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Query: UMLS:C0017536 (giardiasis)
 1,714 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This case report details a child with coeliac disease and giardiasis. Treatment of the infection without recourse to a gluten-free diet cured the symptoms of diarrhoea and returned the small intestinal morphology to normal. Thus, the patient moved from active to latent coeliac disease. Potential and latent forms of coeliac disease are being increasingly recognized, since markers have become available to identify patients and investigations developed to test for gluten sensitivity in the small intestinal mucosa. This case provides an opportunity to consider potential and latent forms of coeliac disease and how these impact on clinical practice and the wider understanding of the disorder.
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PMID:Potential and latent coeliac disease. 1156 55

In patients with coeliac disease, a regression of intestinal damage without a gluten-free diet is a very rare event. We describe a young child with diarrhoea, intestinal mucosa atrophy and positive serum anti-endomysial and anti-tissue transglutaminase (anti-tTG) antibodies during intestinal giardiasis infection. He showed normal intestinal mucosa architecture and negative anti-endomysial and anti-tTG antibodies after his giardiasis was cured, although he continued to assume a normal diet. Re-evaluations on a 6-monthly basis showed that he was symptom free, and all haemato-chemical parameters were within normal limits. Three years after the initial diagnosis, a third intestinal biopsy showed: normal mucosa architecture; an increase in the intra-epithelial CD3+ and gamma/delta+ lymphocyte counts; and immunoglobulin-A anti-endomysial antibody detection in the supernatant of the intestinal mucosa culture incubated with gliadin. An active coeliac disease status, with intestinal mucosa atrophy, may regress to a latent coeliac disease status with normal intestinal mucosa histology after removal of the environmental factors that have presumably precipitated mucosa damage. Serum anti-endomysial and anti-tTG antibody behaviour is not a permanent, life-long feature and this must recommend the repetition of anti-endomysial or anti-tTG antibody assays in the same patient whenever coeliac disease diagnosis is again suspected, irrespective of previous negativity.
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PMID:Treatment of giardiasis reverses "active" coeliac disease to "latent" coeliac disease. 1156 63

We evaluated the clinical and immunological manifestations of 14 children with IgA deficiency. Four of the patients were asymptomatic, and ten were symptomatic, with recurrent sinopulmonary infections, allergic disease, recurrent intestinal giardiasis or celiac disease. Growth retardation was the second important feature in our patients. One of the seven patients with growth retardation had partial growth hormone deficiency. The levels of serum IgG and IgM were high in five and three patients, respectively. Cellular immunity was normal.
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PMID:Growth retardation in children with IgA deficiency. 1219 32

Effective treatment of malabsorption due to severe pancreatic exocrine insufficiency requires delivery of sufficient enzymatic activity into the duodenal lumen simultaneously with meal nutrients. To achieve this, modern therapeutic concepts recommend administration of 25,000 to 40,000 units of lipase per meal using pH-sensitive pancreatin microspheres. In case of treatment failure, dosage should be increased two to three times. If this still is not successful, compliance may be checked by measurement of fecal chymotrypsin, although this is not a standardized procedure. In the compliant patient, diagnosis of pancreatic exocrine insufficiency needs to be reviewed, particularly cases of celiac disease, (concomitant) bacterial overgrowth, and blind loop syndrome, as well as giardiasis, which need to be excluded or otherwise be treated specifically. Finally, additional acid suppression with application of unprotected pancreatin and/or reduced fat intake may help to control malabsorption. Still, in most patients, lipid digestion cannot be completely normalized by current standard therapy. On the one hand, this leads to loss of energy that may only partly be compensated for by increased nutrient intake. On the other hand, increased nutrient exposition of distal intestinal sites may release excessive amounts of mostly inhibitory distal intestinal neurohumoral mediators, and thereby disturb gastrointestinal secretory and motor functions. Consequently, future developments are needed for optimizing treatment.
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PMID:Pancreatic Enzyme Supplementation Therapy. 1295 43

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.
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PMID:Refractory coeliac disease. 1592 46

T lymphocyte-mediated pathogenesis is common to a variety of enteropathies, including giardiasis, cryptosporidiosis, bacterial enteritis, celiac's disease, food anaphylaxis, and Crohn's disease. In giardiasis as well as in these other disorders, a diffuse loss of microvillous brush border, combined or not with villus atrophy, is responsible for disaccharidase insufficiencies and malabsorption of electrolytes, nutrients, and water, which ultimately cause diarrheal symptoms. Other mucosal changes may include crypt hyperplasia and increased infiltration of intra-epithelial lymphocytes. Recent studies using models of giardiasis have shed new light on the immune regulation of these abnormalities. Indeed, experiments using an athymic mouse model of infection have found that these epithelial injuries were T cell-dependent. Findings from further research indicate that that the loss of brush border surface area, reduced disaccharidase activities, and increase crypt-villus ratios are mediated by CD8+ T cells, whereas both CD8+ and CD4+ small mesenteric lymph node T cells regulate the influx of intra-epithelial lymphocytes. Future investigations need to characterize the CD8+ T cell signaling cascades that ultimately lead to epithelial injury and malfunction in giardiasis and other malabsorptive disorders of the intestine.
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PMID:Immunopathology of giardiasis: the role of lymphocytes in intestinal epithelial injury and malfunction. 1596 21

