Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diarrhoea and malabsorption are common problems in elderly persons. Worldwide, diarrhoea is the second leading cause of mortality. In the developed world, 85% of its mortality affects the elderly. The diagnostic work up for diarrhoea and malabsorption is more complex for the elderly than for the young patient. If diarrhoea persists for more than 24 h, oral rehydration solutions or intravenous fluids must be administered promptly in order to prevent hypotension and organ failure in the often multi-morbid patient. Both the immunocompromised patient and the severely affected out-patient should have stool culture performed. Malabsorption usually presents with weight loss, osteoporosis, anaemia, skin and neurological symptoms. The careful diagnostic work-up must aim at the identification of treatable disorders such as coeliac disease, Crohn's disease and bacterial overgrowth. Often, a detailed drug history is of help in identifying a readily treatable cause.
Best Pract Res Clin Gastroenterol 2002 Feb
PMID:Small bowel disease in the elderly: diarrhoea and malabsorption. 1197 26

Diarrhoea, malabsorption and malnutrition characterize the short-bowel syndrome. Following the initial intestinal resection, complications such as fistulas and intra-abdominal abscesses may occur, but these usually resolve with appropriate surgical care. All residual intestine should be placed in continuity before serious attempts at rehabilitation with oral feedings are initiated. Small hourly oral feedings composed of food items high in complex carbohydrate and low in fat are started when appropriate and the diet is gradually increased as intestinal adaptation occurs. The goal during this process is to prevent diarrhoea and allow the formation of semiformed stools. With time, parenteral nutrition (PN) can be reduced, and the time required depends on both length of residual bowel and the particular anatomy involved-for example, the presence or absence of the colon. A programme of optimal diet plus growth hormone (0.1 mg/kg) and oral glutamine (30 g/day) enhances the adaptive process and allows many patients independence from PN. However, those with extremely short segments of jejuno-ileum (<50 cm) and no colon have excessive fluid and electrolyte losses, and intestinal transplantation may be the only therapy which allows such patients to be independent of PN.
Best Pract Res Clin Gastroenterol 2003 Dec
PMID:Indications for specific therapy in the rehabilitation of patients with the short-bowel syndrome. 1464 56

Carbohydrates are mostly digested to glucose, fructose and galactose before absorption by the small intestine. Absorption across the brush border and basolateral membranes of enterocytes is mediated by sodium-dependent and -independent membrane proteins. Glucose and galactose transport across the brush border occurs by a Na(+)/glucose (galactose) co-transporter (SGLT1), whereas passive fructose transport is mediated by a uniporter (GLUT5). The passive exit of all three sugars out of the cell across the basolateral membrane occurs through two uniporters (GLUT2 and GLUT5). Mutations in SGLT1 cause a major defect in glucose and galactose absorption (glucose-galactose Malabsorption), but mutations in GLUT2 do not appear to disrupt glucose and galactose absorption. Studies on GLUT1 null mice and Fanconi-Bickel patients suggest that there is another exit pathway for glucose and galactose that may involve exocytosis. There are no known defects of fructose absorption.
Best Pract Res Clin Gastroenterol 2003 Dec
PMID:Intestinal absorption in health and disease--sugars. 1464 59

Lactose malabsorption (LM; adult-type hypolactasia), an autosomal recessive condition, results from the down-regulation of the activity of lactase enzyme in the intestinal wall. In previous studies the effect of LM on bone mass, bone turnover rate, development of osteoporosis and osteoporotic fractures has remained controversial. We have recently identified a single nucleotide polymorphism (SNP), a C to T change residing 13910 base pairs upstream of the lactase (LCT) gene at chromosome 2q21-22, which shows complete association with lactase persistence, with the C/C-13910 genotype defining LM and the genotypes C/T-13910 and T/T-13910 lactase persistence. The present study was undertaken to examine the relationship of the C/T-13910 polymorphism to peak bone mass, bone turnover rate, and stress fractures among young Finnish men. The study population comprised 234 young men, aged 18.3 to 20.6 years, 184 men were recruits of the Finnish Army, and 50 were men of similar age who had postponed their military service for reasons not related to health. Bone mineral content (BMC), density (BMD), and scan area were measured in the lumbar spine and upper femur by dual-energy X-ray absorptiometry (DXA). Blood was sampled for genotyping of the C/T-13910 polymorphism and determination of serum 25-hydroxyvitamin D (25OHD), intact parathyroid hormone (iPTH), type I procollagen aminoterminal propeptide (PINP), and tartrate-resistant acid phosphatase 5b (TRACP5b). Second-void urine samples were collected for the determination of type I collagen aminoterminal telopeptide (NTX). The prevalence of the C/C-13910-genotype of these young adults did not differ significantly from the corresponding population prevalence of C/C-13910 (17.1% vs 18.1%) among Finnish blood donors. Fifteen recruits of the army experienced a stress fracture; 3 of them (20%) had the C/C-13910-genotype. Calcium intake was similar for the three genotypes as were the unadjusted BMCs, scan areas, and BMDs at different measurement sites. The adjustments for age, height, weight, smoking, alcohol consumption, and physical exercise in the multiple regression analysis did not reveal any significant relationships between the lactase genotypes and BMDs at lumbar (P = 0.16), femoral neck (P = 0.99) or total hip (P = 0.96) sites. Serum 25OHD, iPTH, and bone marker levels were similar for the C/C-13910 C/T-13910 and T/T-13910 genotypes. In summary, in young Finnish men, molecularly defined lactose malabsorption does not alter bone turnover rate and impair the acquisition of peak bone mass. Moreover, the C/C-13910 genotype does not seem to be a risk factor for stress fractures in army recruits.
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PMID:Molecularly defined lactose malabsorption, peak bone mass and bone turnover rate in young finnish men. 1536 57

