Vitamin D is also known as the “sunshine vitamin” since it is manufactured by the body when the skin is exposed to sunshine. Ten to fifteen minutes of sunshine three times weekly is adequate to produce the body’s requirement of vitamin D. It promotes the body’s absorption of calcium, which is essential for the normal development of healthy teeth and bones. It also helps maintain the adequate blood levels of calcium and phosphorus, which are minerals. Vitamin D is found in cheese, butter, margarine, cream, fortified milk (all milk in the United States is fortified with Vitamin D), fish, oysters, and fortified cereals.

Exposure to sunshine, as any medication, should be in appropriate doses and in safe periods of the day: sun should be avoided between 11 am. and 2 pm. in the spring and autumn, and between 10 am. and 3 pm. in the summer (or maybe in even broader range depending on individual tolerance).
 

BONE DISEASE IN VITAMIN D-DEFICIENT PATIENTS WITH CROHN’S DISEASE.
Vogelsang H; Ferenci P; Woloszczuk W; Resch H; Herold C; Frotz S; Gangl A, 1st Department of Gastroenterology and Hepatology, Allgemeines Krankenhaus; Vienna, Austria. Dig Dis Sci, 1989 Jul, 34:7, 1094-9

Vitamin D deficiency is frequently observed in patients with Crohn’s disease and may be associated with an increased risk of development of metabolic bone disease. To estimate the incidence of metabolic bone disease by noninvasive methods, 31 patients (17-75 years old) with Crohn’s disease and low 25 hydroxyvitamin D (25-OHD) levels in winter were investigated in the following summer by measuring the bone mineral content (BMC) of the distal radius by single photon absorptiometry and the cortical area ratio (CAR) calculated from radiographs of the right hand and by x-ray of the lumbar spine. Forty-five percent of the patients showed signs of metabolic bone disease. BMC and CAR correlated with 25-OHD serum levels (P less than 0.05), especially in men. Furthermore, the amount of sun exposure has an influence not only on 25-OHD serum levels both in summer and in winter (P = 0.0006), but also on the BMC (P = 0.07). Consequently, vitamin D deficiency is of major importance for the development of metabolic bone disease in patients with Crohn’s disease. Vitamin D deficiency can be prevented by increasing sun exposure and long-term vitamin D supplementation.
 

OSTEOPOROSIS IN INFLAMMATORY BOWEL DISEASE
*M. Szathmári, Zs. Tulassay, L. Prónai L, T. Zágoni, A. Németh (2nd Dept. Medicine, *1st Dept. of Medicine, Semmelweis Medical Univ., Clinical Gastroenterology Research Unit, Hungary, Budapest). Fifth International Semmelweis Symposium, 1996

Purpose: The aim of our study was to evaluate bone metabolism in colitis ulcerosa and Crohn's disease and assess whether ostopenia represents rather a symptom of the disease then a consequence of the corticosteroid therapy. Methods: Twenty-two patients with ulcerative colitis (9 male, 13 female, mean age 26 y.o., range 22-71) and 23 with Crohn's disease (13 male, 10 female, mean age 42 y.o., range 19-54) were involved in the study. Mean duration of ulcerative colitis was 8.2 years (range 1-20) and that for Crohn's disease was 5.3 years (range 1-20). The bone mineral content and density of the bone turnover were measured by dual X-ray absorptiometry at the lumbar spine and femoral neck, and by single photon absorptiometry at the non-dominant radius midshaft. Other biochemical parameters of bone mineral turnover were also evaluated. Results: A mild osteopenia was detected in approximately one-third of patients with inflammatory bowel disease (Z-score < -1.0). The mean lumbar spine Z-score was significantly lower in Crohn's patients without corticosteroid therapy (Z-score= -0.65, p<0.0.5) than that of the normal population (0). On the other hand, Z-score values were not lower in Crohn's patients treated with corticosteroid when compared to that in patients without this therapy. Z-score of colitis ulcerosa patients without corticosteroid therapy did not show a significant deviation from the normal population. On the other hand, colitis ulcerosa patients with corticosteroid treatment had a significantly lower Z-score (-0.67, p<0.05) compared to healthy controls. All biochemical parameters of bone resorption and formation were within the normal range. Conclusion: Crohn's disease but not colitis ulcerosa seems to be an independent risk factor to induce osteopenia. Steroid use is associated with a decrease of bone mineral density only in colitis ulcerosa.
 

PREVENTION OF BONE MINERAL LOSS IN PATIENTS WITH CROHN'S DISEASE BY LONG-TERM ORAL VITAMIN D SUPPLEMENTATION
Vogelsang H; Ferenci P; Resch H; Kiss A; Gangl A. Eur J Gastroenterol Hepatol: 7:7:609-14 (1995)

OBJECTIVE: To determine whether long-term dietary supplementation with low doses of vitamin D
helps to prevent bone loss and the development of osteoporosis or osteomalacia in out-patients
with Crohn's disease. DESIGN: A randomized controlled study. SETTING: The out-patient clinic of a tertiary centre (university hospital). PATIENTS: Seventy-five out-patients (31 men and 44 women, aged 16-77 years) with Crohn's disease. INTERVENTIONS: All patients were randomly assigned to receive either an oral supplement of 1000 IU/day vitamin D for 1 year or no supplement. Bone
mineral density, assessed in the distal part of the nondominant forearm using single photon
absorptiometry, and serum levels of 25-hydroxyvitamin D, assessed using a competitive protein
binding assay, were measured before and after the period of dietary supplementation. MAIN
OUTCOME MEASURE: Relative change of bone mineral density. RESULTS: Serum levels of
25-hydroxyvitamin D increased in 57% of patients who received a supplement (compared with 37% of control patients). Bone mineral density decreased significantly in control patients median -7%,
interquartile range -12.6-(+0.4%) but not in patients who received a supplement median -0.2%,
interquartile range -3.8-(+14%); P < 0.005. Increases in bone mineral density were especially
prevalent among patients who received the supplement and had normal serum levels of
25-hydroxyvitamin D (68%), whereas increases occurred in only 18% of patients with low serum
levels of 25-hydroxyvitamin D (P = 0.008). Patients without an intestinal resection and receiving the
vitamin D supplement had a marginally greater increase in bone mineral content than patients who
had undergone a resection (P = 0.05). CONCLUSION: Long-term oral vitamin D supplementation seems to be an efficient means of preventing bone loss in patients with Crohn's disease and could be recommended, especially for patients at high risk of osteoporosis.

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