Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Osteoporosis is a common skeletal disease associated with an imbalance in bone remodeling resulting in a reduction in bone strength and increased fracture risk. The principal regulator of osteoclastic bone resorption is receptor activator of nuclear factor-kappaB ligand (RANKL), a cytokine member of the tumor necrosis factor family. The binding of RANKL to its receptor on the cell surface of osteoclasts and pre-osteoclasts increases the formation, activity, and survival of osteoclasts. Denosumab is an investigational fully human monoclonal antibody to RANKL. By binding to RANKL, denosumab prevents RANKL from binding to its receptor, resulting in a decrease in bone resorption due to reduction in the formation, activity, and survival of osteoclasts. In postmenopausal women with osteoporosis, denosumab 60 mg by subcutaneous injection every 6 months increased bone mineral density (BMD), reduced bone turnover markers, and reduced the risk of vertebral, hip, and non-vertebral fractures. In postmenopausal women with low BMD, denosumab increased BMD and reduced bone turnover markers. It was well tolerated with a safety profile generally similar to placebo. Denosumab is a promising emerging drug for the prevention and treatment of postmenopausal osteoporosis. It may be particularly useful in clinical practice for the treatment of patients with gastrointestinal contraindications or side effects with oral bisphosphonates and for patients with malabsorption.
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PMID:Treatment of osteoporosis with denosumab. 2023 78

Hypocalcemia is a known risk following bariatric surgery and can contribute to the development of osteoporosis. Osteoporosis is commonly treated with denosumab, though denosumab can exacerbate underlying abnormalities in calcium homeostasis. We present the case of a 59-year-old female with severe hypocalcemia who had been treated with denosumab for osteoporosis three months before and had Billroth II gastric bypass surgery 15 years before, for bariatric purposes. Intravenous calcium supplementation was used to correct the initial electrolyte abnormality, and the patient was able to maintain appropriate calcium levels on high doses of oral calcium before discharge. Denosumab-induced hypocalcemia has been previously reported in patients with predisposing conditions including chronic kidney disease, primary sclerosing cholangitis, Crohn's disease, and a history of sleeve gastrectomy for marginal gastric ulcers. A few cases of hypocalcemia have been reported in patients with a history of bariatric surgery secondary to vitamin D deficiency, but this report is unique in demonstrating denosumab-induced hypocalcemia after bariatric surgery with normal vitamin D levels, suggesting a primary malabsorption of calcium. The risk of severe hypocalcemia should be considered before initiating denosumab to treat osteoporosis in patients with a history of bariatric surgery. If denosumab is initiated, serum calcium levels should be closely monitored, and patients should be educated about the importance of adherence to calcium supplementation.
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PMID:Denosumab-Induced Hypocalcemia after Billroth II Gastric Bypass Surgery. 3277 45