Displaying publications 1 - 20 of 65 in total

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  1. Abdalla LF, Chaudhry Ehsanullah R, Karim F, Oyewande AA, Khan S
    Cureus, 2020 May 22;12(5):e8240.
    PMID: 32582499 DOI: 10.7759/cureus.8240
    The process of inflammation occurs due to inflammatory mediators, including prostaglandins, cytokines, and tumor necrosis factor (TNF). All these mediators activate the process of tumorigenesis and dysplasia, leading to colitis-associated cancer. Several drugs used to decrease these mediators will help in the treatment of acute attacks and also help in prolonged remissions of the disease by using nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and biological factors. Reducing these inflammatory mediators also have a role in chemoprevention and prevent progression to colorectal carcinoma. The most researched drugs in this process of chemoprevention are NSAIDs as it has both cyclooxygenase-2 (COX-2) inhibitory and non-inhibitory effects. These drugs should be taken for a long time and in large doses to reach this effect, which puts the patient at risk for various side effects. Researchers will need to do more research in the future to find the lowest effective dose that can reach the chemopreventive effect. We used database Pubmed as the main source for data search and extracted articles exploring the relationship between NSAIDs and their role in chemoprevention of colorectal carcinoma in inflammatory bowel disease (IBD) patients. We chose 23 studies which included seven review articles. We found that inflammatory mediators have a key role in colitis-associated cancer.
    Matched MeSH terms: Inflammatory Bowel Diseases
  2. Abdul Rani R, Raja Ali RA, Lee YY
    Intest Res, 2016 Oct;14(4):297-304.
    PMID: 27799880
    Irritable bowel syndrome (IBS), a common gastrointestinal disorder involving the gut-brain axis, and inflammatory bowel disease (IBD), a chronic relapsing inflammatory disorder, are both increasing in incidence and prevalence in Asia. Both have significant overlap in terms of symptoms, pathophysiology, and treatment, suggesting the possibility of IBS and IBD being a single disease entity albeit at opposite ends of the spectrum. We examined the similarities and differences in IBS and IBD, and offer new thoughts and approaches to the disease paradigm.
    Matched MeSH terms: Inflammatory Bowel Diseases
  3. Al-Jashamy K, Murad A, Zeehaida M, Rohaini M, Hasnan J
    Asian Pac J Cancer Prev, 2010;11(6):1765-8.
    PMID: 21338230
    Colorectal cancer (CRC) is the second most common cause of cancer mortality among men and women worldwide; the risk of its occurrence has been shown to be increased by chronic bacterial infections. A case control study was therefore carried out at Hospital Universiti Sains Malaysia (HUSM) to determine the incidence of colorectal cancer associated with S. bovis infection. A total of 166 stool specimens were collected from diseased patients and healthy individuals and S. bovis isolates were identified. Suspected colon tumor and cancer cases were diagnosed and confirmed. It was found that overall prevalence of S. bovis was 41 (24.7%) out of 166 cases studied. Some 41(48.6%) of these S. bovis isolates was found in patients with colonic polyps, adenocarcinomas, inflammatory bowel disease (IBD) and chronic gastrointestinal tract (GIT). It was also found that colorectal cancer incidence was 24.7%, adenocarinomas accounting for 51% with the highest incidence in the sigmoid part of the colon. Among the IBD and chronic GIT cases, ulcerative colitis featured in the majority of cases (41.4%). In conclusion, there is a high incidence of colorectal cancer associated with S. bovis.
    Matched MeSH terms: Inflammatory Bowel Diseases/complications*; Inflammatory Bowel Diseases/microbiology; Inflammatory Bowel Diseases/epidemiology
  4. Ananthakrishnan AN, Bernstein CN, Iliopoulos D, Macpherson A, Neurath MF, Ali RAR, et al.
    Nat Rev Gastroenterol Hepatol, 2018 Jan;15(1):39-49.
