Serum Sclerostin Levels in Patients with Human Immunodeficiency Virus Infection and Their Association with Bone Turnover Markers and Bone Mineral Densitometry.
10.11005/jbm.2016.23.1.16
- Author:
Abdulrahman Y ALMANSOURI
1
;
Mohammed E ABDULFATAH
;
Omar H BAAQIL
;
Alaa A BAKHEET
;
Sarah A TURKI
;
Mamdouh M KOTB
;
Alaa ALTHUBAITI
;
Majed M ALMAGHRABI
;
Abdulrahman M ALTHUBAITI
;
Badr M MADANI
;
Ali S M JAWAD
Author Information
1. Center of Excellence for Osteoporosis Research, King Abdulaziz University, Jeddah, Saudi Arabia. red.amlor@gmail.com
- Publication Type:Original Article
- Keywords:
Glycoproteins;
HIV;
Osteoporosis;
Saudi Arabia
- MeSH:
Bone Density;
Densitometry*;
Female;
Femur Neck;
Glycoproteins;
HIV*;
Humans;
Humans*;
Inflammation;
Male;
Osteoporosis;
Prospective Studies;
Saudi Arabia;
Spine;
Viral Load
- From:Journal of Bone Metabolism
2016;23(1):16-22
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The aim of the study was to compare serum sclerostin levels in human im-munodeficiency virus (HIV)-infected patients and healthy controls, and to evaluate their relationship with bone turnover markers (BTM) and bone mineral density (BMD). METHODS: We prospectively studied 33 HIV treatment-naive patients and 63 healthy individuals; matched for age and sex. Serum sclerostin levels, BTM, BMD were measured. Viral load and cluster of differentiation 4 (CD4) levels were also assessed in HIV-infected patients. RESULTS: The mean+/-standard deviation (SD) age of sample was 37.6+/-10.3 years (range, 19 to 59 years). Of the 96 subjects, 58 (60.4%) were male and 38 (39.6%) were female. Infection with HIV is associated with significant reduction in serum sclerostin levels (HIV-infected: 39.4+/-28.3 vs. non HIV: 76.6+/-15.7 pmol/L; P<0.001) and a decrease in BMD at femoral neck and lumbar spine compared to healthy controls. Sclerostin however was not correlated with BMD and was not related to age, generally a strong correlation. There were no significant correlations between sclerostin and BTM (P>0.05). CONCLUSIONS: These findings suggest that untreated HIV and the resulting immune deficiency and/or systemic inflammation could be an important regulator of serum sclerostin in this population.
