1,721,018 research outputs found
Osteoporosis in GH deficiency
No full textGH/IGF-1 axis is one of the main regulator of both
bone modeling and remodeling. Therefore, GH deficient
(GHD) patients have a derangment in these processes
leading to impaired linear growth with delayed stature,
reduced peak bone acquisition, reduced bone size, decrease
in bone turnover, low bone mass, osteoporosis and
increased fracture risk in adults. GH replacement therapy
can restore a normal bone linear growth in children and
can improve bone mass, reducing the fractures in GHD
patients, whereas its application in treating osteoporosis
in non-GHD patients is still controversial
Bone organic matrix components: their roles in skeletal physiology
No full textBone matrix is composed mainly of inorganic materials, while the bone organic compartment is a minor and complex structural entity, surrounding and supporting cells. Three major classes of biomolecules are involved in this organic part: structural proteins, specialized proteins, and proteoglycans. This review will briefly summarize our knowledge about the role and regulation of these specific bone components
Serum total estradiol, but not testosterone is associated with reduced bone mineral density (BMD) in HIV-infected men: a cross-sectional, observational study
No full textBy investigating the relationship between serum testosterone, estradiol, and bone mineral density (BMD) in a large cohort of HIV-infected men, estradiol was associated with BMD, relative estrogen deficiency being involved in bone loss in men with hypogonadism, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss.
INTRODUCTION:
The purpose of this study is to evaluate the relationship between serum testosterone, estradiol, and BMD in a large cohort of HIV-infected men.
METHODS:
We investigated biochemical, hormonal parameters, and BMD in 1204 HIV-infected men (age 45.64 ± 7.33 years) participating in a cross-sectional, observational study. Among other parameters, the main outcome measures were serum total testosterone and estradiol, gonadotropins, 25-hydroxyvitamin D [25(OH)D], parathormone (PTH), calcium, phosphorous, femoral, and lumbar BMD.
RESULTS:
In men with HIV, the prevalence of osteoporosis and osteopenia is 15.1 and 63.2 % with 25(OH)D insufficiency being very common (60.1 %). After age adjustment, BMD is positively associated with estradiol, but not testosterone, at linear (p < 0.001) and stepwise (p < 0.05) multiple regression. Lumbar BMD significantly increases across the estradiol quartiles but not among testosterone quartiles. Femoral and lumbar BMD are significantly higher in men with estradiol ≥ 27 pg/mL than in those with estradiol <27 pg/mL. Apart from estradiol, only age, calcium, and BMI predict BMD at stepwise linear multiple regression, but the strength of this association is weak.
CONCLUSIONS:
Estradiol, but not testosterone, is associated with BMD in HIV-infected men and exerts a protective role on bone especially when it is above 27 pg/mL. Relative estrogen deficiency is a potential mechanism involved in bone loss in hypogonadal HIV-infected men, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss. Finally, reduced BMD in young-to-middle-aged HIV-infected men might be considered a peculiar hallmark of HIV infection due to its relevant prevalence, representing one of the several pieces composing the complicated puzzle of premature aging related to HIV infection.Summary: By investigating the relationship between serum testosterone, estradiol, and bone mineral density (BMD) in a large cohort of HIV-infected men, estradiol was associated with BMD, relative estrogen deficiency being involved in bone loss in men with hypogonadism, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss. Introduction: The purpose of this study is to evaluate the relationship between serum testosterone, estradiol, and BMD in a large cohort of HIV-infected men. Methods: We investigated biochemical, hormonal parameters, and BMD in 1204 HIV-infected men (age 45.64 ± 7.33 years) participating in a cross-sectional, observational study. Among other parameters, the main outcome measures were serum total testosterone and estradiol, gonadotropins, 25-hydroxyvitamin D [25(OH)D], parathormone (PTH), calcium, phosphorous, femoral, and lumbar BMD. Results: In men with HIV, the prevalence of osteoporosis and osteopenia is 15.1 and 63.2 % with 25(OH)D insufficiency being very common (60.1 %). After age adjustment, BMD is positively associated with estradiol, but not testosterone, at linear (p < 0.001) and stepwise (p < 0.05) multiple regression. Lumbar BMD significantly increases across the estradiol quartiles but not among testosterone quartiles. Femoral and lumbar BMD are significantly higher in men with estradiol ≥ 27 pg/mL than in those with estradiol <27 pg/mL. Apart from estradiol, only age, calcium, and BMI predict BMD at stepwise linear multiple regression, but the strength of this association is weak. Conclusions: Estradiol, but not testosterone, is associated with BMD in HIV-infected men and exerts a protective role on bone especially when it is above 27 pg/mL. Relative estrogen deficiency is a potential mechanism involved in bone loss in hypogonadal HIV-infected men, in addition to all HIV-related factors. Increased aromatization in adipose tissue does not counteract HIV-related bone loss. Finally, reduced BMD in young-to-middle-aged HIV-infected men might be considered a peculiar hallmark of HIV infection due to its relevant prevalence, representing one of the several pieces composing the complicated puzzle of premature aging related to HIV infection
Asymptomatic primary hyperparathyroidism: surgical and medical management
No full textPrimary hyperparathyroidism (PHPT) is a common endocrine disorder, frequently asymptomatic. Notwithstanding, mild PHPT may cause adverse skeletal effects that include high bone remodeling, reduced bone mineral density (BMD), and increased fracture risk. The definitive therapy for symptomatic and asymptomatic PHPT (aPHPT) is parathyroidectomy, which has been shown to increase BMD. In patients who choose not to be treated surgically or have contraindications for surgery, medical therapy should include drugs designed to protect the skeleton and/or to lower serum calcium, such as bisphosphonates, hormone replacement, and/or calcimimetic agents. However, there are currently no fracture data for any of these options. Obviously, there is the need for larger randomized controlled trials with fractures as end-points to evaluate the efficacy of medical treatment
Phosphate metabolism and pathophysiology in parathyroid disorders and endocrine tumors
No full textThe advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, and also of rarer endocrine metabolic bone diseases, such as hypoparathyroidism and tumor‐induced hypophosphatemia. These rare diseases of mineral metabolism have been and will be a precious source of new information about phosphate and other minerals in the coming years. The parathyroid glands, the kidneys, and the intestine are the main organs affecting phosphate levels in the blood and urine. Parathyroid disorders, renal tubule defects, or phosphatonin‐producing tumors might be unveiled from alterations of such a simple and inexpensive mineral as serum phosphate. This review will present all these disorders from a ‘phosphate perspective’
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Bone mass loss in calcium stone disease: Focus on hypercalciuria and metabolic factors
No full textBackground: Several authors have observed that idiopathic calcium stone formers show a bone mass reduction, which is more evident in those with idiopathic hypercalciuria. The aim of this work was the evaluation of osteopenia and osteoporosis rate in a group of idiopathic calcium stone formers. The influence of hypercalciuria, nutritional factors and anthropometric parameters on bone mass was evaluated in these patients as well. Methods: We enrolled 196 idiopathic calcium stone formers; 102 males, and 94 females. All subjects underwent a metabolic study. BMC and BMD were evaluated as well as QUS. Results: Males showed greater weight, height, BMI, densitometric values and plasma creatinine, uric acid, urea, sodium, magnesium, GFR and urinary osmolarity than females. Moreover males excreted more uric acid, urea, creatinine, sulphate, phosphate, oxalate and citrate than females. The prevalence of osteopenia and osteoporosis, according to T-score, was 54% and 14% respectively. Hypercalciuria was demonstrated in 21.7% of the patients. Hypercalciuric men showed a higher excretion of urea, phosphate, sulphate and magnesium. Conclusions: Our results confirm the importance of QUS in the evaluation of stone formers' bone mass. Anthropometric characteristics and dietary habits seem to play a role in bone loss. We did not demonstrate any influence of hypercalciuria on bone mass. Although the pathogenesis of bone loss in stone formers still remains unclear, it can be hypothesized that a slight degree of metabolic acidosis, probably of alimentary origin, may be involved in the reduction of bone mass
- …