    PMID: 29018271 DOI: 10.1038/nrgastro.2017.136
    A number of environmental factors have been associated with the development of IBD. Alteration of the gut microbiota, or dysbiosis, is closely linked to initiation or progression of IBD, but whether dysbiosis is a primary or secondary event is unclear. Nevertheless, early-life events such as birth, breastfeeding and exposure to antibiotics, as well as later childhood events, are considered potential risk factors for IBD. Air pollution, a consequence of the progressive contamination of the environment by countless compounds, is another factor associated with IBD, as particulate matter or other components can alter the host's mucosal defences and trigger immune responses. Hypoxia associated with high altitude is also a factor under investigation as a potential new trigger of IBD flares. A key issue is how to translate environmental factors into mechanisms of IBD, and systems biology is increasingly recognized as a strategic tool to unravel the molecular alterations leading to IBD. Environmental factors add a substantial level of complexity to the understanding of IBD pathogenesis but also promote the fundamental notion that complex diseases such as IBD require complex therapies that go well beyond the current single-agent treatment approach. This Review describes the current conceptualization, evidence, progress and direction surrounding the association of environmental factors with IBD.
    Matched MeSH terms: Inflammatory Bowel Diseases/diagnosis; Inflammatory Bowel Diseases/etiology*; Inflammatory Bowel Diseases/therapy
  5. Bakshi HA, Mishra V, Satija S, Mehta M, Hakkim FL, Kesharwani P, et al.
    Inflammation, 2019 Dec;42(6):2032-2036.
    PMID: 31377947 DOI: 10.1007/s10753-019-01065-3
    Hypoxia inducible factor (HIF)-prolyl hydroxylase (PHD) inhibitors are shown to be protective in several models of inflammatory bowel disease (IBD). However, these non-selective inhibitors are known to inhibit all the three isoforms of PHD, i.e. PHD-1, PHD-2 and PHD-3. In the present report, we investigated the associated changes in levels of PHDs during the development and recovery of chemically induced colitis in mice. The results indicated that in the experimental model of murine colitis, levels of both, PHD-1 and PHD-2 were found to be increased with the progression of the disease; however, the level of PHD-3 remained the same in group of healthy controls and mice with colitis. Thus, the findings advocated that inhibitors, which inhibited all three isoforms of PHD could not be ideal therapeutics for IBD since PHD-3 is required for normal gut function. Hence, this necessitates the development of new compounds capable of selectively inhibiting PHD-1 and PHD-2 for effective treatment of IBD.
    Matched MeSH terms: Inflammatory Bowel Diseases/drug therapy
  6. Banerjee R, Ali RAR, Wei SC, Adsul S
    Gut Liver, 2020 11 15;14(6):685-698.
    PMID: 33191310 DOI: 10.5009/gnl19209
    The advent of biologics and biologic therapy has transformed the management of inflammatory bowel disease (IBD) with enhanced early and adequate responses to treatment, fewer hospitalizations, a reduced need for surgery, and unprecedented outcomes including complete mucosal and histologic healing. However, an important issue with the use of anti-tumor necrosis factor (anti-TNF) agents in IBD is the increased risk of tuberculosis (TB). This is compounded by the diagnostic dilemma when differentiating between Crohn's disease and gastrointestinal TB, and the potentially serious consequences of initiating an incorrect treatment in the case of misdiagnosis. The interplay between IBD and TB is most relevant in Asia, where more than 60% of the 10.4 million new TB cases in 2016 were reported. A number of studies have reported an increased risk of TB with anti-TNF agents, including in patients who had tested negative for TB prior to treatment initiation. The limited evidence currently available regarding adhesion molecule antagonists such as vedolizumab suggests a comparatively lower risk of TB, thus making them a promising option for IBD management in TBendemic regions. This comprehensive review examines the available literature on the risk of TB with the use of biologics in the TB-endemic regions of Asia, focusing on the diagnostic dilemma, the risk of reactivation, and the optimized management algorithms for latent and active disease.
    Matched MeSH terms: Inflammatory Bowel Diseases*
  7. Chan SN, Low END, Raja Ali RA, Mokhtar NM
    Intest Res, 2018 Jul;16(3):374-383.
    PMID: 30090036 DOI: 10.5217/ir.2018.16.3.374
    Inflammatory bowel disease (IBD), which comprises of Crohn's disease and ulcerative colitis, is an idiopathic relapsing and remitting disease in which the interplay of different environment, microbial, immunological and genetic factors that attribute to the progression of the disease. Numerous studies have been conducted in multiple aspects including clinical, endoscopy and histopathology for the diagnostics and treatment of IBD. However, the molecular mechanism underlying the aetiology and pathogenesis of IBD is still poorly understood. This review tries to critically assess the scientific evidence at the transcriptomic level as it would help in the discovery of RNA molecules in tissues or serum between the healthy and diseased or different IBD subtypes. These molecular signatures could potentially serve as a reliable diagnostic or prognostic biomarker. Researchers have also embarked on the study of transcriptome to be utilized in targeted therapy. We focus on the evaluation and discussion related to the publications reporting the different approaches and techniques used in investigating the transcriptomic changes in IBD with the intention to offer new perspectives to the landscape of the disease.
