Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relatively short-term treatment of paraparesis due to Paget's disease with subcutaneous salmon calcitonin alone produced dramatic relief of sensory loss, pain, and paraparesis. The successful outcomes in 2 patients, one with spinal cord and one with cauda equina compression, indicate a potential alternative to surgery in reversing mild-to-severe neural dysfunction in Pagets disease. The proposed mechanisms of action of calcitonin include reduction of a direct bony impingement on the neural tissue and/or a decrease of neural ischemia. It is suggested that even if paraparesis does not improve with calcitonin alone, the medication given preoperatively would probably serve a useful adjunctive role by decreasing intraoperative bone bleeding. However, those patients whose pagetic bone is already metabolically inactive would probably not benefit from calcitonin therapy.
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PMID:Paget's disease. Reversal of severe paraparesis using calcitonin. 47 94

Thirty-two patients with osteitis deformans were treated with porcine calcitonin for 240 patient-months. Relief of pain occurred in 10 patients, while a fall in the serum alkaline phosphatase level was observed in 22 out of 24 patients whose treatment lasted for more than two weeks. Pain relief occurred predominantly in patients with pain in the lower limbs, although not all patients with lower limb pain showed improvement. Side effects, usually mild in nature, were reported by half the patients. Antiporcine calcitonin antibodies were detected in sera of six out of 14 patients. The presence of circulating antibodies seemed unrelated to the effect of therapy or to the occurrence of side effects.
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PMID:Porcine calcitonin in the treatment of Paget's disease of bone: experience with 32 patients. 55 8

Twenty-eight patients with symptomatic Paget's disease of bone were treated with synthetic salmon calcitonin for periods of 9 to 42 months (average, 23 months). Serum alkaline phosphatase concentration and urinary hydroxyproline excretion, which had been elevated before treatment, were decreased by calcitonin treatment in all patients, and some decrease was sustained in 23 in association with variable decreases in pain, heat and stiffness of major joints. Improvement was sustained further in approximately half of these patients; the other half had partial return of symptoms. Calcium absorption was increased in 9 of 10 patients studied; the increase did not correlate with plasma concentrations of parathyroid hormone. The mean endogenous fecal calcium excretion was decreased significantly but there was no significant change in mean urinary calcium excretion. Mean accretion rate of calcium to bone, studied in 10 patients, was decreased by 35% after 6 months of treatment and by a further 23% 1 year later. There was no consistent effect of calcitonin treatment on bone mineral mass. No serious adverse effects of treatment such as allergic reactions were observed. Calcitonin appears to be effective initially in most patients with Paget's disease of bone, but with long-term treatment resistance may be acquired.
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PMID:Long-term treatment of Paget's disease of bone with salmon calcitonin. 56 31

Sixteen patients with Paget's disease of bone aged from 51 to 80 years was treated daily with 20 micrograms (equivalent to 80 MRCU) synthetic salmon calcitonin. Fourteen patients was observed on a long time. In all cases was observed significant reductions in increased serum alkaline phosphatase. The urinary hydroxyproline excretion was also decreased. Other laboratory dates as serum calcium, serum phosphorus, serum acide phosphatase, urinary calcium and phosphorus excretion was not significantly influenced by the therapy. The treatment produced a clear remission of pain. After treatment of 6 months the dose was reduced (2 or 3 injections subcutaneously of 20 micrograms salmon calcitonin weekly). There was observed a recurrence of pain and an increase of serum alkaline phosphatase, but not until the pretreatment values. These results confirm the effectiveness of calcitonin treatment in Paget's disease of bone.
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PMID:[On the treatment of the osteodystrophia deformans (Paget's disease) with synthetic salmon calcitonin (author's transl)]. 57 Jul 64

