Corticosteroid induced osteoporosis

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Published in John D Firth, Professor Ian Gilmore, MRCP Part 2 Self-Assessment, 2018

The pathogenesis of corticosteroid induced osteoporosis is multifactorial. Corticosteroids reduce osteoblastic activity and the resulting osteoblast / osteoclast imbalance causes loss of bone. They also reduce intestinal calcium absorption and lower circulating sex steroid levels. Corticosteroid induced bone loss is fastest in the first 3–6 months of therapy.

Alendronate-loaded, biodegradable smart hydrogel: a promising injectable depot formulation for osteoporosis

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Journal Information

Published in Journal of Drug Targeting, 2018

Noha Nafee, Mariam Zewail, Nabila Boraie

Alendronate (ALN), a bone resorption inhibitor, is the most commonly prescribed oral amino-bisphosphonate for the treatment of post-menopausal osteoporosis, corticosteroid-induced osteoporosis, Paget’s disease, malignant hypercalcaemia, primary hyperparathyroidism and metastatic bone diseases [1]. ALN acts by inhibiting the resorptive activity of mature osteoclasts causing osteoclast apoptosis [2]. Being a BCS III drug (high solubility and low permeability due to polar hydrophilic nature), ALN is characterised by limited oral absorption and bioavailability (1%). Meanwhile, alendronate administration is associated with side effects including jaw osteonecrosis, oesophageal irritation, musculoskeletal pain, atrial fibrillation and atypical fractures [3]. Patients are advised to take ALN with water on empty stomach before breakfast and to stay in upright position for 30 min to avoid oesophageal irritation and cancer [4]. Recent trials to improve oral ALN delivery include the use of sucrose fatty acid esters as well as N-acyl amino acids and N-acyl taurates as absorption enhancers [5,6].

Corticosteroid induced osteoporosis

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Alendronate-loaded, biodegradable smart hydrogel: a promising injectable depot formulation for osteoporosis