In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma.
BACKGROUND
Epidemiologic studies have demonstrated an inverse correlation between dietary calcium and vitamin D intake and the incidence of colorectal carcinoma. Elevated serum levels of 25-hydroxyvitamin D3 (25-OH-D3) are associated with a major reduction in the incidence of this neoplasm. The reduction in tumor size and number induced by calcium supplements in an experimental carcinogenesis model was neutralized by vitamin D3 deficiency. To the authors' knowledge, vitamin D serum levels have never been determined previously in colorectal carcinoma patients. They compared serum 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), 25-OH-D3, and parathyroid hormone (PTH) levels of colorectal carcinoma patients with those of healthy controls.


METHODS
Serum 1,25(OH)2D3, 25-OH-D3, and PTH levels were determined in 84 colorectal carcinoma patients (10 with Stage I, 29 with Stage II, 25 with Stage III, and 20 with Stage IV) and 30 healthy controls, all of whom were normocalcemic and not taking calcium or vitamin D supplements.


RESULTS
25-OH-D3 serum levels were higher in cancer patients than controls, irrespective of stage. Serum 1,25(OH)2D3 decreased with advancing stage: 73 +/- 18, 48 +/- 16, 39 +/- 12, 34 +/- 13, and 75 +/- 20 pg/mL in Stages I, II, III, IV, and controls, respectively. There was a corresponding increase in serum PTH levels: 58.0 +/- 9.4, 73.7 +/- 14.4, 79.0 +/- 21.3, 100.4 +/- 30.9, and 51.2 +/- 3.9 pg/mL in Stages I, II, III, IV, and controls, respectively. Serum vitamin D metabolite levels did not correlate with gender, age, tumor localization, or histologic grade.


CONCLUSIONS
An inverse correlation between serum levels of the active metabolite of vitamin D and colorectal carcinoma stage has been demonstrated for the first time, to the authors' knowledge, in colorectal carcinoma patients. Because 1,25(OH)2D3 has been shown to inhibit proliferation of colonic epithelial cells, decreased serum levels may facilitate the growth of colorectal carcinoma and influence its biologic behavior.
Niv
Y
Y
Department of Gastroenterology, Rabin Medical Center, Tel-Aviv University, Petah-Tikvah, Israel.
Sperber
A D
AD
Figer
A
A
Igael
D
D
Shany
S
S
Fraser
G
G
Schwartz
B
B
D000368:Aged; D002112:Calcifediol / Q000097:blood*; D002117:Calcitriol / Q000097:blood*; D016022:Case-Control Studies; D003110:Colonic Neoplasms / Q000097:blood* / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D009367:Neoplasm Staging; D010281:Parathyroid Hormone / Q000097:blood*; D012004:Rectal Neoplasms / Q000097:blood* / Q000473:pathology
D010281:Parathyroid Hormone; D002117:Calcitriol; D002112:Calcifediol