FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2326147561> ?p ?o ?g. }

• W2326147561 endingPage "460" @default.
• W2326147561 startingPage "458" @default.
• W2326147561 abstract "Three years after Crohn's disease developed, a 13-year-old boy began having seizures. Cranial computed tomographic and magnetic resonance scans done at age 14.5 years showed a focal area of low density and atrophy in the left frontal lobe. We discuss the association between inflammatory bowel disease, cerebral thromboembolism, and epilepsy. The pathogenesis of thromboembolism in inflammatory bowel disease is also discussed, and other neurologic complications of inflammatory bowel disease are mentioned. CASE REPORT A boy was initially admitted to hospital at the age of 10 years with a 6-month history of abdominal pain, weight loss, intermittent vomiting, bloody diarrhoea, and anorexia. A barium contrast study showed generalized mucosal oedema of the upper and mid-ileum, with some segmentation and flocculation of barium. There were anterior and posterior fissures in the rectal mucosa detected by sigmoidoscopic examination, and histologic analysis of a biopsy specimen of the rectal mucosa showed active chronic inflammation with epithelioid granuloma in the lamina propria. The features were those of Crohn's disease. The patient was treated initially with an intermittent elemental diet for acute exacerbations of the disease. The patient had been born at 34 weeks' gestation, and apart from mild jaundice, there were no significant perinatal problems. His development had been normal, and there was no family history of epilepsy. His neurologic problems started at the age of 13, when he had his first episode of seizure with generalized tonicclonic convulsions. Findings in a physical examination that included a neurologic examination were normal. A subsequent electroencephalogram showed generalized paroxysmal bursts of bilateral synchronous spike and polyspike and wave activity. He had another episode of seizure, which was also generalized, at 14.5 years of age. This time, conjugate deviation of the eyes to the right was noted during the convulsion. A few days before this seizure, acute relapse of Crohn's disease had been diagnosed, and oral corticosteroids had been prescribed. An electroencephalogram showed paroxysmal high-voltage activity, most markedly on the left. Cranial computed tomographic scan showed a focal area of low density in the left frontal region with appearances suggesting atrophy or gliosis. A cranial magnetic resonance scan confirmed these findings. The lesions were thought to be of ischaemic origin and long-standing. The patient has recently had a further seizure, which also happened during an episode of acute Crohn's disease, and he has since been given carbamazepine. DISCUSSION Crohn's disease is an idiopathic inflammatory disorder that affects any part of the gastrointestinal tract from the mouth to the anus. There has been a significant increase in the incidence of Crohn's disease in children(1,2). Extraintestinal manifestations may be observed in 25% to 35% of patients(3) and effects may be observed in various organ systems(4,5). Neurologic complications are rare(6) and usually result from thromboembolic episodes(7). The incidence of neurovascular and thromboembolic complications in adult patients with inflammatory bowel disease ranges between 1.3% and 7% (8), but thombotic events in children occur less frequently (9,10). Findings in one prospective paediatric study (11) showed a 3.3% incidence of vascular complications in children with inflammatory bowel disease. The reported association of epilepsy and Crohn's disease(12) may be related to underlying cerebrovascular disease. General risk factors for thrombogenesis are known to be vessel wall injury, alterations in the coagulation system, and stasis (Virchow's triad). Microvascular injury is seen in Crohn's disease, and granulomatous vasculitis has been suggested to have a primary role in the pathogenesis of the disease(13,14). The cause of the vasculitis is unclear, but it may be autoimmune in origin (15). Circulating immune complexes associated with vasculitis have been described(16), and other evidence supporting an autoimmune process include the presence of such autoantibodies as antineutrophil cytoplasmic (17), antiphospholipid(18), anticardiolipin (19), and antiendothelial cell antibodies (20). Vasculitis has been described in various parts of the body. Nelson et al. have reported morphologically documented necrotizing cerebral vasculitis in a 19-year-old man with ulcerative colitis (21). Vasculitis associated with inflammatory bowel disease has also been seen in the skin(22), the calf muscles (23), and the retina (24). Increased platelet activation and aggregation have been reported in patients with inflammatory bowel disease (25), and this contributes not only to the multifocal microinfarction seen in the mesenteric vasculature (26) but also increases the risk of systemic thromboembolism. Disorders in the coagulation mechanism resulting in a hypercoagulable state have been described and may be responsible for thromboembolic episodes. Increased concentrations of factors V and VIII and depressed levels of antithrombin 3 have been demonstrated in Crohn's disease and in ulcerative colitis (27). In a recent study of the haemostatic systems of patients with inflammatory bowel disease, Chiarantini et al. reported results showing significant increases in the levels of platelet count, fibrinogen, prothrombin fragments F1 and 2 and decreased levels of factor XIII (18). Results in the same study also showed increased platelet aggregation in platelet-rich plasma. The serum concentration of immunoreactive von Willebrand's factor is also increased in Crohn's disease (28). The development of thrombosis is usually related to periods of active inflammation in most patients with Crohn's disease (29). Prolonged dehydration and immobilization secondary to active disease(30) could lead to venous stasis and could contribute to the development of thrombosis. Thromboembolic phenomena have been described in cerebral veins and arteries(31-33). Cerebrovascular disease associated with inflammatory bowel disease may exhibit symptoms of seizures(6,10,11,21,32), speech difficulties (10,32), episodes of confusion(10), hemiparesis (6,10), or coma (10,11). Other neurologic complications of Crohn's disease include polyneuropathy(34), myopathy secondary to granulomatous myositis(35), myasthenia gravis (36), and myelopathy (6). A familial association of multiple sclerosis and Crohn's disease has been reported (37) and an association between multiple sclerosis and ulcerative colitis was reported in 1982 (38). The familial concurrence of multiple sclerosis and inflammatory bowel disease may represent either shared genetic causes or common environmental risk factors. Our patient had no neurodevelopmental problems before Crohn's disease was diagnosed. We postulate that his epilepsy is a reflection of his underlying cerebrovascular disease, which in turn is associated with his Crohn's disease. This provides additional support to the evolving concept that paediatric inflammatory bowel disease, like its adult counterpart, may be accompanied by cerebral thromboembolic events. Paediatricians who treat children and adolescents with inflammatory bowel disease should be aware of this rare but serious complication. Cerebrovascular disease should be considered in any child with inflammatory bowel disease who has seizures, headache, episodes of confusion, coma, or other neurologic signs or symptoms. Screening for cardiovascular risk factors and hypercoagulability might be indicated in patients with active Crohn's disease to prevent major neurovascular complications." @default.
