg ◽  
N. Crama ◽  
...  

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 5023-5023
Author(s):  
Jacob Haaber ◽  
Anne G. Sørensen ◽  
Anne Nibe ◽  
Ole Nielsen ◽  
Niels Abildgaard ◽  
...  

Abstract 192 patients with multiple myeloma (MM) and benign monoclonal gammopathy of undetermined significance (MGUS, n=10) were investigated by interphase fluorescence in-situ hybridisation (iFISH) without (n= 132) and with positive plasma cell identification (PC-ID+) (n= 50). 134 were investigated at diagnosis 32 at time of progression, 7 at time of relapse and 9 were investigated with partial remission or no response. 10 of the MM cases were investigated twice. The patients were investigated with FISH probes detecting 11q23 (n=61), 13q13-14 (n=181), 14q32 ((n=121), 17p13.1 (n=181), t(4;14) (n=76) and t(11;14) (n=73). 61/132 (46%) of patients investigated without PC-ID+ showed abnormalities as opposed to 45/49 of evaluable cases (92%) with PC-ID+. The increase in abnormal cases was mainly due to the detection of more cases with loss of 13q and 17p and der(14)(q32): For patients investigated at diagnosis without and with PC-ID+, respectively: 13q-: 17% and 28%, 17p-: 3% and 15%, and 14q split signals (excluding the specific translocations): 8% and 24%. Based on the relatively small number investigated, the t(4;14) and the t(11;14) were not detected more frequently. G-band cytogenetics was carried out in 72 patients (25 without PC-ID+ and 47 with PC-ID+). 19 cases were abnormal (26%). Concordance for 1 or more aberration was found in 14 patients. t(11;14) was detected by both methods in 4 of 5 patients. Out of 7 cases with either near-tetraploidy/triploidy or hypoploidy in the G-band karyotypes, the modal number in the G-banded karyotypes could not be elucidated with certainty in 4 by iFISH with the applied probes. 7/10 patients investigated twice by iFISH showed new abnormalities on reinvestigation, 5 of these had a normal 1st analysis. 3 of 10 MGUS patients showed abnormalities. In conclusion, PC-ID+ is important for the detection of numerical aberrations and disclosing translocations involving 14q32, as translocations involving the IgH locus are frequent occurring in 64 % (n = 32) at diagnosis. Of these the t(4;14) and the t(11;14) constituted 8% and 20%, respectively. Re-examination of patients with a normal analysis should be considered in non-responders and progressing patients. Lastly, by applying the set of probes we chose in accordance with the proposed recommendations from the European Myeloma Network FISH Workshop, Royal Marsden Hospital, London UK, March 2005, failure to accurately the exsistence of detect near-tetraploid/near-triploid-, and hypoploid clones, is not insignificant (26%) and, based on the small number of cytogenetically abnormal cases it is recommended to include extra probes to classify the patients according to modal number by iFISH.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4755-4755
Author(s):  
Lucie Kovarova ◽  
Ivana Buresova ◽  
Ludek Pour ◽  
Renata Suska ◽  
Zdenek Adam ◽  
...  

Abstract Introduction: Multiple myeloma (MM) is a B-cell neoplasia caused by the proliferation of clonal plasma cells (PCs). MM and benign monoclonal gammopathy of unknown significance (MGUS) are routinely distinguished on the basis of paraprotein concentration, level of PCs infiltration and the presence or absence of other clinical features. Flowcytometric detection of PCs according to the expression of CD38 and CD138 has limitation in discrimination between normal and abnormal PCs, but this is possible in multicolor phenotypic analysis. The aim of this study is to compare the numbers of normal and abnormal PCs in MGUS and MM subjects and to find some parameter useful for evaluation PCs distribution. Materials and methods: 51 newly diagnosed untreated MM patients (63,9±10,0 years old) and 31 non-treated MGUS subjects (64,2±13,8 years old) were analysed. Lysed whole bone marrows were analysed by flowcytometric immunophenotyping and PCs were indentified by expression of CD38, CD138, CD45 and also CD56 and CD19. Results: Discrimination between normal CD19+ PCs and abnormal CD56+ PCs was done on CD38+CD138+ population. Ratio of normal PCs count and abnormal PCs counts (normal/abnormal=N/A) was used to describe a distribution of PCs. Subjects with MGUS had 0,97±1,65% (average±SD) of CD38+CD138+ cells (median 0,45; range 0,03–7,47%) with average N/A ratio 2,91±3,94 (median 1,36; range 0,01–18,44). Newly diagnosed MM patients had 4,96±9,94% of CD38+CD138+ cells (median 0,85; range 0,02–41,80%) with average N/A ratio 1,70±3,03 (median 0,13; range 0–11,5). In 9,7% MGUS subjects evaluation of distibution of PCs showed transformation of MGUS into MM. In some newly diagnosed MM patients (31,4%) CD38+CD138+ plasma cells were positive for CD19 although they were aberrant and these PCs were mostly CD45+. In some patients (9,7% of MGUS; 17,6% of MM) PC did express neither CD19 nor CD56 and this fact may complicate further evaluation of PCs. Conclusions: Results confirmed that in MGUS subjects we can find lower numbers of PCs which are mostly CD45+CD19+. A majority of plasma cells in newly diagnosed MM patients are abnormal CD56+ PCs and these plasma cells are usually CD45−. Further follow-up of patients can confirm the N/A ratio as a predictive factor for transformation of MGUS into MM and its value for evidence of relapse or progression to active myeloma.


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