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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Curr Opin Gastroenterol. Author manuscript; available in PMC 2013 October 22.
Published in final edited form as:
PMCID: PMC3805278

Vitamin D Status in Gastrointestinal and Liver Disease

Structured Abstract

Purpose of the review

The purpose of this review is to report: a) the prevalence of suboptimal vitamin D status in populations with specific gastrointestinal disorders, b) information regarding the impact of vitamin D deficiency on the bone health of patients with these disorders, c) recommendations regarding optimal vitamin D intake to avoid deficiencies specifically for these disorders, d) the state of knowledge regarding the effect of vitamin D on the disease itself, through its actions on the immune system.

Recent findings

The scientific community has revised upward the serum level of vitamin D considered to reflect optimal vitamin D stores.

Evidence is emerging to support that doses of vitamin D much larger than the currently recommended are needed to maintain optimal vitamin D stores especially in individuals with diseases of the gastrointestinal system and the liver.

The relationship between vitamin D and bone health in individuals with gastrointestinal and liver disease is controversial.

The role of vitamin D in the regulation of the immune system continues being elucidated through findings in animal studies and in vitro.


Suboptimal vitamin D status is prevalent among individuals with gastrointestinal and liver disease, and the etiology of this finding is multifactorial and disease dependent. Although replacement and supplementation guidelines have not been well defined and could be different in different diseases and disease states, practitioners should aim for a serum 25OHD level of at least 32 ng/mL when undertaking these tasks. The contribution of vitamin D status to the bone health of individuals with gastrointestinal and liver disease may be different between active and quiescent phases of the disease. Finally, the role of vitamin D in altering disease course through its actions on the immune system remains to be elucidated.

Keywords: Vitamin D, 25 OH vitamin D, gastrointestinal disease, liver disease, inflammatory bowel disease, cystic fibrosis, celiac disease


Adequate skin exposure to solar ultraviolet B (UVB) radiation can satisfy the human requirement for vitamin D. During sunlight exposure, 7-dehydrocholesterol, present in plasma membranes of skin cells is converted to pre-vitamin D3 (pre-D3) which then undergoes thermally induced transformation to vitamin D3 (1). Season, latitude, time of day, skin pigmentation, aging, and sunscreen influence the cutaneous production of vitamin D3 (2). No pre-D3 is produced through skin exposure to sunlight even on cloudless days in Boston (42.2 degrees N) from November through February (3). Thus, patients depend on nutrition and/or oral supplements to satisfy their vitamin D needs during that time. Ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) are the most common forms of oral supplements available. Vitamin D, formed in the skin or ingested, is removed by binding to the plasma transport protein, vitamin D-binding protein (DBP) which delivers vitamin D first to the liver where it undergoes 25-hydroxylation (25OHD), and then to the kidney where it undergoes 1-hydroxylation (4). 1,25-dihydroxyvitamin D (1,25(OH)2D) is the active metabolite and over 30 tissues have receptors for this steroid (5). The most abundant metabolite in the human body is 25OHD and is indicative of overall vitamin D status (4).

Ingested vitamin D is lipid soluble, and as such, its absorption through the gastrointestinal system is dependent on an intact fat absorption mechanism. Patients with gastrointestinal disease may be particularly prone to deficiencies of this vitamin. Low vitamin D intake, fat malabsorption, bile salt deficiency, loss of absorptive surface, increased intestinal permeability, and loss of liver function are conditions frequently associated with gastrointestinal disease, which may account for the suboptimal vitamin D status encountered in this population.

Vitamin D, via the active form 1,25(OH)2D, plays a major role in calcium homeostasis, bone metabolism, and immune system regulation. 1,25-hydroxyvitamin D enhances small intestinal calcium absorption by interacting with the Vitamin D receptor-retinoic acid x receptor complex (VDR-RXR) to enhance the expression of the epithelial calcium channel, (transient receptor potential cation channel, subfamily V, member 6 (TRPV6) and calbindin 9k, a calcium binding protein (CABP), located in the enterocyte (6). Bone is a dynamic tissue which undergoes resorption and formation several times a day. Osteoblasts and osteoclasts, the mature bone cells, are the protagonists in bone formation and resorption respectively.

Activation of osteoclasts is mediated by the receptor activator of NF-κB (RANK), its ligand (RANKL), and the decoy receptor of this ligand, osteoprotegerin (OPG) (711). RANK, which is expressed on the membrane of osteoclastic precursors among other cells (12, 13), is activated by binding to RANKL and leads in turn to activation of osteoclasts (810). RANKL is largely expressed by cells of osteoblastic lineage and T-lymphocytes (8). OPG is produced by a number of cells, including osteoblasts (14) and as a decoy receptor for RANKL limits its availability for RANK activation, providing a limiting step in osteoclast activation (711).

Vitamin D plays an important role in the normal coupling of bone remodeling, promoting both osteoblastic and osteoclastic activity: 1,25(OH)2D3-vitamin D receptor defective mice manifested impaired osteoblastogenesis in the presence of normal PTH (15), and vitamin D enhances osteoblast differentiation and mineralization in humans (16). 1,25(OH)2D3 also stimulates RANKL expression (17), and inhibits OPG production by osteoblasts (18), thus promoting osteoclastogenesis.

The optimal level of serum 25OHD to maximize bone health in the general population, remains controversial(6) Although Vitamin D deficiency has been classically defined as a serum 25OHD level of less than 20ng/ml (50nmole/Liter) (19) ((20), there is recent evidence to suggest that a level of at least 30ng/ml (75nmol/liter) is required to minimize hyperparathyroidism and maximize intestinal calcium transport (6), (21) (22). Intestinal calcium transport increased by 45–65% in healthy women when 25OHD levels were increased from an average of 20 to 32 ng per milliliter (50 to 80 nmol per liter) (22)

It has been well established that vitamin D3 (cholecalciferol) is a more potent form of vitamin D than vitamin D2 (ergocalciferol) (23, 24). There is evidence to support the fact that an intake of 400 IU of vitamin D2/day may not be adequate to maintain optimal vitamin D stores (25OHD ≥ 32 ng/mL), especially during winter in healthy adults and children in the northern hemisphere(2529). Several investigators have suggested that daily doses of vitamin D3 between 1,000 – 4,000 IU/day are needed in order to achieve and maintain serum 25OHD concentrations ≥ 30 ng/mL, starting from a point of vitamin D sufficiency in healthy adults (21, 3033). Adults and children with gastrointestinal disease could have an even greater requirement for vitamin D intake in order to overcome malabsorption, reduced sunlight exposure, and nutrient loss through an inflamed intestine. The US National Academy of Sciences has indicated that the current “no observed adverse effect level” for vitamin D3 intake is 2,000 IU/day (34).