• W2326147561 created "2016-06-24" @default.
• W2326147561 creator A5032527327 @default.
• W2326147561 creator A5037179842 @default.
• W2326147561 creator A5076494290 @default.
• W2326147561 date "1998-04-01" @default.
• W2326147561 modified "2023-09-23" @default.
• W2326147561 title "Epilepsy and Crohn's Disease in Children" @default.
• W2326147561 cites W1559985172 @default.
• W2326147561 cites W166805679 @default.
• W2326147561 cites W1801157143 @default.
• W2326147561 cites W1964749627 @default.
• W2326147561 cites W1969545370 @default.
• W2326147561 cites W1973383592 @default.
• W2326147561 cites W1979147258 @default.
• W2326147561 cites W1988173708 @default.
• W2326147561 cites W1990991302 @default.
• W2326147561 cites W2013636491 @default.
• W2326147561 cites W2017082559 @default.
• W2326147561 cites W2021754696 @default.
• W2326147561 cites W2033813776 @default.
• W2326147561 cites W2046615856 @default.
• W2326147561 cites W2052784269 @default.
• W2326147561 cites W2057806187 @default.
• W2326147561 cites W2059341107 @default.
• W2326147561 cites W2060589228 @default.
• W2326147561 cites W2073522094 @default.
• W2326147561 cites W2100176961 @default.
• W2326147561 cites W2109900681 @default.
• W2326147561 cites W2122491999 @default.
• W2326147561 cites W2126831079 @default.
• W2326147561 cites W2141046689 @default.
• W2326147561 cites W2158211903 @default.
• W2326147561 cites W2428363881 @default.
• W2326147561 cites W4238069173 @default.
• W2326147561 cites W4251167677 @default.
• W2326147561 doi "https://doi.org/10.1097/00005176-199804000-00018" @default.
• W2326147561 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9552145" @default.
• W2326147561 hasPublicationYear "1998" @default.
• W2326147561 type Work @default.
• W2326147561 sameAs 2326147561 @default.
• W2326147561 citedByCount "14" @default.
• W2326147561 countsByYear W23261475612013 @default.
• W2326147561 countsByYear W23261475612014 @default.
• W2326147561 countsByYear W23261475612016 @default.
• W2326147561 crossrefType "journal-article" @default.
• W2326147561 hasAuthorship W2326147561A5032527327 @default.
• W2326147561 hasAuthorship W2326147561A5037179842 @default.
• W2326147561 hasAuthorship W2326147561A5076494290 @default.
• W2326147561 hasBestOaLocation W23261475611 @default.
• W2326147561 hasConcept C118552586 @default.
• W2326147561 hasConcept C126322002 @default.
• W2326147561 hasConcept C177713679 @default.
• W2326147561 hasConcept C187212893 @default.
• W2326147561 hasConcept C2778186239 @default.
• W2326147561 hasConcept C2779134260 @default.
• W2326147561 hasConcept C2779280984 @default.
• W2326147561 hasConcept C2992200296 @default.
• W2326147561 hasConcept C71924100 @default.
• W2326147561 hasConceptScore W2326147561C118552586 @default.
• W2326147561 hasConceptScore W2326147561C126322002 @default.
• W2326147561 hasConceptScore W2326147561C177713679 @default.
• W2326147561 hasConceptScore W2326147561C187212893 @default.
• W2326147561 hasConceptScore W2326147561C2778186239 @default.
• W2326147561 hasConceptScore W2326147561C2779134260 @default.
• W2326147561 hasConceptScore W2326147561C2779280984 @default.
• W2326147561 hasConceptScore W2326147561C2992200296 @default.
• W2326147561 hasConceptScore W2326147561C71924100 @default.
• W2326147561 hasIssue "4" @default.
• W2326147561 hasLocation W23261475611 @default.
• W2326147561 hasLocation W23261475612 @default.
• W2326147561 hasLocation W23261475613 @default.
• W2326147561 hasOpenAccess W2326147561 @default.
• W2326147561 hasPrimaryLocation W23261475611 @default.
• W2326147561 hasRelatedWork W1568450052 @default.
• W2326147561 hasRelatedWork W1971326018 @default.
• W2326147561 hasRelatedWork W1982563674 @default.
• W2326147561 hasRelatedWork W1983516269 @default.
• W2326147561 hasRelatedWork W2085446880 @default.
• W2326147561 hasRelatedWork W2167194258 @default.
• W2326147561 hasRelatedWork W2383988748 @default.
• W2326147561 hasRelatedWork W2388384059 @default.
• W2326147561 hasRelatedWork W2426214947 @default.
• W2326147561 hasRelatedWork W2460082029 @default.
• W2326147561 hasVolume "26" @default.
• W2326147561 isParatext "false" @default.
• W2326147561 isRetracted "false" @default.
• W2326147561 magId "2326147561" @default.
• W2326147561 workType "article" @default.