The development of inhibitory antibodies to human factor VIII in a significant minority

of patients with haemophilia A treated with concentrates derived from human plasma was already well recognized by the early 1970s. The treatment options at the time were limited to either infusions of high doses of human factor VIII or primitive prothrombin complex concentrates (PCCs) like Autoplex and Proplex. Neither of these options could guarantee control of haemostasis and the use of PCCs was also known to be associated with a risk of venous and arterial thromboembolism. A highly purified preparation of porcine Tigecycline research buy factor VIII was developed in the early 1980s using polyelectrolyte chromatographic fractionation. This product was specifically developed to provide another treatment option for patients who had developed inhibitory antibodies to human factor VIII. The rationale was that porcine factor VIII was sufficiently similar to human factor VIII to work just like the natural product, but it was also sufficiently different in structure to render it less susceptible to inactivation by circulating inhibitory antibodies. The very early work was undertaken by Speywood Laboratories

in Nottingham (which later became part of the Ipsen group) in conjunction with researchers in Oxford. An attractive offer from the Welsh Development Agency persuaded Speywood to find more Mirabegron set up its production facility for Hyate:C in Wrexham, where a fractionation plant was built to handle porcine plasma obtained from abattoirs in England [Figs 2–4]. The first published report of the clinical use of Hyate:C appeared in 1984 and described the successful use of the product in eight patients over an 18-month period [6]. A total of 297 infusions were given for the treatment of 45 distinct bleeding episodes. A clear advantage over other products was that measureable levels of factor VIII were obtained after infusion, which could be used to monitor treatment. In most cases,

the inhibitory antibodies against human factor VIII showed little or no cross-reactivity with porcine factor VIII. Where no baseline antibody against porcine factor VIII was detectable, the mean postinfusion rise in plasma factor VIII was 1.29 U dL−1 per unit infused kg−1. Furthermore, there was usually little or no anamnestic rise in antibody titre after treatment with Hyate:C, by contrast with the steep rise frequently reported after treatment with human factor VIII or activated prothrombin complex concentrates. Multiple and prolonged courses of therapy were used in this series without evidence of loss of clinical or laboratory efficacy. Apparently allergic reactions, including fever, were observed after approximately 10% of the infusions.

147 Higher LCFA oxidation was found in liver mitochondria and peroxisomes isolated from ob/ob mice (Table 1).57,149,152,153 Increased mtFAO capacity in ob/ob liver was associated with enhanced CPT activity and/or CPT1 expression,109,152,154 and higher expression BVD-523 chemical structure of other mtFAO enzymes.119,154-157 Moreover,

PPARα expression is augmented in ob/ob liver,109,154,158 although some studies found normal or reduced PPARα expression.157,159 In db/db mice, mtFAO was enhanced in one study,160 whereas total hepatic FAO was decreased in another report (Table 1).161 PPARα expression in db/db liver was either increased,109,162,163 unchanged,164-166 or decreased.167,168 In ob/ob mice, hepatic mitochondrial oxidation of glutamate (providing electrons to complex I) was either unchanged or increased, whereas that of succinate (providing electrons to complex II) was consistently enhanced (Table 1).152,169-171 In db/db liver, glutamate and succinate-driven mitochondrial respiration was increased.170 However, the activity of different hepatic MRC complexes was significantly reduced in ob/ob57,58,172,173 and db/db mice (Table 1).172,174,175 These data, reporting higher (or normal) rates of oxygen consumption and reduced activity of different MRC complexes, are not necessarily Palbociclib order discordant. Indeed, mitochondrial respiration is significantly impaired only when

the activity of MRC complexes is severely inhibited.176 An important ATP depletion was observed in ob/ob liver,171,177 which could be due to OXPHOS uncoupling.171,178 Finally, electron microscopic analysis of ob/ob liver showed enlarged mitochondria with abnormal cristae organization

and granular matrix, but without crystalline inclusions.153 Taken together, these data in ob/ob and db/db indicated higher Bcl-w oxidative capacity of liver mitochondria with different respiratory substrates including FAs, but impaired activity of different MRC complexes. These mitochondrial alterations are leading to ROS overproduction since more substrate-derived electrons are entering the MRC and leak from complexes I and III.5,7,17,63,171 Increased hepatic mtFAO in ob/ob and db/db mice was associated with higher, normal, or even reduced PPARα expression. The exact reasons of this discrepancy are not known, but differences in age and diet could be involved. Three studies assessed whole-body 13C-octanoate oxidation in patients with NASH. In one study, patients with NASH had higher whole-body 13C-octanoate oxidation when compared to the controls,72 whereas the other studies showed no difference (Table 1).179,180 Using indirect calorimetry and KB production as surrogate markers of mtFAO, other investigations found higher fat oxidation in patients with NASH.42,71,97,181 In contrast, reduced PPARα mRNA expression was found in patients with NASH compared to patients with simple fatty liver,111,113,182 thus suggesting that PPARα induction progressively declines when fatty liver progresses to NASH.

