scholarly journals Case Report: Development of Type 1 Autoimmune Pancreatitis in an Adolescent With Ulcerative Colitis Mimicking Pancreatic Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Sujin Choi ◽  
Hae Jeong Lee ◽  
An Na Seo ◽  
Han Ik Bae ◽  
Hyung Jun Kwon ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Autoimmune Pancreatitis ◽  
Pancreatic Enzyme ◽  
Pancreatic Neoplasm ◽  
Gastrointestinal Symptoms ◽  
Corticosteroid Treatment ◽  
Pancreatic Enzymes ◽  
Extraintestinal Manifestation ◽  
Abdominal Ultrasonography

Introduction: Autoimmune pancreatitis (AIP) is a rare extraintestinal manifestation of inflammatory bowel disease (IBD) which is typically responsive to corticosteroid treatment.Case Presentation: We report a case of a 17-year-old male diagnosed with ulcerative colitis who subsequently developed acute pancreatitis. Blood tests demonstrated elevated pancreatic enzyme levels of amylase (1319 U/L) and lipase (809 U/L). Abdominal computed tomography revealed peripancreatic fat stranding and the presence of a perisplenic pseudocyst. Azathioprine and mesalazine were stopped as possible causes of drug-induced pancreatitis. However, pancreatic enzymes remained elevated and corticosteroid treatment was started. Despite corticosteroid therapy, amylase and lipase levels continued to increase. Infliximab was started due to a flare in gastrointestinal symptoms of ulcerative colitis. Follow-up abdominal ultrasonography revealed a pancreatic tail mass. Tumor markers, including CA 19-9, were elevated and atypical cells were seen on histological examination of an endoscopic ultrasonography-guided fine needle aspiration biopsy. Surgical pancreaticosplenectomy was performed for suspected pancreatic neoplasm. Surprisingly, histology revealed chronic pancreatitis with storiform fibrosis and infiltration of IgG4-positive cells, compatible with AIP type 1. Thereafter, pancreatic enzymes gradually decreased to normal levels and the patient has been in remission for 9 months on infliximab monotherapy.Conclusion: Pediatric gastroenterologists should keep in mind that AIP may develop during the natural course of pediatric IBD. Moreover, the development of pancreatic fibrosis may be non-responsive to corticosteroid treatment and mimic pancreatic neoplasia.

scholarly journals Autoimmune Pancreatitis Type 2: Case Report

2017 ◽  
Vol 5 (4) ◽  
pp. 232470961773424 ◽  
Author(s):  
Chidinma Onweni ◽  
Harika Balagoni ◽  
Jennifer M. Treece ◽  
Emmanuel Addo Yobo ◽  
Archi Patel ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Acute Pancreatitis ◽  
Case Report ◽  
Autoimmune Pancreatitis ◽  
Corticosteroid Treatment ◽  
Unknown Etiology ◽  
Inflammatory Bowel ◽  
Igg4 Antibody

A middle-aged man presents with acute pancreatitis of unknown etiology and is found to have a presentation consistent with the diagnosis of type 2 autoimmune pancreatitis (AIP). AIP is a group of rare heterogeneous diseases that are challenging to diagnose. There are 2 types of AIP. Type 1 disease is the more common worldwide than type 2 AIP. While type 1 AIP is associated with IgG4-positive antibodies, type 2 AIP is IgG4 antibody negative. Both types of AIP are responsive to corticosteroid treatment. Although type 1 AIP has more extrapancreatic manifestations and more commonly relapses, this is a case of a patient with type 2 AIP with inflammatory bowel disease and relapsing course.