    Matched MeSH terms: Inflammatory Bowel Diseases
  8. Cheng CW, Feng CM, Chua CS
    J Int Med Res, 2020 May;48(5):300060520922379.
    PMID: 32475192 DOI: 10.1177/0300060520922379
    Amebiasis is a frequently occurring parasitic infection in South East Asia. We present a case of a 54-year-old man with right lower quadrant abdominal pain that persisted for longer than 1 year. He had been diagnosed with inflammatory bowel disease in Indonesia. His abdominal pain persisted, despite therapy, and he visited Malaysia for transnational medical advice. Abdominal ultrasound showed fatty liver, gallbladder polyps, and a small left renal stone. Colonoscopy showed multiple ulcers in the cecum and a histopathological examination confirmed amebic infection of the cecum. The colonic ulcers subsided after anti-amebic treatment. This case highlights the need to consider the differential diagnosis of amebic colitis in patients presenting with manifestations of inflammatory bowel disease, especially in patients who live in or have traveled to endemic areas.
    Matched MeSH terms: Inflammatory Bowel Diseases/diagnosis
  9. Chew D, Zhiqin W, Ibrahim N, Ali RAR
    Intest Res, 2018 10;16(4):509-521.
    PMID: 30369231 DOI: 10.5217/ir.2018.00074
    The patient-physician relationship has a pivotal impact on the inflammatory bowel disease (IBD) outcomes. However, there are many challenges in the patient-physician relationship; lag time in diagnosis which results in frustration and an anchoring bias against the treating gastroenterologist, the widespread availability of medical information on the internet has resulted in patients having their own ideas of treatment, which may be incongruent from the treating physicians' goals resulting in patient physician discordance. Because IBD is an incurable disease, the goal of treatment is to sustain remission. To achieve this, patients may have to go through several lines of treatment. The period of receiving stepping up, top down or even accelerated stepping up medications may result in a lot of frustration and anxiety for the patient and may compromise the patient-physician relationship. IBD patients are also prone to psychological distress that further compromises the patient-physician relationship. Despite numerous published data regarding the medical and surgical treatment options available for IBD, there is a lack of data regarding methods to improve the therapeutic patient-physician relationship. In this review article, we aim to encapsulate the challenges faced in the patient-physician relationship and ways to overcome in for an improved outcome in IBD.
    Matched MeSH terms: Inflammatory Bowel Diseases
  10. Chua KH, Hilmi I, Lian LH, Patmanathan SN, Hoe SZ, Lee WS, et al.
    J Dig Dis, 2012 Sep;13(9):459-65.
    PMID: 22908971 DOI: 10.1111/j.1751-2980.2012.00617.x
    This study was aimed to investigate the possible association of Crohn's disease (CD) with inflammatory bowel disease gene 5 (IBD5) IGR2198a_1 (rs11739135), IGR2096a_1 (rs12521868) and interleukin-23 receptor (IL23R) genetic variant (rs1004819) in the Malaysian population.
    Matched MeSH terms: Inflammatory Bowel Diseases/genetics*
  11. Chua KH, Ng JG, Ng CC, Hilmi I, Goh KL, Kee BP
    PeerJ, 2016;4:e1843.
    PMID: 27069792 DOI: 10.7717/peerj.1843
    Crohn's disease (CD) is a prominent type of inflammatory bowel disease (IBD) that can affect any part of the gastrointestinal tract. CD is known to have higher prevalence in the Western countries, but the number of cases has been increasing in the past decades in Asia, including Malaysia. Therefore, there is a need to investigate the underlining causes of CD that may shed light on its prevention and treatment. In this study, genetic polymorphisms in NOD1 (rs2075820), CXCL16 (rs2277680), STAT6 (rs324015) and TLR4 (rs4986791) genes were examined in a total of 335 individuals (85 CD patients and 250 healthy controls) with PCR-RFLP approach. There was no significant association observed between NOD1 rs2075820 and STAT6 rs324015 with the onset of CD in the studied cohort. However, the G allele of CXCL16 rs2277680 was found to have a weak association with CD patients (P = 0.0482; OR = 1.4310). The TLR4 rs4986791 was also significantly associated to CD. Both the homozygous C genotype (P = 0.0029; OR = 0.3611) and C allele (P = 0.0069; OR = 0.4369) were observed to confer protection against CD. On the other hand, the heterozygous C/T genotype was a risk genotype (P = 0.0015; OR = 3.1392). Further ethnic-stratified analysis showed that the significant associations in CXCL16 rs2277680 and TLR4 rs4986791 were accounted by the Malay cohort. In conclusion, the present study reported two CD-predisposing loci in the Malay CD patients. However, these loci were not associated to the onset of CD in Chinese and Indian patients.
