Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of calcium, phosphate, alkaline phosphatase (A.P.), immunoreactive calcitonin (iC.T.), and immunoreactive parathyroid hormone (iP.T.H.) were measured in fifty-two patients with chronic renal failure on maintenance haemodialysis. On the basis of a bimodal distribution of values for plasma-A.P. the patients were dividied into 2 groups. In those patients with normal A.P. concentratons as well as in twenty-eight normal subjects there was a positive correlation between iP.T.H. and iC.T. which was independent of plasma calcium or phosphate. Patients with increased plasma-A.P. had higher concentrations of iP.T.H., lower concentrations of iC.T., and showed a negative relation between the concentrations of the two hormones. It is suggested that a possible factor in the pathogenesis of renal bone disease is a failure to secrete C.T. in adequate amounts.
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PMID:Evidence that endogenous calcitonin protects against renal bone disease. 6 2

Four patients with thyrotoxicosis, hypercalcaemia and metabolic bone disease are described. One of them had a 'hot nodule', T3 toxicosis and a parathyroid tumour and another had thin bones, subperiosteal cortical bone erosions and complete dysphagia. Hypercalcaemia persisted during treatment with antithyroid drugs in two patients, both of whom had hyperparathyroidism. The administration of salmon calcitonin to these two patients before starting antithyroid treatment produced an immediate and sustained fall in serum calcium and urinary hydroxyproline levels. Calcitonin administration should be of value in the early management of hypercalcaemic patients.
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PMID:Thyrotoxicosis and hypercalcaemia: response to antithyroid drugs and salmon calcitonin. 6 11

Hypercalcemia is very uncommon in small cell (oat cell) carcinoma of the lung. Two cases of this neoplasm associated with symptomatic hypercalcemia are described. Despite normal skeletal roentgenograms, metastatic bone disease was demonstrated by abnormal bone scans and bone biopsies in both patients. The combination of conventional antihypercalcemia therapy, cytotoxic cancer chemotherapy, and synthetic salmon calcitonin corrected the hypercalcemia despite progression of the small cell carcinoma. One patient with elevated serum immunoreactive parathyroid hormone (PTH) had a parathyroid adenoma at autopsy. This association emphasizes that in cases of bronchogenic small cell carcinoma with hypercalcemia, conincidental primary hyperparathyroidism should be considered.
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PMID:Hypercalcemia in small cell (oat cell) carcinoma of the lung. Coincident parathyroid adenoma in one case. 17 Oct 50

Comparison of biopsies from patients with Paget's bone disease before and during long-term treatment with calcitonin reveals that the ration of bone-adherent osteoclasts to free osteoclasts is not modified by the hormone. Nor does treatment alter the average number of nuclei in osteoclasts. Under electron microscopy, all the cytological anomalies of osteoclasts in Paget's bone disease and, in particular, the characteristic nuclear inclusions, persist through treatment. Thus, although such osteoclasts do react to calcitonin as demonstrated by several authors, the specific morphological anomalies remain unaffected by the treatment. It is likely that the osteoclast in Paget's bone disease is an abnormal cell with peculiarities which may be related to the yet unknown etiology of the disease.
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PMID:[Action of calcitonin on osteoclasts in Paget's bone disease during long term treatment (author's transl)]. 20 10

Osteitis deformans is a bone disease of still unknown aetiology which shows characteristic symptoms in the maxillofacial region. An increase in size of the entire calvarium and also of single bones of the facial skeleton belongs to these symptoms. A triad may be seen in the jawbone: osteoporosis, foci of densification and cementum hyperplasia. No possibility of treatment was known in the past. Nowadays, the use of cytostatics, calcitonin and diphosphonates seems to be promising.
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PMID:[Osteitis deformans]. 27 33

Two children with bone dysplasia with hyperphosphatasemia (juvenile Paget's disease) were treated with synthetic human calcitonin. The progress of bone disease was monitored radiographically and histologically. Pretreatment radiographs showed markedly abnormal bone, characterized by lack of discrete cortex and absence of normal modeling. During treatment a discrete cortex was formed composed of compact bone, and more normal modeling occurred. This coincided with a histologic change from woven bone before treatment to a more lamellar type during treatment.
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PMID:Calcitonin treatment in hereditary bone dysplasia with hyperphosphatasemia: a radiographic and histologic study of bone. 40 39

There is currently considerable interest in the pathogenesis of postmenopausal osteoporosis, which is the most common metabolic bone disease. Osteoporosis affects approximately 20 million persons in the United States, 90% of whom are postmenopausal women. Although there is evidence that estrogen deficiency is an important contributory factor, the pathogenesis of osteoporosis is multifactorial and presently poorly understood. There is evidence that pineal melatonin is an anti-aging hormone and that the menopause is associated with a substantial decline in melatonin secretion and an increased rate of pineal calcification. Animal data indicate that pineal melatonin is involved in the regulation of calcium and phosphorus metabolism by stimulating the activity of the parathyroid glands and by inhibiting calcitonin release and inhibiting prostaglandin synthesis. Hence, the pineal gland may function as a "fine tuner" of calcium homeostasis. In the following communication, we propose that the fall of melatonin plasma levels during the early stage of menopause may be an important contributory factor in the development of postmenopausal osteoporosis. Consequently, plasma melatonin levels taken in the early menopause could be used as an indicator or perhaps as a marker for susceptibility to postmenopausal osteoporosis. Moreover, light therapy, administration of oral melatonin (2.5 mg at night) or agents which induce a sustained release of melatonin secretion such as 5-methoxypsoralen, could be useful agents in the prophylaxis and treatment of postmenopausal osteoporosis. Finally, since application of external artificial magnetic fields has been shown to synchronize melatonin secretion in experimental animals and humans, we propose that treatment with artificial magnetic fields may be beneficial for postmenopausal osteoporosis.
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PMID:Is postmenopausal osteoporosis related to pineal gland functions? 130 8

