1,720,983 research outputs found
Risk of vertebral fractures in hypoparathyroidism
No full textParathyroid hormone (PTH) exerts both anabolic and catabolic actions on bone,depending on the duration and periodicity of exposure. Hypoparathyroidism is defined by inadequate production of PTH in the presence oflow serum calcium. In hypoparathyroidism it has been reported an increase in corticaland trabecular bone mass, but it is still unknown if these quantitative variations maybe accompanied by qualitative ones and increased bone strength. Despite the extensive data available on the effects of hypoparathyroidism on bone, itseffect on the hard end point in this area which is the risk of fractures still remainsunresolved and highly debated. As a matter of fact no previous review has focused onthis relevant clinical topic. This review will deal with the various aspects of bone metabolism (turn-over,density, quality) in hypoparathyroidism, focusing on the few data available on therisk of fracture and in particular of morphometric vertebral fractures, the emerging way to assess actual skeletal fragility particularly in secondary forms of osteoporosis
Treatment of hypoparathyroidism
No full textThe goal of the clinical management of hypoparathyroidism is to correct acute and chronic hypocalcemia. Treatment of acute hypoparathyroidism via intravenous infusion of Ca++ salts, is necessary only in symptomatic patients, or in asymptomatic patients in the setting of a rapid decrease in ionized Ca ++ levels. The treatment cornerstones of chronic hypoparathyroidism are oral supplementation of calcium and/or active vitamin D, that can be associated with dietary restriction of sodium and phosphates, thiazide diuretics, and phosphate binders. Notably, PTH replacement is emerging as a innovative treatment of chronic hypoparathyroidism. rhPTH (1–84) has been shown to safely reduce calcium and vitamin D dosage, and increase serum calcium levels in hypoparathyroid patients. Therefore, rhPTH (1–84) appears to represent a new option in patients with chronic hypoparathyroidism “resistant” to conventional treatment
Skeletal fragility: an emerging complication of Ehlers–Danlos syndrome
No full textEhlers-Danlos syndrome (EDS) is an emerging cause of skeletal fragility. Mechanism of bone damage are probably multifactorial in line with the different skeletal phenotypes that can be found in clinical practice. A structured approach to clinical management of bone metabolic complication in EDS is proposed
Glucocorticoid-induced osteoporosis: pathophysiological role of GH/IGF-I and PTH/VITAMIN D axes, treatment options and guidelines
No full textGlucocorticoid-induced osteoporosis is the most frequent form of secondary osteoporosis caused by chronic exposure to glucocorticoid excess. Pathogenesis of glucocorticoid-induced osteoporosis is multifactorial including direct effects of glucocorticoids on bone cells and indirect effects of glucocorticoids on several neuroendocrine and metabolic pathways. Fragility fractures occur early in glucocorticoid-induced osteoporosis and anti-osteoporotic drugs along with calcium and vitamin D should be started soon after exposure to glucocorticoid excess. This paper summarizes some of the main topics discussed during the 9th Glucocorticoid-Induced Osteoporosis Meeting (Rome, April 2016) with a specific focus on the role of growth hormone/insulin-like growth factor-1 and parathyroid hormone/vitamin D axes in the pathogenesis of glucocorticoid-induced osteoporosis and the controversial aspects concerning therapeutic approach to skeletal fragility in this clinical setting
Growth hormone deficiency in treated acromegaly and active Cushing's syndrome
No full textGrowth hormone deficiency (GHD) in adults is characterized by reduced quality of life and physical fitness, skeletal fragility, increased weight and cardiovascular risk. It may be found in (over-) treated acromegaly as well as in active Cushing's syndrome. Hypopituitarism may develop in patients after definitive treatment of acromegaly, although the exact prevalence of GHD in this population is still uncertain because of limited awareness, and scarce and conflicting data so far available. Because GHD associated with acromegaly and Cushing's syndrome may yield adverse consequences on similar target systems, the final outcomes of some complications of both acromegaly and Cushing's syndrome may be further affected by the occurrence of GHD. It is still largely unknown, however, whether GHD in patients with post-acromegaly or active Cushing's syndrome (e.g. pharmacologic glucocorticoid treatment) may benefit from GH replacement. We review the diagnostic, clinical and therapeutic aspects of GHD in adults treated for acromegaly and in those with active Cushing's syndrome
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe 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
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