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Hyperphosphatemia is associated with cardiac valve calcification in chronic hypoparathyroidism
S Polonine1, R G de Santa Rosa2, M L F Farias3
1Division of Endocrinology, Clementino Fraga Filho Hospital, UFRJ, Avenida Professor Rodolpho Paulo Rocco 255, Rio de Janeiro, RJ, 21941-913, Brazil. simonepolonine@gmail.com.
Insights
In patients with chronic hypoparathyroidism (HPP), elevated serum phosphorus levels were linked to cardiac valve calcification (CVC). Further research is needed to determine if managing hyperphosphatemia can lower cardiovascular risk in this population.
Area of Science:
- Endocrinology
- Cardiology
- Metabolic Disorders
Background:
- Chronic hypoparathyroidism (HPP) is associated with metabolic disturbances.
- Cardiovascular disease is a significant concern in patients with HPP.
- Understanding metabolic links to cardiovascular risk factors is crucial for managing HPP patients.
Purpose of the Study:
- To investigate the relationship between metabolic abnormalities and cardiovascular risk factors in individuals with chronic HPP.
- To identify specific metabolic factors contributing to cardiovascular complications in HPP.
Main Methods:
- 37 adult patients with HPP, normal kidney function, and no prior coronary artery disease were enrolled.
- Measurements included serum calcium, phosphorus, glucose, lipids, PTH, 25(OH)D, and FGF23.
- Cardiovascular risk was assessed using the ESC calculator, echocardiography, and carotid ultrasound to evaluate carotid plaques (CP), intima-media thickness (IMT), cardiac valve calcification (CVC), and left ventricular hypertrophy (LVH).
Main Results:
- The prevalence of CP, CVC, and LVH was 24.3%, 24.3%, and 13.5%, respectively. IMT remained within normal limits.
- Fibroblast growth factor 23 (FGF23) did not correlate with CP, IMT, CVC, or LVH.
- Elevated serum phosphorus was significantly associated with CVC in both univariate and multivariate analyses (OR 3.572; p=0.035). A phosphorus level >5.05 mg/dL was the optimal cutoff for predicting CVC.
Conclusions:
- Hyperphosphatemia is a significant metabolic abnormality associated with cardiac valve calcification in patients with chronic hypoparathyroidism.
- These findings suggest that phosphorus control may be a target for reducing cardiovascular risk in HPP.
- Further studies are warranted to confirm the impact of hyperphosphatemia management on cardiovascular outcomes in HPP patients.
Purpose:
To evaluate the association between metabolic abnormalities and cardiovascular risk factors in patients with chronic hypoparathyroidism (HPP).
Patients And Methods:
Patients 18 years and older, glomerular filtration > 30 mL/min/1.73 m2 and no documented coronary artery disease were selected. Serum calcium, phosphorus, glucose, lipids, PTH, 25(OH)D and FGF23 were measured. Cardiovascular risk was estimated by the European Society of Cardiology (ESC) calculator. Transthoracic echocardiogram and carotid ultrasound were performed to detect carotid plaques (CP), carotid intima-media thickness (IMT), cardiac valve calcification (CVC), and left ventricular hypertrophy (LVH).
Results:
Thirty-seven patients (94.6% female), aged 56.0 ± 13.5 years and HPP duration 7.0 (4.0; 11.3) years, were included. Fifteen were classified as low cardiovascular risk, 9 as intermediate risk, 9 as high risk and none as very high risk. The prevalence of CP, CVC and LVH was 24.3%, 24.3% and 13.5%, respectively. IMT values were within normal ranges in all cohort. FGF23 were not associated with CP, IMT, CVC or LVH. After logistic regression, phosphorus was the only significant metabolic variable impacting CVC in univariate analysis (OR 2.795; 95% CI 1.132-6.905; p = 0.026), as well as in the multivariate analysis (OR 3.572; 95% CI 1.094-11.665; p = 0.035). Analysis by ROC curve showed serum phosphorus > 5.05 mg/dL (AUC 0.748; CI 0.584-0.877; p = 0.05) as the best cutoff point associated with valve heart calcification (sensitivity 78%; negative predictive value 91.3%).
Conclusion:
Hyperphosphatemia was associated with CVC in HPP patients. Further studies are needed to investigate whether the control of hyperphosphatemia may reduce cardiovascular risk in this population.
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