The relationship between vitamin D status and the regulation of the immune system is well-established. 1,25(OH)2D appears to play a pivotal role in the development of self-tolerance (35). It regulates T-helper cell (Th-1) function and dendritic cell function, while inducing regulatory T-cell function (35). The net result is a decrease in the Th1-driven autoimmune response and decreased severity of symptoms. The role of vitamin D in the pathogenesis and course of Th-1 cytokine- mediated immune diseases, such as multiple sclerosis (36) (37) (38) (39) (40), rheumatoid arthritis (41) (42), inflammatory bowel disease (43) (44)and type 1 diabetes mellitus (45) (46) (47, 48) is supported by findings in both animal models and epidemiologic studies in humans. Serum 25OHD levels much higher than what we consider “adequate” for bone health may be needed in order to exert beneficial effects on the immune system.

In this article, we intend to review: a) the prevalence of suboptimal vitamin D status in populations with specific gastrointestinal disorders, b) information regarding the impact of vitamin D deficiency on the bone health of patients with these disorders, c) recommendations regarding optimal vitamin D intake to avoid deficiencies specifically for these disorders, d) the state of knowledge regarding the effect of vitamin D on the disease itself, through its actions on the immune system.

Vitamin D status in inflammatory bowel disease

Reports of vitamin D status in adults with IBD place the prevalence of vitamin D deficiency between 22–70 % for Crohn disease (CD) (4959), and up to 45% for ulcerative colitis (UC) (59). Data concerning the vitamin D status of children with IBD are limited and conflicting (6063) and could be explained by different thresholds for vitamin D deficiency. We found this prevalence to be as high as 34.5% among pediatric patients with IBD, and higher than that encountered among healthy New England adolescents studied in our hospital using the same 25OHD assay (24.1%) (63, 64).

In pediatric subjects with IBD, cross-sectional studies have associated lower 25OHD levels with winter season, dark skin complexion, upper gastrointestinal disease, higher lifetime corticosteroid exposure, lower Z-scores for weight and body mass index (BMI), higher erythrocyte sedimentation rate (ESR), not taking vitamin D supplements, and lower serum albumin levels (60, 63). Absorption of vitamin D was normal in reports of adults with IBD and hypovitaminosis D (65, 66).

Hypovitaminosis D has been associated with low BMD in studies of healthy adults (6770) and adolescents, the latter suggesting that hypovitaminosis D may compromise the attainment of peak bone mass (71, 72). The relationship between 25OHD levels and BMD is controversial among adults with IBD. Some investigators found a positive association between 25OHD levels and BMD (52, 54). Others reported low BMD, despite the presence of normal 25OHD levels (7375), and some found no relationship (53, 59).

The contribution of vitamin D status to bone mineral accrual in children with IBD is unknown. A few cross-sectional studies report no relationship between BMD and vitamin D levels (60, 61, 63). Others report a positive relationship between these variables in corticosteroid-treated children, including children with IBD (76). The relationship between vitamin D status and bone quality (as represented by bone biomechanical properties measured by peripheral quantitative computerized tomograhy) has not been studied. Vitamin D regulates the release of several cytokines (77) (78, 79). There are reports of decreases in the levels of bone-resorption promoting cytokines that parallel increases in 25OHD serum concentration and improvement in BMD in inflammatory conditions (80, 81). These properties of vitamin D could counteract the effects of systemic inflammation on bone health. Clinical trials showed that supplementation with vitamin D and its analogues protected against bone loss in subjects with rheumatoid arthritis and lupus erythematosus (8285). The capacity of vitamin D to promote both osteoblastic and osteoclastic activity, may be of great importance especially in children, since both osteoblastic and osteoclastic activity seem to be depressed, at least in the initial stages of inflammation in children (86).

Studies in animal models support the hypothesis that the vitamin D endocrine system may play a role in the maintenance of normal immune responses in the gut. A lack of expression of the vitamin D receptor (VDR) aggravates symptoms in murine experimental colitis models (43);1,25(OH)2D3 prevents and ameliorates IBD symptoms in an experimental mouse model (IL-10 ko. mouse) (44), and calcium and 1,25(OH)2D3 together target the TNF-α pathway to suppress experimental IBD (87). One in vitro human study found a synergistic inhibitory effect of cyclosporin A and vitamin D derivatives on T-lymphocyte proliferation in active ulcerative colitis (88). Another found that calcipotriol (a vitamin D analogue) inhibits rectal epithelial cell proliferation in ulcerative proctocolitis (89). A study of the effect of vitamin D supplementation on disease activity is under way at our center.

The optimal vitamin D intake for repletion and maintenance of vitamin D stores in this population has not been identified yet. Studies regarding this are underway in our center, including a controlled clinical trial of two forms of vitamin D replacement.

Vitamin D status in celiac disease

Celiac disease is an immune mediated enteropathy that can occur in response to the ingestion of gluten proteins present in wheat, barley and rye. The disease can affect genetically susceptible individuals and is closely associated with genes that code class II human leukocyte antigens predominantly HLA- DQ2 and less frequently HLA-DQ8 classes (90). Celiac Disease is now considered a common condition affecting a variety of organ systems including the skeleton. The prevalence of celiac disease is estimated at 0.7% to 2.0% of the general population (91). Diagnosis includes screening serologic antibodies for tissue transglutaminase antibody and anti-endomysial antibody and obtaining the gold standard diagnostic duodenal biopsy revealing characteristic inflammation and tissue injury(91, 92). Adherence to a lifelong strict gluten free diet (GFD) leads to symptomatic and histopathologic remission, serologic normalization, and recovery of many of the affected organ systems (93) (94).