Consequently, there is a need for antiviral compounds such as TDF, which is a well-tolerated, potent therapy with a high threshold for resistance development. The addition of FTC occurred in only 5% of patients and did not appear to affect the subsequent rate of HBV DNA decline because comparable PF-562271 supplier declines occurred in eligible patients who opted to remain on TDF monotherapy. Our analysis demonstrated no detectable TDF resistance among 641 HBeAg+ and HBeAg− patients with CHB infection who received TDF for up to 144 weeks. “
“Although there have been numerous reports describing the isolation of liver progenitor cells from the adult liver, their exact origin

has not been clearly defined; and the role played by mature

hepatocytes as direct contributors to the hepatic progenitor cell pool has remained largely unknown. Here, we report strong evidence that mature hepatocytes in culture have the capacity to dedifferentiate into a population of adult liver progenitors without genetic or epigenetic manipulations. By using highly purified mature hepatocytes, which were obtained from untreated, healthy rat liver and labeled with fluorescent dye PKH2, we found that hepatocytes in culture gave rise to a population of PKH2-positive liver progenitor cells. These cells, liver-derived progenitor cells, which share phenotypic similarities with oval cells, were previously reported to be capable of forming mature hepatocytes, both in culture and in animals. click here Studies done at various time points during the course of dedifferentiation cultures revealed that hepatocytes rapidly transformed CHIR-99021 mouse into liver progenitors within 1 week through a transient oval cell-like stage. This finding was supported by lineage-tracing studies involving double-transgenic AlbuminCreXRosa26 mice expressing β-galactosidase exclusively in hepatocytes. Cultures set up with hepatocytes obtained from these mice resulted in the generation of β-galactosidase-positive liver progenitor cells, demonstrating that they were a direct

dedifferentiation product of mature hepatocytes. Additionally, these progenitors differentiated into hepatocytes in vivo when transplanted into rats that had undergone retrorsine pretreatment and partial hepatectomy. Conclusion: Our studies provide strong evidence for the unexpected plasticity of mature hepatocytes to dedifferentiate into progenitor cells in culture, and this may potentially have a significant effect on the treatment of liver diseases requiring liver or hepatocyte transplantation. (HEPATOLOGY 2012;) The liver is a unique organ with an enormous capacity to regenerate after injury. Up to 75% of liver mass can be regenerated in the rat within 1 week after partial hepatectomy.1 Under normal conditions and in the absence of toxic injury, hepatocytes are predominantly responsible for this process.

76,173,174 It is not clear if the variation in surgical rates for CD across Asia is due to differences in disease severity or in clinical practice. A study from Hong Kong showed a cumulative surgical rate of 29% at 10 years,24 whereas a much higher rate of 58.3% at 10 years was reported in China.72 From Korea, cumulative surgical rates were 11.9–15.5% at one year, 25% at 5 years and 32.8% at 10 to 15 years.77,172 Eighteen percent of surgical patients from one study required a second resection, with cumulative rate of re-operation

of 2.9% after 1 year, 19.9% after 5 years, and 30.8% after 10 years.77 Japanese studies have reported cumulative rates at 5 years of 25.9–44.4% and 10 years of 46.3–80.1%,76,173,174 which are comparable to Western data of cumulative surgical rates of 37.9% (Norway)168 and 65% (Copenhagen) at 10 years.90 Regarding risk factors for surgery, multivariate analyses from China find protocol have found stricturing and penetrating behaviour,72,172 and smoking habit,72 to be independently associated with increased risk of surgery, whereas female gender and ileal disease were independent risk factors for surgery in Japan.175 Extra-intestinal manifestations.  In the West, MK-2206 price the prevalence of extra-intestinal manifestations (EIM) (Table 5) in IBD is approximately 25–40%,178–181 although comparisons between studies are difficult due to different diagnostic criteria. Previous reviews of IBD in Asia

