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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboembolic events are a known complication in inflammatory bowel disease (IBD). We report on 2 young women with IBD and aortic mural thrombi as a source of arterioarterial embolization to the lower limbs resulting in significant morbidity. The first case was a 36-year-old woman with severe ulcerative colitis who presented with signs of microembolism into two toes of her right foot. A thrombus in the otherwise normal infrarenal aorta with occlusion of the inferior mesenteric artery was revealed by computed tomography (CT) and intrarterial angiography. The digital ischemia resolved without sequelae. The second case was a 41-year-old woman with Crohn's disease complicated by fistulas. She developed acute ischemia of her right leg. Arteriography and CT revealed infrapopliteal embolic occlusions and a thrombus in the distal otherwise normal abdominal aorta and the left iliac artery. A primarily successful thrombectomy had to be repeated 5 times because of reocclusion. Eventually the leg was exarticulated at the knee. In both patients no further thromboembolic event occurred during follow-up of 4 1/2 years and 5 1/2 years, respectively, and aortic thrombi had resolved at follow-up CT scans. Extensive work up for hypercoagulability was negative in both patients. We consider IBD as the most likely trigger for arterioarterial embolization in the absence of thrombophilia in both patients. Finally we give an overview of the literature of similar cases with aortic mural thrombi in IBD patients.
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PMID:Aortic mural thrombi in patients with inflammatory bowel disease: report of two cases and review of the literature. 1547 53

Schering-Plough's interleukin (IL)-10 (ilodecakin) is under investigation for the potential treatment of autoimmune diseases, solid tumors, ulcerative colitis, Crohn's disease and organ transplantation. In June 1996, ilodecakin entered phase II trials for Crohn's disease, ulcerative colitis and rheumatoid arthritis and, as of June 1999 was reported to be in phase III trials for Crohn's disease and rheumatoid arthritis. It has also demonstrated promising effects in the treatment of inflammatory bowel disease. In January 1997, phase I trials began in HIV-infected patients. Initial results from a pilot study, carried out by the National Institute of Allergy and Infectious Disease Control, indicated that a single dose of IL-10 decreases the blood viral load. The results, however, were transient. Early clinical studies are ongoing in acute lung injury, ischemia-reperfusion injury, multiple sclerosis and psoriasis. In February 1999, Morgan Stanley Dean Witter predicted sales of US $50 million in 2000 rising to US $325 million in 2005.
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PMID:Ilodecakin. Schering-Plough Corp. 1611 14

Pouchitis after restorative proctocolectomy for ulcerative colitis is usually of ill-defined etiology and is encountered with sclerosing cholangitis, bacterial overgrowth, and ischemia. Recently, appendiceal involvement, ileitis, and fissures in the colectomy specimen have been associated with short- and long-term development of pouchitis. To corroborate these recent findings, the histology of 40 colectomies (70% males; mean age 46.3 years, age range 20-70 years; mean follow-up period 3.7 years, range 1-13 years) with yearly follow-up biopsies was correlated with pouchitis and clinical symptoms. Appendicitis, fissures, and ileitis were present in 47, 45 and 5% of the patients, respectively. Pouchitis in patients with appendicitis or with fissures was noted in 44 and 50% at first biopsy and in 70 and 58% during follow-up (p = NS). Of the patients without appendicitis or without fissures, 33 and 33% demonstrated pouchitis at the first biopsy and 30 and 55% during follow-up (p = NS). Clinico-histological correlation revealed normal/near-normal biopsies with the lowest clinical severity score in 77% and with the highest clinical score in 43% (p < 0.025). The histological findings of appendiceal involvement, fissuring ulcers, and ileitis in colectomies for ulcerative colitis do not correlate with the finding of pouchitis in early or late pouch biopsies. A high clinical suspicion score is frequently not correlated with significant inflammation of the pouch.
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PMID:Pouchitis in ulcerative colitis: correlation between predictors from colectomy specimens and clinico-histological features. 1686 67

