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Hi!
I don't understand why she was started on 180mg prednisone. This is a HUGE dose! When using prednisone to treat various conditions (not necessarily AA), any doctor would start at 1mg/kg, unless there is a specific rationale to up the dose. Even then, you'd want to start at lower doses and then increase as necessary.
According to the protocol used by Children's Hospital in Denver, glucosteroids are used to attenuate/ prevent serum sickness caused by ATG. Thus the patient receives twice a day methylprednisolone IV (Solumedrol) 1mg/kg for day 1 through 5, and then twice a day prednisone oral 1mg/kg for days 5 through 10, followed by taper till day 13.
N. Goldenberg and al. - Succesfsul treatment of SAA in Children Using Standardized IST with ATG and CsA - Pediatric Blood Cancer 2004; 43; p. 718
My son used a similar protocol from Boston Children's Hospital.
However, having been on such huge dose, it is normal to taper slowly (probably at 10mg/mo), and this discussion would be somehow moot.
About the Neupogen, I honestly believe is a very dangerous drug if used regularly long term as Haylee seems to be doing. I would be extremely reluctant to give to her unless her ANC drops below 200, and even then, only on a case by case basis (as needed per CBC). The following is a commentary that I posted on the Aplastic Central forum (please note that G-CSF is the same thing as Neupogen)
"There is quite a lot of controversy surrounding the use of G-CSF in AA patients. First to sound the alarm were the japanese researchers that found a strong statistical correlation between use of G and latter development to MDS.
Kojima et all - Blood, 2002, 100, p.786
The American researchers were initially skeptical, they pointed out that very large doses of G were administered in the japanese patient cohort (which was indeed true). However, the seeds of doubt were there...
So Young at NIH did his own studies (the following article is very technical, as is mainly lab research, but the title summons all up)
G-CSF preferentially stimulates proliferation of monosomy 7 cells bearing the isoform IV receptor
Sloand, Young et all - Proceedings of the National Academy of Science of USA - 2006, 103, 39, p. 14483
Their findings were that the data "strongly suggest a mechanism by which G expands an existing monosomy 7 clone". They tried to downplay the risks of using G occasionally (as in healthy blood donors that sometimes receive shots after donating blood or surgery patients) but had to caution against long term use.
The Europeans in the meantime did a huge analysis of some 840 patients that received or not G.
Blood First Edition Paper, pre-published online November 16, 2006; DOI 10.1182/blood-2006-07-034272
They found a significant incidence of MDS/AML
in the patients that did take it (the doses were NOT as high as in the japanese study, what matter was length of use) Their findings "emphasise the necessity [..] to alert physicians that adding G-CSF to immunosupressive treatment is currently not standard treatment for SAA"
But, again, since her doctor plans to take her off Neupogen, this discussion is also somehow moot.
May I ask you what was her MCV (mean corpuscular volume) at diagnosis?
Sandra
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