Oxidative stress in middle age males with osteoporosis: correlation of hormonal pattern and plasma total antioxidant capacity

Sebastiano Raimondo; Francesco Ciro Tamburrelli; Segni Chantal Di; Mariasara Persano; Roberto Festa; Andrea Silvestrini; Elisabetta Meucci; Alfredo Pontecorvi; Antonio Mancini

doi:10.1530/endoabs.32.P87

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Endocrine Abstracts (2013) 32 P87 | DOI: 10.1530/endoabs.32.P87

ECE2013 Poster Presentations Bone and Osteoporosis (41 abstracts)

Oxidative stress in middle age males with osteoporosis: correlation of hormonal pattern and plasma total antioxidant capacity

Sebastiano Raimondo ¹ , Francesco Ciro Tamburrelli ² , Chantal Di Segni ¹ , Mariasara Persano ¹ , Roberto Festa ³ , Andrea Silvestrini ⁴ , Elisabetta Meucci ⁴ , Alfredo Pontecorvi ¹ & Antonio Mancini ¹

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¹Division of Endocrinology, Department of Internal Medicine, Catholic University of the Sacred Heart, Rome, Italy; ²Department of Spine Surgery, Catholic University of the Sacred Heart, Rome, Italy; ³Department of Molecular Pathology, Polytechnic University of the Marche, Ancona, Italy; ⁴Institute of Biochemistry and Clinical Biochemistry, Catholic University of the Sacred Heart, Rome, Italy.

Male idiopathic osteoporosis is an underestimated disease, despite its clinical and social importance. The biochemical mechanisms are still poorly understood even if the interaction between genetic factors and hormone environment (especially gonadal steroids and GH) plays a undoubtful role. In previous studies we demonstrated low plasma total antioxidant capacity (TAC) in hypogonadal patients. The aim of this study was to investigate oxidative stress as risk factor for bone fracture, and its relationships with endocrine milieu.

We enrolled 31 male subjects (36–72 years), all affected by back pain/spine fracture as a consequence of trivial trauma and ten healthy controls (30–48 years). TAC was determined using a colorimetric assay, using the system H₂O_2-metmyoglobin as source of radicals and a chromogen (ABTS); the latency time (LAG) in the accumulation of ABTS^.+, spectroscopically detectable, is proportional to antioxidants concentration. An endocrine evaluation including testosterone, estradiol, insulin, IGF1, PRL, FT₃, FT₄, TSH levels was also performed. Finally, bone mineral density was assessed by DEXA. Bone metabolic parameters were evaluated (PTH, vitamin D, osteocalcin, and β-cross laps). Statistical evaluation was performed using Mann–Whitney U test.

The prevalence of IGF1 defects (52.8±15.28 ng/ml) was 5/31 (suggesting GH deficiency (GHD), confirmed by GHRH+arginine test). Hypogonadism (mean testosterone levels 2.03±0.46 ng/ml) was present in 4/31. The 22 patients left did not show alterations in the hormonal parameters studied. Despite mean levels of LAG were not different between patients and controls (72.7±8.5 vs 75.0±6.0 s), 12 out of 31 patients had low LAG levels (between 50 and 60 s) irrespective of hormonal milieu. Moreover, when considering parameters of bone metabolism we found significantly lower vitamin D levels in hypogonadal subjects, than in patients with GHD and patients with normal hormonal parameters (10.7±5.8 ng/ml vs 19.7±17.7 and 22.7±9.7 respectively).

These preliminary data suggest a possible involvement of oxidative stress in unexplained fractures even if further investigations are needed to establish a possible correlation with anabolic hormones involved in bone metabolism. Low vitamin D levels could exert a worsening effect on osteoporosis in hypogonadal patients.