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Antineoplastics



Depletions

Antineoplastics/Nutrient Depletion:
  • ArginineArginine: Data from a clinical trial indicates that certain antineoplastics may have a mechanism of action that starve cancer cells through depletion of arginine (15911102).
  • CarnitineCarnitine: Increased urinary loss of carnitine has been noted in patients taking ifosfamide (10412953). In humans, during one chemotherapy cycle using ifosfamide, an increased urinary loss of carnitine was noted and patients lost about 10% of their carnitine stores (10412953). Based on human study, cisplatin may increase urinary excretion of carnitine and acylcarnitine due to inhibition of carnitine reabsorption by the proximal tubule of the nephron (9832290). Carnitine levels, however, normalized seven days after cessation of chemotherapy. Based on human study, carboplatin may inhibit L-carnitine and its short-chain acetyl-L-carnitine reabsorption in the kidney (16988826).
  • CholesterolCholesterol: Based on a review, boron derivatives may increase lipid excretion from the body and by inhibiting rate-limiting enzyme activities for the de novo synthesis of lipids and cholesterol (16101500).
  • CholineCholine: Based on secondary sources, methotrexate may diminish pools of choline metabolites.
  • DHEADHEA: Based on human evidence, DHEA was lowered compared with pretreatment values in both women and men taking Gefitinib® (15870715).
  • FolateFolate: Secondary sources cite that methotrexate may be a folate antagonist that prevents the conversion of folic acid to its active form and lowers plasma and red blood cell folate levels. Secondary sources also indicate that patients being treated with methotrexate for cancer should avoid folic acid supplements, unless recommended by their oncologist. Secondary sources maintain that folic acid may interfere with the anticancer effects of methotrexate.
  • MagnesiumMagnesium: Human and animal studies indicate that amifostine (WR-2721) may reduce serum magnesium levels by reducing renal tubular reabsorption of magnesium and increasing urinary losses (2837628, 10958599). Carboplatin and cisplatin may cause hypomagnesemia due to renal tubular damage, which increases urinary magnesium losses (11219485). Based on human study, cetuximab (Erbitux®) may increase renal magnesium excretion, resulting in lowered magnesium levels in patients (16945172, 17118852, 18594003, 18473701). According to secondary sources, panitumumab (Vectibix®) may increase renal magnesium excretion, leading to lowered magnesium levels. Based on human study, recombinant interleukin-2 (IL-2) infusions have been associated with hypomagnesia (3260620).
  • Niacin/niacinamideNiacin/niacinamide: Mercaptopurine may reduce niacin levels due to a deficiency of nicotinamide or of its precursor tryptophan (9856171). Based on case reports, fluorouracil may cause a deficiency of vitamin B3 (9856171, 8504053). According to secondary sources, 5-fluorouracil may inhibit the conversion of tryptophan to niacin.
  • PotassiumPotassium:Based on human and animal studies, cisplatin may induce hypokalemia by an increase in renal potassium excretion (15619138, 11219485, 2400647, 14583761). According to a review and human study, both cisplatin and carboplatin may cause hypokalemia due to damage to vasculature or structures of the kidney (11219485, 2400647).
  • RiboflavinRiboflavin: Based on animal evidence, doxorubicin (Adriamycin®) use may cause a depletion of riboflavin due to an increase in urinary excretion of riboflavin (1802973). Based on animal evidence and a review, methotrexate may inhibit the effects of riboflavin in the body (5535183, 4579772). There is preliminary human evidence suggesting that postmenopausal breast cancer patients with low riboflavin levels may normalize their levels following treatment with tamoxifen (9849035). Theoretically, the cause of their low baseline riboflavin, however, may be related to prior treatment with doxorubicin chemotherapy.
  • ThiaminThiamin: Based on secondary sources, 5-fluorouracil (5-fluorouracil, 5-FU, Adrucil®) may inhibit the phosphorylation of thiamin to thiamin pyrophosphate, interfering with activation of thiamin and possibly increasing its breakdown. Secondary sources cite that people receiving fluorouracil-containing chemotherapy regimens may be at risk for developing symptoms and signs of thiamin deficiency. In addition, chemotherapy patients may be at an elevated risk of developing vitamin deficiencies due to decreased dietary intake.
  • Vitamin EVitamin E: Based on human study, in patients with chronic myeloid leukemia, treatment with busulfan appeared to increase serum vitamin E levels (10778591). Levels may increase after treatment without vitamin E supplementation. Based on human study, cisplatin may reduce plasma vitamin E levels (11484987, 12610195). According to secondary sources, cyclophosphamide and cytosine may reduce vitamin E levels. Based on animal studies, alpha-tocopherol levels may be reduced by doxorubicin (18513847). Based on human studies, etoposide may reduce plasma concentrations of alpha-tocopherol possibly as a result of enhanced breakdown of the antioxidant (2513140). According to secondary sources, vitamin E may be reduced after the administration of methotrexate or thiotepa.
  • Vitamin KVitamin K: Based on anecdotal evidence, dactinomycin may decrease the effects of vitamin K and increase vitamin K requirements.
  • ZincZinc: Based on human evidence, cisplatin may increase renal excretion of zinc(7201366). Based on human study, dexrazoxane may increase urinary zinc excretion (11410492). According to secondary sources, dexrazoxane may reduce zinc level through metal-ion chelating activity.

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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