    Matched MeSH terms: Inflammatory Bowel Diseases
  12. Gothai S, Muniandy K, Gnanaraj C, Ibrahim IAA, Shahzad N, Al-Ghamdi SS, et al.
    Biomed Pharmacother, 2018 Nov;107:1514-1522.
    PMID: 30257369 DOI: 10.1016/j.biopha.2018.08.112
    Colorectal cancer (CRC) is ranked as the fourth most lethal and commonly diagnosed cancer in the world according to the National Cancer Institute's latest report. Treatment methods for CRC are constantly being studied for advancement, which leads for more clinically effective cancer curing strategy. Patients with prolonged chronic inflammation caused by ulcerative colitis or similar inflammatory bowel disease are known to have high risks of developing CRC. But at a molecular level, oxidative stress due to reactive oxygen species (ROS) is an important trigger for cancer. Hence, in recent years, exogenous antioxidants have been immensely experimented in pre-clinical and clinical trials, considering it as a potential cure for CRC. Significantly, potential antioxidant compounds especially derivatives of medicinal plants have received great attention in the current research trend for CRC treatment. Though antioxidant compounds seem to have beneficial properties for the treatment of CRC, there are also limitations for pure compounds to be tested clinically. Therefore, this review aims to delineate the pharmacological awareness among researchers on using antioxidant compounds to treat CRC and the measures taken to prove the effectiveness of such compounds as impending drug candidates for CRC treatment in modern medication.
    Matched MeSH terms: Inflammatory Bowel Diseases/complications
  13. Hassan V, Hassan S, Seyed-Javad P, Ahmad K, Asieh H, Maryam S, et al.
    Med J Malaysia, 2013;68(1):34-8.
    PMID: 23466764
    Inflammatory bowel diseases (IBDs) are immune mediated diseases affecting the gastrointestinal tract. Several environmental factors in concert with genetic susceptibilities can trigger IBDs. Recently, one of the important environmental factors contributing to the development of autoimmune diseases is vitamin D (VitD) deficiency. Furthermore, some new evidence points to VitD deficiency and its receptor dysfunction as an underlying factor for the emergence experimental IBDs. The aim of the current study was to evaluate the correlation between serum 25(OH)D concentrations and IBD activity in patients with ulcerative colitis or Crohn's disease. Sixty patients with confirmed diagnosis of IBD were recruited for a cross sectional study. Most of the identified confounders affecting serum VitD concentrations were excluded. Disease activity was assessed using validated questionnaires, including Truelove for Ulcerative Colitis and Crohn Disease Activity Index (CDAI) for Crohn disease. Serum 25(OH)D concentrations were determined by chemiluminescent assay. Serum 25(OH)D≤10 (ng/ml) was considered as VitD deficiency and 11≤25(OH)D<29(ng/ml) as VitD insufficiency. Mean serum 25(OH)D value was 13.1 ± 11.1(ng/ml) in IBD patients. Almost 95% of patients were vitamin D insufficient or deficient. Forty one percent of IBD patients had active disease. VitD deficiency was not associated with IBD activity (p=0.23). However, VitD deficiency was significantly associated with a history of IBD related intestinal surgery (p=0.001). In conclusion, this cross-sectional prospective study suggested that there is no association between vitamin D deficiency and disease activity in a relatively small number of IBD patients in a short period of time.
    Matched MeSH terms: Inflammatory Bowel Diseases
  14. Hilmi I, Sunderesvaran K, Ananda V, Sarji SA, Arumugam K, Goh KL
    J Clin Endocrinol Metab, 2013 Jun;98(6):2415-21.
