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)

The present study was an attempt to assess the cause of persistent pain in lower limbs among children from Kashmir. The study was conducted on one hundred children attending Paediatric out-patient department of Sher-i-Kashmir Institute of Medical Sciences, Srinagar. All the children were in the age group of 5 to 14 years. They showed markedly raised levels of serum alkaline phosphatase, whereas serum phosphorus, serum calcium levels and antistreptolycin O-titres were normal in 93% cases. None of them had any rheumatic or rheumatoid pathology. Among 15 suspected clinical rickets only three were established radiologically. Dietary and socio-economic history revealed deficient vitamin D intake and less exposure to sun. It was hypothesized that sub-clinical vitamin D deficiency could be a major cause of persistent pain in lower limbs and raised serum alkaline phosphatase could be the earliest marker of vitamin D deficiency. It was confirmed by injecting single dose of vitamin D (3 lac I. U.) which relieved bone pain and lowered the levels of serum alkaline phosphatase to normal within 14 weeks of initiation of therapy.
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PMID:Persistent limb pain and raised serum alkaline phosphatase the earliest markers of subclinical hypovitaminosis D in Kashmir. 262 Sep 72

The author examined a group of 143 patients with osteomalacia of different origin before treatment and after adequate treatment with vitamin D, using laboratory tests, assessment of body weight and muscular strength (grip of the dominant hand). After treatment there was a significant rise of calcaemia, phosphataemia and calciuria and a drop of alkaline phosphatase activity. The body weight increased within the first month of treatment on average by 1.27 kg, during the second month by another 1.15 kg. The patients gained a total of 2.42 kg. The muscular strength increased during the first month on average by 3.23 kg and during the second month by another 2.16 kg, i.e. a total of 5.39 kg. From these results it may be concluded that vitamin D may have a certain anabolic effect if used in pharmacological does either due to an increased nutrient absorption from the gut because of hypertrophy of the intestinal wall or indirectly via hypercalcaemia which increases the hydrochloric acid secretion in the stomach as well as pepsin secretion, and promotes activation of trypsin and lipase in the duodenum and moreover causes retardation of the intestinal transit. The increased muscular strength in due to a rise of calcaemia, improved muscle contraction and probably also due to the mentioned nutritional factors. There may be also the factor of an improved lifestyle due to the immunomodulating action of vitamin D and disappearance of bone pain.
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PMID:[Anabolic effects of vitamin D in patients with osteomalacia]. 263 59

Hypophosphataemic osteomalacia occurred in a 38-year-old woman. The leading clinical symptom was severe bone pain. X-ray studies demonstrated fractures of the iliac crest and pubic and ischiadic bone, as well as Looser's zones and demineralization of the skeleton. Computerized densitometry of the bone revealed a 31% reduction of hydroxyapatite. Histological evaluation showed nearly absence of osteoclasts and extensive demineralisation of the bone. Hypophosphataemia (0.48 mmol/l), increased urinary phosphate clearance (36 ml/min), reduced renal-tubular reabsorption for phosphate (73%) and increased alkaline phosphatase (355 U/l) were present. Parathyroid hormone and 1,25-dihydroxyvitamin D were normal. No inborn errors, disturbances of the calcium metabolism or paraneoplastic signs could be detected. Defective renal tubular reabsorption of phosphate is likely to be the underlying cause of the disease. Phosphate supplementation and intermittent vitamin D administration remains the therapy of choice.
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PMID:[Hypophosphatemic osteomalacia in adults]. 270 31

Clinical observations of bone pain, abnormal gait, and unusual fractures during remission of leukemia led us to assess mineral status in a cohort of 16 children with acute lymphoblastic leukemia treated with intensive chemotherapy. During maintenance and 6 months after the completion of therapy, blood and urine were analyzed for calcium and magnesium and blood for osteocalcin, vitamin D, and parathyroid hormone. Bone mineral content and bone width of the distal one third of the radius of the nondominant arm was measured by single-photon absorptiometry. During therapy, mild ionic hypocalcemia (less than 1.19 mmol/L) and hypomagnesemia (less than 0.77 mmol/L) were demonstrated in 9 and 8 of 16 children, respectively; hypercalciuria (8/16) and hypomagnesiuria (12/16) were also observed. Plasma osteocalcin values correlated with plasma magnesium levels (r = 0.54; p less than 0.05). Oral magnesium supplements normalized plasma magnesium, calcium, and osteocalcin levels, all of which were normal at the postchemotherapy study. Plasma 1,25-dihydroxyvitamin D levels were nondetectable (less than 8 ng/ml) in 12 of 13 patients receiving therapy and in 7 of 14 patients not receiving therapy; alkaline phosphatase activity increased significantly after therapy (179 +/- 86 to 340 +/- 101 units/L), and parathyroid hormone levels were normal in both studies. Bone mineral content/bone width ratio was less than 1 SD below the mean for age- and sex-related population standards in 70% of patients. These data indicate that alterations in magnesium, calcium, and vitamin D metabolism in children treated for acute lymphoblastic leukemia may be instrumental in inducing or sustaining altered bone turnover during chemotherapy.
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PMID:Mineral homeostasis and bone mass in children treated for acute lymphoblastic leukemia. 278 92