Hypovitaminosis D and hypocalcemia are reported in some newly diagnosed patients (95) (96). However, the true prevalence of hypovitaminosis D in patients with celiac disease remains unknown. Inadequate intake of calcium and vitamin D is often present in undiagnosed patients as a result of general malnutrition and anorexia related to gastrointestinal complaints including abdominal pain, nausea, and diarrhea. The recommended GFD can lead to suboptimal intake of calcium and vitamin D. Kinsey et al noted that 100% of individuals older than 50 years of age with celiac disease on a GFD reported a vitamin D intake below reference nutrient intake values (97). Similarly, in children complying with a strict GFD, nutritional imbalances were reported (98) although vitamin D status was not examined.

Vitamin D status in newly diagnosed celiac disease appears to be primarily a function of the degree of sunlight exposure and vitamin D ingestion and not intestinal absorption. The intestinal vitamin D receptors in patients with newly diagnosed celiac disease and intestinal villous atrophy have been shown to be equally abundant in the crypts of the duodenal mucosa of patients with active disease as with control subjects(99).

At the time of diagnosis of celiac disease, bone mineral density is decreased in approximately 3–39% of children and adolescents and 22–80% of adults. (100). Osteoporosis has been estimated in approximately one quarter of adult patients. (101). Newly diagnosed patients with celiac disease were reported to have elevated RANKL/OPG ratios compared with controls and patients on a gluten free diet (102). Fiore demonstrated that some patients on a strict GFD and normal follow up duodenal histology continue to display evidence of elevated RANKL/OPG ratio and persistently low spine and femoral bone mineral density compared with controls (103).

The age of the patient at time of diagnosis and initiation of GFD has a marked impact on the long term skeletal health. Children on a GFD for one year often display complete recovery of the bone disease with normalization of the bone mineral density and often achieve peak bone mass similar to controls (104), (105). Following institution of a GFD, adults with newly diagnosed celiac disease will show improvement of bone mineral density but often do not normalize to the levels seen in matched control groups ((106), (96) (103). The etiology of the lack of full normalization of bone health, despite normal follow up intestinal histology reported in some studies (103) remains unknown, but it could be related to ongoing hypovitaminosis D and sub clinical hyperparathyroidism. The relationship between vitamin D status and bone health has not been systematically studied with cross-sectional or longitudinal studies in this population.

New insights into vitamin D requirements and an understanding of the underlying immunologic pathways involved in skeletal mineralization will pave the way for optimizing bone health in all patients with celiac disease. Until specific recommendations for the pediatric population are developed, vitamin D supplementation, whether with ergocalciferol or cholecalciferol, must be sufficient to produce a serum 25OHD value > 32 ng/mL. All adult patients regardless of age with treated celiac disease with or without bone disease should follow the recommendations of the National Osteoporosis Foundation for those over 50 years of age to ingest 800 IU-1000 IU vitamin D3 and 1200 mg calcium daily ( Serum levels of 25OHD must be maintained > 32ng/mL(6).

Vitamin D status in cystic fibrosis

Bone health in patients with cystic fibrosis is becoming a topic of great interest as the mechanisms that control bone accrual and loss become amenable to detailed investigation (107). At present, the term “ CF bone disease” is used to describe a variety of abnormalities in bone found in approximately 50% of adult patients (108). CF bone disease increases in frequency with advancing age, worsening pulmonary status and malnutrition. Among the factors that influence bone composition in CF are pancreatic insufficiency leading to decreased absorption of vitamin D and calcium; reduced exposure to sunlight; sub-optimal nutrition producing poor growth, loss of body fat stores and pubertal delay; diabetes; pulmonary inflammation associated with elevated circulating and tissue cytokines; glucocorticoid use; decreased weight-bearing exercise; and vitamin K deficiency with reduced γ-carboxylation of osteocalcin (107, 109).

While a complete understanding of the causes of low vitamin D stores in CF remains to be delineated, low serum 25OHD levels are commonly found. Five to 10% of CF patients have severe vitamin D deficiency with 25OHD levels <10 ng/mL (25 nmol/L) (107), and the mean level of 25OHD in CF adults is approximately 21.5 ng/mL (median 20.3) (110). Vitamin D deficiency occurs in 25–33% of patients with late-stage CF (107).

The target 25OHD levels that avoid hyperparathyroidism have changed over the years; thus the literature describing supplementation with vitamin D for CF patients must be read in the context of the target level considered optimal at the time of the study (107) (6), (21) (22). For example, it is clear that 800 IU of cholicalciferol (vitamin D3) per day is inadequate as only 30% of patients studied by Hanly et al (111) attained levels of 25OHD >20 ng/mL. If current levels of >32 ng/mL had been used, the number of patients adequately treated would have been much lower. Kelly et al (112) found that 1,800 IU of ergocalciferol (vitamin D2) per day were required to bring the 25OHD levels of CF patients to >25 ng/mL. When a target value of 30 ng/mL was used, Boyle et al found that only 8% of patients receiving 50,000 IU ergocalciferol per week for 8 weeks achieved 25OHD levels >30 ng/mL. A number of those who failed to increase their levels were then given 50,000 IU twice weekly for 8 weeks. Surprisingly, none of them increased their 25OHD levels significantly (110). In contrast, a more recent study of 215 patients (113) demonstrated that 40 patients with baseline 25OHD values <10 ng/mL (<25 nmol/L) achieved mean levels of 53 nmol/L after at least 3 months of therapy (median intake 1800 IU per day). However, only 17% of the 215 patients had follow-up 25OHD values of >75nmol/L (>approximately 30 ng/mL).

On the basis of available data, it is fair to state that vitamin D supplementation, whether with ergocalciferol or cholicalciferol, must be sufficient to produce a serum 25OHD value of >32 ng/mL (approximately >75 nmol/L). If this cannot be accomplished using oral therapy, parenteral vitamin D must be provided. The ultimate challenge will be to monitor outcomes of such therapy, considering that vitamin D has a number of potentially beneficial effects in addition to those on bone metabolism.