    PMID: 23553858 DOI: 10.1210/jc.2013-1147
    INTRODUCTION: Osteoporosis and osteopenia are well-recognized complications of inflammatory bowel disease. Previous studies have suggested that vitamin D deficiency is an important risk factor for the development of osteoporosis. We hypothesized that low vitamin D levels is the main reason for reduced bone mineral density in patients with inflammatory bowel disease. We aimed to study its potential role in Malaysia, which is a tropical country with 3 large ethnic groups. We also sought to examine the relationship between fracture risk and bone mineral density in this group.
    METHODOLOGY: Relevant history as well as 25-hydroxycholecalciferol (vitamin D) levels and bone mineral density were obtained. Normal, inadequate, and low vitamin D levels were defined as 61-160 nmol/L (24-64 ng/mL), 30-60 nmol/L (12-24 ng/mL), and less than 30 nmol/L (<12 ng/mL), respectively.
    RESULTS: Seventy-two patients were recruited. The prevalence of osteopenia and osteoporosis, respectively, were 58% and 17% in the spine and 51% and 14% in the hip. Mean vitamin D level in the group was low at 45.12 ± 17.4 nmol/L (18.05 ± 6.96 ng/mL), but there was no significant association between bone mineral density and vitamin D level. Twelve patients (16.7%) had a fragility fracture after the diagnosis of inflammatory bowel disease. The cumulative fracture incidence was 10% at 5 years and 35% at 10 years. There was a statistically significant association between osteoporosis of hip and a history of fracture (odds ratio 5.889; 95% confidence interval 1.41-24.53, P = .009).
    CONCLUSION: Osteoporosis is prevalent among Malaysian patients with inflammatory bowel disease and is associated with a 6-fold increased risk of fractures. Most inflammatory bowel disease patients had inadequate or low vitamin D levels, but there was no association between vitamin D levels and BMD.
    Matched MeSH terms: Inflammatory Bowel Diseases/complications*
  15. Hilmi I, Kobayashi T
    Intest Res, 2020 Jul;18(3):265-274.
    PMID: 32623876 DOI: 10.5217/ir.2019.09165
    Capsule endoscopy (CE) is emerging as an important investigation in inflammatory bowel disease (IBD); common types include the standard small bowel CE and colon CE. More recently, the pan-enteric CE was developed to assess the large and small bowel in patients with Crohn's disease (CD). Emerging indications include noninvasive assessment for mucosal healing (both in the small bowel and the colon) and detection of postoperative recurrence in patients with CD. Given the increasing adoption, several CE scoring systems have been specifically developed for IBD. The greatest concern with performing CE, particularly in CD, is capsule retention, but this can be overcome by performing cross-sectional imaging such as magnetic resonance enterography and using patency capsules before performing the procedure. The development of software for automated detection of mucosal abnormalities typically seen in IBD may further increase its adoption.
    Matched MeSH terms: Inflammatory Bowel Diseases
  16. Imawana RA, Smith DR, Goodson ML
    Ann Gastroenterol, 2020 06 06;33(5):485-494.
    PMID: 32879595 DOI: 10.20524/aog.2020.0507
    Background: The current literature suggests a protective benefit of Helicobacter pylori (H. pylori) infection against inflammatory bowel disease (IBD). Here we assessed whether this effect varied by IBD subtype-Crohn's disease (CD) or ulcerative colitis (UC)-and geographic region: East Asia, Europe (non-Mediterranean) or Mediterranean region.

    Methods: A database search was performed up to July 2019 inclusive for all studies that compared H. pylori infection in IBD patients vs. non-IBD controls. The relative risk (RR) was used to quantify the association between IBD and H. pylori, and the effects were combined across studies using a mixed-effects meta-regression model, which included IBD subtype and geographic region as categorical moderator variables.

    Results: Our meta-regression model exhibited moderate heterogeneity (I2=48.74%). Pooled RR depended on both region (P=0.02) and subtype (P<0.001). Pooled RRs were <1 for all subtype and region combinations, indicative of a protective effect of H. pylori against IBD. The pooled RR was 28% (9%, 50%; P=0.001) greater for UC vs. CD and 43% (4%, 96%; P=0.02) greater for Mediterranean countries vs. East Asia. The pooled RR was 18% (-13%, 60%; P=0.48) greater for Europe vs. East Asia and 21% (-13%, 68%; P=0.42) greater for Mediterranean vs. Europe, though these differences were not statistically significant.

