Secondary Hyperparathyroidism and Hypovitaminosis D in African-Americans with Decompensated Heart Failure

• Published in: The American journal of the medical sciences 2006-09, Vol.332 (3), p.112-118
• Main Authors: Laguardia, Stephen P., Dockery, Brian K., Nelson, Maeda D., Weber, Karl T., Bhattacharya, Syamal K., Carbone, Laura D.
• Format: Article
• Language: English
• Subjects: Adult; African Americans; Aged; Biological and medical sciences; Calcium - metabolism; Congestive heart failure; Endocrinopathies; Female; General aspects; Heart Failure - complications; Humans; Hyperparathyroidism - etiology; Ionized hypocalcemia; Ionized hypomagnesemia; Magnesium - metabolism; Male; Medical sciences; Middle Aged; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Parathyroid hormone; Parathyroid Hormone - blood; Parathyroids. Parafollicular cells. Cholecalciferol. Phosphocalcic homeostasis (diseases); Vitamin D; Vitamin D - analogs & derivatives; Vitamin D - blood; Vitamin D Deficiency - etiology
• ISSN: 0002-9629; 1538-2990
• DOI: 10.1097/00000441-200609000-00003

We previously noted secondary hyperparathyroidism (SHPT) in African-American patients hospitalized during February, 2005 with either untreated or treated congestive heart failure (CHF) due to ischemic or idiopathic cardiomyopathy. Herein, we hypothesized that housebound African-American patients hospitalized during the period of June 1 through August 31, 2005, with CHF would have SHPT and hypovitaminosis D. Twenty-five African-American patients with an ejection fraction (EF) less than 35% due to ischemic or dilated (idiopathic) cardiomyopathy were monitored: 20 were hospitalized with CHF, stratified on historical grounds as of 4 weeks’ or longer duration or of 1 to 2 weeks’ duration in 11 and 9 patients, respectively, despite medical care that included furosemide; serum parathyroid hormone (PTH) and 25(OH)D at the time of admission in these patients were compared to five asymptomatic outpatients seen during the summer with stable, compensated failure. Serum PTH was elevated (127 ± 13; 82–243 pg/mL) in all patients with CHF of 4 weeks’ or longer duration (normal, 12–65 pg/mL) and was elevated in three of nine patients (59 ± 8; 18–99 pg/mL) with CHF of 1 to 2 weeks’ duration. Ionized hypocalcemia (1.09 ± 0.03 and 1.08 ± 0.02mmol/L; normal, 1.12–1.30) and hypomagnesemia (0.47 ± 0.02 and 0.46 ± 0.03mmol/L; normal, 0.53–0.67) were respectively found in long- or short-duration CHF. No compensated patient had elevated PTH (42 ± 5; 17–53). Hypovitaminosis D (≤30ng/mL) was universally present in patients with CHF of 4 weeks’ or longer duration (15.1 ± 1.4; 7.0–23.8ng/mL) and was also prevalent in the other groups (20.3 ± 5.1, 7.0–54.1ng/mL in CHF of 1 to 2 weeks’ duration and 23.1 ± 4.9; 17.2–42.7ng/mL in compensated failure). In African-American patients with CHF, hypovitaminosis D, aldosteronism, and loop diuretic treatment each exaggerate Ca2+ and Mg2+ losses to stress a fragile Ca2+ balance leading to ionized hypocalcemia and hypomagnesemia with SHPT.