Vitamin D status in liver disease

Both cholestatic and non-cholestatic liver disease is associated with suboptimal vitamin D stores. Cholestasis reduces the intestinal availability of bile salts which are needed for the absorption of fat-soluble vitamins such as vitamin D. Among 6 subjects (mean age 12.1 years) with cholestasis since infancy, most displayed a significantly blunted absorption response to enteral vitamin D2 as compared to healthy children, and baseline serum 25OHD values were undetectable in five out of the six subjects (114). Cholestatic children may also have defective hepatic conversion of vitamin D2 or D3 to the hydroxylated molecule. In five cholestatic children admitted to a research unit with controlled exposures to ultraviolet light, circulating levels of 25OHD3 were low or undetectable on admission and continued to be so after 8 days of therapy (115).

Non-cholestatic diseases may also result in abnormalities of vitamin D physiology, with the burden on patients with cirrhosis. Impaired conversion of vitamin D to the 25 hydroxylated form in the liver is the major mechanism for the resulting vitamin D insufficiency, since photo conversion in the skin is normal in patients with liver disease (116). In 100 adult subjects (1/3 women; mean age 49 years) with non-cholestatic chronic liver disease, Fisher et al reported serum levels of 25OHD <50nmol/L (20ng/mL) in 86% of the cirrhotic versus 49% of the non-cirrhotic patients (P=0.001), and this level correlated inversely with the international normalized ratio (INR), suggesting that Vitamin D status may be determined in part by chronic liver disease severity (117).

Vitamin D insufficiency is present in up to 96 percent of patients before liver transplantation (118). In contrast, vitamin D deficiency post-transplantation is uncommon. Some investigators found that serum 25OHD levels were low in only 5 of the 87 pediatric liver transplant recipients, with a cut off value set relatively low at 15ng/ml (119), and others found that vitamin D stores normalize within 1 year following liver transplantation in children (120).

Metabolic bone disease such as osteomalacia and osteopenia is relatively common in patients with liver disease, particularly cholestatic liver diseases. Potential mechanisms for this include inadequate calcium intake, and suboptimal vitamin D status. Other non-vitamin D related factors may be important, such as hypogonadism (121), vitamin K deficiency (122), medications (123), and alcohol intake (124) in adults.

The relationship between bone health and vitamin D status in liver disease is unclear. Investigators did not find any relationship between bone mineral content and serum 25OHD levels in subjects with cholestatic disease(125)(126). There is evidence that osteoblastic dysfunction may play a major role in the pathogenesis of metabolic bone disease in patients with chronic liver disease, and this dysfunction may not be explained by abnormalities in vitamin D metabolites alone (127).

The most robust relationship between bone health and vitamin D status is found in patients post liver transplantation. Low serum 25OHD levels were highly associated with the risk for osteoporosis post-transplantation (128), and spinal bone mass gains in adults post liver transplantation were related to higher serum 25OHD levels(129). It is known that both bone mineral density and vitamin D stores normalize within 1 year following liver transplantation in children (120).

Vitamin D is known to have non-skeletal functions, including serving as a modulator of immune responses via paracrine mechanisms (6). Although the effect of vitamin D or vitamin D analogues on the course of liver disease has not been studied in humans, polymorphisms in the vitamin D receptor have been associated with autoimmune hepatitis and primary biliary cirrhosis (130).


Supported in part by General Clinical Research Grant M01 002172 from the National Institutes of Health


