Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

19 patients with Paget's disease were treated orally for 6 months with disodium dichloromethylene diphosphonate. 1600 mg/day (10 patients) significantly reduced urine hydroxyproline, serum alkaline phosphatase, urine calcium, and the number of pagetic bone osteoclasts. Tetracycline double labelling revealed undisturbed bone mineralisation. There was improvement on quantitative bone-scans and bone pain diminished. There was a transient increase in parathyroid hormone level in 13 of the 19 patients during treatment, which was associated with a high serum 1,25 (OH)2D3. No adverse clinical side-effects have been observed and biochemical remission has persisted for 9 months.
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PMID:Effects of disodium dichloromethylene diphosphonate on Paget's disease of bone. 9 Feb 15

Thirty-five patients with bone disease and chronic renal failure (twenty-four on maintenance haemodialysis) were treated for 7--39 months with 1alpha-hydroxyvitamin D3, 2--2.5 microgram daily by mouth. Symptoms (bone pain and muscle weakness) and radiographic appearances improved and plasma alkaline phosphatase returned to normal in the majority of patients (87, 76 and 75% respectively). In contrast, histological appearances in bone improved in only 46% twenty-three patients from whom paired biopsies were available, and this change was not greatly different from that seen in a comparable group of untreated patients. Significant correlations were noted in individual patients between the changes in symptoms, X-rays, plasma alkaline phosphatase and immunoreactive parathyroid hormone and these, in turn, were related to histological changes in bone, although these latter changes were often small. It is concluded that 1alpha-hydroxyvitamin D3 is a useful new drug in the treatment of renal bone disease, but that the evaluation of the response depends critically on the method of assessment used.
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PMID:Correlation of clinical, biochemical and skeletal responses to 1alpha-hydroxyvitamin D3 in renal bone disease. 60 24

A 17 year old man with longstanding hypocalcemia and hyperphosphatemia presented with incapacitating bone pain and progressive weakness nad bowing of the legs. The serum abnormalities were due to idiopathic hypoparathyroidism as evidenced by a decreased serum concentration of parathyroid hormone and an appropriate rise in urinary cyclic AMP and phosphate excretion, and serum calcium concentration, in response to exogenously administered parathyroid extract. The serum concentration of 1,25-dihydroxycholecalciferol was appropriately decreased. The bone findings were due to osteomalacia as documented by physical findings, bone roentgenograms, and bone biopsy. Normal renal tubular function, blood pH, and serum concentration of 25-hydroxycholecalciferol and elevated serum alkaline phosphatase excluded the common causes of osteomalacia. The data are consistent with the hypothsis that lack of parathyroid hormone causes both hypocalcemia and a decreased serum concentration of 1,25-dihydroxycholecalciferol which, in turn, limit the availability of calcium and cause defective synthesis of bone matrix resulting in abnormal mineralization.
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PMID:Hypoparathyroidism: a possible cause of osteomalacia . 87 58

Five adult patients with chronic renal failure and associated renal osteodystrophy have been treated for 6 months with 1-alpha-hydroxycholecalciferol (1 alpha-OH-D3), a synthetic vitamin D analogue. All 5 patients had severe metabolic bone changes as estimated by bone scintigraphy. Three patients were hypocalcemic, 4 had elevated serum alkaline phosphatases, 5 had elevated serum immunoreactive parathyroid hormone (i-PTH) concentration and 3 had bone pains. During treatment serum calcium increased in all patients (mean 11.4%) and 3 originally hypocalcemic patients became normocalcemic. Serum alkaline phosphatases decreased (mean 27.3%) and became normal in 4 patients, who initially had elevated values. A pronounced decline in the serum concentration of i-PTH (mean 53%) was seen in all patients and 1 patient obtained normal i-PTH levels after 4 months of treatment. The intestinal calcium absorption, which was low initially, even when calcium intake was considered, rose almost threefold (mean 273%) and reached normal values in all cases. The bone mineral content increased in all patients, but the changes were small (mean 4.9%) and insignificant. Finally, bone pain disappeared in 2 patients and improved in 1 of 3 patients exhibiting this symptom. A linear correlation (r = 0.48, p less than 0.001) was found between the dose of 1 alpha-OH-D3 and serum calcium. But in spite of this and the frequent control, all patients developed one episode of hypercalcemia. This disappeared within 48 hours after discontinuing the drug. It is concluded that treatment with 1 alpha-OH-D3 appears to be of therapeutic value in metabolic bone disease associated with chronic renal failure, but frequent control of blood biochemistry seems mandatory.
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PMID:L-alpha-hydroxycholecalciferol treatment of adults with chronic renal failure. 96 64

