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Plasma homocysteine is not a major risk factor for vascular disease in growth hormone deficient adults
T A Abdu1, T A Elhadd, M Akber
1Department of Medicine, School of Postgraduate Medicine, Keele University, North Staffordshire Hospital NHS Trust, Stoke on Trent, UK.
Insights
Adult growth hormone deficiency (GHD) does not significantly increase plasma homocysteine levels, a known risk factor for atherosclerosis. Therefore, elevated homocysteine is unlikely to be a primary driver of vascular disease in GHD patients.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Adult growth hormone deficiency (GHD) is associated with increased vascular mortality.
- Plasma homocysteine is an established independent risk factor for atherosclerosis.
- The contribution of homocysteine to cardiovascular risk in adult GHD remains unclear.
Purpose of the Study:
- To investigate whether plasma homocysteine levels are elevated in adults with GHD.
- To determine if homocysteine contributes to the increased cardiovascular risk observed in GHD patients.
Main Methods:
- Plasma homocysteine was measured in 45 GHD adults and 55 matched controls using fluorescence polarization immunoassay.
- Subjects were assessed for cardiovascular risk factors, including blood pressure, BMI, and waist-hip ratio.
- Serum levels of vitamin B12 and folate, crucial for homocysteine metabolism, were also measured.
Main Results:
- No significant difference in plasma homocysteine levels was found between GHD patients and controls.
- Serum vitamin B12 levels were comparable between the groups.
- Serum folate levels were significantly lower in GHD patients, particularly in females.
Conclusions:
- Plasma homocysteine levels are not significantly elevated in adults with GHD.
- Elevated homocysteine is unlikely to be a major contributor to vascular disease risk in this population.
Objective:
Several cardiovascular risk factors have been investigated in patients with adult growth hormone deficiency (GHD) to explain the observed increase in vascular mortality. Plasma homocysteine concentration has been identified recently as an independent risk factor for atherosclerosis. We wished to determine whether plasma homocysteine contributes to cardiovascular risk in adult GHD.
Method:
Plasma homocysteine was measured by fluorescence polarization immunoassay in 45 GH-deficient adults on stable conventional hormone replacement (25M, 20F), age range 23-76 years, and compared with 55 matched controls (30M, 25F), age range 21-77 years. All subjects were free from clinical hypertension, diabetes, ischaemic heart disease and peripheral vascular disease. Blood pressure, body mass index and waist hip ratio were recorded. Serum creatinine and fasting lipids were measured. Serum vitamin B12 and folate levels, important cofactors in the homocysteine metabolic pathways, were also measured.
Results:
Homocysteine levels were not different in patients and controls (9.75 [7.8-11.6] micromol/l vs. 9.65 [8.3-11.5] micromol/l, respectively, P = 0.88). Serum vitamin B12 was also not different (320.5 [262.0-427.5] pmol/l vs. 313.5 [277.0-460.5] pmol/l, respectively, P = 0.77). Serum folate levels were significantly lower in the patient group (7.05 [5.12-8.27] ng/ml vs. 7.80 [6.52-10.60] ng/ml, respectively, P = 0.03). When separated by gender, in males folate was not significantly different between patients and controls 7.05 [5.17-9.19] vs. 7.65 [6.15-10.22], P = 0.264, whereas in females, folate was significantly lower in patients at 7.05 [4.57-7.75] compared to controls at 8.4 [6.60-12.20], P = 0.01.
Conclusion:
Plasma homocysteine levels are not significantly elevated in GH-deficient adults and are unlikely to be a major risk factor for vascular disease in these individuals.
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