Immunology of type 1 diabetes mellitus

2011 ◽  
pp. 1723-1733
Author(s):  
Mark Peakman
Keyword(s):  
Bone Marrow ◽  
Type 1 Diabetes ◽  
T Lymphocytes ◽  
Immune Cells ◽  
Pancreatic Enzyme ◽  
Gastrointestinal Symptoms ◽  
Adaptive Immune Cells ◽  
Established Disease ◽  
Sub Saharan

The concept that the pathological hallmark of type 1 diabetes—namely, irreparable damage to β‎ cells—is the result of an autoimmune process has gained sustained credence since it was first intimated in the 1970s. Forty years on, a robust set of criteria can be applied to settle this important question. As a result of numerous, reproducible research findings (Table 13.2.3.1), there is now an overwhelming case to support the assertion that type 1 diabetes is an autoimmune disease. Perhaps the most persuasive evidence is provided by the case reports of diabetes arising in recipients of bone marrow from patients with type 1 diabetes (1, 2). In these cases, the recipients underwent bone marrow ablation as part of the treatment for their underlying condition (e.g. relapsed haematological cancers) that effectively removed all autologous innate and adaptive immune cells. To reconstitute their immune system, they then received bone marrow from a sibling with type 1 diabetes. They developed the disease themselves some years later. It is hard to argue against the proposal that immune cells transferred in the bone marrow inoculum were responsible for β‎ cell destruction. Indeed, current practice in these circumstances is to ensure immune depletion of any mature T lymphocytes that may be present in the transplanted bone marrow using specific monoclonal antibodies. This successfully circumvents the problem—and also provides clear evidence for the pivotal role for T lymphocytes in causing β‎ cell damage. It should be noted that the overwhelming majority of patients with type 1 diabetes—especially those inhabiting the Western, developed world—have evidence of the underlying autoimmune processes, as discussed in this chapter. However, there is a recognition that type 1 diabetes may be heterogeneous, as, in some patients, evidence of autoimmunity is lacking (WHO diabetes classification type 1B). In Japan, a fulminant form of diabetes has been described as representing 15–20% of type 1 disease (15). Presentation is characterized by a high prevalence of preceding common cold-like and gastrointestinal symptoms, a near-normal level of HbA1c (despite very high plasma glucose levels and ketoacidosis), raised serum pancreatic enzyme levels, and absent C-peptide—but only rarely any evidence of autoantibodies against islet cell autoantigens (16). Some cases of type 1 diabetes arising in sub-Saharan Africa have also been described as lacking evidence of autoimmunity against islet cells (see Chapter 13.4.3.4); however, these data require clarification, since it is known that the autoantibodies decline and may disappear from the circulation soon after diagnosis, making retrospective classification of cohorts with established disease highly problematic (17). Future studies in these locations will need to establish evidence of autoimmunity at diagnosis in currently equivocal situations, using the most comprehensive, up-to-date range of serological markers (see Table 13.2.3.2, below), as well as to establish the clinical and immunogenetic features of the disease.

scholarly journals Difficulties in Evaluating Urinalysis following Combined Pancreas–Kidney Transplantation

1997 ◽  
Vol 34 (6) ◽  
pp. 664-667 ◽  
Author(s):  
Dirk R Bernard ◽  
Joris R Delanghe ◽  
Michel R Langlois
Keyword(s):  
Kidney Transplantation ◽  
Pancreatic Enzyme ◽  
Pancreatic Enzymes ◽  
Marker Proteins ◽  
Kidney Transplantations ◽  
Pancreas Kidney Transplantation ◽  
Postoperative Problems ◽  
Proteins And Peptides

Combined pancreas–kidney transplantation has been introduced in the treatment of patients with type 1 diabetes and renal failure 20 years ago. By 1985 374 combined pancreas–kidney transplantations had been reported to the International Pancreas Transplant Registries.1 Surgical drainage of the transplanted exocrine pancreas into the urinary bladder solves most of the postoperative problems encountered with the exocrine secretions. Furthermore, monitoring of pancreatic enzyme (amylase) activity in urine has been shown to be useful in diagnosis of rejection of the pancreatic graft.2 However, little attention has been paid to the biochemical consequences of high activities of proteolytic pancreatic enzymes on the determination of urinary proteins. The present case illustrates the difficulties in interpreting proteinuria in patients with combined pancreas–renal transplant with pancreaticocystostomia. In the propositus, interpretation of the urinary protein electrophoresis is hampered by the presence of pancreatic juice proteins and peptides originating from digestion of proteins by activated pancreatic enzymes. Results of immunochemically determined marker proteins ([micro]albumin, transferrin, β2-microglobulin) are unreliable due to digestion by pancreatic enzymes.

