Publications by authors named "Siri A Urquhart"

5 Publications

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Primary Sclerosing Cholangitis-Associated Pouchitis: A Distinct Clinical Phenotype.

Clin Gastroenterol Hepatol 2021 Feb 4. Epub 2021 Feb 4.

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. Electronic address:

Background & Aims: Patients with primary sclerosing cholangitis (PSC) commonly undergo ileal pouch-anal anastomosis (IPAA) for medically-refractory ulcerative colitis (UC) or colorectal dysplasia. Pouchitis develops more frequently in patients with PSC, potentially leading to increased morbidity. We aimed to assess clinical characteristics and treatment outcomes for pouchitis in patients with PSC compared to a matched, non-PSC cohort.

Methods: All patients with PSC who underwent IPAA and were diagnosed with pouchitis (PSC-pouchitis) were identified. A matched cohort composed of non-PSC patients who underwent IPAA for UC and subsequently developed pouchitis (UC-pouchitis) was developed. Relevant demographic, clinical, endoscopic, histologic, and treatment data were collected and compared between groups.

Results: Of those with PSC-pouchitis (n=182), 53.9% and 46.1% underwent IPAA for medically-refractory disease and dysplasia, respectively, compared to 88.7% and 11.3% in the UC-pouchitis group (P < .001). Patients with PSC-pouchitis were more likely to develop chronic pouchitis (68.1% vs 34.1%; P < .001), have moderate-to-severe pouch inflammation (54.9% vs 32.4%; P < .001), and prepouch ileitis (34.1% vs 11.5%; P < .001) compared to UC-pouchitis. Of those with PSC-pouchitis, 50.6% and 17.6% developed chronic antibiotic-dependent or antibiotic-refractory pouchitis, respectively, compared to 25.8% and 7.7% with UC-pouchitis. There was no difference in treatment response between the two groups with use of thiopurines, anti-tumor necrosis factor agents, and newer biologics.

Conclusions: PSC-associated pouchitis presents with a unique clinical phenotype, characterized by increased risk of chronic pouchitis, moderate-to-severe pouch inflammation, prepouch ileitis, and less response to conventional antimicrobial therapy.
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http://dx.doi.org/10.1016/j.cgh.2021.02.006DOI Listing
February 2021

Jejunal Polyps out of Place: A Case of Gastric Heterotopia of the Jejunum.

Case Rep Gastrointest Med 2020 20;2020:8822019. Epub 2020 Aug 20.

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA.

Heterotopia is the presence of normal physiologic tissue in an atypical location. Gastric heterotopia has been described in various locations throughout the gastrointestinal tract, including the small intestine. Gastric heterotopia of the small intestine typically is asymptomatic but may present in several ways with symptoms of obstruction, bleeding, perforation, intussusception, or pain. However, gastric heterotopia is rare beyond the duodenum except for its frequent association with Meckel's diverticulum. This entity should be considered in the differential diagnosis of polypoid lesions presenting with symptoms of bleeding or obstruction especially in younger patients. We present a case of gastric heterotopia of the jejunum in a patient with a prior history of Meckel's diverticulectomy after he presented with obstructive symptoms. His symptoms improved following resection of two jejunal polyps via antegrade double-balloon assisted enteroscopy with fluoroscopy. On histopathlogical examination, findings were consistent with gastric heterotopia. This case highlights the importance of considering gastric heterotopia in the differential diagnosis of polypoid lesions located beyond the ligament of Treitz in younger patients presenting with obstructive symptoms.
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http://dx.doi.org/10.1155/2020/8822019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7455846PMC
August 2020

An Unusual Cause of Abdominal Pain.

Gastroenterology 2020 Feb 1. Epub 2020 Feb 1.

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.

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http://dx.doi.org/10.1053/j.gastro.2020.01.041DOI Listing
February 2020

Brain changes associated with thromboxane receptor antagonist SQ 29,548 treatment in a mouse model.

J Neurosci Res 2015 Aug 22;93(8):1279-92. Epub 2015 Feb 22.

Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, North Dakota.

The purpose of this study was to characterize behavioral and physiological effects of a selective thromboxane (TP) receptor antagonist, SQ 29,548, in the C57Bl/6 mouse model. At 6 months of age, male mice were given either sham or drug i.p. injections for 3 days at a dose of 2 mg/kg each day. On the day after the final injection, mice were subjected to behavioral testing before brain collection. Left hemisphere hippocampi were collected from all mice for protein analysis via Western blot. Right brain hemispheres were fixed and embedded in gelatin and then serially sectioned. The sections were immunostained with anti-c-Fos antibodies. Prostaglandin analysis was performed from remaining homogenized brain samples, minus the hippocampi. Injection of SQ 29,548 decreased selective brain prostaglandin levels compared with sham controls. This correlated with robust increases in limbic-region c-Fos immunoreactivity in the SQ 29,548-injected mice. However, drug-treated mice demonstrated no significant changes in relevant hippocampal protein levels compared with sham treatments, as determined from Western blots. Surprisingly, injection of SQ 29,548 caused mixed changes in parameters of depression and anxiety-like behavior in the mice. In conclusion, the results indicate that administration of peripheral TP receptor antagonists alters brain levels of prostanoids and influences neuronal activity, with only minimal alterations of behavior. Whether the drug affects neurons directly or through a secondary pathway involving endothelium or other tissues remains unclear.
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http://dx.doi.org/10.1002/jnr.23578DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478107PMC
August 2015

Overexpression of mutant amyloid-β protein precursor and presenilin 1 modulates enteric nervous system.

J Alzheimers Dis 2015 ;44(4):1263-78

Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, USA.

Alzheimer's disease (AD) is a neurodegenerative disorder histologically characterized by amyloid-β (Aβ) protein accumulation and activation of associated microglia. Although these features are well described in the central nervous system, the process and consequences of Aβ accumulation in the enteric nervous system have not been extensively studied. We hypothesized that Aβ also may accumulate in the enteric nervous system and lead to immune cell activation and neuronal dysfunction in the digestive tract not unlike that observed in diseased brain. To test this hypothesis, ileums of the small intestine of thirteen month old AβPP/PS1 and C57BL/6 (wild type) mice were collected and analyzed using immunohistochemistry, western blot analysis, cytokine arrays, and ELISA. AβPP/PS1 mice demonstrated no differences in intestinal motility or water absorption but elevated luminal IgA levels compared to wild type mice. They also had increased protein levels of AβPP and the proteolytic enzyme, BACE, corresponding to an increase in Aβ1-40 in the intestinal lysate as well as an increase in both Aβ1-40 and Aβ1-42 in the stool. This correlated with increased protein markers of proinflammatory and immune cell activation. Histologic analysis localized AβPP within enteric neurons but also intestinal epithelial cells with elevated Aβ immunoreactivity in the AβPP/PS1 mice. The presence of AβPP, Aβ, and CD68 immunoreactivity in the intestines of some patients with neuropathologically-confirmed AD are consistent with the findings in this mouse model. These data support the hypothesis that in AD the intestine, much like the brain, may develop proinflammatory and immune changes related to AβPP and Aβ.
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http://dx.doi.org/10.3233/JAD-142259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6295343PMC
November 2015