Malabsorption

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Malabsorption

  • carbohydrate malabsorption
  • fat malabsorption
  • fructose malabsorption
  • intestinal malabsorption
  • lactose malabsorption

  • Terms modified by Malabsorption

  • malabsorption syndrome

  • Selected Abstracts


    Comparison of indices of vitamin A status in children with chronic liver disease,

    HEPATOLOGY, Issue 4 2005
    Andrew P. Feranchak
    Malabsorption of fat-soluble vitamins is a major complication of chronic cholestatic liver disease. The most accurate way to assess vitamin A status in children who have cholestasis is unknown. The goal of this study was to assess the accuracy of noninvasive tests to detect vitamin A deficiency. Children with chronic cholestatic liver disease (n = 23) and noncholestatic liver disease (n = 10) were studied. Ten cholestatic patients were identified as vitamin A,deficient based on the relative dose response (RDR). Compared with the RDR, the sensitivity and specificity to detect vitamin A deficiency for each test was, respectively: serum retinol, 90% and 78%; retinol-binding protein (RBP), 40% and 91%; retinol/RBP molar ratio, 60% and 74%; conjunctival impression cytology, 44% and 48%; slit-lamp examination, 20% and 66%; tear film break-up time, 40% and 69%; and Schirmer's test, 20% and 78%. We developed a modified oral RDR via oral coadministration of d-alpha tocopheryl polyethylene glycol-1000 succinate and retinyl palmitate. This test had a sensitivity of 80% and a specificity of 100% to detect vitamin A deficiency. In conclusion, vitamin A deficiency is relatively common in children who have chronic cholestatic liver disease. Our data suggest that serum retinol level as an initial screen followed by confirmation with a modified oral RDR test is the most effective means of identifying vitamin A deficiency in these subjects. (HEPATOLOGY 2005;42:782,792.) [source]


    Indirect evidence for increased mechanosensitivity of jejunal secretomotor neurones in patients with idiopathic bile acid malabsorption

    ACTA PHYSIOLOGICA, Issue 2 2009
    A. Bajor
    Abstract Aim:, The interdigestive motor rhythm, the migrating motor complex (MMC), is accompanied by active secretion of chloride during periods of distally propagating maximal motor activity (MMC phase III). We studied the behaviour of this system in bile acid malabsorption (BAM), a relative common cause of chronic diarrhoea. We measured motor activity and transmucosal potential difference (PD, reflecting active chloride secretion), in the proximal jejunum in healthy controls (n = 18) and in a group of patients with BAM (n = 11). The phase III-generated voltage was related to the degree of BAM quantified by the 75SeHCAT test. Methods:, We used a multi-channel intestinal infusion system to simultaneously measure jejunal pressure and PD. Saline passing calomel half-cells was infused into the jejunum and subcutaneously. Pressure and PD were recorded in the fasting state and after a test meal. Results:, In the absence of motor activity, jejunal PD was not significantly different from zero in either group. During MMC phase III, PD reached significantly higher mean and peak levels in BAM patients. The product of MMC phase III length multiplied by voltage, over 3 h, was also significantly higher in BAM patients (controls: median 307 mV × cm, range 70,398; BAM: median 511, range 274,2271, P < 0.01). This value was also significantly correlated with the degree of BAM as reflected by the 75SeHCAT test (P < 0.05). Conclusion:, Phase III induced jejunal secretion may be upregulated in BAM patients, resulting in overload of colonic reabsorption capacity. [source]


    Prevalence of autoimmune diseases in islet transplant candidates with severe hypoglycaemia and glycaemic lability: previously undiagnosed coeliac and autoimmune thyroid disease is identified by screening

    DIABETIC MEDICINE, Issue 2 2007
    M. Walter
    Abstract Aims, Autoimmune diseases such as Addison's or coeliac disease can contribute to hypoglycaemia or malabsorption and are more common in Type 1 diabetes (T1DM). This brief report describes the prevalence of known and newly detected autoimmune disease in clinical islet transplant candidates with longstanding T1DM and severe hypoglycaemia and/or glycaemic lability who are routinely screened for coexisting autoimmune disease. Methods, One hundred and twenty-four C-peptide negative T1DM subjects [77 (62%) female, mean age 44 ± 9 years, diabetes duration 28 ± 11 years, body mass index 24.9 ± 3.5 kg/m2] with indications for clinical islet transplantation at the University of Alberta were screened for autoimmune disease by history and measurement of anti-transglutaminase antibodies (positive > 10 U/ml), 09.00 h cortisol (followed by adrenocorticotrophic hormone-stimulation if < 495 nmol/l) and thyroid-stimulating hormone to determine the prevalence of coeliac disease, Addison's disease and autoimmune thyroid disease, respectively. Results, Forty per cent of subjects had one or more coexisting autoimmune disease. The prevalence of autoimmune disease was 35%, coeliac disease 8% and Addison's disease 1.6%. In 11 individuals (9%), one or more autoimmune disease were newly detected (seven coeliac disease and five thyroid disease). Seven of 10 cases of coeliac disease were newly detected. A gluten-free diet in individuals with newly diagnosed coeliac disease reduced gastrointestinal symptoms, but indications for clinical islet cell transplantation persisted. Conclusions, Coexisting autoimmune disease is common in candidates for clinical islet cell transplantation. Screening in this group identified a substantial number of previously unrecognized cases. Clinicians should consider the presence of autoimmune disease even in the absence of classical symptoms. [source]