During pregnancy, calcium is continuously transferred directly from the maternal intestine to the fetal bone, a transfer that is mainly induced by the interrelated actions of the calcium-regulating hormones parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcitonin. It has recently been demonstrated in animals that PTH-related protein (PTHrP) is the fetal equivalent of PTH. Human PTHrP, originally described as a product of a human lung cancer cell line and implicated in the pathogenesis of humoral hypercalcemia of malignancy, is a protein with 141 amino acids, and it has biochemical actions similar to PTH. It is believed that fetal PTHrP is mainly derived from the placenta during early gestation and from the fetal parathyroid glands during further development and that this protein has the role of maintaining the maternal-fetal calcium gradient either alone or in concert with 1,25(OH)2D. With birth, the placental supply of calcium ceases abruptly, stimulating the increase of PTH and 1,25(OH)2D, which are the main regulators of postnatal calcium metabolism. Alterations in the placental calcium (and phosphate) gradient may be caused by maternal hypo- or hypercalcemia and placental insufficiency and may be followed by transient disorders of calcium metabolism in the newborn. Due to abrupt cessation of the calcium and phosphate supply after delivery at a time when mineral demands are the highest, preterm infants are especially prone to hypocalcemia and osteopathy. If bone disease of prematurity is to be prevented, the amounts of calcium and phosphate must be adequate, as demonstrated by laboratory tests, the most important being calcium and phosphate in urine and alkaline phosphatase activity in serum.
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PMID:[Perinatal calcium metabolism. Physiology and pathophysiology]. 143 20

The ability of low-dose tetracyclines to inhibit collagenase activity and inactivate osteoclasts suggests that these compounds have great potential as a prophylaxis for metabolic bone disease. However, the cellular mechanism by which tetracyclines interact with skeletal tissue is not yet clear. To better understand the effects of tetracyclines on bone metabolism, we examined their effect on osteoclast activity in vitro. Because tetracyclines can enter the cell and bind calcium and have been reported to directly interact with osteoclasts, we postulated that exposure to either of two tetracyclines, minocycline or doxycycline, would alter cytosolic Ca2+ regulation in rat osteoclasts. [Ca2+]i was measured in single rat osteoclasts utilizing fura-2. Addition of extracellular Ca2+ (5 mM CaCl2), a potent osteoclast inhibitor, increased [Ca2+]i in all osteoclasts, but 10(-6) M salmon calcitonin (sCT) did so only in a subpopulation of osteoclasts. Neither minocycline nor doxycycline (10 micrograms/ml) altered steady-state osteoclast [Ca2+]i. Further, neither minocycline nor doxycycline pretreatment affected the sCT-mediated increases in [Ca2+]i. However, tetracycline pretreatment significantly decreased the cytosolic Ca2+ response to extracellular CaCl2. Our results strongly suggest that tetracyclines have a specific effect on extracellular Ca(2+)-stimulated cytosolic Ca2+ mobilization in osteoclasts, which is not solely dependent on their ability to buffer Ca2+. Furthermore, these results point to the potential use of tetracyclines as probes to study cytosolic Ca2+ regulation. However, that tetracyclines attenuate a signal response associated with decreased osteoclastic resorption suggests that the reported antiresorptive attributes of tetracyclines must be achieved independently of an effect on osteoclastic cytosolic Ca2+.
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PMID:Regulation of cytoplasmic calcium concentration in tetracycline-treated osteoclasts. 146 56

Increasing pain in the region of the lumbar vertebrae occurred in a 23-year-old woman known for the past 6 1/2 years to have Crohn's disease affecting the ileocolon. Radiology revealed marked osteopenia with collapse and deformation of the vertebral bodies. The only pointer to a bone disease was a markedly lowered serum level of 25-OH-vitamin D (less than 10 ng/ml). Biopsy from the ileal crest revealed pure osteoporosis without osteomalacia. Decisive pathogenetic factors were, in the main, glucocorticoid medication, malnutrition and the long duration of Crohn's disease. During treatment with monofluorophosphate, 152 g daily, in fixed combination with 600 mg calcium as well as calcitonin (initially 100 I.U. daily subcutaneously for two weeks, then 100 I.U. every other day s.c.) and vitamin D (3 x 1,000 I.U. daily by mouth) she became free of symptoms, and she has remained so for 9 months.
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PMID:[Severe osteoporosis in a young female patient with Crohn's disease]. 164 71


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