Thyroid diseases and bone health.

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Term Occurence Count Dictionary
thyrotoxicosis 6 endocrinologydiseases
congenital hypothyroidism 3 endocrinologydiseases
hyperthyroidism 11 endocrinologydiseases
hypothyroidism 13 endocrinologydiseases
osteoporosis 8 endocrinologydiseases
thyroglobulin 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
thyroglobulin 17171 cancerThyroid cancer cells express TSH receptor, and TSH stimulates cell proliferation, iodine uptake and thyroglobulin secretion from tumour cells. This is also true in metastatic cells in about 65% of cases. There is,
Select Disease Character Offset Disease Term Instance
congenital hypothyroidism 21089 (TSHR)Loss-of-function mutations in TSHB, encoding the TSHβ subunit, result in biologically inactive TSH and congenital hypothyroidism (OMIM 275100). Loss- and gain-of-function mutations in TSHR, encoding the TSH receptor, result in TSH
congenital hypothyroidism 21233 Loss- and gain-of-function mutations in TSHR, encoding the TSH receptor, result in TSH resistance with congenital hypothyroidism (OMIM 275200) or autosomal dominant hyperthyroidism (OMIM 609152), respectively. Few reports have documented
congenital hypothyroidism 21627 supplementation or thyroidectomy/ablation [[1]]. Nevertheless, normal growth occurs in individuals with congenital hypothyroidism following proper thyroid hormone replacement [[60]–[62]], and improvement of skeletal developmental
hyperthyroidism 1318 are rare because of prompt diagnosis and treatment. Recent data, however, indicate that subclinical hyperthyroidism is associated with low bone mineral density (BMD) and an increased risk of fracture. Population studies
hyperthyroidism 10780 closure of the cranial sutures can result in craniosynostosis with neurological sequelae. Untreated hyperthyroidism during pregnancy is also associated with craniosynostosis and may be a causative risk factor [[20]].Summary
hyperthyroidism 13463 formation that results in a net loss of approximately 10% of bone per remodelling cycle [[23], [24]]. Thus, hyperthyroidism is an established cause of high bone turnover with accelerated bone loss leading to osteoporosis and
hyperthyroidism 13750 untreated thyrotoxicosis is now rare because of early diagnosis and treatment, although undiagnosed hyperthyroidism is an important risk factor for secondary bone loss and osteoporosis in patients presenting to hospital
hyperthyroidism 14314 reference ranges in the presence of a TSH level elevated above its reference range. Conversely, subclinical hyperthyroidism occurs when T4 and T3 levels are within their reference ranges, but the TSH concentration is suppressed
hyperthyroidism 14870 association with fracture [[28]].More studies have investigated the relationship between subclinical hyperthyroidism and BMD or fracture risk [[1]] and large population studies have suggested an increase in bone turnover,
hyperthyroidism 15457 with a 2- and 3.5-fold increased risk of hip and spine fractures, respectively. Overall, subclinical hyperthyroidism was associated with bone loss and fracture, particularly in individuals with endogenous disease [[28]].
hyperthyroidism 18468 admissions for fracture was 2.5× higher in patients with TSH <0.05 mU/l [[29]]. In patients with hyperthyroidism , there was a 3× increase in hip and 4× increase in vertebral fracture if TSH was suppressed <0.01 mU/l
hyperthyroidism 19461 susceptibility to fracture. This complication is now rare because of prompt diagnosis and treatment. Subclinical hyperthyroidism is also associated with an increased risk of fracture in both men and women, but especially those with
hyperthyroidism 21295 receptor, result in TSH resistance with congenital hypothyroidism (OMIM 275200) or autosomal dominant hyperthyroidism (OMIM 609152), respectively. Few reports have documented the skeletal consequences of these genetic
hyperthyroidism 21814 and improvement of skeletal developmental manifestations is seen in patients with autosomal dominant hyperthyroidism following thyroidectomy and normalization of thyroid status [[63], [64]]. Overall, the limited available
hypothyroidism 343 essential for skeletal development and are important regulators of bone maintenance in adults. Childhood hypothyroidism causes delayed skeletal development, retarded linear growth and impaired bone mineral accrual. Epiphyseal
hypothyroidism 772 growth and bone maturation, but recovery may be incomplete dependent on the duration and severity of hypothyroidism prior to treatment. A severe phenotype characteristic of hypothyroidism occurs in children with resistance
hypothyroidism 844 the duration and severity of hypothyroidism prior to treatment. A severe phenotype characteristic of hypothyroidism occurs in children with resistance to thyroid hormone due to mutations affecting THRA encoding thyroid
hypothyroidism 10175 adult height may not always be achieved and in such cases the deficit correlates with the severity of hypothyroidism and its duration prior to commencement of thyroid hormone replacement [[17]].HyperthyroidismThyrotoxicosis
hypothyroidism 11525 deposition, but may also result in short stature. Thus, the opposing skeletal consequences of childhood hypothyroidism and thyrotoxicosis, together with the rapid response of the hypothyroid skeleton to thyroid hormone
