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1.
Sci Rep ; 12(1): 18668, 2022 11 04.
Artigo em Inglês | MEDLINE | ID: mdl-36333367

RESUMO

In general, IBD increases arteriovenous thromboembolic events, though the association between UC and cerebrovascular complications remains inconclusive. Some studies suggest young women with UC have an increased risk of cerebrovascular accidents (CVA). The focus of this study was to characterize the rates, anatomic distribution, and risk factors for CVA in patients with UC. We developed a retrospective cohort of patients with UC at a single health care system from June 2010 to June 2015. Neuroimaging was used to document presence, location and type of stroke and traditional risk factors were considered. Prevalence of CVAs in patients with UC was compared to that of the general population of Minnesota (MN) and the United States (U.S.). A total of 2,183 UC patients were identified (1088 females [f-UC], 1095 males [m-UC]). The prevalence of CVA in UC patients (4.7%, 95% CI 3.9-5.6) was higher than in the U.S. (2.5-2.7%, p < 0.0001) and in Minnesota (1.8% CI 1.5-2.2, p < 0.0001) . The prevalence increased in both sexes with a peak prevalence of 24.7% (95% CI 17.1-34.4) in women with UC over the age of 80. Older age, cancer and atrial fibrillation were risk factors for CVA in univariate analysis for both sexes. In multifactorial analysis, both age and atrial fibrillation were risk factors for CVA in the m-UC cohort, but only age was associated with CVA in f-UC. The most common type of CVA was ischemic stroke (77.7%). The most common locations for CVAs in UC patients were frontal and occipital lobes (19% and 18%, respectively). UC patients have an increased risk for CVA, with women over 80 demonstrating the highest risk. Providers should be aware of these risks in making treatment decisions for UC.


Assuntos
Fibrilação Atrial , Colite Ulcerativa , Acidente Vascular Cerebral , Masculino , Humanos , Feminino , Estados Unidos/epidemiologia , Fibrilação Atrial/complicações , Colite Ulcerativa/complicações , Colite Ulcerativa/epidemiologia , Estudos Retrospectivos , Prevalência , Acidente Vascular Cerebral/epidemiologia , Acidente Vascular Cerebral/etiologia , Fatores de Risco
2.
Med Hypotheses ; 107: 78-80, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28915969

RESUMO

Among 700,000 new and recurrent ischemic stroke patients per year, forty percent are hyperglycemic on admission. In-vitro, hyperglycemia is toxic to neurons. Acute ischemic stroke patients who are hyperglycemic on admission experience higher morbidity and mortality. Results of multiple trials have provided no evidence supporting benefit in achieving normoglycemia. On the contrary, there is some evidence that tight glycemic control in acute brain injury is associated with poor outcome. Current consensus derived guidelines from the American Heart Association/American Stroke Association recommend an upper limit of blood glucose of 140-180mg/dl, as there is no evidence to support strict control. The lack of improved outcomes with normoglycemia in this population dictates reconsideration of assumptions regarding the underlying pathophysiology of hyperglycemia. Review of the current data suggests there are two distinct pathophysiologic entities of hyperglycemia in acute ischemic stroke patients: diabetic and non-diabetic. We propose that the lack of positive results from well-designed intention-to-treat trials in hyperglycemic acute ischemic stroke patients could be attributed to treating these distinct groups as one.


Assuntos
Hiperglicemia/complicações , Acidente Vascular Cerebral/complicações , Animais , Glicemia/metabolismo , Complicações do Diabetes/sangue , Complicações do Diabetes/terapia , Humanos , Hiperglicemia/sangue , Hiperglicemia/terapia , Insulina/sangue , Modelos Biológicos , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/terapia
3.
Intern Med ; 54(11): 1433-6, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26028002

RESUMO

Cerebral toxoplasmosis is a rare disease predominantly found in immunocompromised hosts. However, cerebral toxoplasmosis has not been frequently described in association with the use of immunosuppressive medications. We herein report a case of cerebral toxoplasmosis in a 76-year-old Caucasian woman on methotrexate and infliximab for rheumatoid arthritis. The patient presented with right facial droop, slurred speech and difficulty walking. In addition to receiving methotrexate and infliximab and owning a cat, she had no other obvious risk factors. Imaging studies were not conclusive; however, brain biopsy confirmed the diagnosis. Serology was positive for anti-toxoplasma immunoglobulin G. Cerebral toxoplasmosis should be included in the differential diagnosis of patients under immunosuppressive medication who present with neurological manifestations.


