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Results for “Bone Diseases, Endocrine”

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At least 19 recordsLinked to original sources
PubMed1989

Bone scanning in metabolic and endocrine bone disease.

99mTc diphosphonate bone scanning has proved to be a sensitive, though nonspecific, way of detecting a wide variety of metabolic bone disorders. Classic scan appearances of generalized increased tracer uptake throughout the skeleton are found in many types of metabolic bone disease, and whole-body retention measurements can be used to detect early forms of disease. Focal disease identified on bone scanning such as pseudofractures and brown tumors are clearly identified on the 99mTc diphosphonate bone scan, with isotope scan changes preceding radiological changes by up to 18 months. The use of whole-body retention measurements will further increase sensitivity of detection in patients with metabolic bone disease.

Bone Diseases↗
PubMed2002

Gender differences in serum markers of bone resorption in healthy subjects and patients with disorders affecting bone.

To assess how two different serum markers of bone resorption may reflect changes in bone turnover, we compared age- and sex-related changes in serum C-terminal telopeptide of type I collagen (betaCTx) and tartrate-resistant acid phosphatase activity (TRAP) in 136 healthy men and 184 normal women. Serum levels of the two markers were also assessed in several groups of patients of both sexes presenting with the most common metabolic and endocrine bone diseases: established osteoporosis (n = 77), primary hyperparathyroidism (n = 44), glucocorticoid excess (n = 17), chronic renal failure (n = 39), active Paget's disease of bone (n = 5), humoral hypercalcemia of malignancy (n = 3), osteomalacia (n = 3), hyperthyroidism (n = 10), post-surgical hypoparathyroidism (n = 10), acromegaly (active disease, n = 8) and Cushing's syndrome (n = 10). In men the regression of betaCTx with age showed an initial decrease in bone resorption followed by an increase thereafter, starting from the sixth decade of life. No age-related change in serum TRAP activity was observed. In women, by contrast, a slight but significant linear correlation of both serum betaCTx and TRAP with age (r = 0.223, p<0.003 and r = 0.333, p<0.0001, respectively) was found, the two markers being positively correlated (r = 0.238, p<0.002). In each class of patients the mean Z-scores of betaCTx were significantly higher than those of TRAP activity. Moreover, compared with normal subjects, serum betaCTx seems to be characterized by a superior sensitivity relative to TRAP measurement, at least in the disorders studied.

Acid Phosphatase↗
PubMed2006

P450 oxidoreductase deficiency: a new form of congenital adrenal hyperplasia.

PURPOSE OF REVIEW: P450 oxidoreductase deficiency--a newly described form of congenital adrenal hyperplasia--typically presents a steroid profile suggesting combined deficiencies of steroid 21-hydroxylase and 17alpha-hydroxylase/17,20-lyase activities. These and other enzymes require electron donation from P450 oxidoreductase. The clinical spectrum of P450 oxidoreductase deficiency ranges from severely affected children with ambiguous genitalia, adrenal insufficiency and the Antley-Bixler skeletal malformation syndrome to mildly affected individuals with polycystic ovary syndrome. We review current knowledge of P450 oxidoreductase deficiency and its broader implications. RECENT FINDINGS: Since the first report in 2004, at least 21 P450 oxidoreductase mutations have been reported in over 40 patients. The often subtle manifestations of P450 oxidoreductase deficiency suggest it may be relatively common. P450 oxidoreductase deficiency, with or without Antley-Bixler syndrome, is autosomal recessive, whereas Antley-Bixler syndrome without disordered steroidogenesis is caused by autosomal dominant fibroblast growth factor receptor 2 mutations. In-vitro assays of P450 oxidoreductase missense mutations based on P450 oxidoreductase-supported P450c17 activities provide excellent genotype/phenotype correlations. The causal connection between P450 oxidoreductase deficiency and disordered bone formation remains unclear. SUMMARY: P450 oxidoreductase mutations cause combined partial deficiency of 17alpha-hydroxylase and 21-hydroxylase. Individuals with an Antley-Bixler syndrome-like phenotype presenting with sexual ambiguity or other abnormalities in steroidogenesis should be analyzed for P450 oxidoreductase deficiency.

