Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 20-year-old man suffering from Crohn's disease developed coma and generalized seizures following ileocecal resection. During postoperative parenteral feeding he received xylitol in an unusually high concentration. CT examinations a few days before death showed intense hypodensity and swelling of brainstem and basal ganglia and increasing triventricular dilatation. Autopsy revealed, mainly in the brainstem and cerebellum, a destruction of intracerebral, intracerebellar and leptomeningeal vessel walls by birefringent crystals (probably calcium oxalate), an early inflammatory reaction and severe brain edema with final tonsillar herniation. The same crystalloid deposits were found in the kidneys.
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PMID:Reno-cerebral oxalosis induced by xylitol. 643 46

A patient with Crohn's disease and generalized seizures who lacked the distal small bowel and ascending colon required 600 mg of intravenous phenytoin daily (11 mg/kg/24 h) to maintain her plasma phenytoin levels in the 12-24 micrograms/ml range. She received no oral phenytoin. Stool volumes ranged from 1,125 to 1,875 ml/24 h, and stool fraction phenytoin levels from 15 to 41 micrograms/ml. Urinary 5-(p-hydroxyphenyl)-5-phenylhydantoin and phenytoin levels in three 24-h samples were sufficient to account for 26, 46, and 57% of the administered drug, compared with the expected 70-90%. This was most likely due to an alteration of the normal cycle of absorption and reexcretion between the intestinal lumen and the blood resulting in net excretion of phenytoin into the bowel.
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PMID:Enhanced gastrointestinal excretion of phenytoin in a patient with Crohn's disease. 672 91

We report on a 6-year-old boy with mosaic trisomy 9. The patient was born at 42 weeks of gestation to a 27-year-old G1 white woman. Birth weight was 2,820 g, length 52 cm, and Apgar scores were 4 and 6 at 1 and 5 min, respectively. The infant presented with apparently low-set ears, overfolded helices, epicanthal folds, prominent nasal bridge, high-arched palate, micrognathia, bilateral dislocated hips, left genu recurvatum, and cryptorchidism. Chromosome analysis showed an unusual karyotype: 47,XY,+inv(9qh+)/47,XY,+mar. The marker chromosome was thought to be a remnant of the inv(9qh+) chromosome. The mother's karyotype was 46,XX,inv(9qh+), while the father's was 46,XY. At age 5 months, the patient developed seizures and gastroesophageal reflux. Crohn disease was diagnosed at age 2 years, although symptoms began at age 1 year. Recurrent bouts of pneumonia have occurred since the patient's birth. Severe psychomotor retardation was also noted. Trisomy 9 syndrome was first reported in 1973. Over 30 cases have been reported since then. Of these cases reports, only 5 patients were older than 1 year. Inflammatory bowel disease has been reported in association with other chromosome abnormalities, but to our knowledge, has not been reported in trisomy 9 syndrome.
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PMID:Trisomy 9 syndrome: report of a case with Crohn disease and review of the literature. 777 85

Arterial thrombo-embolism is an unusual complication in inflammatory bowel disease in adults and children. Cerebral arterial disease has been reported on only a few occasions. There are only two previous case reports of arterial disease occurring in a child with Crohn disease. However in both instances the arterial disease was part of a generalised Takayasu arteritis which resulted in multi-organ involvement. This report describes a 14-year-old boy who developed seizures before a histological diagnosis of Crohn disease was made. These seizures were the result of a vascular lesion which was confined to the right middle cerebral artery. CONCLUSION. Crohn disease as well as ulcerative colitis should be considered as a possible cause of cerebrovascular accidents in children.
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PMID:Isolated cerebral thrombo-embolism and Crohn disease. 852 79

An increased incidence of cerebral thromboembolic events has been reported in young patients with inflammatory bowel disease (IBD). It has been suggested that a hypercoagulable state is associated with clinical activity of the disease, with elevation of factors V, VIII, fibrinogen and platelets and a lowering of anti-thrombin III. We present the case of a 35 y/o male with refractory Crohn's disease who complained of headaches, blurred vision and tonic-clonic seizures. The studies demonstrated an ischemic stroke of the left cerebral hemisphere, without vascular abnormalities. Elevation of factor VIII, platelets, and antithrombin III were found. The symptoms were relieved with medical treatment and the patient has continued in good health after resection of the diseased terminal ileum.
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PMID:Cerebral thrombosis associated with active Crohn's disease. 988 77

