Hyperhomocysteinemia and low folate levels as the only risk factors in pseudo-Foster Kennedy syndrome

Rahhal-Ortuño, Miriam; Fernández-Santodomingo, A.S.; Marín-Payá, Emma; Aguilar-González, Marina; Villena-Alvarado, C K; Ramos-González, L

doi:10.1016/j.jfo.2020.09.014

Cited by 2 publications

(2 citation statements)

References 8 publications

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“…El síndrome de Foster-Kennedy (FKS) como conjunto signos y síntomas, tiene como síntoma cardinal la pérdida progresiva de la agudeza visual unilateral, generada por la atrofia secundaria a la compresión directa del nervio óptico, causados por una masa compresiva en la fosa anterior y asociado a papiledema contralateral secundario al aumento de la presión intracraneana (1). Adicionalmente, los pacientes pueden manifestar cefalea en 84% la cual puede ser de características migrañosas (52%) o tensionales (22%); así como tinnitus (52%) o anosmia (2)(3)(4)(5). En el caso que se describe, el paciente inicialmente se presenta con afectación visual crónica en ojo izquierdo y un deterioro agudo en campos visuales de ojo derecho.…”

Section: Discussionunclassified

Pseudo Foster-Kennedy: Reporte de un caso.

Aristizabal Colorado,

Marín Hoyos,

Moreno

et al. 2023

Acta Med Col

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El síndrome de Foster Kennedy es una entidad caracterizada por una pérdida monocular de la visión generada por un tumor que genera presión directa sobre el nervio óptico, posterior a esto producto de la hipertensión endocraneana el nervio óptico contralateral se ve afectado, presentando pérdida visual progresiva. En el caso que discutiremos a continuación presentamos un caso de pérdida visual con atrofia del nervio óptico secundaria a hipertensión endocraneana idiopática, el cual posteriormente comienza con deterioro progresivo monocular contra lateral simulando un foster kennedy. El paciente finalmente requirió derivación ventrículo peritoneal por alto riesgo de pérdida visual total.

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Section: Discussionunclassified

Pseudo Foster-Kennedy: Reporte de un caso.

Aristizabal Colorado,

Marín Hoyos,

Moreno

et al. 2023

Acta Med Col

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“…У плазмі крові до 40% фолатів зв'язуються з білками-носіями: альбуміном і трансферином. У клітинах організму фолієва кислота за допомогою NADPH-H+залежних ферментів відновлюється у активну форму -5-метилтетрагідрофолієву кислоту [11,12].…”

Section: результати дослідженьunclassified

Homocysteine as a Biomarker of Vascular Pathology

Vynogradova¹,

Minko²,

Slaba³

et al. 2023

Ukr. ž. med. bìol. sportu

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The purpose of the study was to analyze professional literature sources devoted to the influence of homocysteine on the development of vascular disorders. The role of homocysteine as a biomarker of vascular pathology is considered. Materials and methods. Bibliosemantic and analytical methods were used in the study. The analysis of the specialized literature (47 sources) was carried out using information in the scientific-metric databases MEDLINE/PubMed, Scopus and Google Scholar. Results and discussion. Homocysteinemia is a pathological condition associated with quite serious consequences for the body; the endothelium of vessels suffers mostly: systemic endothelial dysfunction develops (including disruption of the synthesis and exchange of the endothelium-relaxing factor – nitric oxide), oxidative stress, activation of platelet aggregation, hypercoagulation occurs (due to a decrease in the activity of heparin, thrombomodulin and an increase in the activity of thromboxane A2). The prevalence of hyperhomocysteinemia in Ukraine is quite high and reaches 10% among healthy adults, 2% among young people and adolescents, from 13% to 43% in patients with cardiovascular pathology. The C677T polymorphism of the methylenetetrahydrofolate reductase gene is widespread among the population of Ukraine (40.7%). Researchers believe that hyperhomocysteinemia is an independent and modifiable risk factor for vascular pathology. Conclusion. Homocysteine is recognized as one of the markers of vascular pathology. Scientists consider the activation of oxidative stress, damage to the endothelium, stimulation of the proliferation of smooth muscle cells, and pro-inflammatory effects to be the main mechanisms of vascular damage in hyperhomocysteinemia. The described pathological changes are accompanied by a violation of the regulation of vascular tone, mostly due to a decrease in the synthesis of nitric oxide. Unbalanced synthesis of nitric oxide causes and potentiates oxidative stress, the processes of atherothrombogenesis. The professional literature presents enough scientific data that convincingly prove the role of homocysteine in the development of cardiovascular and neurological pathology. However, there is a small number of studies devoted to the relationship between hyperhomocysteinemia and periodontal diseases, and the pathogenetic mechanisms of the influence of hyperhomocysteinemia on the development of vascular disorders in coronavirus disease are not fully disclosed

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Hyperhomocysteinemia and low folate levels as the only risk factors in pseudo-Foster Kennedy syndrome

Cited by 2 publications

References 8 publications

Pseudo Foster-Kennedy: Reporte de un caso.

Pseudo Foster-Kennedy: Reporte de un caso.

Homocysteine as a Biomarker of Vascular Pathology

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