{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T14:49:21Z","timestamp":1790261361852,"version":"4.1.0"},"reference-count":35,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2024,8,26]],"date-time":"2024-08-26T00:00:00Z","timestamp":1724630400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Foot Ankle Int."],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Charcot neuroosteoarthropathy (CNO) is characterized with increased osteoclastic activity that can be curbed with antiresorptive agents. Chronic kidney disease (CKD) precludes bisphosphonates but anti\u2013receptor activator of nuclear factor-B ligand (anti-RANKL) antibody, denosumab, can be contemplated in CKD. We investigated denosumab for active CNO of foot in CKD for CNO remission.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>During the study period, 446 persons of diabetes with unilateral, active CNO of foot and CKD were identified and 78 were finally enrolled. Patients received either 60\u2009mg denosumab (single-dose, subcutaneous) along with standard of care (SoC) as total contact cast (TCC) (group A; n\u2009=\u200926) or SoC (group B; n\u2009=\u200952) only. Patients were followed every 4\u2009weeks until CNO remission and subsequently every 8 weeks until 48\u2009weeks following remission. Remission was defined as temperature difference &lt;2 \u00b0C between 2 feet confirmed twice (4\u2009weeks apart) with clinical resolution of signs of inflammation. The primary outcome studied was proportion of patients achieving remission within 48\u2009weeks and the time to remission.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Median age was 56.5 (48.8-65) and 57 (48.5-61.2)\u2009years, P\u2009=\u2009.57; duration of diabetes 16 (10-25.3) and 14.9 (10-19)\u2009years, P\u2009=\u2009.151; and estimated glomerular filtration rate 44.8 (21.1-65.6) and 45.7 (32.9-55.7) mL\/min\/1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      , P\u2009=\u2009.771, in group A and B, respectively. Median temperature difference at presentation between the affected and opposite foot was 3.4 \u00b0C (2.7-6.9) and 3.2 \u00b0C (2.2-4.0), P\u2009=\u2009.119, respectively. All patients achieved remission in group A (100%) compared with 42 (80.8%) in group B ( P\u2009=\u2009.006) (hazard ratio 0.52, 95% CI: 0.32-0.87; P\u2009=\u2009.012). The median time to remission was similar in the 2 groups (15 [11-25] and 17.5 [14-31.5] weeks, P\u2009=\u2009.229, respectively). 25-Hydroxyvitamin D\n                      <jats:sub>3<\/jats:sub>\n                      &gt;14\u2009ng\/mL was significantly associated (OR 9.5, 95% CI 1.04-87.5, P\u2009=\u2009.045) with remission.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Anti-RANKL antibody added to SoC (TCC) induces remission of active foot CNO in greater proportions of patients with diabetes and CKD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/10711007241268147","type":"journal-article","created":{"date-parts":[[2024,8,27]],"date-time":"2024-08-27T02:44:37Z","timestamp":1724726677000},"page":"1122-1130","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Anti-RANKL Antibody For Active Charcot Foot Neuro-Osteoarthropathy in Patients with Diabetes and Chronic Kidney Disease"],"prefix":"10.1177","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9375-3102","authenticated-orcid":false,"given":"Ashu","family":"Rastogi","sequence":"first","affiliation":[{"name":"Deptartment of Endocrinology, PGIMER, Chandigarh, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raveena","family":"Singh","sequence":"additional","affiliation":[{"name":"Deptartment of Endocrinology, PGIMER, Chandigarh, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jayaditya","family":"Ghosh","sequence":"additional","affiliation":[{"name":"Deptartment of Endocrinology, PGIMER, Chandigarh, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajat","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Alchemist Hospitals, Panchkula, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2024,8,26]]},"reference":[{"key":"bibr1-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.080616"},{"key":"bibr2-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1016\/j.bone.2010.11.020"},{"key":"bibr3-10711007241268147","doi-asserted-by":"publisher","DOI":"10.2337\/dc06-0376"},{"key":"bibr4-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1007\/s00198-019-05020-8"},{"key":"bibr5-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1210\/clinem\/dgaa851"},{"key":"bibr6-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1359\/jbmr.0809010"},{"key":"bibr7-10711007241268147","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-017-00563-4"},{"key":"bibr8-10711007241268147","volume":"41","author":"Busch-Westbroek TE","year":"2017","journal-title":"Diabetes 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