    Prospective screening for biopsy proven coeliac disease, autoimmunity and malabsorption markers in Belgian subjects with Type 1 diabetes

    DIABETIC MEDICINE, Issue 7 2005
    M. Buysschaert
    Abstract Aims To determine prospectively the prevalence of biopsy proven coeliac disease (CD) in an adult Type 1 diabetic population from Belgium with regards to associated auto-immunity and malabsorption. Methods and results Determination in 400 Type 1 diabetic patients of serum anti-endomysial and/or anti-transglutaminase auto-antibodies. All subjects with abnormal serology underwent an intestinal biopsy. Ten patients (2.5%) had positive antibodies. Diagnosis of CD was confirmed by an intestinal biopsy. Eight patients were symptom-free, although laboratory findings suggesting malabsorption were prominent in the presence of CD [microcytic anaemia, iron and folate deficiencies, low levels of 25(OH)vitamin D3, calcium and cholesterol]. Other auto-immune conditions, especially vitiligo, were found in patients with CD. Conclusions Asymptomatic coeliac disease occurs frequently in adult Type 1 diabetic patients, and is often associated with subclinical malabsorption. Screening should be part of routine evaluation, to implement life-long dietary gluten avoidance. [source]


    A rare case of multiple myeloma initially presenting with pseudoachalasia

    DISEASES OF THE ESOPHAGUS, Issue 6 2009
    Georgia Lazaraki
    SUMMARY Pseudoachalasia is a rare clinical entity with clinical, radiographic, and manometric features often indistinguishable from achalasia. Primary adenocarcinomas arising at the gastroesophageal junction or a tumor of the distal esophagus are the most frequent causes of pseudoachalasia. Rarely, processes other than esophagogastric cancers including chronic idiopathic intestinal pseudo-obstruction, amyloidosis, sarcoidosis, Chagas' disease, vagotomy, antireflux surgery, pancreatic pseudocysts, von Recklinghausen's neuroinomatosis, gastrointestinal stromal tumor, and other malignancies and rare genetic syndromes, may lead to the development of pseudoachalasia. Secondary achalasia is extremely rare, with less than 100 cases reported in the literature so far. Gastrointestinal manifestations in primary or secondary amyloidosis include abdominal pain, diarrhea, constipation, malabsorption, obstruction, motility disturbance, intestinal infarction, perforation, and hemorrhage; however, gastrointestinal tract involvement is asymptomatic in most instances. We present here a rare case of multiple myeloma initially presenting with dysphagia because of esophageal amyloidosis and manometric findings typical of achalasia. [source]


    Small intestinal malabsorption in an aged mare

    EQUINE VETERINARY EDUCATION, Issue 3 2000
    K. Chandler
    [source]


    Do horses suffer from irritable bowel syndrome?

    EQUINE VETERINARY JOURNAL, Issue 9 2009
    J. O. HUNTER
    Summary Irritable bowel syndrome (IBS) in man is not a single entity but has several causes. One of the most common forms has similarities with colic and laminitis in horses. Undigested food residues may pass from the small intestine into the colon where bacterial fermentation produces chemicals that lead to disease. In horses the consequences may be disastrous, but in healthy humans such malabsorption may not be harmful. After events such as bacterial gastroenteritis or antibiotic treatment, an imbalance of the colonic microflora with overgrowth of facultative anaerobes may arise, leading to malfermentation and IBS. It is not known whether such subtle changes may likewise be present in the microflora of horses who are susceptible to colic and laminitis. Metabolomic studies of urine and faeces may provide a suitable way forward to identify such changes in the horse's gut and thus help to identify more accurately those at risk and to provide opportunities for the development of improved treatment. [source]


    Impaired nutritional status in common variable immunodeficiency patients correlates with reduced levels of serum IgA and of circulating CD4+ T lymphocytes

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2001
    M. Muscaritoli
    Background Common variable immunodeficiency (CVI) is a primary defect of the immune system. Infections, persistent diarrhoea and malabsorption may result in malnutrition, which may in turn contribute to increased morbidity. In this paper, the prevalence of malnutrition in CVI was evaluated. Patients and methods Forty CVI patients (20 male, 20 female, aged 17,75 years) underwent anthropometric measurements from which body mass index, arm fat and muscle area were calculated. Body mass index values <,18·5 and arm fat and muscle area values <,10th percentile were considered indicative of malnutrition. Patients were divided into four groups according to circulating CD4+ T cells (lower or greater than 300 µL,1) and serum immunoglobulin A (IgA) levels (detectable and undetectable). Results Body mass index <,18·5, arm fat and muscle area <,10th percentile were observed in 23%, 58% and 44%, respectively, of patients. Lower values of body mass index, arm fat and muscle area were more frequent in patients with low CD4+ cells and undetectable IgA. Low arm fat values were more frequent in patients with diarrhoea (P = 0·03). Infectious episodes were more frequent in undetectable IgA than in detectable IgA patients (P = 0·04). Conclusions Anthropometric measurements revealed an increased rate of malnutrition in CVI patients, particularly in those with low CD4+ and undetectable IgA, suggesting that selected CVI subjects could be considered for standard or specialized nutritional support. [source]


    Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001
    S. Gabsi
    Ataxia with vitamin E (Vit E) defciency (AVED) is an autosomal recessive disorder caused by mutations of the , tocopherol transfer protein gene. The Friedreich ataxia phenotype is the most frequent clinical presentation. In AVED patients, serum Vit E levels are very low in the absence of intestinal malabsorption. As Vit E is a major antioxidant agent, Vit E deficiency is supposed to be responsible for the pathological process. Twenty-four AVED patients were fully investigated (electromyography, nerve conduction velocity (NVC) studies, somatosensory evoked potentials, cerebral computed tomography scan, sural nerve biopsy, genetic studies) and supplemented with Vit E (800 mg daily) during a 1-year period. Clinical evaluation was mainly based on the Ataxia Rating Scale (ARS) for cerebellar ataxia assessment and serum Vit E levels were monitored. Serum Vit E levels normalized and ARS scores decreased moderately but significantly suggesting clinical improvement. Better results were noted with mean disease duration , 15 years. Reflexes remained abolished and posterior column disturbances unchanged. Vitamin E supplementation in AVED patients stabilizes the neurological signs and can lead to mild improvement of cerebellar ataxia, especially in early stages of the disease. [source]


    Down-regulation of reduced folate carrier may result in folate malabsorption across intestinal brush border membrane during experimental alcoholism

    FEBS JOURNAL, Issue 24 2007
    Abid Hamid
    Folate plays a critical role in maintaining normal metabolic, energy, differentiation and growth status of all mammalian cells. The intestinal folate uptake is tightly and diversely regulated, and disturbances in folate homeostasis are observed in alcoholism, attributable, in part, to intestinal malabsorption of folate. The aim of this study was to delineate the regulatory mechanisms of folate transport in intestinal absorptive epithelia in order to obtain insights into folate malabsorption in a rat model of alcoholism. The rats were fed 1 g·kg,1 body weight of ethanol daily for 3 months. A reduced uptake of [3H]folic acid in intestinal brush border membrane was observed over the course of ethanol administration for 3 months. Folate transport exhibited saturable kinetics and the decreased intestinal brush border membrane folate transport in chronic alcoholism was associated with an increased Km value and a low Vmax value. Importantly, the lower intestinal [3H]folic acid uptake in ethanol-fed rats was observed in all cell fractions corresponding to villus tip, mid-villus and crypt base. RT-PCR analysis for reduced folate carrier, the major folate transporter, revealed that reduced folate carrier mRNA levels were decreased in jejunal tissue derived from ethanol-fed rats. Parallel changes were observed in reduced folate carrier protein levels in brush border membrane along the entire crypt,villus axis. In addition, immunohistochemical staining for reduced folate carrier protein showed that, in alcoholic conditions, deranged reduced folate carrier localization was observed along the entire crypt,villus axis, with a more prominent effect in differentiating crypt base stem cells. These changes in functional activity of the membrane transport system were not caused by a general loss of intestinal architecture, and hence can be attributed to the specific effect of ethanol ingestion on the folate transport system. The low folate uptake activity observed in ethanol-fed rats was found to be associated with decreased serum and red blood cell folate levels, which might explain the observed jejunal genomic hypomethylation. These findings offer possible mechanistic insights into folate malabsorption during alcoholism. [source]


    The analysis of the fine specificity of celiac disease antibodies using tissue transglutaminase fragments

    FEBS JOURNAL, Issue 21 2002
    Daniele Sblattero
    Celiac disease is an intestinal malabsorption characterized by an intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and an autoantigen located in the endomysium. The latter has been identified as the enzyme tissue transglutaminase which belongs to a family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis. In a recent paper, we described the selection and characterization of anti-transglutaminase Igs from phage antibody libraries created from intestinal lymphocytes from celiac disease patients. In this work, using transglutaminase gene fragments, we identify a region of tissue transglutaminase recognized by these antibodies as being conformational and located in the core domain of the enzyme. This is identical to the region recognized by anti-transglutaminase Igs found in the serum of celiac disease patients. [source]


    Helicobacter pylori -Associated Chronic Gastritis and Unexplained Iron Deficiency Anemia: a Reliable Association?