have surmised lower EIM in Asian countries compared to the West.45,182 Studies in China and Hong Kong have demonstrated that joint manifestations in IBD were seen in 2.7–7.9% of patients.24,70,73,81 In India, up to one quarter of patients have joint manifestation.137 Primary sclerosing cholangitis (PSC) associated with UC is less prevalent in Asia (0–1.7%)56,70,81,84,137,176,183 compared with the West (2–7%).184 A recent Korean study of 1849 UC patients demonstrated

the cumulative probability of PSC after diagnosis was 0.71% after 1–5 years, 1.42% after 10 years, 2.59% after 15 years, and 3.35% after 20–25 years.176 In the West the likelihood of having IBD in patients diagnosed with PSC was 62–76%.185–188 GPX6 In contrast, 20% of PSC patients in Japan and 50% in India had IBD.189 A case series of 10 patients with PSC in Singapore revealed that only 20% were associated with symptomatic IBD.190 Studies comparing different ethnicities within the one country have found differing EIM between ethnic groups. In Malaysia, there was a higher prevalence of EIM among the Indians compared with Malays (P = 0.04) and Chinese (P = 0.002).56 In Singapore the frequency of EIM was higher in Indians (14%) than Chinese (6%).55 The use of corticosteroids for UC and CD is variable in studies from Asia. A recent questionnaire, designed according to European and US Guidelines of IBD, was distributed to IBD specialists throughout Asia with the aim of assessing IBD management practices.

Giorgini, Massimo Zuin, Andrea Salmi, Silvia Colombo, Osvaldo Fracassetti, Paolo Del Poggio, Savino Bruno, Stefano Fagiuoli, Marco Andreoletti, Agostino Selleck ATR inhibitor Colli, Alberto Eraldo Colombo, Giorgio A. Bellati, Carlo F. Magni, Elena Angeli, Guido A. Gubertini, Massimo Fasano, Teresa A. Santantonio, Natalia M. Terreni, Giampaolo Mangia Background & Aims Given the substantial evidence that early hepatitis B virus (HBV) DNA response after oral antiviral therapy

can strongly predict prolonged virologic outcomes, treatment adaptation at an early phase is strongly recommended for chronic hepatitis B (CHB) patients with primary non-response during treatment. The purpose of this study is to assess whether the definition of primary virologic response to guide the CHB treatment algorithm suggested Palbociclib clinical trial by the AASLD guidelines was optimal for treatment with entecavir, a newer and more potent antiviral agent. Methods This retrospective study included 1,262 treatment-naïve CHB patients receiving entecavir (0.5mg/day) monotherapy for over six months: median age 47 years, 63 % Male, 55% HBeAg-positive, and 42% cirrhosis. All patients had an HBV DNA level of at least 2,000 IU/mL at

the start of their entecavir treatment. “”Primary

non-response”" was defined as <2 log decrease in the serum HBV DNA level from the baseline after at least six months Phloretin of therapy, according to the AASLD guidelines. The primary endpoint of this study was the virologic response, evidenced by achieving the serum HBV DNA to an undetectable level (<15 IU/mL) during the study period. The cumulative probability of a virologic response was evaluated and compared between the groups using Kaplan-Meier analysis and the log-rank test. Results In our study, the median duration of entecavir therapy was 31 months (range, 6 to 72 months). A total of 19 (1.5%) patients were categorized as primary non-responders. The cumulative rates for achieving a virologic response over time were 68.3%, 88%, 95%, and 95.7%, respectively, at 12, 24, 36, and 48 months, and which were significantly greater than the 29.4%, 64%, 88%, and 88%, respectively, seen in the primary non-responders (P=0.002). At 48 months, the proportion of virologic respon-ders (95.6% vs 100%) and the mean reduction in the serum HBV DNA levels (-5.08 vs. -6.79 log 10 IU/mL) were not associated with the presence of a primary response (P=NS for both).

