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It has long been recognized that treatment with glucocorticoids can produce a significant loss of bone mass (1,2). The mechanism for this steroid-induced bone loss is not fully understood. but is associated with a marked decrease in intestinal calcium absorption and an increased urinary calcium excretion that frequently accompanies administration of supraphysiologic doses of glucocorticoids (3.4).It has been proposed that steroid-induced alterations in vitamin D metabolism are responsible for the decrease in intestinal calcium absorption produced by glucocorticoid therapy. Reports to date have suggested that 25-hydroxyvitamin D (25[OH]D) concentrations are low ( 5 ) or normal in patients treated with corticosteroids (6,7). More importantly, it has been reported that the circulating concentration of 1, 25[OHI7_D). the physiologically active form of vitamin D, is low (8) or normal (7,9-11) in subjects receiving glucocorticoids. These contradictory results are due, in part, to the dosage and length of glucocorticoid administration used in the previous studies. All studies to date have utilired a supraphysiologic dose of glucocorticoid. In order to assess whether long-term administration of low-dose glucocorticoids affects vitamin D metabolism, we measured the circulating concentrations of the vitamin D metabolites, calcium, phosphorus, alkaline phosphatase, and immunorcactive parathyroid hormone (iPTH) in patients with rheumatoid arthritis receiving 5 mg of prednisone per day for up to 6 months (12). Since the study was conducted as a double-blind trial, an age-matched group of patients with rheumatoid arthritis who received placebo served as the control group.Patients and methods. The details of the patient population and study protocol have been previously reported (12). Briefly, 34 patients were initiated into a double-blind trial that lasted 32 weeks. Patients were admitted who were receiving nonsteroidal antiinflammatory drugs including salicylates, or who were receiving a constant dose of gold salts or D-penicillamine for at least I 2 weeks prior to beginning the study. Excluded were patients with active peptic ulcer disease or rectal bleeding, diabetes mellitus, symptomatic idiopathic osteoporosis, or active renal or hepatic disease. Patients who had received intraarticular glucocorticoid injections, vitamin D, or calcium preparations less than 6 weeks prior to entering the study were also excluded. prednisone 24 weeks into the study. The final evaluation of patients in both groups was made at 32 weeks.

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Many gastrointestinal diseases have a predilection for the terminal ileum. Retrograde ileography is a valuable technique for evaluating this region. However, this procedure necessitates reflux of barium (with or without air) into the terminal ileum. This does not often spontaneously occur during a barium enema study. The use of glucagon in double-contrast studies of the colon has been recommended for various reasons, one of which is to facilitate reflux of barium into the terminal ileum. This randomized, double-blind trial confirms that glucagon does promote reflux. Multiple regression analysis indicates that the independent variables of patient age, weight, and sex have little effect on the frequency of reflux. It is concluded that glucagon can facilitate examination of the distal small bowel during a double-contrast colon examination.