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Member
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Join Date: Jan 2009
Location: Paradise
Posts: 855
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Member
Join Date: Jan 2009
Location: Paradise
Posts: 855
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Interesting Mike. Great job! While HPV B19 no doubt enters into the equation in some capacity, I am not sure that it enters into the causative side rather that in some way, it is simply a side effect of CRPS.
Seropositive existence of HPV B19 increases with age. By the age of 15, about 50% of individuals have serologic evidence of a past infection, which may present as the common childhood disease erythema infectiosum. At the age of 70, seroprevalence reaches 80 to 100%. This is according to a paper: Human parvovirus B19: relevance in internal medicine. Van Elsacker-Niele AM, Kroes AC. And Sève P, Ferry T, Charhon A, Calvet A, Broussolle C, in a paper titled Systemic manifestations of Parvovirus B19 infections, found that "B19 infection associated with virus clearance suggesting that B19 can act as a trigger of systemic disease. However, studies in large series indicate that in fact B19 is probably an extremely rare cause..."
And then Van de Vusse AC, Goossens VJ, Kemler MA, Weber WE. found in their study entitled Screening of patients with complex regional pain syndrome for antecedent infections, that "seroprevalence in lower extremity CRPS 1 (94%) was significantly higher than in upper extremity CRPS I patients (68%)." Why would there be such a huge difference in seroprevelance simply by virtue simply of location of symptoms? And that would also then mean that HPV B19 was not present at all in the blood of 32% of the patients with upper extremity CRPS I.
The B19 DNA seems to also cross over to many, many other illnesses like aplastic crisis in chronic haemolytic anaemias, exanthemathous disease and arthropathy, mainly in women, and chronic anaemia in the immunocompromised host. Even heart disease as discovered by Schenk T, Enders M, Pollak S, Hahn R, Huzly D, High prevalence of human parvovirus B19 DNA in myocardial autopsy samples from subjects without myocarditis or dilative cardiomyopathy, which stated that "B19 DNA was found in myocardial samples from 46 of 48 seropositive and in none of 21 seronegative individuals."
I think Gross et. al. may have it right in their abstract when they "suggest the involvement of parvovirus B19.......in the pathogenesis of CRPS." Perhaps there exists some defect or attack on the immune system to where HPV B19 then becomes a key player? Much like Pneumocystis carinii/jirovecii pneumonia is a very rare infection in people with normal immune systems but can become deadly in the immunocompromised.
Very interesting paper though. Thanks for sharing!
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