Phlebotomy was performed within 48 hours of starting steroids. Patient demographics (age, sex, alcohol history) were documented as well as serum biochemistry results taken on days 0 and 7. GAHS and Lille model prognostic scores were calculated as described.2, 23, 24 All patients were treated daily with 40 mg prednisolone orally for a minimum

of 10 days and full supportive care. All patients either had undergone liver biopsy within the 6 months prior to inclusion or underwent biopsy during the current hospital admission to exclude alternative causes of liver disease. Primary outcome was mortality at 6 months. Fall in bilirubin in the first 7 days following treatment was a secondary outcome measure. A suppression of lymphocyte proliferation of <60% of the maximal proliferation count (Imax) was used as a criterion of in vitro steroid resistance as described.16, 17 Imax = 1 − (cpm with dexamethasone − cpm with phytohemagglutinin [PHA] alone) × 100% (cpm = count per million). In all, 20-40 mL of blood was taken from each patient within 48 hours of starting steroid therapy. PBMCs were isolated by Ficoll-paque Plus density gradient centrifugation of heparinized venous blood and cell viability

assessed by the Trypan blue dye exclusion test. A total of 4 × 105 PBMCs were resuspended in RPMI 1640 media Autophagy activator solution (Invitrogen) and cultured in triplicate in a round-bottom, 96-well

plate containing 10% heat-inactivated fetal calf serum and 20 μg/mL PHA as described.16, 17 To study the effects of IL-2 blockade on steroid resistance, 10 μg/mL final concentration of basiliximab (Simulect, Novartis) was added to a triplicate of cultures at baseline. Cells were cultured in the presence or absence of dexamethasone 10−6 M for 42 hours. Ten Methocarbamol μL of 3H thymidine (Amersham International, Amersham, UK) was then added to each well and left for a further 6 hours. The plate was harvested onto a glass fiber filter paper (Wallac Oy, Turku, Finland) using a cell harvester apparatus (Tomtec, Orange, CT) and the incorporated radiolabel was counted using a Micro β emission scintillation counter (Wallac) expressing triplicate culture data as counts per minute. In all but five individuals tritiated thymidine incorporation after PHA stimulation alone was >10,000 cpm. Where the induction of proliferation was inadequate (cpm with PHA alone <10,000), the assay was repeated within 3 months and the data included in the analysis if on repeat testing the value was >10,000 (two individuals). Three individuals were excluded from the analysis because of repeated failure of the proliferation assay. Of these, one-third died within 6 months. There was no difference between the median proliferated cell counts in either the steroid-resistant or steroid-sensitive groups (P = 0.84).

Western blotting data showed bands of C3 subunits C3α and β and

FH in the HSC culture supernatant (serum-free medium) (Supporting Fig. 3C). Depletion of C3 (by GDC-0199 mouse addition of specific mAb into HpSC supernatant, precipitated, and removed using protein-A agarose followed by centrifugation) markedly reduced (not entirely inhibited) the ability to induce H-MC (Supporting Fig. 3D), suggesting a crucial role of C3 produced by HSC, and other factor(s) may also be involved. Indeed, flow analysis of intracellular staining showed that almost all HSC that were used for cotransplantation were C3-positive (Supporting Fig. 3E). Consistently, the histochemical staining of islet/HSC grafts demonstrated that the islets were surrounded by HSC (alpha smooth

muscle actin [α-SMA]+) cells that were C3-positive. Single α-SMA+ cells scattered in the islet grafts were vessel smooth muscle cells (Supporting Fig. 3F). The immune stimulatory activity of H-MC was examined in a one-way MLR assay. H-MC elicited significantly lower proliferative responses in allogeneic T cells compared to DC (Fig. 6A). Intracellular staining revealed that, compared to DC, T cells stimulated by H-MC produced less IFN-γ, but more IL-10 (Fig. 6A). The impact of H-MC on generation of Treg cells was examined mTOR inhibitor by multiple color staining for CD4, CD25, and Foxp3. Compared to this website DC, H-MC inhibited generation of CD25+Foxp3− effector cells, but preferentially enhanced the frequency of CD25+Foxp3+ Treg cells, resulting in a marked increase in the Treg:effector ratio (0.6 in DC versus 2.0 in the H-MC group) (Fig. 6B). To test the ability of H-MC to suppress T-cells responses, H-MC were added into an MLR culture in which CFSE-labeled T cells

