1.
[Thromboembolic event and metabolic hyperhomocysteinemia: A case report and review of literature].
Biron, F, Rousseau, JF, Baulin, JM, Guérin-Boyer, M, Lanéelle, D
Annales de cardiologie et d'angeiologie. 2021;(3):177-182
Abstract
INTRODUCTION Venous thromboembolic diseases have an incidence of 1.57/1000. Among patients under 50 years old, thrombophilia is assessed, the indications for which are increasingly stringent. Today, the need of plasma homocysteine assay is uncertain. OBSERVATION Our case is a 42 year-old man, in whom a pulmonary embolism associated with macrocytosis made us discover a B12 deficiency secondary to Biermer's disease. In the literature, patients are men with an average age limit to the realisation of the assessment of thrombophilia. Not all of these patients had any causal other than hyperhomocysteinemia secondary to Biermer's disease. The support is not detailed. CONCLUSION Hyperhomocysteinemia is probably not the only thromboembolic factor. The patient received anticoagulation and vitamin B12 supplementation. A good reading of the complete blood count is essential.
2.
[Acute arterial thrombosis in a context of hyperhomocysteinemia: Case report and literature review].
Raybaud, G, Lambert, M, Douillard, C, Dessein, AF, Morell-Dubois, S, Guillou, M, Haulon, S, Hatron, PY
La Revue de medecine interne. 2016;(12):849-853
Abstract
INTRODUCTION Hyperhomocysteinemia is a biological marker that could be identified in the venous thrombotic events and rarely during acute arterial thrombotic events. The consequences can be serious. Effective diagnostic strategy is needed to optimize the management. CASE REPORT Following bariatric surgery, a 40-year-old patient was admitted with an acute encephalopathy associated with peripheral lower limb arterial ischemia. The diagnostic work-up identified a major hyperhomocysteinemia whose causes were several. Surgical treatment and anticoagulation was associated with vitamins and trace elements supplementation. Correcting deficiencies allowed delirium and hyperhomocysteinemia improvement. Once treatment established, the patient did not present a recurrent thrombotic episode. CONCLUSION Major hyperhomocysteinemia seems to be associated with an increased risk of acute arterial thrombosis. This marker might be considered in nutritional deficiency situations with appropriate support on the vascular, metabolic and nutrition level.
3.
Homocysteine and cognitive impairment; a case series in a General Practice setting.
McCaddon, A
Nutrition journal. 2006;:6
Abstract
BACKGROUND An elevated blood level of homocysteine is a risk factor for cognitive impairment and dementia. Homocysteine can be lowered by folate and/or vitamin B12 supplementation; antioxidants might also be required for optimal reduction in neurovascular tissue. This report presents clinical and radiological findings from administering the antioxidant N-acetylcysteine together with B vitamins to cognitively impaired patients with hyperhomocysteinaemia. METHODS A case series (n = 7) performed in a semi-rural General Practice setting. Formal cognitive assessments were performed in five patients, and radiological assessments in one patient, before and after supplementation. RESULTS AND DISCUSSION The addition of N-acetylcysteine resulted in subjective clinical improvement in all patients, and an objective improvement in cognitive scores in five patients. One patient had radiological evidence of halted disease progression over a twelve month period. CONCLUSION N-acetylcysteine, together with B vitamin supplements, improves cognitive status in hyperhomocysteinaemic patients. Randomized controlled clinical trials are required to formally evaluate this treatment approach.
4.
Venous thrombosis associated with pernicious anaemia. A report of two cases and review.
Barrios, M, Alliot, C
Hematology (Amsterdam, Netherlands). 2006;(2):135-8
Abstract
Since homocystinuria, an inborn metabolism error is complicated by venous thrombosis in about half of the patients, hyperhomocysteinemia has been suspected of favouring thrombosis. Several case-control studies and even meta-analysis have confirmed a link between venous thrombosis and mild hyperhomocysteinemia. Nevertheless, the proper role of homocysteine remains debated. Hyperhomocysteinemia is induced by vitamin B9 or B12 deficiencies in a vast majority of cases. The authors report on two patients with venous thrombosis revealing pernicious anemia and review nine similar cases found in the world literature. The literature concerning the relationships between homocysteine and venous thrombosis is briefly reviewed.