Diss. (sammanfattning) Uppsala : Sveriges lantbruksuniv. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Stockholm universitet, 2007. / Härtill 4 uppsatser.

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Inflammatory bowel disease (IBD) is a group of diseases in the gastrointestinal field that is becoming more commonly diagnosed among patients. IBD is usually characterized as a group of chronic diseases affecting the digestive tract that are caused by a multitude of factors including genetic, environmental, mucosal, and immune contributors. One of the subgroups of IBD is very early onset IBD (VEO-IBD), which is diagnosed in children under the age of 6. VEO-IBD is a rare yet unique case of IBD, which reports poor response to conventional adult-onset IBD treatments. Nutrition is an alternative treatment that can decrease inflammation and allow IBD patients to achieve remission. This proposed study explores whether formula-based diets, which have been strongly correlated with reduced IBD inflammation and symptoms, will impact VEO-IBD patients. A mouse model will be set up with one control group of healthy mice and two variable groups of VEO-IBD characteristic mice, with 60 mice in each group. The mice will be fed three formula-based dietary regiments including camel’s milk, Pediasure, and liquid vitamin D3 twice daily for 90 days. All three of these dietary treatments have been proven to decrease inflammation in adult-onset IBD patients. The inflammation and severity of symptoms will be monitored every two days through Western blotting protein levels of IL10 (a genetic marker for VEO-IBD) and physiological tests. If nutrition has a positive effect on the VEO-IBD induced mice, then a decrease in inflammation and VEO-IBD symptoms should be observed. This study is vital to future treatment plans by determining the influence of formula-based diets in alleviating symptoms of VEO-IBD patients.

The aim of the present study was to assess whether the changes in the epithelial glycoproteins seen in the mucosa adjacent to tumors are specific premalignant markers or secondary reactive phenomena. A secondary objective was to assess whether ulcerative colitis and Crohn's Disease could be distinguished from one another histochemically. The carbohydrate prosthetic groups from colonic epithelial glycoproteins were characterized histologically and histochemically from 17 cases of ulcerative colitis, 21 cases of Crohn's Disease and 19 cases of diverticular disease. Two histochemical parameters - the relative proportion of sulpho- and sialomucin and the side-chain substitution pattern of O-acetylated sialic acid - were assessed using a battery of seven histochemical techniques. Serial sections from each specimen were also evaluated morphologically, using hematoxylin and eosin. In addition, the patterns of O-acetylated side-chain sialic acid from the three inflammatory bowel diseases were compared to data previously acquired from the mucosa adjacent to colonic tumors. Results indicate that neither focal changes nor the predominance of sialomucins are specific to the mucosa adjacent to tumors. As well, changes in one histochemical parameter were independent of changes in the other parameter. No histochemical class of epithelial glycoproteins was specific to any of the inflammatory bowel diseases and, therefore, it was not possible to distinguish between ulcerative colitis and Crohn's Disease on the basis of the histochemical techniques used in the present study. It was also noted that the histochemical changes in ulcerative colitis, Crohn's Disease and diverticular specimens were not related to the degree of inflammation. Finally, as a group, Crohn's Disease specimens showed a loss of sulphomucin-sialomucin gradient along the length of the crypts. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

Stomal varices are a rare phenomenon that can infrequently develop in patients with enterostomies and portal hypertension. Acute gastrointestinal bleeding from stomal varices can be life threatening and is often a diagnostic challenge. We present a case of severe gastrointestinal hemorrhage from stomal varices requiring emergent intervention with transjugular intrahepatic portosystemic shunt (TIPS) and plug embolization. A 61 year old male patient with a history of colorectal adenocarcinoma status post chemotherapy, radiation, along with low anterior colon resection with ostomy creation presented with a one day history of sudden onset of bright red blood from his colostomy site. He had a known history of decompensated cirrhosis related to hepatitis C and alcohol abuse. On arrival, the patient was tachycardic with borderline low blood pressure with evidence of bright red bleeding from his ostomy site. After initial resuscitation, a colonoscopy through the stoma revealed active bleeding from what appeared to be submucosal colonic varices. The patient continued to experience large volumes of blood loss and became more hemodynamically unstable. Cross sectional imaging showed colonic varices being fed by a branch of the inferior mesenteric vein. The patient underwent TIPS followed by Amplatzer plug embolization of the branch of the interior mesenteric vein that was feeding the colonic stomal varices. The patient’s bleeding was stopped by the combination of these therapeutic modalities and he recovered without complication. The current standard of care for treatment of such varices is with either (1) local therapy with ligation or sclerotherapy, (2) surgical interventions such as stomal manipulation or vessel shunting, either transhepatic or portosystemic to reduce portal pressures, or (3) liver transplantation. Our patient required an unusual combination of TIPS and Amplatzer plug embolization to control his massive hemorrhage. This combination of therapies has been shown effective for the management of select cases of esophageal or gastric variceal bleeding; however, our case demonstrates that the application of the TIPS plus Amplatzer plug embolization can be applied more broadly to the rare scenario of colonic stomal varices.

