Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboembolic complications occurring in patients with Crohn's disease are increasingly reported and are associated with a high mortality. The mechanism by which the thrombogenic process occurs is unclear. As recent findings suggest that Crohn's disease is a chronic vasculitis with multifocal gastrointestinal infarctions secondary to an imbalance of the cellular hemostatic pathway, extradigestive thrombotic complications might be mediated by the same vascular immune reaction. We report an unusual case of recurrent venous thrombosis associated with regional enteritis, the main point of interest being two-fold: first, this case provides a morphological evidence for an angiitic process as the cause of extradigestive thrombosis; second, the gastrointestinal disease remained subclinical for more than four years although the patient developed major venous thrombotic complications.
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PMID:Venous thromboangiitis associated with regional enteritis. 146 Mar 59

Vasculitis in many forms has been reported rarely in association with ulcerative colitis. We report the occurrence of necrotizing vasculitis in a 48-year-old man 19 years after the onset of ulcerative colitis and 5 years after total colectomy with rectal preservation. The disease was limited to small arteries of skin and muscle consistent with the syndrome of cutaneous polyarteritis nodosa that has been reported with regional enteritis but not previously with ulcerative colitis.
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PMID:Cutaneous polyarteritis nodosa and ulcerative colitis. 167 18

The histology from rectal biopsy specimens taken 1980-1990 on 131 occasions from 116 horses, age 1-18 years, with clinical signs of intestinal disease was evaluated and classified retrospectively. In 40 horses, autopsy results were studied for comparison. Biopsy specimens (21 horses) and post mortem rectal tissue (9 horses) from 30 healthy horses, age 4-22 years, were used as controls. In 105 clinical cases, a biopsy was performed on only one occasion, while repeat biopsy was performed in 11 cases. Specimens showed pathological changes in 60 horses. The findings were classified into acute, chronic or chronic active simple proctitis, granulomatous enteritis, eosinophilic granulomatosis/gastroenteritis, eosinophilic proctitis, erosive/ulcerative proctitis, pseudomembranous proctitis, proctitis with vasculitis and malignant lymphoma. Mild scattered neutrophil infiltration in the lamina propria was found in controls, but neutrophils in crypt or surface epithelia were abnormal findings. Depletion or hyperplasia of goblet cells sometimes accompanied inflammation. Simple proctitis occurred in association with malignant lymphoma and various inflammatory disorders of the gastrointestinal tract apparent at autopsy. Eosinophilic granulomatosis/gastroenteritis and granulomatous enteritis were diagnosed from biopsy specimens in 6 of 12 and 4 of 9 cases, respectively, of these diseases confirmed at autopsy. Reduction of acid mucins in goblet cells was a prominent feature of eosinophilic granulomatosis. Rectal biopsy was found to be a useful adjunct for evaluation of intestinal disease in the horse.
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PMID:Rectal biopsy diagnosis in horses with clinical signs of intestinal disorders: a retrospective study of 116 cases. 881 89

The clinico-pathologic entity of idiopathic granulomatous gastritis is a form of granulomatous gastritis, distinct from Crohn's disease, sarcoidosis, infections, foreign bodies, malignancy or vasculitis. The case of a 61-year-old female is described who was admitted on account of progressive weight loss, diffuse abdominal pains, post-prandial vomiting. Gastroscopy revealed a pyloric stenosis managed surgically. Pathological examination of the resected stomach showed numerous non-caseating granulomas in the lamina propria. No definite aetiological factor could be detected. A diagnosis of idiopathic granulomatous gastritis was made. She remains well 5 years later and has not developed regional enteritis, sarcoidosis, or any other generalized diseases.
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PMID:Granulomatous gastritis presenting as gastric outlet obstruction: a case report. 978 39

In the late fall of 2004 more severe lesions of porcine circovirus-2 associated disease (PCVAD) than usual occurred during an outbreak of porcine circovirus-2 (PCV-2) infection in Ontario nursery and grower/finisher pigs. The lesions were of unprecedented severity and included diffuse bronchointerstitial pneumonia, granulomatous enteritis, vasculitis, interstitial nephritis, and new lesions of splenic infarction. Some affected herds had up to 50% mortality. The outbreak correlated with the sudden emergence of a variant PCV-2, with PCR restriction fragment length polymorphism (RFLP) type 321. Phylogenetic comparison of ORF2 sequences and full genome sequences showed the new variant to be different from the previously dominant RFLP type 422 viruses, and similar to viruses that had occurred in France and other European and Asian countries. A subsequent retrospective study showed a statistically significant increase in the frequency of histological lesions in lymph node, spleen, lung, small intestine, colon and kidney, for pigs spontaneously infected with RFLP type 321, compared with the older RFLP type 422 strain. Viral burden, based on IHC staining in lymph node, also showed a statistically significant increase in pigs infected with the newer variant RFLP type 321, compared with the older RFLP type 422 strain. This enhanced virulence in pigs infected with PCV-2 RFLP type 321 strain may be related to the genetic differences in this new strain of PCV-2. This virus is now the dominant strain of PCV-2 virus found in Ontario and Quebec swine.
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PMID:The emergence of a new strain of porcine circovirus-2 in Ontario and Quebec swine and its association with severe porcine circovirus associated disease--2004-2006. 1850 90

Prognosis in Crohn's disease (CD) and ulcerative colitis (UC) varies substantially between patients. Accordingly, no single treatment strategy will be suitable for everyone. 'Top-down' strategies inevitably overtreat patients destined to experience indolent disease (and risk unnecessary immunosuppression), whilst 'step-up' strategies expose patients with aggressive disease to avoidable disease-related morbidity. Accordingly, for personalised medicine to succeed in IBD, a reliable method of predicting prognosis is critical. In oncology, gene expression profiling enables reliable prediction of several aspects of tumour behaviour. Unfortunately, this technology has been less successful in other disease areas - often because heterogeneous cell populations are studied, producing gene signatures that simply reflect compositional differences in the starting material. This can be overcome by analysing purified cell populations. Previously, we discovered a prognostic gene expression signature in purified CD8+ T cells from patients with systemic lupus erythematosus and ANCA-associated vasculitis. We therefore investigated whether the same signature might exist in other relapsing-remitting diseases driven by immune responses to antigen, and detected an analogous signature in CD and UC. This signature was detectable from diagnosis, but did not correlate with contemporaneous clinical or biochemical data. A significant association with prognosis was detected in both UC and CD, with patients who were enriched for the signature (subgroup 'IBD1') experiencing a more aggressive disease course, characterised by frequent flares and a higher incidence of treatment failure. This suggests that gene expression profiling could stratify patients with CD or UC at diagnosis according to their future disease course, and represents a step towards personalised therapy.
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PMID:Predicting the course of IBD: light at the end of the tunnel? 2307 76