    HELICOBACTER, Issue 6 2003
    Stéphane Nahon
    Abstract Background and aim., About 35% of iron deficiency anemia cases remain unexplained after a gastrointestinal evaluation. An association between Helicobacter pylori and iron malabsorption has been suggested. The aim of this study was to determine whether H. pylori -associated chronic gastritis is linked to unexplained iron deficiency anemia in adults. Methods., From 1996 to 2001, we identified 105 patients with unexplained iron deficiency anemia after upper endoscopy, colonoscopy, small bowel radiographic examination and duodenal biopsies. Two biopsies were obtained from the gastric antrum and two from the corpus of each patient. Gastritis status was described according to the Sydney System and H. pylori infection was assessed by an immunohistochemical test on biopsy specimens. This group was compared to a control group matched for sex and age. Results., There were 76 women and 29 men (mean age 57.4 ± 21.4 years) examined in the study. A H. pylori -associated chronic gastritis was identified in 63 cases (60%) vs. 45 cases (43%) cases in the control group (p < .01). Atrophic gastritis was significantly associated with iron deficiency anemia compared with the control group [16 (15%) vs. 6 (6%); p < .03]. In the unexplained iron deficiency anemia group, (1) patients with chronic gastritis were significantly younger (52 ± 22 vs. 64 ± 20 years; p < .005), and (2) chronic gastritis was not linked to sex [sex ratio (male/female): 0.5 vs. 0.34, p = .34]. The prevalence of H. pylori infection was similar between premenopausal and postmenopausal women [28 (27%) vs. 26 (25%); p = .7] with iron deficiency anemia. Conclusion.,H. pylori infection and chronic gastritis, especially atrophic gastritis, are significantly associated with unexplained iron deficiency anemia. Relationships between H. pylori -associated chronic gastritis and unexplained iron deficiency anemia should be considered. [source]


    Bile acid treatment alters hepatic disease and bile acid transport in peroxisome-deficient PEX2 Zellweger mice,

    HEPATOLOGY, Issue 4 2007
    Megan H. Keane
    The marked deficiency of peroxisomal organelle assembly in the PEX2,/, mouse model for Zellweger syndrome provides a unique opportunity to developmentally and biochemically characterize hepatic disease progression and bile acid products. The postnatal survival of homozygous mutants enabled us to evaluate the response to bile acid replenishment in this disease state. PEX2 mutant liver has severe but transient intrahepatic cholestasis that abates in the early postnatal period and progresses to steatohepatitis by postnatal day 36. We confirmed the expected reduction of mature C24 bile acids, accumulation of C27,bile acid intermediates, and low total bile acid level in liver and bile from these mutant mice. Treating the PEX2,/, mice with bile acids prolonged postnatal survival, alleviated intrahepatic cholestasis and intestinal malabsorption, reduced C27,bile acid intermediate production, and prevented older mutants from developing severe steatohepatitis. However, this therapy exacerbated the degree of hepatic steatosis and worsened the already severe mitochondrial and cellular damage in peroxisome-deficient liver. Both untreated and bile acid,fed PEX2,/, mice accumulated high levels of predominantly unconjugated bile acids in plasma because of altered expression of hepatocyte bile acid transporters. Significant amounts of unconjugated bile acids were also found in the liver and bile of PEX2 mutants, indicating a generalized defect in bile acid conjugation. Conclusion: Peroxisome deficiency widely disturbs bile acid homeostasis and hepatic functioning in mice, and the high sensitivity of the peroxisome-deficient liver to bile acid toxicity limits the effectiveness of bile acid therapy for preventing hepatic disease. (HEPATOLOGY 2007;45:982,997.) [source]


    Phage display of human antibodies from a patient suffering from coeliac disease and selection of isotype-specific scFv against gliadin

    IMMUNOLOGY, Issue 2 2003
    Claudio Rhyner
    Summary Coeliac disease (CD), a gastrointestinal illness characterized by intestinal malabsorption, results from gluten intolerance accompanied with immunological responses towards gliadin, an ethanol-soluble protein fraction of wheat and other cereals. The role of gliadin in eliciting immune responses in CD is still partly unclear; however, the occurrence of anti-gliadin in the sera of patients suffering from CD correlates well with clinical symptoms. In this work we report the construction of isotype-specific, phage-displayed scFv libraries from peripheral blood lymphocytes of a patient with CD and from a healthy control individual. VH and VL chains were amplified by reverse transcription,polymerase chain reaction (RT,PCR) using a set of oligonucleotides recognizing all human variable gene families. The three scFv libraries (IgA, IgG and IgM) were selectively enriched for gliadin-binding phage. After four rounds of affinity selection, polyclonal enrichment of gliadin-binding phage was observed in all libraries from the CD patient but in none from the healthy donor. Phagemid particles generated from single clones were demonstrated to be gliadin-specific, as shown by strongly positive enzyme-linked immunosorbent assay (ELISA) and BiaCore signals. The VH and VL chains from samples of these monoclonal isotype-specific phage were sequenced to identify the most common variable regions used by the immune system to elicit antibody responses against gliadin. [source]


    Pilot study on the effect of reducing dietary FODMAP intake on bowel function in patients without a colon

