Riboflavin use as a drug marker in Veterans Administration cooperative studies.

Most Veterans Administration (VA) cooperative studies have used only the pill count method to measure and describe patient adherence to a drug regimen. The use of a drug marker is considered when adherence is expected to be a problem in a study, especially if the therapeutic drug or metabolite cannot be measured in the blood or urine of all patients or if reliability of pill counts is open to serious question. In a VA-NHLBI hypertension study using riboflavin as a marker for assessing patient adherence, group data suggest that similar adherence scores can be expected when comparing pill counts and urine tests. However, when an individual patient's adherence was examined by each method at a particular visit, discrepancies were noted. In a VA cooperative study on disulfiram for the treatment of alcoholism, riboflavin used as a marker provided additional information that was needed to assess the adherence of the study population. By employing this second measure of adherence in this study, we were able to obtain at least one measure of adherence at 84% of all clinic visits. If the pill count method had been the sole adherence measure, only 60% of visits would have produced an adherence score. At 65% of clinic visits, the pill count and urine test were in agreement. Results of urine tests taken in the interval between visits were similar to those taken at the clinic visit. Patient cooperation in providing urine specimens or in returning pills to the clinic was slightly associated with positive adherence scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Platelets and malignancy. Rationale and experimental design for the VA Cooperative Study of RA-233 in the treatment of cancer.

Considerable evidence has accumulated in recent years which implicates blood coagulation reactions in the growth and spread of malignancy. In particular, platelets may accumulate on embolic tumor cells and facilitate their adhesion to the endothelium at distant sites perhaps by enhancing blood coagulation reactions. Alternatively, platelets may promote tumor cell proliferation by contributing a growth-promoting factor or through interactions mediated by prostaglandins. Inhibition of tumor growth and spread by platelet-inhibitory drugs has been demonstrated in several experimental tumor systems. Preliminary data suggest that similar effects may be seen in human malignancy. The purpose of this paper is to review relevant literature which provides the rationale for therapeutic trials of platelet-inhibitory drugs in human malignancy and to describe the experimental design for a trial involving one such drug, RA-233, in a recently established VA Cooperative Study.