Enhancement of 24,25-Dihydroxyvitamin D Levels in Patients Treated with Continuous Ambulatory Peritoneal Dialysis

Shany, Shraga; Rapoport, Jayson; Zuili, I.; Yankowitz, N.; Chaimovitz, Cidio

doi:10.1159/000183653

Cited by 18 publications

(6 citation statements)

References 8 publications

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“…25‐OH‐D 3 and 1,25(OH) 2 D 3 fractions were separated by the Sep‐Pak separation procedure using C‐18 and silica columns 25. The 25‐OH‐D 3 fraction was submitted to a competitive protein binding assay using diluted rachitic rat serum as the binding protein 26. The 1,25(OH) 2 D 3 fraction was determined quantitatively by a vitamin D receptor (VDR) binding assay27 using calf thymus VDR as the ligand binder (Nichols Co.).…”

Section: Methodsmentioning

confidence: 99%

In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma

Niv

Sperber

Figer

et al. 1999

Cancer

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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. Cancer 1999;86:391–7. © 1999 American Cancer Society.

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Section: Methodsmentioning

confidence: 99%

In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma

Niv

Sperber

Figer

et al. 1999

Cancer

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“…25-(OH)D and 1,25-(OH) 2 D fractions were separated by a Sep-Pak (Waters, Milford, MA) separation procedure using C-18 and silica columns (33). The 25-(OH)D fraction was submitted to a competitive protein-binding assay using diluted rachitic rat serum as the binding protein (34). Quantification of the 1,25-(OH) 2 …”

Section: Serum 25(oh)d and 125(oh) 2 D Determinationmentioning

confidence: 99%

Estrogen Increases 1,25-Dihydroxyvitamin D Receptors Expression and Bioresponse in the Rat Duodenal Mucosa

Liel

1999

Endocrinology

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Menopause and estrogen deficiency are associated with apparent intestinal resistance to vitamin D, which can be reversed by estrogen replacement. The in vivo influence of estrogens on duodenal vitamin D receptor (VDR) was studied in three groups of rats: ovariectomized (OVX), sham-operated, and ovariectomized rats treated daily with estrogen (40 g/kg BW) for 2 weeks (OVX ϩ E). Estrogen administration to OVX rats resulted in a 2-fold increase in VDR messenger RNA transcripts. 1,25(OH) 2 D 3 was shown to bind specifically to one class of receptors in duodenal mucosal extracts, with a dissociation constant of 0.03 nM. Binding was significantly increased in duodenal extracts from OVX ϩ E rats, compared with OVX rats (735 Ϯ 81 vs. 295 Ϯ 26 fmol/mg protein; P Ͻ 0.001); a comparable, 1.5-to 2-fold increase in VDR protein expression was observed in Western blot analyzes of the duodenal mucosa. Markers of VDR activity were increased in estrogen-exposed rats: calbindin-9k messenger RNA transcript content was 1.4-to 1.6-fold higher, and alkaline phosphatase activity was 1.4-to 3-fold higher in sham-operated and OVX ϩ E, respectively, compared with OVX. 25(OH)D, 1,25(OH) 2 D, or PTH levels were not altered by estrogen treatment. Cumulatively, these findings suggest that estrogen up-regulates VDR expression in the duodenal mucosa and concurrently increases the responsiveness to endogenous 1,25(OH) 2 D. Modulation of intestinal VDR activity by estrogen, and subsequent influence on intestinal calcium absorption, could be one of the major protective mechanisms of estrogen against osteoporosis. (Endocrinology 140: 280 -285, 1999) I NTESTINAL calcium absorption takes place via two main mechanisms: passive diffusion, which occurs when luminal calcium is high; and active absorption, a complex and not fully understood process mediated by 1,25(OH) 2 D 3 , which predominates when luminal calcium is low (1). Under physiological circumstances, 1,25(OH) 2 D 3 is primarily produced in the kidneys under the influence of PTH stimulation. PTH secretion, in turn, is dependent on extracellular free calcium concentration, as sensed by calcium-sensing-receptors located in parathyroid cells' membranes (2). Overall, the rate of active intestinal calcium absorption is determined by physiologic interactions between various components of the PTH-vitamin D-endocrine system organized in a multilevel negative feed-back loop structure.Intestinal calcium absorption declines with age, both in humans (3, 4) and in rats (5). A widely held hypothesis suggests that the decrease in intestinal calcium absorption results from a sequence of events initiated by low estrogen levels, causing increased bone resorption; released calcium increases extracellular space calcium concentration, which suppresses PTH secretion, followed by a subsequent decrease in 1,25(OH) 2 D 3 production and in 1,25(OH) 2 D 3 plasma concentration, and finally results in decreased intestinal calcium absorption (6).Nevertheless, there is evidence that estrogen may be more directly i...

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“…Shany et al [24] demonstrated that CAPD patients with kidneys in situ appear to be able to produce an adequate serum level of 1,25 and 24,25(OH)3D3 if administered 1-a-OH-D alone. Salusky et al [25] suggest high-dose l,25(OH)2D3 for control of renal osteodystrophy, and Delmez et al [26] suggest intraperitoneal dialysate supplemented with 4.0 mEq/1 cal cium and 0.5 ug l,25(OH)2D3.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Ionized Calcium and 1,25-Dihydroxycholecalciferol Loss from Peritoneal Fluid during Peritonitis in Patients Treated with Continuous Ambulatory Peritoneal Dialysis

Lin

Huang²

1991

Nephron

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This study was to evaluate whether peritoneal loss of vitamin D metabolites during peritonitis leads to more depletion of 1,25-hydroxycholecalciferol [1,25(OH)₂D₃] and 25-hydroxycholecalciferol [25(OH)D] in continuous ambulatory peritoneal dialysis (CAPD) patients, especially in the high peritonitis occurrence group (HPOG). A series of ionized calcium, pH values, 1,25(OH)₂D₃ and 25(OH)D levels in dialysate during peritonitis were studied in 30 CAPD patients. In addition, bone mineral content (BMC) was determined during peritonitis. On the basis of peritonitis occurrence, 14 patients were in the low peritonitis occurrence group (LPOG) and 6 patients in the HPOG. Increase in peritoneal loss of ionized calcium, 1,25(OH)₂D₃, 25(OH)D and a decrease of pH value in dialysate may appear in the early period of peritonitis in both groups. When peritonitis occurs too frequently in a short period, the peritoneal membrane function cannot recover completely. Frequent peritonitis may impair peritoneal function and cause persistent loss of calcium. 1,25(OH)₂D₃ amd 25(OH)D loss is also higher in the HPOG than in the LPOG. The persistent loss of calcium, low plasma vitamin D levels and increased parathyroid hormone level with hyperparathyroidism in the HPOG are the important factors contributing to renal osteodystrophy. The lower BMC in the bone study confirmed this. Therefore, adequate calcium and vitamin D supplementation is necessary in the HPOG.

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Enhancement of 24,25-Dihydroxyvitamin D Levels in Patients Treated with Continuous Ambulatory Peritoneal Dialysis

Cited by 18 publications

References 8 publications

In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma

In colorectal carcinoma patients, serum vitamin D levels vary according to stage of the carcinoma

Estrogen Increases 1,25-Dihydroxyvitamin D Receptors Expression and Bioresponse in the Rat Duodenal Mucosa

Enhancement of Ionized Calcium and 1,25-Dihydroxycholecalciferol Loss from Peritoneal Fluid during Peritonitis in Patients Treated with Continuous Ambulatory Peritoneal Dialysis

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