    INFLAMMATORY BOWEL DISEASES, Issue 12 2007
    Catherine Croagh MB
    Abstract Background: Poorly absorbed short-chain carbohydrates (FODMAPs) in the diet should, by virtue of their osmotic effects, increase fecal output following colectomy and ileal pouch formation or ileorectal anastomosis (IRA). The aim was to perform a proof-of-concept evaluation of this hypothesis. Methods: Fifteen patients (13 pouch, 2 IRA) had dietary and symptomatic evaluation before and during a low FODMAP diet. Carbohydrate malabsorption was evaluated by breath tests. Pouchitis was assessed clinically/endoscopically or by fecal lactoferrin. Results: Of 8 patients with a breath hydrogen response to lactulose, 7 had fructose malabsorption, 3 with lactose malabsorption, and 1 had lactose malabsorption alone. Five of 7 studied retrospectively improved stool frequency (from median 8 to 4 per day; P = 0.02), this being sustained over 0.5,3 years of follow-up. Five of 8 patients completed a prospective arm of the study. One patient had sustained improvement in stool frequency and 1 had reduced wind production. Overall, none of 8 patients who had pouchitis improved. In contrast, median daily stool frequency fell from 8 to 4 (P = 0.001) in the 7 without pouchitis. The degree of change in FODMAP intake also predicted response. There was a tendency for pouchitis to be associated with low baseline FODMAP intake. Conclusions: There is a high prevalence of carbohydrate malabsorption in these patients. Reduction of the intake of FODMAPs may be efficacious in reducing stool frequency in patients without pouchitis, depending on dietary adherence and baseline diet. (Inflamm Bowel Dis 2007) [source]


    Impaired intestinal iron absorption in Crohn's disease correlates with disease activity and markers of inflammation

    INFLAMMATORY BOWEL DISEASES, Issue 12 2006
    Gaith Semrin MD
    Abstract Background: Anemia in patients with Crohn's disease (CD) is a common problem of multifactorial origin, including blood loss, malabsorption of iron, and anemia of inflammation. Anemia of inflammation is caused by the effects of inflammatory cytokines [predominantly interleukin-6 (IL-6)] on iron transport in enterocytes and macrophages. We sought to elucidate alterations in iron absorption in pediatric patients with active and inactive CD. Methods: Nineteen subjects with CD (8 female, 11 male patients) were recruited between April 2003 and June 2004. After an overnight fast, serum iron and hemoglobin levels, serum markers of inflammation [IL-6, C-reactive protein (CRP), and erythrocyte sedimentation rate], and a urine sample for hepcidin assay were obtained at 8 am. Ferrous sulfate (1 mg/kg) was administered orally, followed by determination of serum iron concentrations hourly for 4 hours after the ingestion of iron. An area under the curve for iron absorption was calculated for each patient data set. Results: There was a strong inverse correlation between the area under the curve and IL-6 (P = 0.002) and area under the curve and CRP levels (P = 0.04). Similarly, the difference between baseline and 2-hour serum iron level (,[Fe]2hr) correlated with IL-6 (P = 0.008) and CRP (P = 0.045). When cutoff values for IL-6 (>5 pg/mL) and CRP (>1.0 mg/dL) were used, urine hepcidin levels also positively correlated with IL-6 and CRP levels (P = 0.003 and 0.007, respectively). Conclusions: Subjects with active CD have impaired oral iron absorption and elevated IL-6 levels compared with subjects with inactive disease. These findings suggest that oral iron may be of limited benefit to these patients. Future study is needed to define the molecular basis for impaired iron absorption. [source]


    Report on the vitamin D status of adult and pediatric patients with inflammatory bowel disease and its significance for bone health and disease

    INFLAMMATORY BOWEL DISEASES, Issue 12 2006
    Helen M. Pappa MD
    Abstract Vitamin D is a hormone responsible for calcium homeostasis and essential for bone mineralization throughout the lifespan. Recent studies revealed a high prevalence of hypovitaminosis D among healthy adults and children, especially in the northern hemisphere, and a link between this condition and suboptimal bone health. Moreover, maintenance of what are today considered optimal vitamin D stores has not been achieved throughout the year with currently recommended daily intake for vitamin D. The prevalence of hypovitaminosis D is even higher among adults with inflammatory bowel disease (IBD), a situation that may be caused by malabsorption and gastrointestinal losses through an inflamed intestine, among other factors. In children with IBD, existing reports of vitamin D status are scarce. The relationship between vitamin D status and bone health, although well-established in healthy adults and children, has been controversial among adults and children with IBD, and the reasons for this have not been investigated to date. Studies in animal models of colitis and in vitro human studies support a role of vitamin D in the regulation of the immune system of the gut and the potential of vitamin D and its derivatives as therapeutic adjuncts in the treatment of IBD. This role of vitamin D has not been investigated with translational studies to date. Currently, there are no guidelines for monitoring vitamin D status, treating hypovitaminosis D, and maintaining optimal vitamin D stores in patients with IBD. These tasks may prove particularly difficult because of malabsorption and gastrointestinal losses that are associated with IBD. [source]


    IBD and skeletal health: Children are not small adults!

    INFLAMMATORY BOWEL DISEASES, Issue 11 2005
    Francisco A Sylvester MD
    Abstract Patients with inflammatory bowel disease often have decreased bone mass, and fragility fractures can occur. Multiple disease- and treatment related factors, including malnutrition, inflammation, malabsorption, decreased weight-bearing physical activity, and corticosteroids negatively influence bone metabolic activity. Because low-impact fracture is the pathologic expression of critically reduced bone mass and bone quality, knowing the relative risk of fractures in patients with IBD is of great interest. The absolute risk for incident fractures in these patients is still being debated. Clinical and laboratory research is clarifying mechanisms by which IBD can affect the function of osteoblasts and osteoclasts. In this concise review, we aim to provide an update on this topic, with focus on how pediatric IBD affects bone health. [source]


