[Pathogenesis of corticoid-induced osteoporosis].
Corticoid osteoporosis is the most important of the so-called secondary forms of osteoporosis. Although, in recent years, our knowledge of the pathomechanisms involved have been expanded, at the cellular and molecular-biological level, it remains incomplete. In practical-clinical terms, however, the following main effects of corticoids on bone metabolism and the calcium balance can be identified: inhibition of osteoblastic bone matrix synthesis and enhancement of osteoclastic bone absorption. This latter is promoted by inhibition of intestinal calcium absorption and tubular reabsorption of calcium with subsequent mild secondary hyperparathyroidism. These mechanisms suggest possibilities for the prevention and treatment of this form of osteoporosis.
Med. Klinik IV (Geriatrie), Städtisches Krankenhaus Leverkusen, Akademisches Lehrkrankenhaus der Universität zu Köln.
J D
JD
Ringe
D000305:Adrenal Cortex Hormones / Q000009:adverse effects*; D002118:Calcium / Q000378:metabolism; D006801:Humans; D007408:Intestinal Absorption; D007684:Kidney Tubules / Q000378:metabolism; D010006:Osteoblasts / Q000187:drug effects; D010010:Osteoclasts / Q000187:drug effects; D010024:Osteoporosis / Q000139:chemically induced* / Q000517:prevention & control
D000305:Adrenal Cortex Hormones; D002118:Calcium
Pathogenese der Kortikoidosteoporose.