Adrenal Hyperplasia, Congenital↗
PubMed1999

[Osteoporosis and metabolic bone diseases; clinical relationship].

Metabolic bone diseases with disturbed bone remodeling lead to loss of biomechanical quality and atraumatic fractures. Differential diagnosis, prevention and adequate treatment should already start early in the course of these disorders to prevent fractures. Thus, clinical osteology is more than the simplified connection "low bone mineral density--fractures--osteoporosis". This review summarizes physiological relations between bone tissue and calcium homoeostasis as well as the relation between structure and function. In addition, the main metabolic osteopathies "osteoporosis, primary hyperparathyroidism and osteomalacia" are presented from a clinical point of view. The importance and the diagnostic values of biochemical parameters and of the transiliacal biopsy are discussed. In this respect the quantitative measurement of the mineralization density (bone mineral density distribution = BMDD) seems to be of high value and extends the well established bone histomorphometry. This recently introduced method has the power to distinguish between small differences in the degree of mineralization of the matrix with high precision and reproducibility. The results of quantitative backscattered electron imaging in the scanning electron microscope improve the differential diagnosis of bone diseases with alterations in mineralization density, helps to detect mixed etiology (e.g. osteoporosis plus osteomalacia) and facilitate decision making for treatments. The value of biochemical, radiological, osteodensitometric and histopathological tests for diagnosis and treatment depends on the knowledge of the clinical relations and the complex interactions between calcium-, phosphate- and bone metabolism.

Age Factors↗
PubMed1995

Endocrine causes of bone disease.

Hyperthyroidism, glucocorticoid excess, hyperparathyroidism, hypogonadism, and acromegaly decrease bone mineral density and aggravate the osteoporotic tendencies of elderly individuals. After effective treatment of endocrinopathy, the bone attempts to return to the normal mineral density. In most circumstances, however, this attempt is incomplete. Early diagnosis and treatment of these endocrine problems in older patients helps to maintain their skeletal integrity and prevent osteoporotic fractures.

Adrenal Gland Diseases↗
PubMed1990

[Different behavior of bone turnover markers in endocrine (extrinsic) and structural (intrinsic) osteopathies].

Alkaline phosphatase, osteocalcin and hydroxyproline levels were evaluated in patients with the following conditions: primary hyperparathyroidism, renal dialysis, hyperthyroidism, Cushing's syndrome, long term corticosteroid therapy, Paget's disease, osteoblastic metastases, osteolytic or mixed metastases, and nutritional osteomalacia. In all cases the levels of the three substances were increased, with the following exceptions: a) in endogenous or exogenous hypercortisolism states osteocalcin level was reduced and those of alkaline phosphatase and hydroxyproline were unchanged; and b) in blastic or lytic metastases osteocalcin level was unchanged. In general, alkaline phosphatase and hydroxyproline levels had a higher sensitivity than those of osteocalcin in structural bone disease (Paget's disease, blastic or lytic metastases), whereas the converse was true for endocrine bone disease (the remaining conditions except osteomalacia, which is mixed, both structural and endocrine; in this syndrome, the three substances showed the same sensitivity.

Adolescent↗
PubMed1991

[Diagnostic value of alkaline phosphatase isoenzymes].

Among the serum enzymes used for diagnostic purposes the alkaline phosphatase (AP) is one of the oldest and the most frequently applied laboratory tests. Increased activity found in the serum is a consequence of certain hepato-biliary disorders, different bone diseases, endocrine syndromes, kidney illnesses and malignant tumors as well. From the study of the pattern of the isoenzymes of the serum-AP information of practical importance may be gained by which many differential-diagnostic problems can be solved. For the clinical-chemical laboratories methods that use electrophoretic separation on different membranes or gels are recommended. Patterns characteristic for different diseases may well be differentiated from normal constellation. AP-isoenzymes help to reveal cholestases at early stages, some disorders of bone metabolism and malignant processes as well.

Alkaline Phosphatase↗