Clinical profile and quality of life scores in Chronic Hypoparathyroidism: a transversal retrospective study

Abstract

Introduction: In patients with hypoparathyroidism, conventional therapy maintains parathyroid hormone (PTH)-dependent mineral metabolism homeostasis but is unable to prevent emergence of comorbidities and low quality of life. Objectives: To evaluate long-term progression of patients with hypoparathyroidism receiving conventional therapy and their quality of life compared with patients with primary hypothyroidism and healthy controls. Design and Setting: Retrospective cohort study for quality-of-life analysis and transversal cut on clinical profile. Patients with hypoparathyroidism from four public referral centers in endocrinology and bone metabolism in the metropolitan region of Rio de Janeiro. Material and Methods: Quality of life by SF-36 protocol, and clinical profile by medical record analysis. Results: 243 individuals with hypoparathyroidism (n=113), hypothyroidism (n=65), and healthy controls (n=65) included. Median time since diagnosis and duration of conventional therapy was 8 years (IQR 4–17 years). Data on type of conventional therapy (median, minimum–maximum daily dose, percentage of patients with hypoparathyroidism using each medication): calcium supplementation (2000 mg/day, 200–6000 mg/day, 95%), cholecalciferol (2000 IU/day, 200–40000 IU/day, 44%), calcitriol (0.5 μg/day, 0.25–2 μg/day, 77%), thiazides (25 mg/day, 12.5–100 mg/day, 44%). Conclusions: Conventional therapy is associated with homeostasis of serum mineral levels, but not with improved quality of life. Compared to patients with hypothyroidism, those with additional hypoparathyroidism had lower scores in six SF-36 domains. Conventional therapy successfully maintained normal calcium levels with often high doses of calcium, vitamin D, and thiazides but could not prevent low quality of life scores and comorbidities.

Hypoparathyroidism: Early Detection and Diagnosis Approaches

“…Manifestasi neurologis hipokalsemia ditunjukkan dengan sentakan mioklonik, kedutan, kejang onset baru karena hipokalsemia serebral, atau kejang yang memburuk (Bilezikia, 2020). Manifestasi jantung digambarkan dengan pemanjangan interval QT dan alternan gelombang T, kardiomiopati akut, dan gagal jantung kongestif karena penurunan kontraktilitas jantung yang berhubungan dengan rendahnya kalsium serum dan kemungkinan defisiensi PTH, karena terdapat reseptor PTH di miosit jantung (De Alencar et al, 2023;Sitges-Serra, 2021).…”