Despite limited understanding of therapeutic aetiopathogenesis of ulcerative colitis and Crohn's disease, there is a strong evidence base for the efficacy of pharmacological and biological therapies. It is equally important to recognise toxicity of the medical armamentarium for inflammatory bowel disease (IBD). Sulfasalazine consists of sulfapyridine linked to 5-aminosalicylic acid (5-ASA) via an azo bond. Common adverse effects related to sulfapyridine 'intolerance' include headache, nausea, anorexia, and malaise. Other allergic or toxic adverse effects include fever, rash, haemolytic anaemia, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible sperm abnormalities. The newer 5-ASA agents were developed to deliver the active ingredient of sulfasalazine while minimising adverse effects. Adverse effects are infrequent but may include nausea, dyspepsia and headache. Olsalazine may cause a secretory diarrhoea. Uncommon hypersensitivity reactions, including worsening of colitis, pancreatitis, pericarditis and nephritis, have also been reported. Corticosteroids are commonly prescribed for treatment of moderate to severe IBD. Despite short term efficacy, corticosteroids have numerous adverse effects that preclude their long term use. Adverse effects include acne, fluid retention, fat redistribution, hypertension, hyperglycaemia, psycho-neurological disturbances, cataracts, adrenal suppression, growth failure in children, and osteonecrosis. Newer corticosteroid preparations offer potential for targeted therapy and less corticosteroid-related adverse effects. Azathioprine and mercaptopurine are associated with pancreatitis in 3 to 15% of patients that resolves upon drug cessation. Bone marrow suppression is dose related and may be delayed. The adverse effects of methotrexate include nausea, leucopenia and, rarely, hypersensitivity pneumonia or hepatic fibrosis. Common adverse effects of cyclosporin include nephrotoxicity, hypertension, headache, gingival hyperplasia, hyperkalaemia, paresthesias, and tremors. These adverse effects usually abate with dose reduction or cessation of therapy. Seizures and opportunistic infections have also been reported. Antibacterials are commonly employed as primary therapy for Crohn's disease. Common adverse effects of metronidazole include nausea and a metallic taste. Peripheral neuropathy can occur with prolonged administration. Ciprofloxacin and other antibacterials may be beneficial in those intolerant to metronidazole. Newer immunosuppressive agents previously reserved for transplant recipients are under investigation for IBD. Tacrolimus has an adverse effect profile similar to cyclosporin, and may cause renal insufficiency. Mycophenolate mofetil, a purine synthesis inhibitor, has primarily gastrointestinal adverse effects. Biological agents targeting specific sites in the immunoinflammatory cascade are now available to treat IBD. Infliximab, a chimeric antibody targeting tumour necrosis factor-or has been well tolerated in clinical trials and early postmarketing experience. Additional trials are needed to assess long term adverse effects.
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PMID:Comparative tolerability of treatments for inflammatory bowel disease. 1108 48

We report the case of a girl with a severe perianal fistulizing Crohn's disease who during intravenous infusion of cyclosporine developed headache, general seizures and cortical blindness. Head magnetic resonance imaging showed spread, cortical-subcortical nonenhancing signal changes. Full neurological recovery was achieved in 24 hours. Cyclosporine was stopped and a single dose of infliximab was infused with rapid improvement of the fistula that at 7 months' follow-up is still closed.
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PMID:A girl with severe fistulizing Crohn's disease. 1121 60

Hypomagnesaemia as a primary cause of a generalized seizure is uncommon. A 60-year-old woman with Crohn's disease, who had had recent small bowel surgery and a total colectomy 10 years previously, was admitted complaining of severe nausea, vomiting, fatigue and thirst. Despite oral magnesium therapy she had a generalized seizure due to severe hypomagnesaemia of 0.09 mmol/l (normal range 0.65 to 1.05 mmol/l). Her serum calcium was 1.91 mmol/l (2.03 to 2.63 mmol/l). Hypomagnesaemia can cause generalized convulsions but is usually associated with hypocalcaemia. This patient had an almost normal serum calcium level, and therefore hypomagnesaemia would seem to have been the direct cause of her seizure. Long-term intravenous magnesium was necessary to prevent further seizures.
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PMID:Severe convulsant hypomagnesaemia and short bowel syndrome. 1143 1

A 13-yr-old boy with severe Crohn's disease was admitted with persistent hematochezia requiring transfusion. Cyclosporine A was begun on hospital day 22 because of continued diarrhea and rectal bleeding despite high doses of i.v. corticosteroids. Six days into cyclosporine therapy, the patient developed multiple episodes of generalized tonic-clonic seizures accompanied with magnetic resonance imaging findings typical, although not pathognomonic, of cyclosporine A central nervous system neurotoxicity. Further investigations demonstrated that severe cyclosporine neurotoxicity may occur in the absence of previously reported clinical risk factors. Experience from the pediatric and adult GI transplant and neurological literature is discussed.
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PMID:Cyclosporine-Induced neurotoxicity during treatment of Crohn's disease: lack of correlation with previously reported risk factors. 1156 12

Neurological manifestations of gastrointestinal disorders are described, with particular reference to those resembling multiple sclerosis (MS) on clinical or MRI grounds. Patients with celiac disease can present cerebellar ataxia, progressive myoclonic ataxia, myelopathy, or cerebral, brainstem and peripheral nerve involvement. Antigliadin antibodies can be found in subjects with neurological dysfunction of unknown cause, particularly in sporadic cerebellar ataxia ("gluten ataxia"). Patients with Whipple's disease can develop mental and psychiatric changes, supranuclear gaze palsy, upper motoneuron signs, hypothalamic dysfunction, cranial nerve abnormalities, seizures, ataxia, myorhythmia and sensory deficits. Neurological manifestations can complicate inflammatory bowel disease (e.g. ulcerative colitis and Crohn's disease) due to vascular or vasculitic mechanisms. Cases with both Crohn's disease and MS or cerebral vasculitis are described. Epilepsy, chronic inflammatory polyneuropathy, muscle involvement and myasthenia gravis are also reported. The central nervous system can be affected in patients with hepatitis C virus (HCV) infection because of vasculitis associated with HCV-related cryoglobulinemia. Mitochondrial neurogastrointestinal encephalopathy (MNGIE) is a disease caused by multiple deletions of mitochondrial DNA. It is characterized by peripheral neuropathy, ophthalmoplegia, deafness, leukoencephalopathy, and gastrointestinal symptoms due to visceral neuropathy. Neurological manifestations can be the consequence of vitamin B1, nicotinamide, vitamin B12, vitamin D, or vitamin E deficiency and from nutritional deficiency states following gastric surgery.
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PMID:Neurological manifestations of gastrointestinal disorders, with particular reference to the differential diagnosis of multiple sclerosis. 1179 74


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