very small study by NIH (why so small? weren't they interested in what they were doing? they could hardly lack funding)
It is not evident how they defined recovery ("no symptoms attributed to Lyme disease"; the verbage does not necessarily indicate they were clear of symptoms altogether), and the healthy volunteers are not characterized at all.
I know nothing of the players in the Lyme politics wars. Are these the Reeves and Wesselys of the Lyme world?
Or should this be taken as a geniune contradictory result, though in pilot-sized numbers, so not as significant as, say, this study:
http://www.ncbi.nlm.nih.gov/pubmed/11222912
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2725528/It has been reported that patients with chronic Lyme disease have a decreased number of natural killer cells, as defined by the CD57 marker. We performed immunophenotyping in 9 individuals with post-Lyme disease syndrome, 12 who recovered from Lyme disease, and 9 healthy volunteers. The number of natural killer cells was not significantly different between the groups.
It is not evident how they defined recovery ("no symptoms attributed to Lyme disease"; the verbage does not necessarily indicate they were clear of symptoms altogether), and the healthy volunteers are not characterized at all.
I know nothing of the players in the Lyme politics wars. Are these the Reeves and Wesselys of the Lyme world?
Or should this be taken as a geniune contradictory result, though in pilot-sized numbers, so not as significant as, say, this study:
http://www.ncbi.nlm.nih.gov/pubmed/11222912
(extra paragraph breaks added)Methods: We evaluated 73 patients with chronic LD for lymphocyte subset abnormalities using flow cytometry. Of these, 53 patients had predominant musculoskeletal symptoms, while 20 patients had predominant neurologic symptoms.
The estimated duration of infection ranged from 3 months to 15 years, and all patients had positive serologic tests for B. burgdorferi. Ten patients with acute LD (infection less than 1 month) and 22 patients with acquired immunodeficiency syndrome (AIDS) served as disease controls.
Results: All 31 chronic LD patients who were tested prior to antibiotic treatment had significantly decreased CD57 lymphocyte counts (mean, 30+/-16 cells per microl; normal, 60-360 cells per microl, P<0.001).
Nineteen of 37 patients (51%) who were tested after initiating antibiotic therapy had decreased CD57 levels (mean, 66+/-39 cells per microl), and all five patients tested after completing antibiotic treatment had normal CD57 counts (mean, 173+/-98 cells per microl).
In contrast, all 10 patients with acute LD and 82% of AIDS patients had normal CD57 levels, and the difference between these groups and the pre-treatment patients with chronic LD was significant (P<0.001).
Patients with chronic LD and predominant neurologic symptoms had significantly lower mean CD57 levels than patients with predominant musculoskeletal symptoms (30+/-21 vs. 58+/-37 cells per microl, P=0.002).
CD57 levels increased in chronic LD patients whose symptoms improved, while patients with refractory disease had persistently low CD57 counts.