The osteoblastic effect of inorganic phosphorus and the inhibitory action of calcium on parathyroid hormone secretion formed the basis for a therapeutic trial in which both elements were given intravenously in an alternating sequence for one year to five patients with severe osteoporosis. During treatment, calcium and phosphorus balances were positive, and serum phosphorus concentrations decreased. Iliac crest bone biopsy specimens obtained one year after beginning treatment demonstrated an increase in the thickness of cortical bone. All patients experienced lasting relief of bone pain, and the rate of spontaneous fractures decreased from at least one fracture per year to none following the beginning of treatment. These findings suggest that long-term treatment with alternating phosphorus and calcium infusions may result in lasting relief of symptomatic osteoporosis. It is proposed that the observed improvement reflects an increase in bone mass resulting from enhanced bone formation.
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PMID:Effects of alternating phosphorus and calcium infusions on osteoporosis. 97 42

Ten patients with calcitriol-resistant rickets caused by a defect in the ligand-binding domain of the vitamin D receptor are described. Eight patients, 1.7 to 13.8 years of age, received high doses of elemental calcium (range, 0.4 to 1.4 gm/m2) through indwelling intracaval catheters for periods of 1.8 to 3.8 years. Two other patients, aged 1.1 and 2.2 years, were given oral calcium therapy as the sole mode of treatment. In five of the intravenously treated patients, oral calcium therapy was initiated after radiologic evidence of healing of the rickets. To maintain normal serum calcium concentration, the patients required daily doses of elemental calcium of 3.5 to 9 gm/m2 body surface area. Clinical improvement was observed within a week of the start of intravenous therapy, with disappearance of bone pain; several of the younger patients started to walk for the first time. Growth velocity increased within 2 to 3 months, from a pretreatment rate of -0.8 to -6.3 standard deviation score (SDS), to a posttreatment rate of +0.1 to +5.1 (SDS). Serum calcium, parathyroid hormone, phosphorus, and alkaline phosphatase values returned to normal within a year. Radiologic signs of healing occurred more rapidly in the intravenous treatment groups and in younger patients. Episodes of septicemia occurred frequently in those receiving parenteral therapy and required replacement of the catheter. We recommend that in the treatment of calcitriol-resistant rickets, oral calcium therapy be started at the youngest possible age, in doses to the limit of intestinal tolerance. When rickets is present, calcium should be infused through a large vessel in doses high enough to produce normocalcemia, normophosphatemia, and suppression of parathyroid hormone. Only after radiologic healing has been observed can oral calcium therapy be introduced.
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PMID:Calcium therapy for calcitriol-resistant rickets. 133 89

Despite recent improvements of hemodialysis (HD) techniques, symptoms due to secondary hyperparathyroidism (HPT) contribute to longtime complications of HD patients. The aim of the present retrospective study was to determine the incidence and localization of radiological joint and bone lesions in 175 patients on chronic HD. In 108 patients the diagnosis of HPT was made by radiologic criteria. 56% had radiomorphologic lesions of the hands, 45% of the acromio-clavicular (AC) joint, 31% of the shoulder, and 27% of the pelvis. No sex difference was found for prevalence of HPT in these patients, nor was one found for any of the underlying renal diseases. There was a negative correlation between elevated serum parathyroid hormone and serum aluminum concentrations. In 111 patients the history of bone and joint pain was evaluated. 54% of these patients suffered from bone pain, arthralgia, and morning stiffness. Radiological lesions of AC-joint correlated with shoulder pain in 38%. Our data show that even in the predialytic phase of renal insufficiency x-rays of the shoulder are helpful in early diagnosis of HPT. Skeletal manifestations specific for one of the underlying renal diseases do not exist. Elevated PTH levels are a good indicator of HPT in these patients, whereas low levels of PTH do not exclude radiological manifestations. In contrast to beta 2-microglobulin amyloidosis, pain does not occur during rest and is not worsened during HD. Treatment with non-steroidal antiinflammatory drugs led to pain relief in the majority of patients. Pain history in patients on chronic HD provides important information concerning the differential diagnosis of HPT/beta 2-microglobulin amyloidosis.
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PMID:[Rheumatologic and radiologic symptoms of secondary hyperparathyroidism: retrospective long-term study of 175 chronic hemodialysis patients]. 177 68