Introduction: Sclerosing mesenteritis is a rare autoimmune disease that eventually evolves into fibrotic changes affecting the adipose tissue around the mesenteric vessels. It can present through a myriad of gastroenterological as well as constitutional symptoms including but not limited to abdominal pain, diarrhea, fever, nausea or vomiting. Although the exact etiology of the disease is yet to be determined, there are several predisposing factors the most common of which is history of previous abdominal trauma and/or surgery. This is a case report of abdominal mesenteric panniculitis that presented with abdominal pain in a middle-aged male with history of cholecystectomy. Case Presentation: The patient was a 53-year-old male with past medical history of hypertension who presented with a 2-week history of intolerance to food and liquids and abdominal pain, colicky in nature, radiating to both flanks with no alleviating or relieving factors. One year before, the patient had cholecystectomy due to biliary dyskinesia. His hospital stay at that time was complicated by biliary leak treated with biliary stenting. He later also developed multiloculated abscess collection in the gallbladder fossa that was managed with external drainage and IV antibiotics. In the ER his vital signs were as the following: BP between 120-130/70-80, HR 70s, temperature 97, oxygen saturation was more than 95%. On physical examination, he had abdominal tenderness in all four quadrants with no rigidity, rebound tenderness, masses or skin changes. CBC showed WBC of 7K with no shift to the left, hemoglobin of 15.6 and platelets of 107. CMP showed Na of 142, K 4.2, Chl 19, Glu 99, Ca 9.5, AG 18, lactic acid 1, lipase 50, phos 2.7, beta-hydroxybutyrate 0.12 and Mg of 1.9. urine analysis and Troponins were within normal limits. EKG showed sinus rhythm. Urine drug screen was negative. CRP and ESR were within normal limits. Porphyria workup was negative. Alpha-1-antitrypsin was 123. Ceroluplasmin level was 17. Actin antibody was negative as well as mitochondria M2 antibody. CT angiogram of the abdomen showed patent mesenteric vessels. However, fat stranding was noticed especially at the root of the mesenteric vessels. The patient was placed on prednisone 40mg once daily and tamoxifen. His abdominal pain greatly improved after 2 days. He was discharged with a prolonged prednisone taper. He was scheduled for an appointment with his primary care at discharge but didn’t show up and was lost to follow up. Conclusion: Mesenteric panniculitis is a rare cause of abdominal pain. it is divided based on histological features into sclerosing (retractile) mesenteritis, mesenteric panniculitis and mesenteric lipodystrophy. Diagnoses is usually rarely inferred from the clinical presentation and is often suggested by radiological features. Distinctive findings on CT include fat ring sign and pseudotumor capsule. Although radiological characteristics are helpful, histological proof is essential for definitive diagnosis, especially with an atypical clinical and radiological appearance. There is no consensus on the optimal treatment option but prolonged steroid taper has been used with various degrees of success.

No description available.

The triple antibiotic formulation, known as anti-MAP therapy, exhibits unique synergistic antimicrobial activity and should be effective for treatment of Crohn's disease (CD) associated with Mycobacterium avium subspecies paratuberculosis (MAP). The absence of MAP detection in some CD cases may be linked to poor diagnostics or lack of association with the disease. To understand the therapeutic response of some CD patients to anti-MAP therapy in absence of MAP detection, the immunomodulatory potency of anti-MAP therapy and its major ingredients, clarithromycin (CLA) and rifabutin (RIF), in THP-1, Caco-2, and Jurkat T-cells were investigated. Anti-MAP formulation at 2.0 µg/mL decreased MAP viability in macrophages by 18-fold over 72 h. Additionally, M1/M2 macrophage polarization ratio was reduced by 6.7-fold, and expression and protein levels of TNF-a and IL-6 were reduced by 2.9-fold, whereas IL-10 increased by 5.0-fold in these cells. Mechanistically, the effect of anti-MAP formulation on NF-kB activation was dose-dependent and decreased to 13.4% at 2.0 µg/mL. Anti-MAP therapy also reversed the pro-inflammatory response in lipopolysaccharide (LPS)-induced macrophages, which shows that the anti-inflammatory effect of the treatment is not just due to a decrease in MAP viability. Furthermore, this study shows that anti-MAP therapy exhibits anti-cytotoxic effects in Caco-2 monolayers infected with MAP or treated with dextran sodium sulfate (DSS). Anti-MAP therapy decreased T-cell proliferation by up to 4.8-fold following treatment with phytohemagglutinin (PHA) or MAP purified protein derivative (PPD). Overall, the data demonstrate that anti-MAP therapy plays a significant role in modulating and eliciting a protective immune response in macrophages, endothelial cells, and T lymphocytes, even in absence of infection. This may explain the therapeutic response of some CD patients to treatment, even in absence of MAP detection, infection, or total eradication. The study supports anti-MAP therapy as an alternate treatment option for CD, especially in absence of reliable MAP diagnostics.