Two boys aged six and four with the syndrome of hereditary resistance to 1,25-dihydroxyvitamin D3 with rickets alopecia and growth retardation are presented. After unsuccessful therapeutic trials with pharmacologic doses of vitamin D or its active metabolites, the patients were treated by long-term intracaval infusions of calcium through an implantable catheter. A total of 0.5 to 0.9 g of elemental calcium was infused daily for 18 months and the serum calcium concentration was maintained at 9 to 10 mg/dl. Bone pain subsided within one week of treatment. Serum phosphorus, immunoreactive parathyroid hormone, and 1,25-dihydroxyvitamin D concentrations and alkaline phosphatase activity were normalized within four to nine months. Radiographs of the knees and hands revealed progressive healing of rickets with complete resolution after one year of treatment. The patients gained 12 cm and 8 cm per year in height as compared with 3 cm and 2 cm, respectively, in the previous year. A transilial bone biopsy obtained from one patient prior to treatment revealed severe osteomalacia associated with osteitis fibrosa. A follow-up biopsy examined after 12 months of therapy showed almost complete healing of osteomalacia and normal mineralization. These observations indicate the following: (1) Long-term intracaval calcium infusions are an effective mode of therapy for these patients, and (2) When adequate serum calcium and phosphorus concentrations are maintained, healing of rickets and normal growth rate could be achieved even in the absence of a normal 1,25-dihydroxyvitamin D3 receptor-effector system.
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PMID:Long-term intracaval calcium infusion therapy in end-organ resistance to 1,25-dihydroxyvitamin D. 282 6

Although more than 50 patients with the tumor-induced osteomalacia syndrome, characterized by remission of unexplained osteomalacia after resection of a coexisting tumor, have been reported, the pathogenesis of this syndrome is still not clear. We investigated the cause of biopsy-confirmed osteomalacia which was resistant to treatment with 1 alpha-hydroxyvitamin D3 in a 54-yr-old man. He had severe hypophosphatemia, a high serum alkaline phosphatase level, a low plasma 1,25-dihydroxyvitamin D level, and remarkably increased urinary phosphorus excretion. A tumor, with histological characteristics of a hemangiopericytoma, was found on his left thigh. After surgical removal of this tumor, his plasma 1,25-dihydroxyvitamin D and serum phosphorus levels increased to normal levels, and his bone pain subsided. The tumor was transplanted to athymic nude mice. A nodule formed in each mouse, with histological features identical to those of the original tumor, and the tumor-bearing mice had hypophosphatemia, high serum alkaline phosphatase levels, and increased urinary phosphorus excretion. When extracts of the original tumor were added to primary cultures of renal tubular cells, renal cAMP levels did not change, but 25-hydroxyvitamin D-1 alpha-hydroxylase activity was significantly inhibited. These data indicate tumoral production of some humoral factor(s) inhibiting 25-hydroxyvitamin D-1 alpha-hydroxylase activity and phosphorus reabsorption unrelated to adenylate cyclase-cAMP production in proximal renal tubules.
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PMID:Hemangiopericytoma-induced osteomalacia: tumor transplantation in nude mice causes hypophosphatemia and tumor extracts inhibit renal 25-hydroxyvitamin D 1-hydroxylase activity. 283

We retrospectively reviewed the roentgenographic and pathologic staging of 64 patients with renal cell carcinoma to assess the role of the various staging modalities (ie, angiography, venacavography, bone scanning, ultrasound, computed tomography [CT], and magnetic resonance imaging). Specific attention was directed at detecting vena cava thrombus and metastatic bone disease, factors with a significant impact on the therapeutic approach. The findings support the role of CT as the principle tool for overall staging and the observation that venacavography is not indicated if CT has excluded caval thrombus. Similarly, routine bone scans are not warranted in the absence of an elevated alkaline phosphatase level or bone pain. The key to the more efficient utilization of imaging resources is understanding the capabilities of the technology available.
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PMID:Staging renal carcinoma. What is sufficient? 291 Feb 51