Many children report chronic abdominal pain that is severe and disruptive to normal lifestyle and schooling. Assessment and management depends on indentifying those with underlying organic disease, such as chronic infection, celiac disease or inflammatory bowel disease, but avoiding unnecessary invasive investigations. In those with a functional gut disorder, the aim of therapy is reassurance, a return to normal activity and symptom control. We address the evidence for the use of investigative and management strategies in situations where recurrent abdominal pain is likely to be a functional disorder. Epidemiological studies of European and American populations show that organic causes are uncommon, and that chronic abdominal pain is a risk factor for functional gut disorders in adulthood. There is a paucity of high quality therapeutic trials, none showing conclusive evidence of benefit. Psychological interventions, such as cognitive behavioral and family therapy are effective, reducing symptoms and improving school attendance. Asian studies suggest gastrointestinal infection, such as giardiasis, are common causes of recurrent abdominal pain, but that functional abdominal pain is also prevalent.
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PMID:Recurrent abdominal pain in childhood: the functional element. 1947 50

The gastrointestinal tract possesses a huge epithelial surface area and performs many different tasks. Amongst them are the digestive and absorptive functions. Disorders of intestinal absorption and secretion comprise a variety of different diseases, e.g. coeliac disease, lactase deficiency or Whipple's disease. In principle, impaired small intestinal function can occur with or without morphological alterations of the intestinal mucosa. Therefore, in the work up of a malabsorptive syndrome an early small intestinal biopsy is encouraged in conjunction with breath tests and stool analysis to guide further management. In addition, there is an array of functional tests, the clinical availability of which becomes more and more limited. In any case, early diagnosis of the underlying pathophysiology is most important, in order to initiate proper therapy. In this chapter, diagnostic procedure of malabsorption is discussed with special attention to specific disease like coeliac disease, Whipple's disease, giardiasis and short bowel syndrome. Furthermore, bacterial overgrowth, carbohydrate malabsorption and specific nutrient malabsorption (e.g. for iron or vitamins) and protein-losing enteropathy are presented with obligatory and optional tests as used in the clinical setting.
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PMID:Disorders of intestinal secretion and absorption. 1950 67

Giardia lamblia is the most common human parasite with a worldwide distribution and fecal-oral way of transmission. Diagnostic procedures include stool examination and gastroduodenoscopy with biopsy or secret aspiration. In most cases histology reveals a dense accumulation of the parasites on the surface of the duodenal mucosa with no or only slight inflammation. In rare cases, a dense inflammatory infiltrate with severe mucosal atrophy and increased count of intraepithelial lymphocytes may be seen. If in such cases the amount of parasites is low, the histological picture may mimic celiac disease. The two presented cases demonstrate the close morphological relationship and show the importance of considering giardiasis in the differential diagnosis in patients with suspected celiac disease.
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PMID:[Lambliasis as differential diagnosis of MARSH type 3b]. 2068 19

The aim of this study is to assess the prevalence of isolated short stature as a clinical presentation of celiac disease in Saudi Arab children and whether some of the routine laboratory tests performed to determine the cause of short stature could suggest the diagnosis of celiac disease. A total of 91 children with short stature were included in the study. Extensive endocrine and biochemical assessments, including total protein, serum albumin, calcium phosphate and alkaline phosphatase assays; renal function tests; coagulation profile; anti-endomysial antibodies and anti-tissue transglutaminase antibody, growth hormone, thyroid stimulating hormone, free-thyroxin (FT4) assays; stool tests for giardiasis; bone age; and endoscopic intestinal biopsies, were done for all children. Ten of the 91 children had positive intestinal biopsies in the form of total villous atrophy, an increase in crypt height, and an increase in intra-epithelial lymphocyte (IEL) numbers up to >40 IEL/100 EC (Type 3C) according to the Oberhuber classification, confirming the diagnosis of celiac disease. Five children had mild villous atrophy according to this classification (Type 3A), and they were considered to have potential celiac disease. Seventy-six children had normal intestinal biopsies. Therefore, the prevalence of celiac disease among Saudi children with short stature was 10.9%, and 4.3% of the children were diagnosed as having potential celiac disease. After confirming the diagnosis of celiac disease, all children were kept on a gluten-free diet and all of them showed improvement in their growth rate. We concluded that celiac disease is a very important cause of short stature in children without gastrointestinal complaints in Saudi Arabia. We highly recommend anti-tissue transglutaminase and anti-endomysial antibody screening tests, and a small bowel biopsy to confirm the diagnosis of celiac disease irrespective of the results of the antibody assays, in children with short stature in Saudi Arabia. Once the diagnosis is confirmed, children should be kept on a gluten-free diet so they can catch up their growth early before they develop permanent short stature.
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PMID:Isolated short stature as a presentation of celiac disease in Saudi children. 2158 40


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