scholarly journals Severe, Symptomatic Hypocalcemia due to Denosumab Administration: Treatment and Clinical Course

2019 ◽  
Vol 9 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Jarred Strickling ◽  
Michael J. Wilkowski

Denosumab is a receptor activator of nuclear factor kappa-B (RANK) ligand inhibitor used in the treatment of osteoporosis. Blockade of RANK ligand prevents osteoclastic resorption of bone, but in doing so impairs the parathyroid hormone (PTH)-driven maintenance of serum calcium. A subsequent elevation of PTH remains active at sites other than bone, potentially lowering serum phosphate by inhibiting proximal tubular reabsorption. We present 2 patients who developed severe, symptomatic hypocalcemia after administration of denosumab. These patients provide an opportunity to describe the clinical course and treatment, including the need to consider a continuous calcium infusion, of severe, symptomatic hypocalcemia caused by denosumab.

2002 ◽  
Vol 117 (2) ◽  
pp. 210-216 ◽  
Author(s):  
Sophie Roux ◽  
Larbi Amazit ◽  
Geri Meduri ◽  
Anne Guiochon-Mantel ◽  
Edwin Milgrom ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Afdhal Afiq Abd Jalil ◽  
Sharifah Faradila Wan Muhamad Hatta ◽  
Aimi Fadilah Mohamad ◽  
Mohammed Fauzi Abdul Rani

Denosumab is a human monoclonal antibody that binds to RANKL (receptor activator of nuclear factor-kappa B ligand). It has mainly been used in the treatment of osteoporosis for a variety of causes especially in situations refractory to bisphosphonates or when kidney function is impaired. It is also used in cases of malignancy-associated hypercalcemia. There are many causes of hypercalcemia, but only rarely it is associated with granulomatous diseases such as tuberculous pleural effusion. We report a case of hypercalcemia from tuberculous pleural effusion that was initially admitted with left medium abundance pleural effusion and a serum corrected calcium level of 3.48 mmol/L. The calcium level was successfully normalized within 72 hours of subcutaneous denosumab administration after other interventions have failed.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Xuefei Li ◽  
Longkang Cui ◽  
Wenhua Chen ◽  
Yuan Fang ◽  
Gaobo Shen ◽  
...  

QiangGuYin (QGY) is a common Traditional Chinese medicine prescription for the treatment of osteoporosis. Previous clinical studies have found that QGY effectively improves bone mineral density (BMD) in postmenopausal women, but its underlying mechanism remains unclear. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK) pathway is a classic pathway involved in osteoporosis. Secretin levels are a serum marker of osteoporosis, but their effect on the OPG/RANKL/RANK pathway has not been reported. Hence, we investigated the relationship between the OPG/RANKL/RANK pathway and secretin and further revealed the mechanism underlying the effect of QGY in the treatment of osteoporosis. Mice were divided into secretin knockdown, secretin overexpression, and corresponding control groups. Micro-computed tomography was used to detect BMD in different groups, and the results show that QGY significantly improved BMD in mice of the secretin knockdown group. To further verify this, the serum levels of OPG, RANKL, RANK, and secretin were measured by enzyme-linked immunosorbent assays, and femur levels of OPG, RANKL, RANK, and secretin were evaluated by real-time quantitative PCR and western blotting. The results show that the expression of OPG was inhibited and that of RANKL and RANK was increased in mice from the secretin knockdown group, whereas the expression of OPG was upregulated and that of RANKL and RANK was downregulated after QGY intervention. Therefore, QGY inhibited bone resorption by promoting the expression of secretin and modulating the OPG/RANKL/RANK pathway. In addition to the effect of QGY, we also revealed the general regulatory effect of secretin on the OPG/RANKL/RANK pathway. We conclude that QGY modulates the OPG/RANKL/RANK pathway by increasing secretin levels during treatment of primary type I osteoporosis. This work provides a theoretical basis for the clinical use of QGY in the treatment of osteoporosis.


2017 ◽  
Vol 225 (4) ◽  
pp. S196
Author(s):  
Jeffery M. Chakedis ◽  
Heather Lewis ◽  
Priyani V. Rajasekera ◽  
Eliza W. Beal ◽  
Carl R. Schmidt ◽  
...  

Author(s):  
Legiran Legiran

Latar Belakang: Penelitian tentang hubungan obesitas dan pengeroposan tulang telah banyak dilakukan dan secara epidemiologik menunjukkan obesitas berhubungan dengan peningkatan massa tulang. Penelitian lainnya menemukan bahwa obesitas menjadi faktor risiko terjadinya osteoporosis. Berat badan lebih dianggap sebagai faktor protektif bagi terjadinya proses pengeroposan tulang terutama pada wanita pascamenopause akibat dipertahankannya kadar estrogen selama masa menopause. Bagaimana hubungan obesitas dalam menghambat terjadinya proses pengeroposan tulang?Tujuan: Mendiskusikan hubungan obesitas sebagai faktor protektif proses pengeroposan tulang.Isi: Tulang sebagai bagian dari rangka tubuh manusia memiliki fungsi utama sebagai kerangka yang keras untuk mendukung, melindungi, dan memudahkan fungsi jaringan lunak. Jika ukuran rangka semua orang sama berapapun berat badannya, pasti beberapa tulang akan kesulitan memenuhi tugasnya dan akan tidak menguntungkan jika rangka yang ada secara signifikan lebih berat dari kebutuhannya. Pada individu yang gemuk maka dibutuhkan rangka yang lebih kuat dibanding kurus. Ini secara sederhana ingin menyebutkan bahwa gemuk memiliki hubungan dengan rangka. Penelitian membuktikan bahwa obesitas berhubungan dengan peningkatan kadar adipokin-adipokin seperti leptin, adinopektin, visfatin, resistin, apelin, dan lainnya yang dapat berpengaruh terhadap makronutrien metabolisme dan selanjutnya adipokin-adipokin tersebut mungkin saja berinteraksi dengan modulator energy jangka panjang  seperti insulin. Hal ini masih belum bisa diungkap hubungan erat antara obesitas, hormon-hormon yang dipengaruhinya, dan efek fisiologi yang ditimbulkan. Obesitas dapat menguntungkan bagi kesehatan tulang karena efek mekanik dari berat badan pada pembentukan tulang karena obesitas berkaitan dengan inflamasi kronik dimana terjadi peningkatan sitokin proinflamasi di jaringan dan sirkulasi yang dapat meningkatkan aktivitas osteoklas dan resorpsi tulang melalui modifikasi receptor activator nuclear kappa B, RANK Ligand, dan Osteoprotegerin (RANK/RANKL/OPG) pathway. Obesitas juga dapat menjadi sebuah mekanisme patofisiologi berupa efek metabolic toksik asam lemak bebas dan adipokin yang berpengaruh pada metabolisme tulang.Kesimpulan: Obesitas mungkin berhubungan dengan penghambatan proses pengeroposan tulang dan sebaliknya obesitas mungkin juga menjadi faktor yang menyebabkan pengeroposan tulang. Nyatanya proses pengeroposan tulang sangat dipengaruhi baik oleh faktor genetik dan faktor lingkungan.


2017 ◽  
Vol 2 (1) ◽  
pp. 23-29
Author(s):  
Sousan Kolahi ◽  
Amir Ghorbanihaghjo ◽  
Nadereh Rashtchizadeh ◽  
Alireza Khabbazi ◽  
Mehrzad Hajialilo ◽  
...  

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