Patrusha,
It is unfortunate that your total and absolute white blood cell counts were too low for you to get your scheduled chemotherapy. However, the truth is that both cancer and chemotherapy are often times unpredictable.
About the DPD deficiency. It, too, was suspected that I might be DPD deficient and I recieved the blood test. I pasted this information last week under liver resection but will paste here as well for you to peruse.
Keep kickin' a little cancer a@#!
Holly
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Rodney,
You are correct. DPD deficiency is rare. If you are DPD deficient, you would lack an enzyme which would not allow you to metabolize 5-FU. There is a blood and breathe test available. I had the blood test done through the University of Alabama at Birmingham. I have included the information below for you to peruse. With the complications that you experienced with 5-FU, you may wish to reintroduce the topic with your physician.
Holly
Background
Although introduced as a chemotherapy agent almost 45 years ago, 5-fluorouracil (5-FU) remains one of the most successful and widely used cancer chemotherapy drugs. 5-FU can be used as a single agent but is typically administered in combination with other drugs for the treatment of a number of different malignancies including, carcinomas of the breast, colon, and skin (three of the most frequently occurring cancers). In general, 5-FU is relatively well tolerated at standard doses with typical toxic effects occurring in the gastrointestinal mucosa and bone marrow. Neurologic toxicity presenting as cerebellar ataxia and somnolence occurs much less frequently (<5%). Like many other antineoplastic drugs, 5-FU has a relatively narrow therapeutic window, such that toxicity is likely to increase as the dose is increased. The success of 5-FU has led to several new generation 5-FU-based drugs including Xeloda (Roche) and Tegafur (Taiho).
Metabolism
The anticancer effects and toxicity of 5-FU are directly related to anabolism of the drug to its nucleotides, which can then exert effects through inhibition of thymidylate synthase activity or incorporation into RNA and/or DNA. In humans, more than 85% of an administered dose of 5-FU is degraded through the catabolic pathway. Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting step in pyrimidine catabolism. Over the last decade, it has become clear that DPD regulates the amount of 5-FU available for anabolism thereby affecting its pharmacokinetics, toxicity, and efficacy.
Unanticipated Toxicity to 5-FU
Several reports have described an inherited (pharmacogenetic) disorder in which individuals with absent or significantly decreased DPD activity develop life-threatening toxicity following exposure to 5-FU. Since the catabolic pathway does not function in DPD deficient patients, administration of standard doses of 5-FU results in altered 5-FU pharmacokinetics and severe toxicity including mucositis, granulocytopenia, neuropathy and death. The cause for this toxicity appears to be decreased drug clearance, resulting in markedly prolonged exposure to 5-FU. It has been estimated that approximately 3-5% of the population has DPD activity less than 95% of the lower limit (<0.064 nmol/min/mg for frozen samples) for the normal population. Recent studies by our laboratory have demonstrated a large over-representation of both profoundly (12 %) and partially (31%) DPD deficient patients who developed unanticipated toxicity following treatment with 5-FU.
But there is more......
http://www.dpdenzyme.com/