Heart Failure is predicted by PTH (but vitamin D both prevents and treats HF)

The Role of Parathyroid Hormone and Vitamin D Serum Concentrations in Patients with Cardiovascular Diseases.

Dis Markers. 2018 Jan 31;2018:5287573. doi: 10.1155/2018/5287573. eCollection 2018.

Kolaszko A1, Nowalany-Kozielska E1, Ceranowicz P2, Morawiec B1, Kubiak G1.

1 2nd Department of Cardiology, Medical Faculty, Medical University of Silesia, Katowice 10 M. Skłodowskiej-Curie Street, 41-800 Zabrze, Poland.

2 Department of Physiology, Medical Faculty, Jagiellonian University Medical College, 16 Grzegorzecka Street, 31-531 Krakow, Poland.

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25-hydroxyvitamin D (25(OH)D) plays a crucial role in human homeostasis. Its deficiency (vitamin D deficiency-VDD), being common in European population, combined with elevated concentration of parathyroid hormone (PTH), represents a vicious cycle of mechanisms leading to heart failure (HF). Despite several papers published in that field, the effect of VDD and PTH concentration on cardiovascular system remains unequivocal; thus, the aim of the study was to compare these data among HF and non-HF patients being prospectively enrolled into the study during hospital stay in the cardiology ward.

Patients with HF had higher PTH concentration (85.0 ± 52.6 versus 64.5 ± 31.7, p ≤ 0.02) compared to non-HF patients.

image

Mean PTH values were associated with the clinical status expressed by the New York Heart Association class (NYHA class)

  • ("0"-66.04,

  • "I"-56.57,

  • "II"-72.30,

  • "III"-85.59, and

  • "IV"-144.37 pg/ml, p ≤ 0.00004).

Interestingly,

  • neither 25(OH)D (31.5 versus 29.7 ng/ml, p ≤ ns)

  • nor phosphorus (P) (1.23 versus 1.18 mmol/l, p ≤ ns)

  • nor total calcium (Ca2+) concentration (2.33 versus 2.37 mmol/l, p ≤ ns)

differed among the groups.

Reassuming PTH serum concentration in contrary to 25(OH)D, P and Ca2+ are significantly raised among the patients with HF and shows significant relationship with the clinical status expressed by the NYHA class.

PMID: 29599854 PMCID: PMC5831602 DOI: 10.1155/2018/5287573