Twenty patients with stage D2 prostatic carcinoma were treated for up to 18 months with D-Trp-6-LH-RH. Results of more than 3 months of treatment on these 20 patients are reported. The analog was given SC once daily at a dose of 1,000 micrograms/day. All patients had bone pain and high levels of acid and alkaline phosphatase. After the first week of D-Trp-6-LH-RH administration, major decreases in bone pain and reversal of the signs of prostatism were observed. Acid phosphatase gradually fell, achieving normal values after 12 weeks. Initial plasma testosterone was within normal limits, but during treatment with D-Trp-6-LH-RH it fell to castration levels. Resting values of PRL, GH, TSH, and cortisol did not show significant changes. After TRH, TSH increased in five patients, but five did not respond. However, at 2 and 4 months, all patients released TSH in response to TRH. Two patients died during the treatment with D-Trp-6-LH-RH despite initial subjective responses and decreases in testosterone levels. The rise in acid phosphatase levels in these two patients was accompanied by a general deterioration, suggesting that they had androgen-independent cancer. One patient who developed progressive hepatic, bone, and pulmonary metastases in spite of previous orchiectomy was also treated with the analog. Three months later his acid phosphatase levels were within normal values, and partial regression of metastases was observed. These results demonstrate that D-Trp-6-LH-RH and other LH-RH agonists can be used as an effective endocrine therapy for advanced prostate carcinoma, thereby avoiding the side effects of estrogens or the psychological impact of surgical castration.
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PMID:Treatment of advanced prostatic carcinoma with D-Trp-6-LH-RH. 293 92

Since Schmid (115) and Kruse (74) reported on osteopathies occurring after antiepileptic treatment in children, there have been numerous publications concerning the influence of antiepileptics on mineral metabolism in the bones. The investigators' results range from slight anomalies of the plasma levels of calcium, phosphate, alkaline phosphatase, parathormone and 25-hydroxycholecalciferol to severe bone alterations. In the majority of cases, the severe pictures occurred in retarded, neurologically abnormal, institutionalised children who were treated with a high-dose combination of several antiepileptics for epilepsy which was difficult to treat. The first case reports from adults were published by Dent et al. (26). These patients had also been treated since their early youth with an antiepileptic combination. They displayed fractures and suffered from bone pain and muscular weakness. The good response of the rachitic bone alterations to vitamin D treatment both in children and in adults indicated vitamin D deficiency. These reports prompted systematic investigations on the influence of antiepileptics on bone metabolism in numerous hospitals and outpatient departments. According to the available literature, it can be stated that antiepileptic therapy can lead to shifts in calcium and phosphate metabolism and to a raised activity of serum alkaline phosphatase. In studies comprising control groups, the patient treated with anticonvulsants more frequently displayed variations of clinical laboratory parameters. The frequent observation of vitamin D hypovitaminosis led to the assumption that alterations in vitamin D metabolism by enzyme induction are the cause of the disorders in calcium and vitamin D metabolism. This hypothesis was frequently contradicted in recent years after hypocalcaemia and alterations in the mineral content of the bone after antiepileptic therapy had been reported irrespective of the vitamin D level. Besides a restricted intestinal calcium absorption, an influence of antiepileptics on the hormones regulating calcium and phosphate metabolism was found. Thus, a multifactorial genesis of the disorders in bone mineral balance must be assumed. The fact that the vast majority of outpatients with long-term anticonvulsant therapy do not display any disorders of bone metabolism indicate that there are individually different compensation capabilities (possibly of genetic origin). According to the literature, the probability that adults will develop osteomalacia under antiepileptic therapy is associated with the joint presence of various risk factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Osteopathia antiepileptica in adolescents and adults]. 306 13

Clinical effects of EHDP on relief of bone pain, changes in bone lesions on X-ray and 99mTc-MDP scintigram and performance status were investigated in 19 patients with bone metastasis from urogenital cancers (4 renal cell cancers, 1 renal pelvic cancer, 4 bladder cancers and 10 prostatic cancers). EHDP was effective in relieving bone pain in prostatic cancer patients with osteoblastic lesions. Bone lesions on X-ray and 99mTc-MDP scintigram were slightly improved in prostatic cancer patients with osteoblastic lesions. Administration of EHDP did not improve the performance status. Changes in laboratory data such as serum alkaline phosphatase, serum calcium and urinary total hydroxy-proline following EHDP administration indicated inhibition of osteolytic activity with no effect on bone formation in the early period of treatment (in 4 weeks) and development of both osteolytic activity and bone formation in the later period (from 8 to 12 weeks). No marked side effects were observed. EHDP seems to be effective in relieving bone pain in prostatic cancer patients with osteoblastic bone metastasis. Moreover, some diphosphonate groups including EHDP are expected to be useful to the patients with malignant hypercalcemia.
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PMID:[Effects of etidronate disodium (EHDP) on urogenital malignancies with bone metastasis: a multicentered collaborative evaluation]. 313 34


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