A physician's approach to patients with ulcerative colitis (UC) who are refractory to standard first-line therapies must be thoughtful and systematic and include the individual's physical and emotional state as the physician examines the various dietary, medical, and surgical options currently available. It is of foremost importance to confirm that the refractory patient's symptoms are not simply due to dietary indiscretion, concomitant bowel infection (especially with Clostridium difficile), an incorrect diagnosis (eg, colitis due to infection, NSAIDs, ischemia, diverticulitis, or Crohn's disease), or even a concomitant diagnosis (eg, celiac sprue, pancreatic insufficiency, functional bowel disorder, laxative or sorbitol intake). The ability to quickly assess the status of the colonic mucosa with flexible sigmoidoscopy aids in the ability to distinguish patients with refractory inflammation from those with other diagnoses. The initiation and optimization of the long-term purine analogues azathioprine (AZA) or 6-mercaptopurine (6-MP) remain the backbone of medical therapy for patients with refractory UC. For those unresponsive to corticosteroids, quicker induction of remission may necessitate infliximab, cyclosporine, or tacrolimus. Successful induction and maintenance with AZA, 6-MP, and/or infliximab should be followed by long-term therapy with these agents. Cessation of therapy often leads to relapse. Novel therapies under investigation hold the promise of offering more options for both the induction and maintenance of remission in refractory UC patients. Discussions of surgical intervention should not be put off as a last resort but rather included in the overall treatment plan offered to the patient.
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PMID:Management of refractory ulcerative colitis. 1690 87

Hepatic portal venous gas (HPVG) is an uncommon disease entity that usually has grave prognosis. It is generally associated with bowel necrosis, and has been reported in a wide variety of conditions such as ulcerative colitis, Crohn's disease, diverticulitis, intestinal ischemia, or infarction. We experienced two cases of HPVG associated with acute pancreatitis. HPVG was found in patients with severe necrotizing pancreatitis and concurrent bowel ischemia. Despite aggressive resuscitation with fluids and broad spectrum antibiotics, each patient developed multiorgan failure, and died within few days. Acute pancreatitis is a potential cause of severe intraabdominal systemic catastrophe. Moreover, HPVG is associated with bowel ischemia in the setting of acute pancreatitis which could lead to rapid aggravation of symptom and complicated clinical course. Therefore, vigilant and aggressive management should be warranted in such condition.
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PMID:[Hepatic portal venous gas associated with acute pancreatitis: reports of two cases and review of literature]. 1792 58

The short bowel syndrome (SBS) can result from a variety of conditions, including postoperative complications and malignancy. Continence-preserving operations are generally performed for either ulcerative colitis (UC) or familial polyposis (FAP). These procedures can be associated with high morbidity and the potential for future malignancy. Our aim was to determine the causes and consequences of SBS in patients undergoing these procedures. Twenty-four patients (12 men and 12 women) 18 to 64 years of age were identified with SBS after continence-preserving procedures. Eighteen had pelvic procedures, and six had continent ileostomies. All SBS patients had a proximal ostomy. Remnant length measured <60 cm in five patients, 60-120 cm in ten patients, and >120 cm in nine patients. Overall 13 patients required long-term PN. Four FAP patients with desmoid tumors died. One patient with UC underwent intestinal transplant and expired. Follow-up ranges from 6 to 192 months. Overall 14 patients had UC, nine had FAP, and one had functional disease. Eight patients with an initial diagnosis of UC had subsequent Crohn's disease necessitating further resection and pouch excision. Eight patients (five with UC, two FAP, and one with functional disease) had postoperative complications, including obstruction or mesenteric ischemia requiring resections. One UC patient developed adenocarcinoma in a continent ileostomy. Seven of the nine FAP patients required resection for desmoid tumors. Six of these underwent resection alone. Three died at 10, 11, and 13 months after SBS from liver failure and sepsis while awaiting transplant. One patient has recurrent desmoid at 30 months, another is alive and well at 48 months, and the other patient, who was not a transplant candidate, died from an unrelated cardiac operation at 23 months. A single patient underwent resection with simultaneous multivisceral transplantation. SBS can develop after continence-preserving procedures. This occurs with inflammatory bowel disease when unsuspected Crohn's disease is present or complications occur. SBS related to desmoid tumors has a poor prognosis in patients undergoing resection alone. A more aggressive approach to intestinal transplantation in these patients may be warranted.
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PMID:Short bowel syndrome after continence-preserving procedures. 1796 30