Bone scintigraphy with 99mTc-MDP was performed on 8 patients with Paget's disease of bone. The radionuclide uptake by all the involved lesions was markedly increased, even in subclinical lesions without pain. Bone scintigraphy with 99mTc-phosphorous compounds were thought to be the most simple and sensitive technique to define the precise extent of the lesions, and to detect asymptomatic occult cases with Paget's disease. Possible A-V shunt was estimated in 3 cases by measuring the radioactivity over the lungs after the injection of 99mTc-MAA through a catheter into an artery which supplied the lesion. A-V shunt was calculated as 14.5%, 10.0% and 12.0%, respectively. An uptake study of 99mTc-MDP was attempted to quantify the effect of calcitonin treatment using a gamma camera combined with a computer. An "uptake ratio" was obtained for each lesion by dividing the count rate over the bone lesion by that over the control bone. Three cases of Paget's disease were treated with synthetic eel calcitonin analogue ([Asu1,7] E-CT) in a dose of 40 MRC unit per day. The effectiveness of CT therapy was evaluated by the X-ray film, the serum alkaline phosphatase activity (S-Al-P), the serum phosphate level, the serum calcium level and the "uptake ratio". No remarkable changes were obtained on bone X-ray films at one year after the initiation of the CT treatment in all cases. The S-Al-P levels did not show significant difference in the 2 cases, in which the S-Al-P levels were within the normal range before the treatment. In all cases, however, the "uptake ratio" of the diseased bone fell remarkably within the first three months and the rate of the fall was parallel to the decrease in the bone pain. It was considered that the "uptake ratio" on bone scintigraphy offered the most sensitive and reliable information in evaluating the CT treatment for Paget's disease.
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PMID:[Clinical feature and calcitonin therapy on Paget's disease of bone (author's transl)]. 57 27

Sixteen patients with painful Paget's disease of the bone were treated with high doses of ascorbic acid. Of these patients, 8 experienced lessening of pain within a period of 5 to 7 days after commencing the vitamin therapy. In 3 of these patients pain was completely abolished. Subsequent treatment with calcitonin caused improvement in most cases. There was little change in plasma alkaline phosphatase levels but the excretion of hydroxyproline was elevated following administration of the vitamin. The highest excretions were found in those patients who experienced complete relief of pain. In patients treated with calcitonin alone, the excretion of hydroxyproline was reduced and urinary levels of ascorbic acid dropped in parallel. It seems clear that ascorbic acid and calcitonin have different effects upon bone metabolism.
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PMID:Ascorbic acid therapy for the relief of bone pain in Paget's disease. 58 75

Five women with Paget's disease of the tibia were seen with pain in the knee, ankle, or both, as well as with tibial bone pain. All had tibia vara and internal torsion of the tibial shaft. Osteotomy to correct the deformities was preceded by a course of calcitonin which relieved the bone pain but did not relieve the articular pain. Relief after satisfactory correction of the tibial deformity was achieved in all patients. Calcitonin effectively minimized bleeding at the osteotomy site and complications were not encountered.
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PMID:Osteotomy for tibia vara in Paget's disease under cover of calcitonin. 70 16

The efficacy of long term treatment of senile osteoporosis by low doses of calcitonin was established using five parameters of calcium kinetics and a quantitative pain scale. Under treatment the calcium balance improved, due predominantly to a decrease in bone resorption associated with an increase in bone accretion and intestinal absorption of calcium. In addition, the hormone had a marked analgesic effect, which increased with the length of the treatment. Principal components analysis enables to establish the value of a therapeutic agent for the management of a progressive disease with period of regression like osteoporosis, for which the eficacy of previously advocated treatments had never been proven.
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PMID:Calcitonin treatment of post-menopausal osteoporosis. Evaluation of efficacy by principal components analysis. 80 68

Two cases with spinal cord compression due to Paget's disease (osteodystrophia deformans) are reported, which were treated with calcitonin (Salmon Calcitonin) during 12 and 24 months after decompressive laminectomy. Both presented a favourable clinical course with improvement of sensory and bladder disturbances, paraparesis and pain. Diagnostic criteria as X-ray investigation, scintigraphy of bones, biochemical parameters and the long-term treatment whith calcitonin, are discussed.
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PMID:Paget's disease with spinal cord compression. Favourable course after decompression and calcitonin treatment in two cases. 85 66

Four cases of familial bone dysplasia with hyperphosphatasaemia were treated with synthetic human calcitonin. Prior to therapy, all four cases were characterized by marked bone deformity, pain, tenderness and elevated levels of serum alkaline phosphatase and urinary hydroxyproline. Treatment with calcitonin produced in each case a striking clinical, biochemical and radiographic remission. Pain and tenderness was greatly diminished and urinary hydroxyproline and serum alkaline phosphatase levels were significantly decreased. Radiographic regression of the bony abnormalities was apparent as early as 4 1/2 months after the start of treatment. Prior to therapy bones exhibit no real organization. After calcitonin treatment, the radiographic appearance of a normal cortex and medullary cavity was clearly evident for the first time.
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PMID:Hereditary bone dysplasia with hyperphosphatasaemia: response to synthetic human calcitonin. 105 83


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