Assuntos
Artrite Reumatoide/tratamento farmacológico , Hospedeiro Imunocomprometido , Imunossupressores/uso terapêutico , Infliximab/uso terapêutico , Metotrexato/uso terapêutico , Toxoplasmose Cerebral/diagnóstico , Idoso , Animais , Gatos , Diagnóstico Diferencial , Feminino , Humanos , Imunossupressores/efeitos adversos , Infliximab/efeitos adversos , Metotrexato/efeitos adversos , Toxoplasmose Cerebral/imunologia , Toxoplasmose Cerebral/patologia
4.
Neurocrit Care ; 20(1): 106-10, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24002892

RESUMO

BACKGROUND: Macroglossia has been reported in patients undergoing posterior fossa neurosurgical procedures and is thought to be as a result of venous engorgement from intubation or mechanical positioning during these prolonged procedures. METHODS: We report three patients who developed macroglossia and dysautonomia of central neurogenic origin following brainstem injury. RESULTS: The three patients developed macroglossia and dysautonomia with wide hemodynamic fluctuations in the setting of posterior fossa injury of the lower brainstem structures, necessitating tracheostomy placement. Macroglossia was managed with dexamethasone and there was complete resolution of dysautonomia while treated with beta-blockers and gabapentin. CONCLUSIONS: Neurointensivists should be aware of macroglossia with dysautonomia complicating brainstem injury, which may have perilous consequences in the setting of cerebral edema or intracranial hypertension.


Assuntos
Lesões Encefálicas/complicações , Tronco Encefálico/lesões , Macroglossia/etiologia , Adolescente , Antagonistas Adrenérgicos beta/uso terapêutico , Idoso , Aminas/uso terapêutico , Anti-Inflamatórios/uso terapêutico , Lesões Encefálicas/etiologia , Bloqueadores dos Canais de Cálcio/uso terapêutico , Fossa Craniana Posterior/lesões , Ácidos Cicloexanocarboxílicos/uso terapêutico , Dexametasona/uso terapêutico , Feminino , Gabapentina , Humanos , Macroglossia/tratamento farmacológico , Macroglossia/cirurgia , Masculino , Pessoa de Meia-Idade , Disautonomias Primárias/tratamento farmacológico , Disautonomias Primárias/etiologia , Traqueostomia/métodos , Resultado do Tratamento , Ácido gama-Aminobutírico/uso terapêutico
5.
J Vasc Interv Neurol ; 7(5): 82-5, 2014 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25566347

RESUMO

BACKGROUND: Pompe's disease is a glycogen storage disease that manifests as progressive neuropathy, and myopathy. There are a few reports of vasculopathy in this disease, thought to be from small- and medium-vessel arteriopathy. We present a case of late-onset Pompe's disease with microhemorrhages and review of the pertinent literature. METHODS: We describe a case of microhemorrhages in a patient with known late-onset Pompe's disease. RESULTS: Our patient was noted to have numerous microhemorrhages concentrated in the posterior circulation distribution in what can best be described as central microhemorrhages, distinct from the pattern seen in amyloid angiopathy. Previous autopsy studies have found vacuoles in the vessel wall, resulting in small aneurysms as a part of the Pompe syndrome. CONCLUSIONS: There is an accumulating body of evidence that suggests cerebral vasculopathy as one of the primary manifestations of adult-onset Pompe's disease. This is manifested as dolichoectasia of basilar artery, aneurysms, and microhemorrhages that are central in distribution. The primary pathology is thought to be glycogen deposition in small- and medium-sized intracranial vessels. Controlling blood pressure aggressively and screening intracranial vascular imaging are recommended. Further definition of the syndrome is continuing from phenotypic and genotypic dimensions.

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