All the currently available evidence suggests that the two types of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC), involve a conflict between the immune system of the intestinal mucosa and intraluminal antigens, mainly the intestinal microflora, which are normally tolerated by the immune system. This conflict is modulated by numerous environmental factors and a clear polygenetic predisposition. The present article reviews the behavior of all the etiologic circumstances (microbial, genetic and environmental) and subsequently analyzes the possible pathogenic factors in which the etiologies can be found, namely: dysfunction of the intestinal epithelium, innate immune system alterations, and distortion of the cellular and humoral arms of the acquired immune system. The role of tissue ischemia in CD and expression of "extraintestinal inflammatory metastases", both in CD and UC, are briefly discussed. Finally, the view that IBD may be a spectrum of pathological processes provoked by distinct etiopathogenic factors and the possible biological significance of the growing incidence of this disease in the western world, coinciding with the decline in infectious diseases in this geographical area, are discussed.
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PMID:[Multifactorial etiology and pathogenic factors in inflammatory bowel disease]. 1964 92

Inflammatory bowel disease (IBD) is a chronic intestinal disorder comprising 2 distinct but often overlapping diseases: Crohn's disease and ulcerative colitis. Although much research to identify the etiology of IBD has focused on genetic constitution, infectious causes, and immune dysregulation, its exact cause and pathogenesis remain incompletely understood. Mesenteric blood flow, the intestinal microcirculation, and intestinal ischemia also have been proposed as etiologic, although they remain less-explored themes despite evidence suggesting a contributory role in IBD pathogenesis. The anatomy, architecture, and function of the splanchnic microcirculation will be reviewed here with regard to the development of intestinal microvascular ischemia, a pathologic process that appears to precede the classic changes that characterize IBD.
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PMID:On the role of ischemia in the pathogenesis of IBD: a review. 1968 50

Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) is the surgical treatment of choice for the majority of patients with medically refractory ulcerative colitis (UC) or UC with dysplasia, or familial adenomatous polyposis. Various forms of pouchitis frequently occur after surgery. In fact, pouchitis is the most frequent long-term complication of IPAA in patients with UC, with a cumulative prevalence of up to 50%. The etiology and pathogenesis of pouchitis are not entirely clear. It is generally believed that the initiation and development of the disease process of pouchitis is associated with dysbiosis of pouch reservoir, as evidenced by a favorable response to antibiotic therapy. However, the majority of the patients do not show identifiable etiopathogenetic or triggering factors, therefore being labeled to have idiopathic pouchitis. In contrast, a subgroup of patients, particularly those with antibiotic-refractory pouchitis, may have obvious triggering factors for disease flare-up and progression and may be considered to have secondary pouchitis. Therefore, pouchitis can be classified on the basis of etiology into idiopathic and secondary causes. Approximately 20-30% of patients who present with chronic pouchitis have secondary identifiable and triggering factors, including cytomegalovirus or Clostridium difficile infection, ischemia, concurrent immune-mediated disorders, radiation, collagen deposition, and use of nonsteroidal anti-inflammatory drugs. Careful evaluation of these secondary causes of pouchitis that may contribute to resistance to antibiotics should be performed before the introduction of next-line medical therapy.
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PMID:Secondary pouchitis: those with identifiable etiopathogenetic or triggering factors. 1975 72

Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease, is a chronic and recurrent inflammatory disorder of the intestinal tract. Since the precise pathogenesis of IBD remains unclear, it is important to investigate the pathogenesis of IBD and to evaluate new anti-inflammatory strategies. Recent evidence suggests that heme oxygenase-1 (HO-1) plays a critical protective role during the development of intestinal inflammation. In fact, it has been demonstrated that the activation of HO-1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in various animal intestinal injury models induced by ischemia-reperfusion, indomethacin, lipopolysaccharide-associated sepsis, trinitrobenzene sulfonic acid or dextran sulfate sodium. In addition, carbon monoxide (CO) derived from HO-1 has been shown to be involved in the regulation of intestinal inflammation. Furthermore, administration of a low concentration of exogenous CO has a protective effect against intestinal inflammation. These data suggest that HO-1 and CO may be novel therapeutic molecules for patients with gastrointestinal inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 and CO in intestinal inflammation.
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PMID:The role of heme oxygenase and carbon monoxide in inflammatory bowel disease. 2106 34


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