China
Africa
Explore chapters and articles related to this topic
Pharmacokinetic-Pharmacodynamic Correlations of Corticosteroids
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Helmut Möllmann, Stefan Baibach, Günther Hochhaus, Jürgen Barth, Hartmut Derendorf
Osteoporosis is an undesirable side effect of chronic corticosteroid therapy.13 An impaired balance between bone absorption and bone formation results from corticosteroid effects on mineral metabolism and direct effects on the bone tissue to cause a loss of bone mass,185,186 Osteocalcin, a protein secreted by osteoblast cells during osteogenesis,187 is a sensitive marker of bone formation.186,188 Physiological plasma concentrations normally have a circadian pattern with a peak at night and a trough in the morning (Figure 7).186 The suppression of osteocalcin plasma concentrations can be utilized to quantify a corticosteroid-induced suppression of bone formation.185 Osteocalcin is measured with RIA.186,189
Optimizing Metabolism to Treat Fractures and Prevent Nonunion
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Jacob Wilson, Scott Boden, Kenneth Cintron, Mara Schenker
While not nearly to the extent of vitamin D, vitamin K has also received some attention with regard to its role in maintaining bone health and prevention of fractures. Vitamin K serves as a co-factor for the enzyme gamma carboxylase, which is responsible for osteocalcin carboxylation. Osteocalcin is a hormone produced by osteoblasts and functions primarily to promote bone formation and mineralization.71,72 Only a handful of RCTs have examined vitamin K and the risk of fracture.73–76 Unfortunately, almost all of the trials reporting on fracture rates were conducted in Japan and are of relatively low quality, bringing into question their generalizability.76
Metabolic and endocrine bone disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Other non-collagenous proteins exist in small amounts in the mineralized matrix – mainly sialoproteins (osteopontin), osteonectin, osteocalcin (bone Gla protein) and alkaline phosphatases. Their functions have not been fully elucidated but they appear to be involved in the regulation of bone cells and matrix mineralization. Osteocalcin is produced only by osteoblasts and its concentration in the blood is, to some extent, a measure of osteoblastic activity. Bone matrix also has large concentrations of local regulatory factors including TFG-beta, which stimulate osteoblast differentiation, and may act as coupling factors whereby degradation of bone matrix during resorption leads to release of factors that recruit osteoblasts for the subsequent formation phase.
Suppression of joint destruction with subcutaneous tocilizumab for Japanese patients with rheumatoid arthritis in clinical practice
Published in Modern Rheumatology, 2020
Yasuharu Nakashima, Masakazu Kondo, Eisuke Shono, Takashi Ishinishi, Hiroshi Tsukamoto, Koji Kuroda, Akira Maeyama, Hiroshi Harada, Masayuki Maekawa, Takashi Shimauchi, Ryuji Nagamine, Hiroshi Jojima, Seiji Yoshizawa, Tomomi Tsuru, Takeshi Otsuka, Hisaaki Miyahara, Eiichi Suematsu, Ken Wada, Shigeru Yoshizawa, Yasushi Inoue, Takaaki Fukuda, Satoshi Ikemura, Akihisa Haraguchi
TCZ administration has frequently been reported to increase bone formation markers. Gernero et al. have reported that serum osteocalcin, a bone formation marker, increased in the OPTION study [27]. In the same way, BAP increased significantly from the baseline in the present study showing the positive effects on bone formation. However, it is not consistent with the bone resorption markers with TCZ treatment. The OPTION study showed that carboxy-terminal pyridinoline cross-linked telopeptide of type I collagen (CTX1), a bone resorption marker, decreased after TCZ administration, but the LITHE study showed the increased CTX1 at 52 weeks after TCZ treatment [28]. In this study, both BAP and TRACP5b increased. This paradoxical increase of TRACP5b was also seen with TNF inhibitor. Toussirot et al reported elevated TRAP5b despite increase in lumber spine bone mineral density [29]. There is no clear explanation for these findings at present, and it needs further clarification.
Puberty and resultant increased bone turnover as a possible etiology of an increased lead concentration in a pre-adolescent girl
Published in Clinical Toxicology, 2020
Rebecca E. Bruccoleri, Alan D. Woolf
Osteocalcin, a protein mainly synthesized by osteoblasts, is used as a biomarker of bone formation [3]. It increases during ages that correlate with puberty [4]. Lead is absorbed from the gastrointestinal tract into the blood where it then equilibrates between the blood and bone and soft tissues compartments. Lead is moved into the bone with osteoblasts and out of the bone with osteoclasts [5]. In children with a considerable body burden of lead stored in bone, increased bone turnover could leach lead back into the bloodstream. There is limited literature examining lead poisoning in adolescents. One study of adolescent girls taking depomedroxy-progesterone acetate found a higher proportion had BLL >4 mcg/dl compared to subjects who did not use hormones. Depomedroxy-progesterone acetate is a birth control associated with bone mineral loss [6]. In this patient, a plot of the BLL and osteocalcin levels through time as well as her BLL and change in growth per 30-day periods are shown in Figures 1 and 2. These data suggest changes in BLL correspond to elevated osteocalcin values and changes in growth per 30-day period. In her case, given that lead can persist in bones for decades and no identifiable exposure was found, it was thought that her BLL of 10 mcg/dl prior to her increase represented a slow decline from the initial exposure in early childhood.
Osteocalcin and regulatory cytokine imbalance in children with congenital cleft lip and palate
Published in Immunological Medicine, 2020
Irina Nesterova, Marina Mitropanova, Galina Chudilova, Lyudmila Lomtatidze
Currently, periods of active bone growth in healthy children of different ages are described in detail. At the age of one year old (from 1 day of life to 12 months), active growth and overmodulation of 50–70% of bone tissue occurs. From the age of 3 to 4 to 5 years, and then from 6 to 9 years, periods of active bone growth are again observed. The puberty period (from 10 to 15 years old) is characterized by an active period of bone growth, which in some adolescents can last up to 16–18 years old. Osteocalcin is the main vitamin K-dependent non-collagen bone matrix protein that binds calcium and hydroxyapatites, which is a fundamental process in the formation and metabolism of bone tissue. Osteocalcin is synthesized by osteoblasts and odontoblasts of bone tissue. The bulk of the protein is part of the extracellular matrix of bone tissue, which is then mineralized to form a new bone, and the remainder enters the bloodstream. Osteocalcin is considered a marker of bone remodeling and the most important factor affecting bone growth and restoration. The level of osteocalcin reflects the degree of osteoblast activity and the nature of bone metabolism [19].