Hi Dedi,
I'm sorry to hear that you have this genetic metabolic disorder, and
fear that your case is far from clear. As Njbagel notes below, the
question of whether aspirin is bad for people with G6PD Deficiency is
being called into doubt after being pretty much accepted fact for 15
years. I'm pasting in four abstracts from the PubMed MEDLINE database
(www.pubmed.gov) that look at studies of the effect of aspirin
(acetylsalicylic acid) on the blood of people (particularly children)
with G6PD deficiency.
I have a feeling that part of the reason that aspirin reacts
differently in different people with your disease is that the disease
itself varies greatly from person to person. As a genetic disease, it
has many different levels of expression - so my feeling (and I'm not a
doctor) is that some people may react more significantly to aspirin
than others. More information than you'll ever really want to know
about G6PD deficiency is available from the OMIM: Online Mendelian
Inheritance in Man database (free article:
http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=305900).
There is also a very basic overview of G6PD deficiency available from
the Nemours Foundation:
http://kidshealth.org/parent/general/aches/g6pd.html that mentions
aspirin as one of the many drugs and other substances that should not
be given to people with this condition (others are sulfa drugs,
quinines, fava beans, and mothballs). I found this site through
MedlinePlus, the National Library of Medicine's consumer health index
(www.medlineplus.gov).
As for alternatives to aspirin for cardiac health, I think Njbagel and
others have done an excellent job of summarizing some of the major
options. You'll also find some great help at the MedlinePlus health
topic Heart Diseases - Prevention:
http://www.nlm.nih.gov/medlineplus/heartdiseasesprevention.html.
There is no direct non-aspirin corollary for heart disease prevention
- and aspirin is not recommended for generally healthy people (see the
FDA's page on Daily Aspirin Therapy at
http://www.fda.gov/fdac/features/2003/503_aspirin.html). I would
strongly suggest you talk this issue over with your physician. He/she
will have good recommendations about what you can do to lower your
risk of heart attack that will fit within the constraints of G6PD
deficiency (as we understand it).
Here are those articles I mentioned:
1: East Mediterr Health J. 1999 May;5(3):457-64.
Haemolytic potential of three chemotherapeutic agents and aspirin in
glucose-6-phosphate dehydrogenase deficiency.
Ali NA, al-Naama LM, Khalid LO.
The potential haemolytic effect of three chemotherapeutic drugs and aspirin was
tested in vitro by gluthathione stability tests. Blood was collected from the
local population of Basra, Iraq where previous studies had found a high
frequency of glucose-6-phosphate dehydrogenase (G6PD) deficiency. Primaquine,
chloramphenicol and sulfanilamide caused significant concentration-dependent
reductions of glutathione levels in G6PD-deficient red cells when compared to
normal red cells. Acetylsalicylic acid had no effect on glutathione level. The
G6PD-deficient erythrocytes behaved as previously reported, probably due to
similar patterns in the distribution of its variants. Studies on each local
variant are warranted and new drugs should be tested for haemolytic potential
prior to their introduction in areas where the deficiency is common.
2: DICP. 1991 Oct;25(10):1074-5.
Long-term, low-dose aspirin is safe in glucose-6-phosphate dehydrogenase
deficiency.
Shalev O.
Forty-four patients with Mediterranean-type glucose-6-phosphate dehydrogenase
(G-6-PD) deficiency receiving long-term, low-dose aspirin were monitored over
three months for evidence of hemolysis. Complete blood count, reticulocyte count
and serum bilirubin were normal in all patients before treatment and upon
periodic retesting. We conclude that there is sufficient current evidence to
remove the hemolytic stigma of aspirin in G-6-PD deficiency, thereby
establishing its safety for long-term therapy in this condition.
3: Ann Trop Paediatr. 1990;10(4):335-8.
Drug-induced haemolysis and renal failure in children with glucose-6-phosphate
dehydrogenase deficiency in Afghanistan.
Choudhry VP, Ghafary A, Zaher M, Qureshi MA, Fazel I, Ghani R.
Twenty children (18 boys and 2 girls) with a proven or presumptive diagnosis of
glucose-6-phosphate dehydrogenase (G-6-PD) deficiency developed intravascular
haemolysis following administration of antimalarials in 9, chloroquine and
chloramphenicol in 1, chloroquine, chloramphenicol and aspirin in 1,
chloramphenicol and aspirin in 3, and aspirin alone in 4. Eleven of these
children developed acute renal insufficiency. All were managed with supportive
care, including blood transfusion, forced diuresis and peritoneal dialysis
wherever indicated. Only 16 children recovered completely. The occurrence of
G-6-PD deficiency is being reported for the first time in Afghanistan.
4: Acta Haematol. 1989;81(4):208-9.
Aspirin-induced acute haemolytic anaemia in glucose-6-phosphate
dehydrogenase-deficient children with systemic arthritis.
Meloni T, Forteleoni G, Ogana A, Franca V.
In a 4-year 7-month-old boy with glucose-6-phosphate dehydrogenase deficiency
and systemic arthritis a severe haemolytic anaemia occurred after the
administration of acetylsalicylic acid. Erythrocyte fragmentation, with
haemoglobin condensation zones next to clear zones, was observed on peripheral
blood smears. Since viral or bacterial infections were excluded on the basis of
the laboratory data, the anaemia was ascribed to aspirin.
These were found by doing a PubMed (www.pubmed.gov) search as follows:
"acetylsalicylic acid AND g6pd deficiency Field: All Fields, Limits:
English"
Let me know if anything needs clarifying, otherwise, good luck!
Librariankt |