    Conclusions: The protective effect of H. pylori on IBD varied by both subtype (more protection against CD vs. UC) and region (East Asia more protected than Mediterranean regions). Variation due to these effects could provide insight into IBD etiology.

    Matched MeSH terms: Inflammatory Bowel Diseases
  17. Jayalakshmi P, Wong NW, Malik AK, Goh KL
    JUMMEC, 1996;1(2):39-42.
    A review of all colonic biopsies received by the Department of Pathology during a 8-year period revealed 41 cases of ulcerative colitis (UC). The diagnosis was based on histological and clinical features. The age range of patients was between 14 - 76 years with a median age of 35.4 years. The disease was more prevalent among Indians. The common presenting sysmptoms were diarrhoea (100%) and haematochezia (83%). The extent of colonic involvement varied. Twelve patients (29.2%) had pancolitis and 8 (19.5%) had proctitis.Extraintestinal manifestations were rare and only one patient had pyoderma gangrenosum. One patient developed multifocal colorectal cancer 10 years after the inial diagnosis of UC and died 2 years later due to metastases. Histology plays an important role in the diagnosis and management of patients with UC. We noted a good correlation between clinical and pathological features. The most recent colonic biopsy showed features of chronic UC with activity in 34 cases and features of remission in 4 cases.
    Matched MeSH terms: Inflammatory Bowel Diseases*
  18. Kew, Siang-Tong
    MyJurnal
    Melanosis coli denotes brownish discoloration of the colonic mucosa found on endoscopy
    or histopathologic examination. The condition has no specific symptom on its own. It is a fairly frequent incidental finding of colonic biopsies and resection specimens. The pigmentation is caused by apoptotic cells which are ingested by macrophages and subsequently transported into the lamina propria, where lysosomes use them to produce lipofuscin pigment, not melanin as the name suggests. Melanosis coli develops in over 70% of persons who use anthraquinone laxatives (eg cascara sagrada, aloe, senna, rhubarb, and frangula), often within 4 months of use. Long-term use is generally believed to be necessary to cause melanosis coli.The condition is widely regarded as benign and reversible, and disappearance of the pigment generally occurs within a year of stopping laxatives. Although
    often due to prolonged use of anthraquinone, melanosis can probably result from other factors or exposure to other laxatives. It has been reported as a consequence of longstanding inflammatory bowel disease. Some investigators suggested that increase in apoptosis of
    colonic mucosa by anthraquinone laxatives increased the risk of colonic cancer. Recent data, including those from large-scale retrospective, prospective and experimental studies, did not show any increased cancer risk.
    Matched MeSH terms: Inflammatory Bowel Diseases
  19. Kho ZY, Lal SK
    Front Microbiol, 2018;9:1835.
    PMID: 30154767 DOI: 10.3389/fmicb.2018.01835
    Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. In this review, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them.
    Matched MeSH terms: Inflammatory Bowel Diseases
  20. Kotlarz D, Marquardt B, Barøy T, Lee WS, Konnikova L, Hollizeck S, et al.
    Nat Genet, 2018 Mar;50(3):344-348.
    PMID: 29483653 DOI: 10.1038/s41588-018-0063-6
    Transforming growth factor (TGF)-β1 (encoded by TGFB1) is the prototypic member of the TGF-β family of 33 proteins that orchestrate embryogenesis, development and tissue homeostasis1,2. Following its discovery 3 , enormous interest and numerous controversies have emerged about the role of TGF-β in coordinating the balance of pro- and anti-oncogenic properties4,5, pro- and anti-inflammatory effects 6 , or pro- and anti-fibrinogenic characteristics 7 . Here we describe three individuals from two pedigrees with biallelic loss-of-function mutations in the TGFB1 gene who presented with severe infantile inflammatory bowel disease (IBD) and central nervous system (CNS) disease associated with epilepsy, brain atrophy and posterior leukoencephalopathy. The proteins encoded by the mutated TGFB1 alleles were characterized by impaired secretion, function or stability of the TGF-β1-LAP complex, which is suggestive of perturbed bioavailability of TGF-β1. Our study shows that TGF-β1 has a critical and nonredundant role in the development and homeostasis of intestinal immunity and the CNS in humans.
    Matched MeSH terms: Inflammatory Bowel Diseases/complications*; Inflammatory Bowel Diseases/genetics*; Inflammatory Bowel Diseases/pathology
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