Short bowel syndrome (SBS) is a global malabsorption syndrome that results from extensive intestinal resections. It used to be a typical complication of repetitive bowel resections in patients with Crohn's disease. However, due to improved medical and surgical therapies for these patients it currently occurs more frequently as a consequence of vascular disorders in adults (intestinal infarction) and congenital aberrations in children, respectively. Adequate therapy depends on the degree of (small) bowel losses and on resulting functional disturbances. Moreover, it must be adjusted to the postoperative adaptation process, which consists of three phases: The immediate acute phase lasts less than 4 weeks and serves to stabilise the patient. The subsequent year should be used to induce maximal adaptation by gradually increasing nutrient exposure. When maximal stimulation of nutrient absorption has been achieved, permanent maintenance nutrition treatment should be defined individually, dependent on extent and quality of nutritive deficits. In patients with Crohn's disease, optimal treatment of the underlying disease is of pivotal importance in order to avoid a further reduction of absorptive capacity or other complications. Current investigations aim at improving the adaptation process by administration of specific diets and growth hormones. With these, it appears possible to treat even some patients with very short bowel, i.e. less than 50 cm of small intestine left, with oral nutrition, only. Still, a considerable proportion of patients will need long-term parenteral nutrition. If young patients experience intolerable complications of parenteral nutrition, intestinal transplantation may be considered as a high risk therapy of last choice.
Best Pract Res Clin Gastroenterol 2004 Oct
PMID:Management of the short bowel syndrome after extensive small bowel resection. 1549 90

Anaemia is typically the first clue to iron deficiency, but an isolated haemoglobin measurement has both low specificity and low sensitivity. The latter can be improved by including measures of iron-deficient erythropoiesis such as the transferrin iron saturation, mean corpuscular haemoglobin concentration, erythrocyte zinc protoporphyrin, percentage of hypochromic erythrocytes or reticulocyte haemoglobin concentration. However, the changes in these measurements with iron deficiency are indistinguishable from those seen in patients with the anaemia of chronic disease. The optimal diagnostic approach is to measure the serum ferritin as an index of iron stores and the serum transferrin receptor as a index of tissue iron deficiency. The treatment of iron deficiency should always be initiated with oral iron. When this fails because of large blood losses, iron malabsorption, or intolerance to oral iron, parenteral iron can be given using iron dextran, iron gluconate or iron sucrose.
Best Pract Res Clin Haematol 2005 Jun
PMID:Diagnosis and management of iron-deficiency anaemia. 1573 93

There has been an increasing awareness recently of subtle, non-bleeding gastrointestinal conditions that may result in abnormal iron absorption leading to iron-deficiency anaemia (IDA) in the absence of gastrointestinal symptoms. Thus, the importance of coeliac disease as a possible cause of IDA refractory to oral iron treatment, without other manifestations of malabsorption syndrome, is increasingly being recognized. In addition, Helicobacter pylori has been implicated in several recent studies as a cause of IDA refractory to oral iron treatment, and the anaemia responds favourably to H. pylori eradication. Likewise, achlorhydric gastric atrophy or atrophic body gastritis (ABG), a condition associated with chronic idiopathic iron deficiency, has been shown to be responsible for refractory IDA in over 20% of patients with no evidence of gastrointestinal blood loss. It has also been suggested that H. pylori gastritis may represent an early phase of ABG in which infection may trigger an autoimmune process directed against gastric parietal cells by means of antigenic mimicry. In this review we examine in a critical manner the role of H. pylori gastritis in the causation of IDA, the role of ABG in the pathogenesis of iron malabsorption, the evidence supporting a possible cause-and-effect relationship between H. pylori gastritis and ABG, and the implications of these findings for the diagnostic work-up and management of IDA.
Best Pract Res Clin Haematol 2005 Jun
PMID:Gastropathic sideropenia. 1573 96