were stimulated by allogeneic DC. Addition of H-MC suppressed proliferative responses (CFSE dilution) in both CD4+ and CD8+ T cells in a dose-dependent manner. T-cell inhibition was not due to overcrowding of APC in the culture because addition of the same number of DC did not inhibit T-cell proliferation (Fig. 6C), indicating that the T-cell response was inhibited by H-MC. We first tested the inhibitory effect of H-MC in vivo using the OVA-HEP transgenic mice in which membrane-bound OVA is specifically expressed on hepatocytes.23 Adoptive transfer of OVA-specific CD4+ (2 × 106) and CD8+ T cells (5 × 106) led to elevation of alanine aminotransferase (ALT) in OVA-HEP mice, peaking on day 3 posttransfer (Fig. 7A). This was associated with infiltration of CD4+ and CD8+ T cells in the portal areas of the liver peaking on day 6 (Fig. 7B). When 1.5 × 106 DC were intravenously injected immediately after adoptive transfer of OVA-specific CD4+ and CD8+ T cells, serum ALT was elevated. However, H-MC treatment maintained ALT levels comparable to controls (Fig. 7A).

Malnutrition was associated with active H. pylori infection. Helicobacter pylori (H. pylori) is a gram-negative, curved-shaped bacterium, classified in Group I carcinogen, clinically associated with gastritis, peptic ulcer disease

and NVP-BGJ398 gastric cancer [1, 2]. In developing countries, more than 80% of adults and 50% of children are colonized by H. pylori compared to 30% of adults and 10% of children in developed countries [3]. In Mexico, in 1988 a seroepidemilogical survey estimated H. pylori prevalence of 66% [4, 5]. Twenty percent of infants of 1 year and younger were colonized by H. pylori, and colonization had reached 50% in children before they reached 10 years of age [6]. In a study carried out in 2001 in boarding schools of the National Indigenous Institute of Hidalgo State in Mexico, prevalence of active H. pylori infection was 52% [7]. In a population study, in Mexico City, 38% of school children had active H. pylori. Children with H. pylori infection Rapamycin concentration averaged 1.32 cm (CI 95% −2.22 to −0.42) less in height than children without infection [8]. In the same population, the colonization by H. pylori was a dynamic phenomenon, with an incidence rate of 64 new cases/year/1000 school children and a spontaneous infection clearance rate of 47 cases/year/1000 school children [9]. There are different

H. pylori strains with genetic variability. Bacterial characteristics, host characteristics, and environmental factors determine the degree of damage that the infection can cause in the gastric mucosa [10]. H. pylori displays factors that determine its virulence; one of them is the cytotoxin-associated gene A (cagA) [11]. In learn more most populations, approximately 50% of H. pylori strains have this virulence

factor. The cagA island encodes a bacterial type IV secretion system that translocates CagA into host cells. Intracellular CagA affects multiple pathways that alter host cell morphology, signaling, and inflammatory responses [11]. H. pylori infection with this virulence factor has been associated with the development of severe diseases such as gastric and duodenal ulcer, gastric atrophy, and gastric cancer [12-14]. The infection by H. pylori in children has also been associated with extra-gastric manifestations such as lower growth rate and iron deficiency (ID) or iron deficiency anemia (IDA) [15-21]. Some authors suggest that a chronic infection is a prerequisite for the development of diseases such as symptomatic gastritis, gastric and duodenal ulcers, gastric cancer [22], ID or IDA [23, 24]. Studies on the effect of active infection on the speed of child growth have shown that there is a greater negative effect in the months after the onset of the infection. This effect is maintained and affects infected children’s growth cumulatively throughout time [18, 19, 21]. The majority of H. pylori-infected people remain asymptomatic; thus, the infection is not detected in the acute phase.

4% clinical response) and 77% for CD patients (74% remission, 3.2% clinical response). Sakata et al.33 has conducted a small prospective randomized trial to compare the clinical efficiency for active Inhibitor Library chemical structure UC between LCAP and GMA;

however, they could not detect any significant difference between them. Therapeutic mechanism of GMA for UC.  The therapeutic mechanism of GMA for UC can be judged from the following background. In patients with active IBD, peripheral blood granulocyte and monocytes/macrophage levels are elevated, and cells show activation behavior and increased survival time.34–39 As these leukocytes are a major source of inflammatory cytokines,40,41 the level of neutrophil infiltration into the mucosal tissue in patients with active IBD has been directly related to the severity of intestinal inflammation and clinical relapse.42,43 Adacolumn has been developed to “tame the exuberant immune system” in patients in whom an overactive immune system, namely elevated peripheral blood neutrophils, is associated with disease progression.34 However, interestingly, the observed clinical efficacy cannot be fully explained by the BVD-523 effects of the procedure on peripheral blood leukocytes per se. We have proven that peripheral Treg (CD25HighCD4+ T-cells) expression,

