Eugènia Negredo1, Adolfo Diez-Pérez2, Anna Bonjoch3, Pere Domingo4, Núria Pérez-Álvarez5, Mar Gutierrez4, Gracia Mateo4, Jordi Puig6, Patricia Echeverría6, Roser Escrig6, Bonaventura Clotet7. 1. Lluita contra la Sida Foundation, Servicio de Medicina Interna, Germans Trias i Pujol University Hospital, Badalona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain Universitat de Vic-Universitat Central de Catalunya, Vic, Barcelona, Spain. 2. Institut Hospital del Mar d'Investigació Mèdica (IMIM), Universitat Autònoma de Barcelona and RETICEF, Barcelona, Spain Instituto Carlos III Madrid, Spain. 3. Lluita contra la Sida Foundation, Servicio de Medicina Interna, Germans Trias i Pujol University Hospital, Badalona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain abonjoch@flsida.org. 4. Santa Creu i Sant Pau Hospital, Barcelona, Spain. 5. Lluita contra la Sida Foundation, Servicio de Medicina Interna, Germans Trias i Pujol University Hospital, Badalona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain Statistics and Operations Research Department, Universitat Politècnica de Catalunya, Barcelona, Spain. 6. Lluita contra la Sida Foundation, Servicio de Medicina Interna, Germans Trias i Pujol University Hospital, Badalona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain. 7. Lluita contra la Sida Foundation, Servicio de Medicina Interna, Germans Trias i Pujol University Hospital, Badalona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain Universitat de Vic-Universitat Central de Catalunya, Vic, Barcelona, Spain Irsicaixa Foundation, Germans Trias i Pujol University Hospital, Badalona, Spain.
Abstract
BACKGROUND:Tenofovir is involved in accelerated bone mineral density (BMD) loss. METHODS: We recently published a hip BMD improvement at week 48 [+2.1% (95% CI: -0.6, 4.7) (P = 0.043)] in HIV-infected patients with osteopenia/osteoporosis randomized to switch from tenofovir to abacavir (n = 26), although without reaching statistical significance compared with those who maintained tenofovir (n = 28). Here, we present changes at week 48 in bone markers [C-terminal telopeptide of collagen type 1 (CTX), osteocalcin and procollagen type1 N propeptide (P1NP)] as well as in circulating levels of three proteins involved in bone regulation [osteoprotegerin, receptor activator for NF-κB ligand (RANKL) and sclerostin, a selective regulator of bone formation through the Wnt pathway] in 44 of these patients. χ(2) or Fisher and Student t-tests were performed according to the distribution of the variables. RESULTS:Bone markers decreased only in the abacavir group [mean (SD) CTX changed from 0.543 (0.495) to 0.301 (0.306) ng/mL; mean (SD) osteocalcin changed from 23.72 (22.20) to 13.95 (12.40) ng/mL; and mean (SD) P1NP changed from 54.68 (54.52) to 28.65 (27.48) ng/mL (P < 0.001 in all cases)], reaching statistical significance between the groups at week 48. Osteoprotegerin did not vary, but sclerostin significantly increased in the abacavir group [from 29.53 (27.91) to 35.56 (34.59) pmol/L, P = 0.002]. No significant differences in osteoprotegerin and sclerostin were detected between the groups at week 48. RANKL values were below the limit of detection in all samples. CONCLUSIONS: The switch from tenofovir to abacavir seems to induce a positive effect on bone tissue, since bone turnover markers decreased. In addition, circulating sclerostin levels increased, a change associated with improved bone properties.
RCT Entities:
BACKGROUND:Tenofovir is involved in accelerated bone mineral density (BMD) loss. METHODS: We recently published a hip BMD improvement at week 48 [+2.1% (95% CI: -0.6, 4.7) (P = 0.043)] in HIV-infectedpatients with osteopenia/osteoporosis randomized to switch from tenofovir to abacavir (n = 26), although without reaching statistical significance compared with those who maintained tenofovir (n = 28). Here, we present changes at week 48 in bone markers [C-terminal telopeptide of collagen type 1 (CTX), osteocalcin and procollagen type 1 N propeptide (P1NP)] as well as in circulating levels of three proteins involved in bone regulation [osteoprotegerin, receptor activator for NF-κB ligand (RANKL) and sclerostin, a selective regulator of bone formation through the Wnt pathway] in 44 of these patients. χ(2) or Fisher and Student t-tests were performed according to the distribution of the variables. RESULTS: Bone markers decreased only in the abacavir group [mean (SD) CTX changed from 0.543 (0.495) to 0.301 (0.306) ng/mL; mean (SD) osteocalcin changed from 23.72 (22.20) to 13.95 (12.40) ng/mL; and mean (SD) P1NP changed from 54.68 (54.52) to 28.65 (27.48) ng/mL (P < 0.001 in all cases)], reaching statistical significance between the groups at week 48. Osteoprotegerin did not vary, but sclerostin significantly increased in the abacavir group [from 29.53 (27.91) to 35.56 (34.59) pmol/L, P = 0.002]. No significant differences in osteoprotegerin and sclerostin were detected between the groups at week 48. RANKL values were below the limit of detection in all samples. CONCLUSIONS: The switch from tenofovir to abacavir seems to induce a positive effect on bone tissue, since bone turnover markers decreased. In addition, circulating sclerostin levels increased, a change associated with improved bone properties.
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