Skeletal and nonskeletal consequences of hypoparathyroidism

Abstract

Hypoparathyroidism, despite the conventional therapy with calcium and active vitamin D, can lead to skeletal and nonskeletal abnormalities. Chronic hypoparathyroidism is associated with a significant reduction in bone remodeling, increases in areal and volumetric bone density, and improvement in trabecular microarchitecture and in trabecular bone score. Regardless of these advantages in bone mass and microarchitecture, recent data suggest an increased vertebral fracture risk in patients with nonsurgical hypoparathyroidism. Moreover, chronic hypoparathyroidism can lead to abnormalities in multiple organ systems, including the neurological, cardiovascular, renal, neuropsychiatric, ocular, and immune systems. Nephrocalcinosis, nephrolithiasis, and renal insufficiency, as well as decreased quality of life and cataracts, are common in patients with hypoparathyroidism. An increased incidence of hospitalization due to infections and a greater risk of cardiovascular diseases are observed in patients with hypoparathyroidism, particularly in those with nonsurgical disease. All these abnormalities may be because of the disease itself or complications of therapy. We herein reviewed the skeletal and nonskeletal consequences of hypoparathyroidism in patients conventionally managed with calcium and active vitamin D.

Clinical manifestations of chronic hypoparathyroidism

“…PTH vplýva na remodeláciu kostí, kostnú minerálovú hustotu (BMD) a mikroarchitektúru, čo môže viesť k zvýšenej náchylnosti k fraktúram (11). Uvedené zmeny sa objavujú napriek štandardnej substitúcii vitamínom D, no môžu byť reverzibilné pri podávaní rekombinantného PTH (12).…”

“…Títo pacienti podstupovali operáciu katarakty v skoršom veku oproti kontrolnej vzorke. Napriek vyššiemu riziku vzniku tejto komplikácie, je podozrenie, že katarakta zostáva poddiagnostikovaná predovšetkým u tých pacientov, u ktorých neprebieha jej aktívny skríning (11).…”

“…Pacienti s hypoparatyreózou dosahovali v oblasti lumbálnej chrbtice a proximálneho femuru vyššie hodnoty BMD v porovnaní s bežnou populáciou. Zvýšená BMD býva pri oboch hlavných príčinách hypoparatyreózy(11).Príčinou týchto pozorovaní je vyššie spomínaná znížená remodelácia kosti a zmeny trabekulárnej kosti -predovšetkým zväčšenie jej objemu, čo sa potvrdilo pri histomorfometrickom vyšetrení spomínanom vyššie. Keďže lumbálne stavce a proximálny femur sú bohaté na trabekulárnu kosť, tieto zmeny sú najviac viditeľné práve v týchto miestach.…”

Pivotal Role of Intestinal Microbiota and Intraluminal Metabolites for the Maintenance of Gut–Bone Physiology

“…Low and intermittent doses of PTH exhibit anabolic effects on bone volume and microarchitecture. In contrast, a continued hypersecretion of PTH, such as that which occurs in primary hyperparathyroidism, leads to bone resorption [ 40 , 41 ]. Acting as an opponent of PTH, calcitonin reduces calcium concentrations in the blood, for example, due to the inhibition of bone suppression or the suppression of calcium release from the bone [ 42 ].…”