Bone changes occur during normal aging in both men and women. Changes are both quantitative and qualitative in nature, and include: 1) alterations in the dynamics of bone cell populations, resulting in uncoupling of the normal process of bone resorption and formation; 2) changes in bone architecture (e.g., rearrangement of trabecular struts) and cross-sectional geometry (characterized by subperiosteal expansion and enlargement of the medullary cavity); 3) accumulation of microfractures; 4) localized disparity in the concentration of deposited minerals, with hypomineralization in some areas and hypermineralization in others; 5) changes in the crystalline properties of mineral deposits; and 6) changes in the protein content of matrix material. In addition, there are age-related changes in the status of calcium and phosphate regulating hormones: parathyroid hormone increases, and production of the most active metabolites of vitamin D3 decreases. These hormonal changes undoubtedly affect the maintenance of normal bone homeostasis. Other important factors which can profoundly influence bone status in the elderly are decreased physical activity and dietary inadequacies. Bone tissue is particularly responsive to mechanical loading, and the magnitude of bone mass loss as a consequence of decreased physical activity may not be fully appreciated. Interactions of the above mentioned changes are not completely understood, and the degree to which these changes have been documented in humans varies considerably. Clearly, however, the overall net result is the occurrence of age-related loss of bone tissue and bone strength. This process is accelerated after menopause in women, resulting in the clinical condition commonly known as osteoporosis. In addition to loss of bone mass (usually reported as a decrease in bone mineral content), osteoporosis is accompanied by bone pain, spinal deformity, loss of height, and fractures.
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PMID:Age-related bone changes. 191 89

A patient with late-onset hypophosphatemic osteomalacia was treated with oral supplements of phosphate (1.5 g/day) and calcitriol (1.5-3.0 micrograms/day) for 17 months, before a slowly growing tumor in the first metatarsal space became evident. Before treatment concentrations of inorganic phosphate (Pi) and calcitriol in serum and tubular reabsorption of phosphate (TRP) were very low, calcium and parathyroid hormone (PTH) in serum were normal, urinary cyclic adenosine monophosphate (cAMP) was strongly elevated. During the first weeks of conservative treatment urinary cAMP returned to normal; concomitantly there was a transient slight fall in PTH. Serum calcium was in the low normal range and did not significantly change during conservative therapy. During the further course PTH rose to pretreatment values, but urinary cAMP remained normal. When the dose of calcitriol was elevated to 3 x 1.0 micrograms/day, leading to slightly elevated serum concentrations of this substance, Pi in serum rose to the low normal range, but TRP remained low and bone pain, although improved, did not subside. The tumor was locally excised. Postoperatively calcitriol concentration became elevated within 48 hours and remained so for several weeks. The rise in calcitriol concentration preceded the elevation of Pi in serum, not, however, the increase of TRP. The elevation of urinary cyclic AMP before therapy may have been due to a direct action of the substance secreted by the tumor.
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PMID:Tumor-induced osteomalacia: pre- and postoperative biochemical findings. 196 76

Recently, the role and timing of surgery for treating secondary and tertiary hyperparathyroidism (HPT) have been questioned. In order to delineate the indications for surgery in these patients, a retrospective analysis of 53 consecutive patients treated with parathyroidectomy was conducted. Subtotal thyroidectomy was done in 37 of 45 patients undergoing their initial operations for HPT. Eight additional patients were referred after failed operations. Of 33 patients with preoperative bone pain, 70% improved. Joint pain improved in 87% of 30 patients, pruritus improved in 81% of 27 patients, and preoperative malaise improved in 73% of 33 patients after parathyroidectomy. Abdominal pain and irritated eyes were unlikely to improve. The best predictors of a successful outcome were a markedly elevated preoperative immunoreactive parathyroid hormone (mid-region) level and an elevated alkaline phosphatase level. There were no perioperative deaths. One patient (1.6%) had a recurrent laryngeal nerve injury, and one patient required reoperation for a neck hematoma. No patient had permanent hypoparathyroidism, but transient hypocalcemia (less than 7 mg/dL) occurred in 22%. Postoperative hypocalcemia correlated with elevated preoperative alkaline phosphatase levels (r2 = 0.247).
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PMID:Results of surgical treatment for hyperparathyroidism associated with renal disease. 222 Dec 30


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