    Porotic lesions in immature skeletons from Stara Torina, late medieval Serbia

    INTERNATIONAL JOURNAL OF OSTEOARCHAEOLOGY, Issue 5 2008
    M. Djuric
    Abstract Porotic lesions of immature skeletons have been attracting scientific attention for more than a century. These changes have been documented worldwide and are considered to be one of the indicators of health and/or nutritional status of past human populations. These lesions have frequently been referred to as a nutritional stress indicator, a manifestation of iron-deficiency anaemia, and a condition caused by chronic infections. In this study, 327 immature skeletons from the medieval graveyard of Stara Torina (Serbia) were examined for macroscopic signs of four types of porotic lesions: cribra orbitalia, femoral cribra, humeral cribra, and porotic hyperostosis. Femoral cribra was observed in 83.25% of femora, humeral cribra in 58.46% of cases, cribra orbitalia in 46.12% of orbits, while porotic hyperostosis was recorded in only 2.94% of skulls. The majority of skeletons affected by cribra presented symmetrical lesions. Association between all types of cribra was recorded in 33.33% of skeletons. Historical data supported the hypothesis that the investigated population was exposed to frequent infections, especially parasitic ones, which led to the development of porotic bone lesions via several mechanisms: parasite-induced blood loss and diarrhoea (both iron and magnesium malabsorption) or anaemia as a hepcidin-mediated body adaptive response to infection. Copyright © 2008 John Wiley & Sons, Ltd. [source]


    Fifty years of Australian pediatric gastroenterology

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2009
    Don Cameron
    Abstract When the Gastroenterological Society of Australia (GESA) began 50 years ago there were very few pediatric gastroenterologists in the world. The ,Mother' of Paediatric Gastroenterology was Australian Charlotte (,Charlo') Anderson who established one of the world's first pediatric gastroenterology units in Melbourne in the early 1960s. Her earlier work in Birmingham had identified gluten as the component of wheat responsible for celiac disease and helped separate maldigestion (cystic fibrosis) and mucosal malabsorption. The first comprehensive textbook of Paediatric Gastroenterology was edited by Charlotte Anderson and Valerie Burke in 1975. Rudge Townley succeeded Charlotte Anderson in Melbourne and went on to further develop small bowel biopsy techniques making it a safe, simple, and quick procedure that led to much greater understanding of small bowel disease and ultimately the discovery of Rotavirus by Ruth Bishop et al. and subsequently to Rotavirus immunization. Australian Paediatric Gastroenterology subsequently developed rapidly with units being established in all mainland capital cities by the end of the 1970s. The Australian Society of Paediatric Gastroenterology Hepatology and Nutrition (AuSPGHAN) was established in the 1980s. Australians have contributed significantly in many areas of gastroenterology in infants, children, and adolescents including celiac disease, cystic fibrosis, liver disease, transplantation, gastrointestinal infection, allergy, indigenous health, inflammatory bowel disease, gastrointestinal motility, and the development of novel tests of gastrointestinal function and basic science. There have also been major contributions to nutrition in cystic fibrosis, end-stage liver disease, and intestinal failure. The future of Australian Paediatric Gastroenterology is in good hands. [source]


    New growth factor therapies aimed at improving intestinal adaptation in short bowel syndrome

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006
    Prue M Pereira
    Abstract Short bowel syndrome (SBS) is used to describe a condition of malabsorption and malnutrition resulting from the loss of absorptive area following massive small bowel resection. The key to improved clinical outcome after massive small bowel resection is the ability of the residual bowel to adapt. Although still in experimental stages, a major goal in the management of SBS may be the augmented use of growth factors to promote increased adaptation. A number of growth factors have been implicated in promoting the adaptation process. The best-described growth factors are reviewed: glucagon-like peptide-2 (GLP-2), epidermal growth factor (EGF), and growth hormone (GH). This article reviews the ability of recombinant GLP-2, EGF and GH to modulate structural and functional aspects of intestinal adaptation following small bowel resection. Although these growth factors have shown promise, small sample size, inconsistent measurement parameters and uncontrolled study designs have hampered the acquisition of strong data advocating the use of growth factor treatment for SBS. Multicenter trials using well-defined outcome measures to assess clinical efficacy are needed to direct the clinical indications, timing and duration of therapy and assess potential risks associated with growth factor therapies. [source]


    A15. Public attitudes towards the healthiness of fruit juices

    JOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 5 2000
    K. I. France
    Background Fruit juice is a major part of children's diets and accounts for a large proportion of their fruit and vegetable servings. People may confuse fruit juice with fruit drinks. This can cause problems as people could possibly substituting a portion of fruit for a drink, which contains little or no fruit. Studies have shown that excessive consumption of fruit juice can lead to health problems in children, including short stature, obesity, nonorganic failure to thrive and carbohydrate malabsorption. An increase in dental erosion has also been noted which appears to correlate with an increase in fruit juice and carbonated beverage consumption. Aims The aim of this study was to find out what the general public's attitudes are towards the healthiness of fruit juice. Methods A mini focus group and a questionnaire were the methods used for data collection. The subjects were parents of children aged 12 or under in a local primary school. Results Overall, the study group had a poor knowledge of the difference between fruit juice and drinks, and knowledge of sugar content was poor. The group had a good knowledge of fruit content. Fruit juice was regarded as being a health drink. They were unsure if excessive consumption could damage children's health or not. Their main concern was regarding their children's teeth. The factor identified as being most influential when choosing a drink was flavour, followed closely by healthiness. Nutritional knowledge was generally poor. The average daily intake of juice was 650 mL (22.8 floz), considerably more than the value recommended by several experts. Conclusion There is a need for nutritional education regarding the consumption of fruit juice. The public should be made more aware of the potential problems associated with excessive fruit juice consumption without discouraging fruit juice intake altogether, as it is an important source of fruit in the diets of young children. [source]


