256 HYPERPARATHYROIDISM AND HYPOVITAMINOSIS D IN AFRICAN AMERICANS WITH HEART FAILURE. (1st January 2006)

• Record Type: Journal Article
• Authors: LaGuardia, S. P.; Dockery, B. K.; Bhattacharya, S. K.; Nelson, M. D.; Carbone, L. D.; Weber, K. T.
• Is Part Of: Journal of investigative medicine. Volume 54:Number 1(2006)
• Page Start: S302
• Page End: S302
• Publication Date: 2006-01-01
• Subjects: Clinical medicine -- Periodicals; Medicine -- Research -- Periodicals; Medicine; Research -- United States; Clinical medicine; Medicine -- Research; Periodicals; 616.075
• DOI: 10.2310/6650.2005.X0008.255
• Languages: English
• ISSNs: 1081-5589

Abstract

Abstract : Purpose: Congestive heart failure (CHF), with aldosteronism, includes a systemic illness. Our working hypothesis of this illness invokes secondary hyperparathyroidism (SHPT) induced by exaggerated urinary and fecal losses of Ca 2+ and Mg 2+ and their fallen plasma-ionized levels that accompany aldosteronism and furosemide treatment. We previously found serum parathyroid hormone (PTH) levels to be elevated in predominantly African American (AA) patients hospitalized during the winter (February 2005) because of their symptomatic CHF. However, we did not discount hypovitaminosis D. Melanin is a natural sunscreen. Herein we hypothesized that housebound AA, who were hospitalized during June 1-August 31, 2005 with chronic, treated CHF, would have SHPT and hypovitaminosis D. Methods: Twenty-five AA (50.6 6 2.3 years; 9 women) with systolic dysfunction (EF < 35%) due to ischemic or dilated cardiomyopathy were monitored: 20 were hospitalized with signs and symptoms of CHF, stratified on historical grounds as protracted CHF ($ 4 wk) in 11 or of short duration (1-2 wk) in 9. Patients with CHF had been treated with an ACE inhibitor or AT1 receptor antagonist, furosemide, and in many cases spironolactone. Serum PTH and 25(OH)D, obtained in these 20 patients within 48 hours of admission, were compared to 5 asymptomatic outpatients with stable, compensated failure seen during this time period and who were similarly treated. Results: Serum PTH in the 11 AA with protracted decompensated failure (127 6 13; 82-243 pg/mL) was greater than the normal range (12-65 pg/mL); it was elevated in 3 of 9 with short-term CHF (59 6 8; 18-99 pg/mL). In both groups with CHF, ionized hypocalcemia (1.09 6 0.03 and 1.08 6 0.02 mmol/L; normal 1.12-1.30) and ionized hypomagnesemia (0.47 6 0.02 and 0.46 6 0.03 mmol/L; normal 0.53-0.67) were found. None of the compensated patients had elevated PTH (42 6 5; 17-53 pg/mL). Hypovitaminosis D (# 30 ng/mL) was seen in all 11 with protracted CHF (15.1 6 1.4; 7.0-23.8 ng/mL); 8 of 9 with short-duration CHF (20.3 6 5.1; 7.0-54.1 ng/mL); and 4 of 5 with compensated failure (23.1 6 4.9; 17.2-42.7 ng/mL). Conclusions: In housebound AA with symptomatic CHF, hypovitaminosis D is prevalent, even during the summer. The aldosteronism of protracted CHF and chronic furosemide use each exaggerate Ca 2+ and Mg 2+ losses to compromise cation balance, leading to ionized hypocalcemia and hypomagnesemia with SHPT. Raising 25(OH)D levels in AA with CHF remains to be addressed.