Is hearing loss an extraintestinal manifestation of ulcerative colitis?

2001 ◽  
Vol 120 (5) ◽  
pp. A269-A269
Author(s):  
V MANI ◽  
C HEW ◽  
N KUMAR ◽  
J MATHEWS ◽  
A HARIKRISHNAN ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Hearing Loss ◽  
Extraintestinal Manifestation

scholarly journals Recurrent myocarditis in a patient with active ulcerative colitis: a case report and review of the literature

2021 ◽  
Vol 8 (1) ◽  
pp. e000587
Author(s):  
Giacomo Caio ◽  
Lisa Lungaro ◽  
Fabio Caputo ◽  
Maria Muccinelli ◽  
Maria Caterina Marcello ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Case Report ◽  
Inflammatory Bowel Diseases ◽  
Drug Toxicity ◽  
Active Ulcerative Colitis ◽  
Extraintestinal Manifestations ◽  
Review Of The Literature ◽  
Extraintestinal Manifestation ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel diseases such as ulcerative colitis (UC) may be complicated by several extraintestinal manifestations. These involve joints, skin, eyes and less commonly lungs and heart. Myocarditis may result from the toxic effect of drugs (ie, mesalazine) commonly used for the treatment of UC or due to infections (eg, Coxsackieviruses, enteroviruses, adenovirus). Here, we report a case of a 26-year old man affected by UC and complicated by two episodes of myocarditis. Both episodes occurred during two severe exacerbations of UC. However, in both cases the aetiology of myocarditis remains uncertain being ascribable to extraintestinal manifestation, drug toxicity or both.

scholarly journals Impact of 2′-Fucosyllactose on Gut Microbiota Composition in Adults with Chronic Gastrointestinal Conditions: Batch Culture Fermentation Model and Pilot Clinical Trial Findings

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 938
Author(s):  
Jennifer Joan Ryan ◽  
Andrea Monteagudo-Mera ◽  
Nikhat Contractor ◽  
Glenn R. Gibson
Keyword(s):  
Ulcerative Colitis ◽  
Batch Culture ◽  
Pilot Trial ◽  
Gastrointestinal Symptoms ◽  
Short Chain Fatty Acids ◽  
Open Label ◽  
Gastrointestinal Conditions ◽  
Fermentation Model ◽  
Quality Of Life Index

Intestinal dysbiosis has been described in patients with certain gastrointestinal conditions including irritable bowel syndrome (IBS) and ulcerative colitis. 2′-fucosyllactose (2′-FL), a prebiotic human milk oligosaccharide, is considered bifidogenic and butyrogenic. To assess prebiotic effects of 2′-FL, alone or in combination with probiotic strains (potential synbiotics), in vitro experiments were conducted on stool from healthy, IBS, and ulcerative colitis adult donors. In anaerobic batch culture fermenters, Bifidobacterium and Eubacterium rectale-Clostridium coccoides counts, and short-chain fatty acids (SCFAs) including butyrate increased during fermentation with 2′-FL and some of the 2′-FL/probiotic combinations. In a subsequent open-label pilot trial, the effect of a 2′-FL-containing nutritional formula was evaluated in twelve adults with IBS or ulcerative colitis. Gastrointestinal Quality of Life Index (GIQLI) total and gastrointestinal symptoms domain scores, stool counts of Bifidobacterium and Faecalibacterium prausnitzii, and stool SCFAs including butyrate, increased after six weeks of intervention. Consistent with documented effects of 2′-FL, the batch culture fermentation experiments demonstrated bifidogenic and butyrogenic effects of 2′-FL during fermentation with human stool samples. Consumption of the 2′-FL-containing nutritional formula by adults with IBS or ulcerative colitis was associated with improvements in intra- and extra-intestinal symptoms, and bifidogenic and butyrogenic effects.