    Search for occult secondary osteoporosis: impact of identified possible risk factors on bone mineral density

    JOURNAL OF INTERNAL MEDICINE, Issue 5 2002
    H. A. Deutschmann
    Abstract. Deutschmann HA, Weger M, Weger W, Kotanko P, Deutschmann MJ, Skrabal F (Krankenhaus der Barmherzigen Brüder, Marschallgasse, Teaching Hospital of the Karl-Franzens University Graz, Austria). Search for occult secondary osteoporosis: impact of identified possible risk factors on bone mineral density. J Intern Med 2002; 252: 389,397. Objectives. To determine whether the use of more elaborate diagnostic tests can identify possible risk factors for secondary osteoporosis and to evaluate the impact of these possible risk factors on the severity of bone disease in the study population. Design. Cross-sectional study. Setting and participants. ,We have investigated 377 subjects (285 females, 92 males) with osteoporosis (T-score less than ,2.5 in dual energy X-ray absorption) or nontraumatic lumbar vertebral fractures; these patients were referred to our hospital, a secondary care centre, for evaluation and treatment of osteoporosis. Results. Osteoporosis without attributable risk factor was diagnosed in 106 women (37%) and 30 men (33%). In 241 patients (179 women, 62 men) one or more possible risk factors for osteoporosis (in this paper also called subclinical disease) were revealed. The most common were lactose malabsorption, disturbed exocrine pancreatic function and renal tubular disturbances, including renal hypercalciuria, incomplete renal tubular acidosis and mild phosphate diabetes. The number of possible risk factors in the individual patient was significantly related to the severity of osteoporosis as assessed by Z-scores (Spearman correlation r = ,0.43, P < 0.001, n = 172 for females; r = ,0.28, P < 0.05, n = 65 for males). Conclusions. All the identified subclinical diseases would have remained undetected if the currently accepted guidelines for the investigation of patients with osteoporosis were applied. The statistically significant correlation between the number of identified possible risk factors and the severity of bone disease in the individual patient strongly suggests the pathogenetic significance of the identified subclinical diseases. It is yet to be shown, whether specific treatment of these subclinical diseases yields additional improvement of bone mass as compared with standard treatment of osteoporosis. [source]


    Prevalence of undiagnosed coeliac syndrome in osteoporotic women

    JOURNAL OF INTERNAL MEDICINE, Issue 4 2001
    R. Nuti
    Abstract.,Nuti R, Martini G, Valenti R, Giovani S, Salvadori S, Avanzati A (Institute of Internal Medicine, Metabolic Disease Unit, University of Siena, Siena, Italy). Prevalence of undiagnosed coeliac syndrome in osteoporotic women. J Intern Med 2001; 250: 361,366. Objectives.,The aims of the study were to quantify the prevalence of asymptomatic coeliac disease (CD) in a cohort of osteoporotic females, and to investigate the features of bone loss. Design and subjects.,We studied 255 women (mean age 66.6 ± 8.5 SD) with primary osteoporosis (WHO diagnostic criteria). After the first CD screening with the measure of serum IgG antigliadin antibodies (IgG-AGA), 53 women showed a positive test: antibodies to tissue transglutaminase (TG-ab) were subsequently determined to confirm the diagnosis of CD. Bone metabolism was evaluated by: serum and urinary calcium, serum and urinary phosphate, serum alkaline phosphatase, urinary crosslaps, serum 25(OH)D and serum parathyroid hormone. Results.,High levels of IgG-AGA and TG-ab were observed in 24 patients with a prevalence of serological disease of 9.4%. These women were characterized, in comparison with the other patients, by a statistically significant reduction in serum 25(OH)D (17.8 ± 7.2 vs. 55.1 ± 20.3 nmol L,1, P < 0.01) together with a significant increase of iPTH (65.1 ± 29.7 vs. 35.1 ± 20.0 pg mL,1; P < 0.01). Patients with high TG-ab levels showed also slightly raised values of urinary crosslaps (288 ± 88 vs. 270 ± 90 ,m mol,1 Cr). In IgG-AG positive patients a statistically significant inverse correlation was found between 25(OH)D serum levels and log-transformed TG-ab values (r: ,0.95, P < 0.001). Intestinal biopsies were obtained in 10 TG-ab positive women and verified CD in six patients. Conclusions.,These data support the hypothesis that patients with undiagnosed celiac disease develop high remodelling processes related to calcium malabsorption, secondary hyperparathyroidism and unavailability of vitamin D with a consequent more marked bone loss. [source]


    Ataxia with isolated vitamin E deficiency: A clinical, biochemical and genetic diagnosis

    JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2000
    G Alex
    Abstract: A case of ataxia with isolated vitamin E deficiency, in conjunction with supportive genetic studies, is reported. This is a neurodegenerative condition that involves a mutation in the tocopherol (,) transfer protein gene (TTPA). Measurement of serum vitamin E concentration should be included as part of the investigations in children with progressive ataxia, even in the absence of fat malabsorption. Early treatment with vitamin E may protect such patients against further neurological damage. [source]


    Analysis of the breath hydrogen test for carbohydrate malabsorption: Validation of a pocket-sized breath test analyser

    JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2000
    Ws Lee
    Objective: To assess the validity and clinical application of a hand-held breath hydrogen (H2) analyzer (BreatH2, Europa Scientific, Crewe, UK). Methodology: Breath samples of patients referred to the Gastroenterology Unit, Women's and Children's Hospital, North Adelaide, South Australia, for confirmation of the diagnosis of carbohydrate malabsorption were analysed with the Quintron microlyzer (Quintron Instrument Co., Milwaukee, USA) and the BreatH2 analyser, using the Quintron microlyzer as the gold standard. Results: Twenty-nine breath H2 tests (BHT) were performed in 29 patients aged 2 months to 61 years. The sensitivity and specificity of the BreatH2 analyser in detecting a positive BHT using the Quintron microlyser as the gold standard were 0.90 and 0.95 with positive and negative predictive values of 0.90 and 0.95, respectively. There was one false positive and one false negative reading. Bland,Altman plots showed a high degree of agreement between the values obtained with two different methods. Conclusions: The diagnosis of carbohydrate malabsorption, using a portable breath H2 analyser (BreatH2), achieved an acceptable degree of sensitivity and specificity, enabling it to be used where no alternative is available. [source]


    Lactose intolerance in patients with chronic functional diarrhoea: the role of small intestinal bacterial overgrowth

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010
    J. ZHAO
    Aliment Pharmacol Ther,31, 892,900 Summary Background, Many studies report a high prevalence of lactose intolerance in patients with functional, gastrointestinal disease. Aim, To evaluate the role of small intestinal bacterial overgrowth (SIBO) in condition of lactose intolerance and the mechanism by which SIBO may impact lactose tolerance in affected patients. Methods, Consecutive out-patients with chronic functional diarrhoea (CFD) and healthy controls underwent a validated 20 g lactose hydrogen breath test (HBT). Patients completed also a 10 g lactulose HBT with concurrent assessment of small bowel transit by scintigraphy. Results, Lactose malabsorption was present in 27/31 (87%) patients with CFD and 29/32 (91%) healthy controls (P = 0.708). From the patient group 14/27 (52%) had lactose intolerance and 13/27 (48%) experienced no symptoms (lactose malabsorption controls). Only 5 (17%) healthy controls reported symptoms (P < 0.01). The oro-caecal transit time was similar between patient groups with or without symptoms (P = 0.969). SIBO was present in 11 (41%) subjects and was more prevalent in lactose intolerance than in lactose malabsorption [9/14 (64%) vs. 2/13 (15%), P = 0.018]. Symptom severity was similar in lactose intolerance patients with and without SIBO (P = 0.344). Conclusions, Small intestinal bacterial overgrowth increases the likelihood of lactose intolerance in patients with CFD as a direct result of lactose fermentation in the small intestine, independent of oro-caecal transit time and visceral sensitivity. [source]


    Systematic review: efficacy and safety of pancreatic enzyme supplements for exocrine pancreatic insufficiency

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010
    J. R. TAYLOR
    Summary Background, Pancreatic enzyme supplements are standard therapy for fat malabsorption in patients with exocrine pancreatic insufficiency. The FDA determined that published data are insufficient to support the efficacy and safety of these agents. Aim, To determine if pancreatic enzyme supplements are: (i) superior to placebo for treating fat malabsorption and (ii) superior to other supplements based on randomized cross-over trials. Methods, A computer-assisted search of MEDLINE and EMBASE was performed to identify relevant studies. Data extraction on study design, improvement in coefficient of fat absorption, diarrhoea and adverse events using prespecified forms. Results, A total of 12 manuscripts met inclusion criteria. Most studies (10/12) compared pancreatic enzyme supplements that used different delivery systems, while using similar quantities of enzymes. These studies found no consistent difference in fat malabsorption or gastrointestinal symptoms between different active treatments. Two small placebo-controlled trials (n = 65 patients) demonstrate that pancreatic enzyme supplements are superior to placebo for fat absorption. Data are inadequate to determine if pancreatic enzyme supplements lead to weight gain or improvement in diarrhoea. Conclusions, Based on data from randomized cross-over trials, pancreatic enzyme supplements appear to improve fat malabsorption. No specific branded product or specific delivery system is superior for treatment of fat malabsorption in patients with exocrine pancreatic insufficiency. [source]


    Applicability of the reported prevalence of bile salt malabsorption in irritable bowel

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010
    A. C. Ford
    No abstract is available for this article. [source]


    Applicability of the reported prevalence of bile salt malabsorption in irritable bowel: authors' reply

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010
    L. Wedlake
    No abstract is available for this article. [source]