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High homocysteine is associated with idiopathic normal pressure hydrocephalus in deep perforating arteriopathy: a
Shisheng Ye1, Kaiyan Feng1, Yizhong Li2
1Department of Neurology, Maoming People's Hospital, Maoming, China.
Insights
High homocysteine levels are linked to idiopathic normal pressure hydrocephalus (iNPH) in patients with deep perforating arteriopathy (DPA). This finding suggests homocysteine may play a role in iNPH development within this patient group.
Area of Science:
- Neurology
- Vascular Biology
- Biochemistry
Background:
- Idiopathic normal pressure hydrocephalus (iNPH) pathogenesis is not fully understood.
- Homocysteine may impair cerebral blood vessels and the blood-brain barrier (BBB), potentially contributing to iNPH.
- Deep perforating arteriopathy (DPA) and iNPH share risk factors, indicating a potential link.
Purpose of the Study:
- To investigate the association between serum homocysteine levels and iNPH in patients diagnosed with DPA.
- To explore homocysteine as a potential biomarker or contributing factor in DPA-related iNPH.
Main Methods:
- A cohort study comparing DPA patients with and without iNPH (41 vs. 49 patients).
- Collection of demographic data, vascular risk factors, laboratory results, and neuroimaging.
- Multivariable logistic regression analysis to assess the relationship between homocysteine and iNPH.
Main Results:
- Patients with iNPH exhibited significantly higher serum homocysteine levels compared to those without iNPH (16.34 vs. 14.28 mmol/L, P=0.002).
- Higher homocysteine tertiles were associated with an increased likelihood of iNPH (OR=4.929, P=0.005).
- This association remained significant after adjusting for confounders like age, hypertension, and diabetes.
Conclusions:
- Elevated serum homocysteine is independently associated with iNPH in DPA patients.
- Further research is warranted to elucidate the precise role and predictive value of homocysteine in iNPH pathogenesis.
Background And Objective:
The pathogenesis and pathophysiology of idiopathic normal pressure hydrocephalus (iNPH) remain unclear. Homocysteine may reduce the compliance of intracranial arteries and damage the endothelial function of the blood-brain barrier (BBB), which may be the underlying mechanism of iNPH. The overlap cases between deep perforating arteriopathy (DPA) and iNPH were not rare for the shared risk factors. We aimed to investigate the relationship between serum homocysteine and iNPH in DPA.
Methods:
A total of 41 DPA patients with iNPH and 49 DPA patients without iNPH were included. Demographic characteristics, vascular risk factors, laboratory results, and neuroimaging data were collected. Multivariable logistic regression analysis was performed to investigate the relationship between serum homocysteine and iNPH in DPA patients.
Results:
Patients with iNPH had significantly higher homocysteine levels than those without iNPH (median, 16.34 mmol/L versus 14.28 mmol/L; P = 0.002). There was no significant difference in CSVD burden scores between patients with iNPH and patients without iNPH. Univariate logistic regression analysis demonstrated that patients with homocysteine levels in the Tertile3 were more likely to have iNPH than those in the Tertile1 (OR, 4.929; 95% CI, 1.612-15.071; P = 0.005). The association remained significant after multivariable adjustment for potential confounders, including age, male, hypertension, diabetes mellitus, atherosclerotic cardiovascular disease (ASCVD) or hypercholesterolemia, and eGFR level.
Conclusion:
Our study indicated that high serum homocysteine levels were independently associated with iNPH in DPA. However, further research is needed to determine the predictive value of homocysteine and to confirm the underlying mechanism between homocysteine and iNPH.
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