which has been suppressed in active UC compared with healthy controls, was significantly increased after a single GMA session.44 The increase in CD25High+CD4+ regulatory T-cells after GMA should contribute to improved

immune function of the patient. Moreover, we have proven that the number of CD4+/FoxP3+ mucosal Treg in GMA responders decreased significantly after the fifth GMA session compared with the baseline level.45 It seems possible, therefore, that GMA might impact the circulating as well as the mucosal levels of Tregs. Likewise, several other investigators have reported favorable immunological observations associated with GMA.23,46,47 Reactivation of cytomegalovirus (CMV) infection has often exacerbated UC refractory to immunosuppressive therapies. Yoshino et al. reported the clinical effect of GMA therapy for UC patients with concomitant mucosal CMV infection, and they have proposed that GMA might be a safe and effective treatment for UC patients positive for CMV because selleck the procedure does not induce CMV reactivation.48 Optimization of processing conditions.  Clinical effectiveness of LCAP and GMA should be regulated by blood volume for the procedure (Pv), procedure time, and procedure frequency (Qf). Pv can be calculated as: Pv = Blood flow speed (Qb) × Procedure time (Qt). Basically, slower Qb should reinforce the leukocyte removal performance of the column. Cellsorba, the LCAP column, is unsuitable for proceeding under 20 mL/min of slow Qb conditions since the platelet removal characteristics of the column could cause formation of thromboses in the Cellsorba column.

Key Word(s): 1. Tuberculosis; 2. Crohn’s disease; www.selleckchem.com/screening/anti-infection-compound-library.html 3. Anti-TB therapy; Presenting Author: WEE KHOON NG Additional Authors: WEE CHIAN LIM, CHARLES VU Corresponding Author: WEE KHOON NG Affiliations: Tan Tock Seng Hospital Objective: Vitamin D deficiency and low bone mineral density (BMD) is common amongst patients with inflammatory bowel disease (IBD) [1,2]. It is important to detect vitamin D deficiency as a higher vitamin D status significantly reduces the risk of incident Crohn’s disease (CD). Previous studies also suggested that vitamin D deficiency is a risk factor for low BMD in IBD patients [3,4]. The prevalence of vitamin

D deficiency and the extent of ethnic influence remains poorly documented for Asian patients with IBD. Our aim is to evaluate the prevalence of vitamin D deficiency in patients with IBD in a tropical country like Singapore, with a multi-racial population (predominantly consisting of Chinese, Malay and Indian) and evaluate its association with BMD.* References in appended

file Methods: Case notes and electronic records of patients with IBD who has been treated at our centre were retrospectively reviewed. Vitamin D levels and BMD were Forskolin manufacturer checked at the discretion of the attending physician. The vitamin D levels were initially measured using assay for vitamin D3 (deficiency defined as <20 μg/L, insufficiency 20–30 μg/L), but a new assay acquired in recent years, allowed our centre to monitor total vitamin D levels, which provides a more accurate measurement of vitamin D stores in the body (deficiency defined as <12 μg/L, insufficiency 12–19 μg/L). BMD is measured using Dual-energy X-ray absorptiometry (DEXA). Based on the World Health Organisation (WHO) criteria, T score is defined normal if ≥−1.0, osteopenia

if between −1.0 and −2.5 and osteoporosis if ≤−2.5. Vitamin D and BMD status of each patient were selleck chemicals recorded and the data analysed using the Fisher’s Exact and Chi-Square test. Results: Of the 90 patients with ulcerative colitis (UC) and 54 patients with CD, only 47 UC (52%) and 34 CD (63%) patients had vitamin D levels measured. This adds up to a total of 81 IBD patients and 64 had low vitamin D levels (44 deficiency, 20 insufficiency). Of these, 55 were Chinese, 18 Indians and 8 Malays. Of the 47 UC patients, 39 (83%) had low vitamin D levels (26 deficiency, 13 insufficiency); of the 34 CD patients, 25 (73.5%) had low vitamin D levels (18 deficiency, 7 insufficiency). There was no difference in the prevalence of hypovitaminosis D among UC and CD patients (p = 0.41). Among Chinese patients with IBD, 39 (71%) had low vitamin D levels (29 deficiency, 10 insufficiency) compared to 17 (94%, 11 deficiency, 6 insufficiency) Indian and 8 (100%, 4 deficiency, 4 insufficiency) Malay IBD patients respectively (p = 0.03).