GLUCOCORTICOID-INDUCED BONE DISEASE: MECHANISMS AND IMPORTANCE IN PEDIATRIC PRACTICE.

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Term Occurence Count Dictionary
dexamethasone 2 endocrinologydiseasesdrugs
obesity 4 endocrinologydiseases
osteoporosis 18 endocrinologydiseases
prednisone 1 endocrinologydiseasesdrugs
cortisol 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
cortisol 14859 (11β-HSD1), which converts inactive forms of corticosteroids (cortisone and prednisone) in active forms ( cortisol and prednisolone).[27],[48] Immunohistochemical and in situ hybridization studies showed 11β-HSD1 expression
dexamethasone 15981 GC-inactivating enzyme and HSD 2. The sensitivity of different types of GC to this enzyme varies, and dexamethasone , by having a fluorine atom at the 9α position of the B ring, with site of HSD2 blocked, is the steroid
dexamethasone 18619 response to mechanical overload is also influenced by Wnt β-catenin.[50]An experimental study found that dexamethasone inhibits all Wnt β-catenin pathway from the cell surface to nuclear translocation.[52] In addition,
prednisone 14830 specifically to type 1 (11β-HSD1), which converts inactive forms of corticosteroids (cortisone and prednisone ) in active forms (cortisol and prednisolone).[27],[48] Immunohistochemical and in situ hybridization
Select Disease Character Offset Disease Term Instance
obesity 2616 extrinsic factors - including genetics, puberty, adequate intake of calcium, protein, and vitamin D, obesity , physical activity, chronic inflammatory morbid conditions, and use of medications - affect the occurrence
obesity 13020 unit, with mutual trophic influence. Moreover, chronic corticosteroid therapy promotes adipogenesis and obesity , with capture and reduction of vitamin D.[43],[44]Decreased intestinal calcium absorption, increased
obesity 22209 mode of discontinuing treatment, should be clarified.Nutritional follow-up is essential to prevent obesity , but also to ensure adequate intake of calcium (1,300 mg/day between 9 and 18 years) and proteins, as
obesity 22962 recommended, considering the beneficial action on bone and muscle strength, in addition to the prevention of obesity .The suspicion of spontaneous fractures, especially invertebrae (evidenced by pain or loss of height),
osteoporosis 425 date (epub): 5/2017AbstractABSTRACTObjective: To describe mechanisms by which glucocorticoids cause osteoporosis , with fracture risk, combining this learning with a possible professional behavior change.Data sources:
osteoporosis 839 between 2000 and 2016. Keywords used on the search were the following: glucocorticoids, fractures, osteoporosis , bone health, vitamin D, children, and adolescents.Data synthesis: The review was divided into four
osteoporosis 1023 review was divided into four topics: 1) introduction, with a brief focus on pediatric fractures; 2) osteoporosis in children and adolescents, highlighting it as a silent cause of fractures; 3) glucocorticoids and
osteoporosis 2939 factor.[7]OSTEOPOROSIS IN CHILDREN AND ADOLESCENTSA fracture may indicate underlying bone fragility, that is, osteoporosis , which is not restricted to the elderly. The National Institute of Health (NIH), an American organization,
osteoporosis 3097 National Institute of Health (NIH), an American organization, established the current definition of osteoporosis in 2001 after a consensus: “a skeletal disorder characterized by compromised bone strength predisposing
osteoporosis 4463 will determine bone mass throughout life.[14]It is estimated that 10% increase in PMO can delay senile osteoporosis in 13 years.[15] Approximately 40-60% of adult bone mass is accrued in adolescence, and 25% of the PBM
osteoporosis 4710 two years around the growth spurt.[15],[16] Even without increased bone loss, an adult can develop osteoporosis because he or she has not reached their PBM in childhood and adolescence.[17] As mentioned earlier,
osteoporosis 7153 definition.[20],[22] Therefore, experts gathered in a worldwide consensus established the diagnosis of osteoporosis in children, in addition to the indications, interpretation, and the use of bone densitometry in this
osteoporosis 7701 10 years of age, or three or more fractures of long bones below 19 years of age), are diagnosis of osteoporosis in this age group.[22],[25]The actual incidence and prevalence of osteoporosis in the pediatric population
osteoporosis 7780 age), are diagnosis of osteoporosis in this age group.[22],[25]The actual incidence and prevalence of osteoporosis in the pediatric population are not well defined; however, it is known that osteoporosis may compromise
osteoporosis 7869 prevalence of osteoporosis in the pediatric population are not well defined; however, it is known that osteoporosis may compromise both sexes and occur at any age, being classified as primary or genetic (whose main representative
osteoporosis 8388 calcineurin inhibitors, anticoagulants, and glucocorticoids (GC) are drugs associated with the development of osteoporosis ,[10] with emphasis to the last ones, which are widely used in pediatric prescription.GLUCOCORTICOIDS
osteoporosis 11074 compromise bone health.If used chronically, GC are considered the main cause of secondary and iatrogenic osteoporosis .[27],[35] However, the potential for fractures is often disregarded by the professional who prescribes
osteoporosis 11980 Therefore, the absence of alterations in bone densitometry does not rule out the existence of GC-induced osteoporosis .Extensive study of a British cohort, including individuals aged 4-17 years, revealed that the annual
osteoporosis 13546 direct action of these steroids on bone cells is the main mechanism in the genesis of the resulting osteoporosis .[37],[40]Figure 1 summarizes the pathogenesis of secondary fracture to GC excess.Figure 1:Pathogenesis
osteoporosis 15244 other enzymes.[36]Increased expression of 11β-HSD1 enzyme is considered a risk factor for GC-induced osteoporosis .[12] In its active form, the GC binds with a receiver (GRα or GRβ), a member of the nuclear receptor
osteoporosis 16174 blocked, is the steroid which is most resistant to such inactivation, and therefore is what causes osteoporosis the most.[35]Figure 2 outlines the 11β-HSD enzyme system and the connection with the genomic mechanism
osteoporosis 16400 action. The result of activation or the resistance to inactivation of GC excess in bone contributes to osteoporosis .Figure 2:Genomic mechanism of action of GC and the hydroxysteroid dehydrogenase (HSD) enzymatic system.Owing

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