Abstract 4569

Background:

Monoclonal B-Lymphocytosis (MBL) is the presence of small asymptomatic B-cell clones in the peripheral blood. Prior population studies included only very small numbers in the very elderly age group, but suggested there is a remarkably high prevalence of 50–75% in individuals age ≥90 years (yrs) (Ghia et al, Blood 2004; Nieto et al., Blood 2009). This has led to the hypothesis that MBL clones may be an inevitable consequence of aging, and possibly a phenomenon of immune senescence. The population of Australians aged 90–99 years has increased by 204% (42,234 to 128,654) [0.25% to 0.59%] between 1990 and 2010 compared to a 30% increase in the general population (17M to 22M). At this age bracket the M:F ratio is 1:3 (www.abs.gov.au). Community-based pathology laboratories now see large numbers of patients in this age range. With the aging population, the incidence of MBL, and therefore the risk of progression to CLL, has some practical and not just theoretical relevance.

Methods:

We selected 50 sequential individuals presenting to a large non-hospital based pathology laboratory for a full blood count over 3 separate days. In order to have representation across all age brackets, each one year age bracket (i.e. age 90, age 91, etc) was capped at five patients on each of the 3 separate analysis days. We performed 10-colour flow cytometry on EDTA samples from each individual with an approximate sensitivity down to <0.01×109/L absolute clonal count.

Results:

The age distribution of individuals selected was: 90 yrs – 7, 91 yrs – 6, 92 yrs – 6, 93 yrs – 12, 94 yrs – 6, 95 yrs – 3, 96 yrs - 2, 97 yrs - 2, 98 yrs - 3, 99 yrs - 1, 100 yrs - 1, 101 yrs – 1. Typical of this age bracket, there were 17 males and 33 females, an M:F ratio of 1:2. Five of the 50 tested individuals were identified with an MBL clone, and hence the prevalence was 10%. Two clones were CLL-like, and 3 were non-CLL or lymphoma-like, compared to MBL at other ages where ∼75% are CLL-like and ∼25% NHL-like. All clones were identified in females at ages 92 to 95. No clones were identified in individuals aged >95 years, including the two centenarians aged 100 and 101 years.

Table 1.

Haematology and phenotypic data on 5 of 50 individuals with MBL age≥90 years.

M/FAgeHbANCALCPlatCD20CD 19CD5/19κλClone typeClone level
F 92 135 3.6 1.3 221 15 15 1 14 1 NHL 0.18 × 109/L 
F 93 152 5.9 2.2 249 22 23 11 15 4 CLL 0.24 × 109/L 
F 94 126 5.0 1.2 211 12 12 <1 10 2 NHL 0.12 × 109/L 
F 94 128 4.3 1.9 275 23 24 11 8 5 CLL 0.21 × 109/L 
F 95 102 3.2 2.1 253 14 14 0 2 12 NHL 0.25 × 109/L 
M/FAgeHbANCALCPlatCD20CD 19CD5/19κλClone typeClone level
F 92 135 3.6 1.3 221 15 15 1 14 1 NHL 0.18 × 109/L 
F 93 152 5.9 2.2 249 22 23 11 15 4 CLL 0.24 × 109/L 
F 94 126 5.0 1.2 211 12 12 <1 10 2 NHL 0.12 × 109/L 
F 94 128 4.3 1.9 275 23 24 11 8 5 CLL 0.21 × 109/L 
F 95 102 3.2 2.1 253 14 14 0 2 12 NHL 0.25 × 109/L 
View Large
Conclusion:

The prevalence of MBL in individuals aged 90–100+ years is 10% and hence comparable to the prevalence in individuals aged over 60 years. There were 3 non-CLL, and 2 CLL-like clones. The absolute count of the clones is very low; they would not be detected in routine clinical practice and are highly unlikely to be of clinical significance. Despite the typical M:F ratio of 2:1 for CLL and 1:1 for MBL, there were no males identified with a B-cell clone, probably reflecting in part the fewer surviving males at this age. MBL is therefore not an inevitable consequence of aging or immune senescence.

Disclosures:

Mulligan:Roche: Consultancy, Research Funding, Speakers Bureau; Genzyme: Consultancy, Research Funding, Speakers Bureau.

Topics:
clone cells, lymphocytosis, alteplase, cd20 antigens, edetate disodium, edetic acid, flow cytometry, lymphoma, complete blood count, platelet count measurement

Author notes

*

Asterisk with author names denotes non-ASH members.

© 2012 by The American Society of Hematology
2012
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