Decreased bone mineral density is a frequent finding in patients with inflammatory bowel disease. Factors contributing to this are: 1) malabsorption of vitamin D, calcium and possibly vitamin K and other nutrients, 2) treatment with corticosteroids, 3) inflammatory cytokines in inflammatory bowel disease, and 4) hypogonadism induced by the inflammatory bowel disease. Among patients with Crohn's disease from 32% to 38% have osteopenia (Z-scores <-1), and among patients with ulcerative colitis 23% to 25% have osteopenia. The mean deficit was 0.44+/-0.08 Z-scores in the spine in Crohn's disease and 0.34+/-0.08 in ulcerative colitis. A similar deficit was seen in the hip in both conditions. From these deficits, an increase in overall fracture risk of 1.1-1.3 should be expected. The observed excess fracture risk was limited compared to the general population in both Crohn's disease (RR=1.2, 95% CI: 0.9-1.6 for any fracture and 2.2, 95% CI: 1.2-4.0 for spine fractures) and ulcerative colitis (RR=1.1, 95% CI: 1-1.2 for any fracture, and 1.5, 95% CI: 0.9-2.5 for spine fractures). The observed excess fracture risk was close to that expected from the changes in BMD. Despite the limited excess fracture risk, a relatively large percentage of all fractures may be attributable to corticosteroid use among users of corticosteroids.
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PMID:Prevalence and pathogenesis of osteoporosis in patients with inflammatory bowel disease. 1578 32

A continuing flow of new scientific developments concerning coeliac disease in the last decade asks for the formulation of new concepts of pathophysiology and clinical considerations. Immunogenetic studies have shown a correlation of the disease to the HLA region on the short arm of chromosome 6, immunological research has led to the concept of a T-cell driven immunologic response of the small intestine, with the identification of highly sensitive and specific antibodies. The understanding of the histopathology of coeliac disease has changed dramatically, initiated by the proposition of a spectrum of gluten sensitive enteropathy by Marsh in 1992. Clinical studies report a significant change in patient characteristics and epidemiology. The incidence of the disease has shifted to a majority of adult coeliacs, the disease may present with less severe symptoms of malabsorption and the screening studies suggest an overall prevalence of up to 1 in 200-300. Histopathology has been standardized; lymphocytic enteritis (Marsh I), lymphocytic enteritis with crypthyperplasia (Marsh II), and villous atrophy, subdivided in partial, subtotal and total (Marsh IIIABC). Special attention is given to a subgroup of 'refractory coeliacs', including the identification of pre-malignant T-cells in the intestinal mucosa. The management of coeliacs primarely consists of monitoring for compliance and complications. Dietetic and medical associations need to establish protocols and offer additional training to undergraduetes, internships, general practitioners and other allied health professionals. It might be relevant to have a low threshold for intestinal biopsies. However, screening asymptomatics may be harmful for individuals. Research is needed to assess the benefits of mass-screening in the future. HLA analysis can contribute towards recognising populations at increased risk.
Best Pract Res Clin Gastroenterol 2005 Jun
PMID:Coeliac disease: changing views. 1592 38

A small proportion of coeliac disease (CD) patients fail to improve after a gluten-free diet (GFD) and may be considered as atypical regarding their outcome (refractory coeliac disease). The aim of this study is to diagnose and manage patients with CD who fail to improve after a GFD. Refractory coeliac disease (RCD) is a malabsorption syndrome defined by persisting villous atrophy with, usually, an increase of intraepithelial lymphocytes (IELs) in the small bowel in spite of a strict GFD and comprises a heterogenous group of diseases. Some of these diseases have to be excluded and can be treated by specific therapies like antibiotics in tropical sprue and giardiasis and immune globulin substitution in common variable immunodeficiency, while other malabsorption syndromes are less well defined and may require immunosuppressive therapy. Standardized treatment, however, has not been evaluated in such patients so far. In a subgroup of patients with RCD, an abnormal intraepithelial lymphocyte (IEL) population may be observed with the lack of surface expression of usual T-cell markers (CD3-CD8 and/or the T-cell receptor (TCR)) on IELs associated with T-cell clonality pattern suggest the presence of an early enteropathy-associated T-cell lymphoma (EATL) in a subgroup of patients with RCD. This hypothesis has been supported by studies, which revealed progression into overt intestinal T-cell lymphomas in a subgroup of RCD. Steroid treatment has been reported effective even in patients with underlying early EATL. However, long-term results are unsatisfactory in most of these patients with RCD and parenteral nutrition has to be applied in some of these cases. First results with more aggressive chemotherapies and use of cytokines are under way. Due to the difficulty of diagnostic and therapeutic regimens patients should be referred to tertiary centres for coeliac disease.
Best Pract Res Clin Gastroenterol 2005 Jun
PMID:Refractory coeliac disease. 1592 46


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