hypothyroidism 12443 have strengthened our understanding.HypothyroidismEarly histomorphometry analysis demonstrated that hypothyroidism results in low bone turnover with decreased osteoblastic bone formation and reduced osteoclastic bone
hypothyroidism 13058 imaging techniques. Thus, there are no good clinical data that demonstrate the skeletal consequences of hypothyroidism in adults.HyperthyroidismHyperthyroidism, in contrast, causes high bone turnover with an increased frequency
hypothyroidism 14085 thyrotoxicosis especially in post-menopausal women [[27]–[31]].Subclinical thyroid diseaseSubclinical hypothyroidism is defined biochemically as the occurrence of circulating concentrations of T4 and T3 within their normal
hypothyroidism 14487 ranges, but the TSH concentration is suppressed below its reference range. The effect of subclinical hypothyroidism on bone mineralization and fracture susceptibility has not been studied extensively [[1]], but a recent
hypothyroidism 21100 (TSHR)Loss-of-function mutations in TSHB, encoding the TSHβ subunit, result in biologically inactive TSH and congenital hypothyroidism (OMIM 275100). Loss- and gain-of-function mutations in TSHR, encoding the TSH receptor, result in TSH
hypothyroidism 21244 gain-of-function mutations in TSHR, encoding the TSH receptor, result in TSH resistance with congenital hypothyroidism (OMIM 275200) or autosomal dominant hyperthyroidism (OMIM 609152), respectively. Few reports have documented
hypothyroidism 21638 or thyroidectomy/ablation [[1]]. Nevertheless, normal growth occurs in individuals with congenital hypothyroidism following proper thyroid hormone replacement [[60]–[62]], and improvement of skeletal developmental
hypothyroidism 22742 condition (OMIM 614450) are consistent with the characteristic consequences of congenital and juvenile hypothyroidism , and reflect impaired T3 action in cartilage and bone. To date, 15 THRA mutations in 11 separate codons
osteoporosis 1181 mediates thyroid hormone action in the skeleton. In adults, thyrotoxicosis is well known to cause severe osteoporosis and fracture, but cases are rare because of prompt diagnosis and treatment. Recent data, however, indicate
osteoporosis 5535 demands of mineral homeostasis [[8]]. Uncoupling of these processes leads to accelerated bone loss in osteoporosis or accumulation of bone in osteopetrosis.Fig. 2Bone remodelling cycle. The bone remodelling cycle is
osteoporosis 13563 hyperthyroidism is an established cause of high bone turnover with accelerated bone loss leading to osteoporosis and increased fracture susceptibility. Severe osteoporosis resulting from untreated thyrotoxicosis is
osteoporosis 13622 turnover with accelerated bone loss leading to osteoporosis and increased fracture susceptibility. Severe osteoporosis resulting from untreated thyrotoxicosis is now rare because of early diagnosis and treatment, although
osteoporosis 13822 treatment, although undiagnosed hyperthyroidism is an important risk factor for secondary bone loss and osteoporosis in patients presenting to hospital with fracture [[25], [26]]. Accordingly, population studies have
osteoporosis 18687 <0.01 mU/l [[27]].Overall, post-menopausal women on suppressive doses of T4 may be at risk of bone loss and osteoporosis [[1]].Summary of skeletal consequences of thyroid disease in adultsThyroid hormones act via TRα in
osteoporosis 19308 increased risk of fragility fracture. Thyrotoxicosis is a well-established cause of high bone turnover osteoporosis , resulting in an increased susceptibility to fracture. This complication is now rare because of prompt
osteoporosis 28187 a skeletal phenotype of accelerated bone development in juveniles and increased bone turnover with osteoporosis in adults that is due to increased T3 action in cartilage and bone [[1], [83], [89]–[91]]
thyrotoxicosis 1136 animal studies demonstrating that TRα mediates thyroid hormone action in the skeleton. In adults, thyrotoxicosis is well known to cause severe osteoporosis and fracture, but cases are rare because of prompt diagnosis
thyrotoxicosis 10640 growth plates and early cessation of growth leading to persistent short stature [[18], [19]]. In severe thyrotoxicosis in young children, early closure of the cranial sutures can result in craniosynostosis with neurological
thyrotoxicosis 11544 also result in short stature. Thus, the opposing skeletal consequences of childhood hypothyroidism and thyrotoxicosis , together with the rapid response of the hypothyroid skeleton to thyroid hormone replacement, demonstrate
thyrotoxicosis 13660 to osteoporosis and increased fracture susceptibility. Severe osteoporosis resulting from untreated thyrotoxicosis is now rare because of early diagnosis and treatment, although undiagnosed hyperthyroidism is an important
thyrotoxicosis 13981 fracture [[25], [26]]. Accordingly, population studies have demonstrated an increased risk of fracture in thyrotoxicosis especially in post-menopausal women [[27]–[31]].Subclinical thyroid diseaseSubclinical hypothyroidism
thyrotoxicosis 15803 followed up for 7.5 years. This study demonstrated an exponential association between the duration of thyrotoxicosis and fracture. In euthyroid individuals, the risk of fracture increased with each standard deviation

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