1. Holick MF. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr. 2004;80(6 Suppl):1678S–88S. [PubMed]
2. Holick MF. Environmental factors that influence the cutaneous production of vitamin D. Am J Clin Nutr. 1995;61(3 Suppl):638S–45S. [PubMed]
3. Webb AR, Kline L, Holick MF. Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endocrinol Metab. 1988;67(2):373–8. [PubMed]
4. Haddad JG. Plasma vitamin D-binding protein (Gc-globulin): multiple tasks. J Steroid Biochem Mol Biol. 1995;53(1–6):579–82. [PubMed]
5. Bouillon R, Okamura WH, Norman AW. Structure-function relationships in the vitamin D endocrine system. Endocr Rev. 1995;16(2):200–57. [PubMed]
6. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–81. [PubMed]
7. Simonet WS, Lacey DL, Dunstan CR, et al. Osteoprotegerin: a novel secreted protein involved in the regulation of bone density. Cell. 1997;89(2):309–19. [PubMed]
8. Lacey DL, Timms E, Tan HL, et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell. 1998;93(2):165–76. [PubMed]
9. Malyankar UM, Scatena M, Suchland KL, et al. Osteoprotegerin is an alpha vbeta 3-induced, NF-kappa B-dependent survival factor for endothelial cells. J Biol Chem. 2000;275(28):20959–62. [PubMed]
10. Fuller K, Wong B, Fox S, et al. TRANCE is necessary and sufficient for osteoblast-mediated activation of bone resorption in osteoclasts. J Exp Med. 1998;188(5):997–1001. [PMC free article] [PubMed]
11. Anandarajah AP, Schwarz EM. Anti-RANKL therapy for inflammatory bone disorders: Mechanisms and potential clinical applications. J Cell Biochem. 2006;97(2):226–32. [PubMed]
12. Anderson DM, Maraskovsky E, Billingsley WL, et al. A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function. Nature. 1997;390(6656):175–9. [PubMed]
13. Hsu H, Lacey DL, Dunstan CR, et al. Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand. Proc Natl Acad Sci U S A. 1999;96(7):3540–5. [PubMed]
14. Moschen AR, Kaser A, Enrich B, et al. The RANKL/OPG system is activated in inflammatory bowel disease and relates to the state of bone loss. Gut. 2005;54(4):479–87. [PMC free article] [PubMed]
15. Panda DK, Miao D, Bolivar I, et al. Inactivation of the 25-hydroxyvitamin D 1alpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem. 2004;279(16):16754–66. [PubMed]
16. van Driel M, Koedam M, Buurman CJ, et al. Evidence that both 1alpha, 25-dihydroxyvitamin D3 and 24-hydroxylated D3 enhance human osteoblast differentiation and mineralization. J Cell Biochem. 2006;99(3):922–35. [PubMed]
17. Kitazawa S, Kajimoto K, Kondo T, et al. Vitamin D3 supports osteoclastogenesis via functional vitamin D response element of human RANKL gene promoter. J Cell Biochem. 2003;89(4):771–7. [PubMed]
18. Kondo T, Kitazawa R, Maeda S, et al. 1 alpha, 25 dihydroxyvitamin D3 rapidly regulates the mouse osteoprotegerin gene through dual pathways. J Bone Miner Res. 2004;19(9):1411–9. [PubMed]
19. Holick MF. High prevalence of vitamin D inadequacy and implications for health. Mayo Clin Proc. 2006;81(3):353–73. [PubMed]
20. Bischoff-Ferrari HA, Giovannucci E, Willett WC, et al. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. The American journal of clinical nutrition. 2006;84(1):18–28. [PubMed]
21. Dawson-Hughes B, Heaney RP, Holick MF, et al. Estimates of optimal vitamin D status. Osteoporos Int. 2005;16(7):713–6. [PubMed]
22. Heaney RP, Dowell MS, Hale CA, et al. Calcium absorption varies within the reference range for serum 25-hydroxyvitamin D. J Am Coll Nutr. 2003;22(2):142–6. [PubMed]
23. Trang HM, Cole DE, Rubin LA, et al. Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr. 1998;68(4):854–8. [PubMed]
24. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387–91. [PubMed]
25. Lehtonen-Veromaa M, Mottonen T, Nuotio I, et al. The effect of conventional vitamin D(2) supplementation on serum 25(OH)D concentration is weak among peripubertal Finnish girls: a 3-y prospective study. Eur J Clin Nutr. 2002;56(5):431–7. [PubMed]
26. Lehtonen-Veromaa M, Mottonen T, Irjala K, et al. Vitamin D intake is low and hypovitaminosis D common in healthy 9- to 15-year-old Finnish girls. Eur J Clin Nutr. 1999;53(9):746–51. [PubMed]
27. Lips P, Graafmans WC, Ooms ME, et al. Vitamin D supplementation and fracture incidence in elderly persons. A randomized, placebo-controlled clinical trial. Ann Intern Med. 1996;124(4):400–6. [PubMed]
28. Simonelli C, Weiss TW, Morancey J, et al. Prevalence of vitamin D inadequacy in a minimal trauma fracture population. Curr Med Res Opin. 2005;21(7):1069–74. [PubMed]
29. Antoniucci DM, Vittinghoff E, Blackwell T, et al. Vitamin D insufficiency does not affect bone mineral density response to raloxifene. J Clin Endocrinol Metab. 2005;90(8):4566–72. [PubMed]
30. Heaney RP, Davies KM, Chen TC, et al. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77(1):204–10. [PubMed]
31. Barger-Lux MJ, Heaney RP. Effects of above average summer sun exposure on serum 25-hydroxyvitamin D and calcium absorption. J Clin Endocrinol Metab. 2002;87(11):4952–6. [PubMed]
32. Vieth R, Kimball S, Hu A, et al. Randomized comparison of the effects of the vitamin D3 adequate intake versus 100 mcg (4000 IU) per day on biochemical responses and the wellbeing of patients. Nutr J. 2004;3:8. [PMC free article] [PubMed]
33. Tangpricha V, Koutkia P, Rieke SM, et al. Fortification of orange juice with vitamin D: a novel approach for enhancing vitamin D nutritional health. Am J Clin Nutr. 2003;77(6):1478–83. [PubMed]
34. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes FaNB, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. The National Academies Press; 1997. [PubMed]
35. Cantorna MT, Mahon BD. Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp Biol Med (Maywood) 2004;229(11):1136–42. [PubMed]
