1.
Life-threatening onset of coeliac disease: a case report and literature review.
Guarino, M, Gambuti, E, Alfano, F, Strada, A, Ciccocioppo, R, Lungaro, L, Zoli, G, Volta, U, De Giorgio, R, Caio, G
BMJ open gastroenterology. 2020;(1)
Abstract
BACKGROUND Coeliac disease (CD) results from an immune-mediated reaction to gluten in genetically predisposed individuals. In rare cases CD may occur with acute features deferring the diagnosis and exposing these patients to possible life-threatening complications. Herein we present the case of a young woman with a coeliac crisis, that is, a sudden clinical onset characterised by severe electrolyte imbalance due to an unknown (previously unrecognised) CD. METHODS This is a case report and literature review revealing that coeliac crisis is under-reported, with a total of 48 adult cases so far published. The diagnosis in our case was established by histopathological analysis of multiple duodenal biopsies. The patient's serum was tested by enzyme-linked immunoassay to detect antitransglutaminase IgA antibodies. RESULTS In contrast to cases reported in the literature, with male gender predominance and a mean age of 50±17 years, our patient was a young female case of coeliac crisis. However, like in our patient, a higher incidence of coeliac crisis was associated with the human leucocyte antigen (HLA)-DQ2 haplotype, versus HLA-DQ8, and a severe (Marsh-Oberhüber 3c) duodenal mucosa atrophy. Notably, there is no clear correlation between the antitissue transglutaminase 2 IgA antibody titre and coeliac crisis onset/severity, as confirmed by our case report. CONCLUSIONS The present case highlights that CD may manifest quite abruptly with a severe malabsorption syndrome, that is, electrolyte abnormalities and hypoproteinaemia. Our case should alert physicians, in particular those in the emergency setting, that even a typically chronic disorder, such as CD, may show life-threatening complications requiring urgent management.
2.
Microbial perturbations and modulation in conditions associated with malnutrition and malabsorption.
Jonkers, DM
Best practice & research. Clinical gastroenterology. 2016;(2):161-72
Abstract
The intestinal microbiota is a complex ecosystem, which can be considered an accessory organ. It involves complex microbe-microbe and host-microbe interactions with indispensable functions for the human host with regard to the intestinal epithelium and barrier function, the innate and adaptive immune system, and its large metabolic capacity. Saccharolytic fermentation results in the production of short chain fatty acids, which exert an array of beneficial effects, while proteolytic fermentation leads to an increase in potentially harmful metabolites. In addition, numerous other microbial metabolites are being produced with various intestinal as well as extra-intestinal effects. Their generation depends on the composition of the microbiota as well as the availability of substrates, which both vary along the GI tract. Diet impacts the intestinal microbiota composition and activity in early infancy as well as in adults. Microbial perturbations have been demonstrated in subjects with under-nutrition and/or malabsorption. The bidirectional interactions between the microbiome, nutrient availability and GI function, can contribute to a vicious circle, further impairing health outcome in conditions associated with malnutrition and/or malabsorption. Integrated multivariate approaches are needed to further unravel the complex interaction between microbiome, diet and host factors, as well as possible modulation thereof by prebiotics or probiotics. The present overview will briefly outline the composition and function of the intestinal microbiota, its association with nutrient intake and availability, and will address the role of the intestinal microbiota in malnutrition and malabsorption.
3.
Neurologic manifestations of malabsorption syndromes.
Pfeiffer, RF
Handbook of clinical neurology. 2014;:621-32
Abstract
Although malabsorption is generally considered to be a gastrointestinal problem, the effects of malabsorption extend far beyond the gastrointestinal tract and can include neurologic dysfunction. Malabsorption may occur by a variety of mechanisms, both genetic and acquired, that interfere with the absorption of basic nutrients, vitamins, minerals, and trace elements. Disorders that interfere with fat absorption can lead to neurologic dysfunction as a consequence of associated impairment of fat-soluble vitamin absorption. Thus, individuals with genetic vitamin E deficiency and the familial hypocholesterolemias may develop symptoms of peripheral neuropathy, cerebellar ataxia, and other neurologic signs and symptoms. Disease processes that damage the enteric mucosa and produce malabsorption can trigger neurologic dysfunction both by immune-related processes, as in celiac disease, and by impairing absorption of essential vitamins and other nutrients, as in tropical sprue. Deficiencies of water-soluble vitamins, such as thiamine and niacin, can also develop in the setting of malabsorption and lead to neurologic dysfunction. Neurologists are aware of the neurologic damage that copper excess can cause in Wilson's disease, but copper deficiency due to malabsorption can also produce neurologic dysfunction in the form of myelopathy. It is vitally important for neurologists to be aware of the potential for malabsorptive processes to produce neurologic dysfunction, because effective treatment for such disorders is often available.
4.
Physiology of the small intestine after resection and transplant.
Walther, A, Coots, A, Nathan, J, Kocoshis, S, Tiao, G
Current opinion in gastroenterology. 2013;(2):153-8
Abstract
PURPOSE OF REVIEW Recent studies have evaluated intestinal physiology following bowel resection; understanding changes in small bowel physiology after intestinal transplantation has received less attention. In this review, we will examine recent studies focused on changes in intestinal physiology following resection and intestinal transplantation. RECENT FINDINGS Absorption, immunity, and motility are fundamental components of small bowel physiology. Absorption after resection or transplantation is mediated by adaptation and enterocyte function. After resection, adaptation results in increased villus height and crypt depth. Hepatocyte growth factor and epidermal growth factors cause enterocyte hypertrophy and hyperplasia, allowing greater peptide uptake. Little is known about intestinal adaptation after transplant, but enteral autonomy is attainable. Immunity in small bowel after transplantation relies on a balance of innate and adaptive immune responses in the presence of the luminal microbiota. Intraepithelial lymphocytes are decreased following small bowel resection. After small bowel transplant, the number and the ratio of intraepithelial lymphocytes to enterocytes, as well as changes in the microbiota, can be used to identify rejection. After intestinal transplant, immune-mediated dysmotility is common. Perioperative infliximab in addition to tacrolimus may decrease the inflammation that contributes to dysmotility. SUMMARY As intestinal transplantation becomes more successful, understanding how absorption, immunity, and motility changes will allow for optimization of bowel function.