Survival of human pancreatic enzymes during small bowel transit: effect of nutrients, bile acids, and enzymes

1997 ◽  
Vol 273 (2) ◽  
pp. G553-G558 ◽  
Author(s):  
G. Holtmann ◽  
D. G. Kelly ◽  
B. Sternby ◽  
E. P. DiMagno
Keyword(s):  
Bile Acids ◽  
Enzyme Activities ◽  
Lipolytic Activity ◽  
Pancreatic Enzyme ◽  
Pancreatic Enzymes ◽  
Intestinal Transit ◽  
Small Bowel Transit ◽  
Healthy Humans ◽  
Proximal Intestine ◽  
Distal Jejunum

The activity of pancreatic enzymes declines during aboral intestinal transit. We tested the hypothesis that survival of pancreatic enzyme activities during intestinal transit is affected by amounts or concentrations of calories, nutrients, bile acids, or pancreatic enzymes entering the segments of the small intestine. An oroileal tube was placed in 26 healthy humans. The tube had duodenal, jejunal, and ileal infusion ports for nonabsorbable markers and aspiration ports in the distal duodenum, distal jejunum, and distal ileum. Four infusates of different proportions of protein, fat, and carbohydrate were infused continuously into the duodenum at 40, 90, and 160 kcal/h. Of the nutrients infused into the proximal duodenum, 21 +/- 3, 51 +/- 7, and 39 +/- 5% of fat, protein, and carbohydrate, respectively, were delivered to the distal duodenum. During duodenoileal transit, lipase, chymotrypsin, amylase, and trypsin lost 71 +/- 5, 63 +/- 5, 43 +/- 7, and 38 +/- 9% of activity, respectively (P < 0.01 vs. distal duodenum). During duodenojejunal transit, the activity of each enzyme decreased more than 35% (P < 0.01 vs. distal duodenum), and infusion of more calories into the duodenum improved survival of all enzymes except trypsin (P < 0.05). During jejunoileal transit, greater amounts and concentrations of calories and carbohydrate improved survival of only lipolytic activity (P < 0.01, P < 0.05, respectively), and loss of lipolytic activity correlated directly with delivery of bile acids (r = 0.56, P = 0.05) and chymotrypsin (r = 0.80, P = 0.001) to the distal jejunum. We conclude that intraluminal nutrients increase survival of enzyme activities in the proximal intestine. After absorption of nutrients, the action of chymotrypsin and bile acids decrease lipolytic activity more than activity of other enzymes.

scholarly journals Understanding patient journey in ulcerative colitis prior to biologic initiation: a 5-year exploration

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yiting Wang ◽  
Rupa Makadia ◽  
Christopher Knoll ◽  
Jill Hardin ◽  
Erica A. Voss ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Health Care ◽  
Health Care Utilization ◽  
Corticosteroid Treatment ◽  
Biologic Agent ◽  
Care Utilization ◽  
Biologic Treatment ◽  
Patient Journey ◽  
Care Experience ◽  
Oral Corticosteroids

Abstract Background There has been a more pronounced shift toward earlier, more aggressive therapies in Crohn’s disease than in ulcerative colitis (UC). The aim of this study was to describe the pre-biologic treatment and health care experience, including co-morbidities and overall health care utilization, for UC patients who initiated biologic therapies, in the 5 years prior to the initiation of the first biologic agent. Methods UC patients who initiated a biologic agent approved for UC between 9/15/2005 and 1/30/2018 were identified from the IBM® MarketScan® Commercial Database, a large US database. The date of the first recorded UC biologic exposure was defined as the index date, and ≥ 5 years of pre-index records were required to evaluate patients’ treatment, disease progression and overall health care utilization prior to initiating biologic agents. Results Among the 1891 eligible patients, treatment with oral corticosteroids, 5-aminosalicylates, and other non-biologic immunomodulators, all increased progressively across the 5 years prior to the index. From within year-five to within year-one prior to the index, the median duration of oral corticosteroid treatment increased from 34 to 88 days per year and the proportion of patients who experienced more extensive/pancolitis disease increased from 16 to 59%. Overall, the frequency of all-cause health care visits also increased. Conclusions Patients with UC experienced increasing morbidity and treatment burden in the 5 years prior to initiating biologic therapy. To achieve reduced corticosteroids in UC management, better risk stratification is needed to help identify patients for more timely biologic treatment.

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