36. Cantorna MT, Hayes CE, DeLuca HF. 1,25-Dihydroxyvitamin D3 reversibly blocks the progression of relapsing encephalomyelitis, a model of multiple sclerosis. Proc Natl Acad Sci U S A. 1996;93(15):7861–4. [PubMed]
37. Cantorna MT, Humpal-Winter J, DeLuca HF. Dietary calcium is a major factor in 1,25-dihydroxycholecalciferol suppression of experimental autoimmune encephalomyelitis in mice. J Nutr. 1999;129(11):1966–71. [PubMed]
38. Kurtzke JF, Beebe GW, Norman JE., Jr Epidemiology of multiple sclerosis in U.S. veterans: 1. Race, sex, and geographic distribution. Neurology. 1979;29(9 Pt 1):1228–35. [PubMed]
39. Wallin MT, Page WF, Kurtzke JF. Multiple sclerosis in US veterans of the Vietnam era and later military service: race, sex, and geography. Ann Neurol. 2004;55(1):65–71. [PubMed]
40. Munger KL, Zhang SM, O’Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60–5. [PubMed]
41. Cantorna MT, Hayes CE, DeLuca HF. 1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis. J Nutr. 1998;128(1):68–72. [PubMed]
42. Merlino LA, Curtis J, Mikuls TR, et al. Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women’s Health Study. Arthritis Rheum. 2004;50(1):72–7. [PubMed]
43. Froicu M, Weaver V, Wynn TA, et al. A crucial role for the vitamin D receptor in experimental inflammatory bowel diseases. Mol Endocrinol. 2003;17(12):2386–92. [PubMed]
44. Cantorna MT, Munsick C, Bemiss C, et al. 1,25-Dihydroxycholecalciferol prevents and ameliorates symptoms of experimental murine inflammatory bowel disease. J Nutr. 2000;130(11):2648–52. [PubMed]
45. Mathieu C, Waer M, Laureys J, et al. Prevention of autoimmune diabetes in NOD mice by 1,25 dihydroxyvitamin D3. Diabetologia. 1994;37(6):552–8. [PubMed]
46. Giulietti A, Gysemans C, Stoffels K, et al. Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice. Diabetologia. 2004;47(3):451–62. [PubMed]
47. Casteels K, Bouillon R, Waer M, et al. Immunomodulatory effects of 1,25-dihydroxyvitamin D3. Curr Opin Nephrol Hypertens. 1995;4(4):313–8. [PubMed]
48. Hypponen E, Laara E, Reunanen A, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358(9292):1500–3. [PubMed]
49. Siffledeen JS, Siminoski K, Steinhart H, et al. The frequency of vitamin D deficiency in adults with Crohn’s disease. Can J Gastroenterol. 2003;17(8):473–8. [PubMed]
50. McCarthy D, Duggan P, O’Brien M, et al. Seasonality of vitamin D status and bone turnover in patients with Crohn’s disease. Aliment Pharmacol Ther. 2005;21(9):1073–83. [PubMed]
51. Tajika M, Matsuura A, Nakamura T, et al. Risk factors for vitamin D deficiency in patients with Crohn’s disease. J Gastroenterol. 2004;39(6):527–33. [PubMed]
52. Mezquita Raya P, Munoz Torres M, Lopez Rodriguez F, et al. Prevalence of vitamin D deficiency in populations at risk for osteoporosis: impact on bone integrity. Med Clin (Barc) 2002;119(3):85–9. [PubMed]
53. Jahnsen J, Falch JA, Mowinckel P, et al. Vitamin D status, parathyroid hormone and bone mineral density in patients with inflammatory bowel disease. Scand J Gastroenterol. 2002;37(2):192–9. [PubMed]
54. Andreassen H, Rix M, Brot C, et al. Regulators of calcium homeostasis and bone mineral density in patients with Crohn’s disease. Scand J Gastroenterol. 1998;33(10):1087–93. [PubMed]
55. Vogelsang H, Ferenci P, Resch H, et al. Prevention of bone mineral loss in patients with Crohn’s disease by long-term oral vitamin D supplementation. Eur J Gastroenterol Hepatol. 1995;7(7):609–14. [PubMed]
56. Bischoff SC, Herrmann A, Goke M, et al. Altered bone metabolism in inflammatory bowel disease. Am J Gastroenterol. 1997;92(7):1157–63. [PubMed]
57. Harries AD, Brown R, Heatley RV, et al. Vitamin D status in Crohn’s disease: association with nutrition and disease activity. Gut. 1985;26(11):1197–203. [PMC free article] [PubMed]
58. Driscoll RH, Jr, Meredith SC, Sitrin M, et al. Vitamin D deficiency and bone disease in patients with Crohn’s disease. Gastroenterology. 1982;83(6):1252–8. [PubMed]
59. Silvennoinen J. Relationships between vitamin D, parathyroid hormone and bone mineral density in inflammatory bowel disease. J Intern Med. 1996;239(2):131–7. [PubMed]
60. Sentongo TA, Semaeo EJ, Stettler N, et al. Vitamin D status in children, adolescents, and young adults with Crohn disease. Am J Clin Nutr. 2002;76(5):1077–81. [PubMed]
61. Gokhale R, Favus MJ, Karrison T, et al. Bone mineral density assessment in children with inflammatory bowel disease. Gastroenterology. 1998;114(5):902–11. [PubMed]
62. Issenman RM, Atkinson SA, Radoja C, et al. Longitudinal assessment of growth, mineral metabolism, and bone mass in pediatric Crohn’s disease. J Pediatr Gastroenterol Nutr. 1993;17(4):401–6. [PubMed]
63. Pappa HM, Gordon CM, Saslowsky TM, et al. Vitamin D status in children and young adults with inflammatory bowel disease. Pediatrics. 2006;118(5):1950–61. [PMC free article] [PubMed]
64. Gordon CM, DePeter KC, Feldman HA, et al. Prevalence of vitamin D deficiency among healthy adolescents. Arch Pediatr Adolesc Med. 2004;158(6):531–7. [PubMed]
65. Lo CW, Paris PW, Clemens TL, et al. Vitamin D absorption in healthy subjects and in patients with intestinal malabsorption syndromes. Am J Clin Nutr. 1985;42(4):644–9. [PubMed]
66. Vogelsang H, Schofl R, Tillinger W, et al. 25-hydroxyvitamin D absorption in patients with Crohn’s disease and with pancreatic insufficiency. Wien Klin Wochenschr. 1997;109(17):678–82. [PubMed]
67. Mezquita-Raya P, Munoz-Torres M, Luna JD, et al. Relation between vitamin D insufficiency, bone density, and bone metabolism in healthy postmenopausal women. J Bone Miner Res. 2001;16(8):1408–15. [PubMed]
68. Bischoff-Ferrari HA, Dietrich T, Orav EJ, et al. Positive association between 25-hydroxy vitamin D levels and bone mineral density: a population-based study of younger and older adults. Am J Med. 2004;116(9):634–9. [PubMed]
