Abstract
The effect of large doses of vitamin C (3g ascorbic acid daily) on the ascorbic acid status and urinary excretion of hydroxyproline in 52 early breast cancer patients compared to 10 benign patients has been investigated. The leucocyte ascorbic acid levels of the early breast cancer patients did not increase to those levels found in the patients with benign disease. This may be due to reduced absorption of the vitamin, the effects of radiotherapy and drugs, or, as has been discussed, these patients may have an increased requirement for ascorbic acid due to the presence of residual neoplastic cells. It is possible that these patients could have been excreting the vitamin at a greater rate. Further kinetic studies, involving the administration of a 3g loading dose of the vitamin, were carried out. The excretory profiles of the 3 groups studied (early breast cancer, benign and normal individuals showed dramatic differences, suggesting that the restriction in the rise in leucocyte ascorbic acid concentration following supplementation could be a reflection of a widespread change in the general metabolism and utilisation of the vitamin in early malignant disease. During the course of study (March 1978 - October 1980), 5 of the early breast cancer patients showed clinical signs of skeletal involvement which were confirmed by positive bone scans. The metabolic profiles of these patients have been examined and the relationships between various plasma and urinary parameters are discussed in the light of the chronological development of osseous deposits. Additional longitudinal studies were carried out in advanced breast cancer patients with skeletal metastases. In particular, one patient (age 36 years) was closely observed for a period of 11 months. Sequential plasma ascorbic acid, calcium and alkaline phosphatase were carried out at monthly intervals to within 8 weeks of her death. These results are conflicting. However, the results do indicate that it may be advantageous to use ascorbic acid supplementation in patients with breast cancer as a standard supportive measure. Opportunity was taken to study the tryptophan metabolism in 51 early breast cancer patients compared to 14 patients with benign breast disease. The plasma total tryptophan concentrations were consistently lower in the cancer group, whilst N'-methylnicotinamide excretion was higher. The mean plasma total tryptophan level of the cancerous group increased with time through the study, decreased with age and seemed to be unaffected by the presence of disseminated disease. These trends were not reflected in any of the urinary metabolites studied. The aetiology of these tryptophan disorders has been discussed in the light of the dramatic differences observed between pre and post-menopausal tryptophan status observed, which may be indicative of the possible hormonal control mechanisms operating in this pathway.