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Hyperhomocysteinaemia in black patients with cerebral thrombosis
R Delport1, J B Ubbink, W J Vermaak
1Department of Chemical Pathology, University of Pretoria, South Africa.
Insights
Elevated total homocysteine (tHcy) levels are linked to stroke risk in Black patients. However, this study suggests renal insufficiency, not just hyperhomocysteinemia, may contribute to stroke in this population.
Area of Science:
- Neurology
- Clinical Biochemistry
- Public Health
Background:
- Hyperhomocysteinemia is a known stroke risk factor.
- Its specific role in Black patient populations remains unclear.
- Cerebral thrombosis is a significant cause of stroke.
Purpose of the Study:
- To investigate the association between total homocysteine (tHcy) levels and stroke in Black patients.
- To explore the potential role of renal insufficiency in hyperhomocysteinemia among Black stroke patients.
Main Methods:
- Compared plasma tHcy concentrations in 24 Black patients with cerebral thrombosis to age- and sex-matched healthy controls.
- Assessed vitamin B12, B6, and folate status.
- Analyzed tHcy levels in relation to serum creatinine concentrations.
Main Results:
- Stroke patients exhibited significantly higher plasma tHcy levels than controls (p=0.031).
- This difference was not attributable to vitamin deficiencies.
- Stroke patients with hypercreatininemia showed significantly higher tHcy than controls (p=0.002).
- Stroke patients with normal creatinine did not differ significantly in tHcy from controls.
Conclusions:
- Hyperhomocysteinemia may be partly caused by renal insufficiency in Black stroke patients.
- While hyperhomocysteinemia might increase stroke risk, it may not be the primary initiating factor.
- Further research is needed to elucidate the complex interplay between homocysteine, renal function, and stroke in diverse populations.
Abstract:
Hyperhomocysteinemia is regarded as a risk factor for stroke but its pathogenetic role has not yet been established in Black patients. We studied 24 Black patients admitted with cerebral thrombosis, and compared them with age- and sex-matched apparently healthy controls from the same community. Total homocysteine (tHcy) (free homocysteine, protein-bound homocysteine, the disulfide homocystine and the mixed disulfide homocysteine-cysteine) concentration was 10.91 (4.95-23.05) mumol/l in the stroke patients and 8.73 (3.95-15.10) mumol/l in controls (p = 0.031). This difference could not be explained by differences in vitamin B12, vitamin B6 or folate status. A subgroup of nine stroke patients with hypercreatininaemia (> 90 mumol/l, 75% of control concentrations) had significantly higher plasma tHcy concentrations [median (range) 9.10 (5.40-15.10) mumol/l] compared with controls [8.65 (3.96-13.89) mumol/l] (p = 0.002). Plasma tHcy concentrations of stroke patients with normal serum creatinine concentrations were not significantly different to those of controls. Hyperhomocysteinemia in Black patients with stroke may be partially caused by renal insufficiency. Therefore, while hyperhomocysteinemia may increase the risk of stroke, it is unlikely to be a primary initiating factor.