69. Bhattoa HP, Bettembuk P, Ganacharya S, et al. Prevalence and seasonal variation of hypovitaminosis D and its relationship to bone metabolism in community dwelling postmenopausal Hungarian women. Osteoporos Int. 2004;15(6):447–51. [PubMed]
70. Serhan E, Holland MR. Relationship of hypovitaminosis D and secondary hyperparathyroidism with bone mineral density among UK resident Indo-Asians. Ann Rheum Dis. 2002;61(5):456–8. [PMC free article] [PubMed]
71. Lehtonen-Veromaa MK, Mottonen TT, Nuotio IO, et al. Vitamin D and attainment of peak bone mass among peripubertal Finnish girls: a 3-y prospective study. Am J Clin Nutr. 2002;76(6):1446–53. [PubMed]
72. Valimaki VV, Alfthan H, Lehmuskallio E, et al. Vitamin D status as a determinant of peak bone mass in young Finnish men. J Clin Endocrinol Metab. 2004;89(1):76–80. [PubMed]
73. Abitbol V, Roux C, Guillemant S, et al. Bone assessment in patients with ileal pouch-anal anastomosis for inflammatory bowel disease. Br J Surg. 1997;84(11):1551–4. [PubMed]
74. Ardizzone S, Bollani S, Bettica P, et al. Altered bone metabolism in inflammatory bowel disease: there is a difference between Crohn’s disease and ulcerative colitis. J Intern Med. 2000;247(1):63–70. [PubMed]
75. Scharla SH, Minne HW, Lempert UG, et al. Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn’s disease and ulcerative colitis) Exp Clin Endocrinol. 1994;102(1):44–9. [PubMed]
76. von Scheven E, Gordon CM, Wypij D, et al. Variable deficits of bone mineral despite chronic glucocorticoid therapy in pediatric patients with inflammatory diseases: a Glaser Pediatric Research Network study. J Pediatr Endocrinol Metab. 2006;19(6):821–30. [PubMed]
77. Gurlek A, Pittelkow MR, Kumar R. Modulation of growth factor/cytokine synthesis and signaling by 1alpha,25-dihydroxyvitamin D(3): implications in cell growth and differentiation. Endocr Rev. 2002;23(6):763–86. [PubMed]
78. Shany S, Levy Y, Lahav-Cohen M. The effects of 1alpha,24(S)-dihydroxyvitamin D(2) analog on cancer cell proliferation and cytokine expression. Steroids. 2001;66(3–5):319–25. [PubMed]
79. Cohen ML, Douvdevani A, Chaimovitz C, et al. Regulation of TNF-alpha by 1alpha,25-dihydroxyvitamin D3 in human macrophages from CAPD patients. Kidney Int. 2001;59(1):69–75. [PubMed]
80. Lange U, Jung O, Teichmann J, et al. Relationship between disease activity and serum levels of vitamin D metabolites and parathyroid hormone in ankylosing spondylitis. Osteoporos Int. 2001;12(12):1031–5. [PubMed]
81. Lange U, Teichmann J, Strunk J, et al. Association of 1.25 vitamin D3 deficiency, disease activity and low bone mass in ankylosing spondylitis. Osteoporos Int. 2005;16(12):1999–2004. [PubMed]
82. Buckley LM, Leib ES, Cartularo KS, et al. Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 1996;125(12):961–8. [PubMed]
83. Verstraeten A, Dequeker J, Nijs J, et al. Prevention of postmenopausal bone loss in rheumatoid arthritis patients. A two-year prospective study. Clin Exp Rheumatol. 1989;7(4):351–8. [PubMed]
84. Brohult J, Jonson B. Effects of large doses of calciferol on patients with rheumatoid arthritis. A double-blind clinical trial. Scand J Rheumatol. 1973;2(4):173–6. [PubMed]
85. Yamauchi Y, Tsunematsu T, Konda S, et al. A double blind trial of alfacalcidol on patients with rheumatoid arthritis (RA) Ryumachi. 1989;29(1):11–24. [PubMed]
86. Sylvester FA, Davis PM, Wyzga N, et al. Are activated T cells regulators of bone metabolism in children with Crohn disease? J Pediatr. 2006;148(4):461–6. [PubMed]
87. Zhu Y, Mahon BD, Froicu M, et al. Calcium and 1 alpha,25-dihydroxyvitamin D3 target the TNF-alpha pathway to suppress experimental inflammatory bowel disease. Eur J Immunol. 2005;35(1):217–24. [PubMed]
88. Stio M, Treves C, Celli A, et al. Synergistic inhibitory effect of cyclosporin A and vitamin D derivatives on T-lymphocyte proliferation in active ulcerative colitis. Am J Gastroenterol. 2002;97(3):679–89. [PubMed]
89. Thomas MG, Tebbutt S, Williamson RC. Vitamin D and its metabolites inhibit cell proliferation in human rectal mucosa and a colon cancer cell line. Gut. 1992;33(12):1660–3. [PMC free article] [PubMed]
90. Kaukinen K, Partanen J, Maki M, et al. HLA-DQ typing in the diagnosis of celiac disease. The American journal of gastroenterology. 2002;97(3):695–9. [PubMed]
91. Rewers M. Epidemiology of celiac disease: what are the prevalence, incidence, and progression of celiac disease? Gastroenterology. 2005;128(4 Suppl 1):S47–51. [PubMed]
92. Marsh MN. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity (‘celiac sprue’) Gastroenterology. 1992;102(1):330–54. [PubMed]
93. Kupper C. Dietary guidelines and implementation for celiac disease. Gastroenterology. 2005;128(4 Suppl 1):S121–7. [PubMed]
94. Rostom A, Murray JA, Kagnoff MF. American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease. Gastroenterology. 2006;131(6):1981–2002. [PubMed]
95. Corazza GR, Di Sario A, Cecchetti L, et al. Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease. Bone. 1996;18(6):525–30. [PubMed]
96. Valdimarsson T, Toss G, Lofman O, et al. Three years’ follow-up of bone density in adult coeliac disease: significance of secondary hyperparathyroidism. Scandinavian journal of gastroenterology. 2000;35(3):274–80. [PubMed]
97. Kinsey L, Burden ST, Bannerman E. A dietary survey to determine if patients with coeliac disease are meeting current healthy eating guidelines and how their diet compares to that of the British general population. Eur J Clin Nutr. 2007 [PubMed]
98. Mariani P, Viti MG, Montuori M, et al. The gluten-free diet: a nutritional risk factor for adolescents with celiac disease? Journal of pediatric gastroenterology and nutrition. 1998;27(5):519–23. [PubMed]
99. Colston KW, Mackay AG, Finlayson C, et al. Localisation of vitamin D receptor in normal human duodenum and in patients with coeliac disease. Gut. 1994;35(9):1219–25. [PMC free article] [PubMed]
100. Bernstein CN, Leslie WD, Leboff MS. AGA technical review on osteoporosis in gastrointestinal diseases. Gastroenterology. 2003;124(3):795–841. [PubMed]
101. Kemppainen T, Kroger H, Janatuinen E, et al. Osteoporosis in adult patients with celiac disease. Bone. 1999;24(3):249–55. [PubMed]
102. Taranta A, Fortunati D, Longo M, et al. Imbalance of osteoclastogenesis-regulating factors in patients with celiac disease. J Bone Miner Res. 2004;19(7):1112–21. [PubMed]
103. Fiore CE, Pennisi P, Ferro G, et al. Altered osteoprotegerin/RANKL ratio and low bone mineral density in celiac patients on long-term treatment with gluten-free diet. Hormone and metabolic research Hormon- und Stoffwechselforschung. 2006;38(6):417–22. [PubMed]
104. Mora S. Celiac disease: a bone perspective. Journal of pediatric gastroenterology and nutrition. 2003;37(4):409–11. [PubMed]
105. Kavak US, Yuce A, Kocak N, et al. Bone mineral density in children with untreated and treated celiac disease. Journal of pediatric gastroenterology and nutrition. 2003;37(4):434–6. [PubMed]
106. Pazianas M, Butcher GP, Subhani JM, et al. Calcium absorption and bone mineral density in celiacs after long term treatment with gluten-free diet and adequate calcium intake. Osteoporos Int. 2005;16(1):56–63. [PubMed]
107. Aris RM, Merkel PA, Bachrach LK, et al. Guide to bone health and disease in cystic fibrosis. J Clin Endocrinol Metab. 2005;90(3):1888–96. [PubMed]
108. Elkin SL, Vedi S, Bord S, et al. Histomorphometric analysis of bone biopsies from the iliac crest of adults with cystic fibrosis. Am J Respir Crit Care Med. 2002;166(11):1470–4. [PubMed]
109. Schulze KJ, O’Brien KO, Germain-Lee EL, et al. Calcium kinetics are altered in clinically stable girls with cystic fibrosis. J Clin Endocrinol Metab. 2004;89(7):3385–91. [PubMed]
110. Boyle MP, Noschese ML, Watts SL, et al. Failure of high-dose ergocalciferol to correct vitamin D deficiency in adults with cystic fibrosis. Am J Respir Crit Care Med. 2005;172(2):212–7. [PMC free article] [PubMed]
111. Hanly JG, McKenna MJ, Quigley C, et al. Hypovitaminosis D and response to supplementation in older patients with cystic fibrosis. The Quarterly journal of medicine. 1985;56(219):377–85. [PubMed]
112. Kelly EMR, Pencharz P, Tullis E. Effect of vitamin D supplementation on low serum 25-hydroxyvitamin D in adults with cystic fibrosis. Pediatr Pulmonol. 2002;24(Suppl):344.
113. Stephenson A, Brotherwood M, Robert R, et al. Cholecalciferol significantly increases 25-hydroxyvitamin D concentrations in adults with cystic fibrosis. Am J Clin Nutr. 2007;85(5):1307–11. [PubMed]
114. Heubi JE, Hollis BW, Specker B, et al. Bone disease in chronic childhood cholestasis. I. Vitamin D absorption and metabolism. Hepatology. 1989;9(2):258–64. [PubMed]
115. Klein GL, Soriano H, Shulman RJ, et al. Hepatic osteodystrophy in chronic cholestasis: evidence for a multifactorial etiology. Pediatr Transplant. 2002;6(2):136–40. [PubMed]
116. Jung RT, Davie M, Siklos P, et al. Vitamin D metabolism in acute and chronic cholestasis. Gut. 1979;20(10):840–7. [PMC free article] [PubMed]
117. Fisher L, Fisher A. Vitamin D and parathyroid hormone in outpatients with noncholestatic chronic liver disease. Clin Gastroenterol Hepatol. 2007;5(4):513–20. [PubMed]
118. Trautwein C, Possienke M, Schlitt HJ, et al. Bone density and metabolism in patients with viral hepatitis and cholestatic liver diseases before and after liver transplantation. Am J Gastroenterol. 2000;95(9):2343–51. [PubMed]
119. Guthery SL, Pohl JF, Bucuvalas JC, et al. Bone mineral density in long-term survivors following pediatric liver transplantation. Liver Transpl. 2003;9(4):365–70. [PubMed]
120. Argao EA, Balistreri WF, Hollis BW, et al. Effect of orthotopic liver transplantation on bone mineral content and serum vitamin D metabolites in infants and children with chronic cholestasis. Hepatology. 1994;20(3):598–603. [PubMed]
121. Collier J. Bone disorders in chronic liver disease. Hepatology. 2007;46(4):1271–8. [PubMed]
122. Shiomi S, Nishiguchi S, Kubo S, et al. Vitamin K2 (menatetrenone) for bone loss in patients with cirrhosis of the liver. Am J Gastroenterol. 2002;97(4):978–81. [PubMed]
123. Kurihara N, Roodman GD. Interferons-alpha and -gamma inhibit interleukin-1 beta-stimulated osteoclast-like cell formation in long-term human marrow cultures. J Interferon Res. 1990;10(5):541–7. [PubMed]
124. Mobarhan SA, Russell RM, Recker RR, et al. Metabolic bone disease in alcoholic cirrhosis: a comparison of the effect of vitamin D2, 25-hydroxyvitamin D, or supportive treatment. Hepatology. 1984;4(2):266–73. [PubMed]
125. Floreani A, Carderi I, Ferrara F, et al. A 4-year treatment with clodronate plus calcium and vitamin D supplements does not improve bone mass in primary biliary cirrhosis. Dig Liver Dis. 2007;39(6):544–8. [PubMed]
126. Argao EA, Specker BL, Heubi JE. Bone mineral content in infants and children with chronic cholestatic liver disease. Pediatrics. 1993;91(6):1151–4. [PubMed]
127. Diamond T, Stiel D, Mason R, et al. Serum vitamin D metabolites are not responsible for low turnover osteoporosis in chronic liver disease. J Clin Endocrinol Metab. 1989;69(6):1234–9. [PubMed]
128. Crosbie OM, Freaney R, McKenna MJ, et al. Predicting bone loss following orthotopic liver transplantation. Gut. 1999;44(3):430–4. [PMC free article] [PubMed]
129. Guichelaar MM, Kendall R, Malinchoc M, et al. Bone mineral density before and after OLT: long-term follow-up and predictive factors. Liver Transpl. 2006;12(9):1390–402. [PubMed]
130. Vogel A, Strassburg CP, Manns MP. Genetic association of vitamin D receptor polymorphisms with primary biliary cirrhosis and autoimmune hepatitis. Hepatology. 2002;35(1):126–31. [PubMed]