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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflex sympathetic dystrophy syndrome is a difficult condition to treat. Many modalities have been proposed, all of them being clinically effective but whose efficacy is often difficult to assess, and has not been properly compared. A regimen of physical therapy (pressure therapy, antalgic electrotherapy and exercise therapy) with or without calcitonin was investigated in 24 patients randomly assigned to 2 groups, one given physical therapy alone (Group I) and the other physical therapy plus salmon calcitonin 100 MRC units daily for 3 weeks (Group II). Efficacy assessment was based on clinical (pain, oedema and movement in the affected parts), biochemical (blood and urinary phosphorus and calcium levels, plasma 25-OH-D, plasma parathyroid hormone (PTH), creatinin, alkaline phosphatases and urinary hydroxyproline) and scintigraphic parameters, as well as on the patient's ability to resume working. There was significant improvement in pain in the Group II patients after one week of treatment. As a result the authors advocate the use of calcitonin in addition to physical therapy in reflex sympathetic dystrophy syndrome - and even of calcitonin alone where physical therapy is not possible.
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PMID:Calcitonin and reflex sympathetic dystrophy syndrome. 353 62

A 59 year-old patient had lumbago and pain in hip joints, knees, and ribs of long duration. Severe hypophosphatemia and high serum ionized calcium were found in spite of normal level of total serum calcium. The serum parathyroid hormone and alkaline phosphatase levels were elevated, and diffuse demineralization of the bones and renal stones were found by x-ray examination. Parathyroid adenoma was diagnosed from the subtraction image of the 99mTc O-4 and 201Tl-Cl2 scintigrams. Osteomalacia was demonstrated by bone biopsy at the right iliac crest. A right lower parathyroid adenoma of 2.0 X 1.8 cm, weighing 4.0 g was removed. The long standing phosphate depletion and hypophosphatemia, due to hyperparathyroidism causing renal damage with nephrocalcinosis and reduced synthesis of active vitamin D, and milk tolerance due to gastroduodenostomy were probably responsible for producing the clinical picture of normocalcemic hyperparathyroidism complicated with osteomalacia.
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PMID:A case of normocalcemic primary hyperparathyroidism with osteomalacia. 383 67

Parathyroid hormone, thyrocalciotonin, testosterone, estradiol, aldosterone and renin activity of the blood plasma were radioimmunoassayed in 142 patients with neurological manifestations of lumbar osteochondritis. The blood levels of parathyroid hormone and, to a lesser degree, those of thyrocalciotonin were elevated. The levels depended on the severity and duration of the pain syndrome while thyrocalciotonin excretion depended on the degree of the degenerative dystrophic process in the spinal column. Prolonged pain syndrome was associated with an inhibited function of the gonads and the mineralocorticoid layer of the adrenals. A hypothesis is advanced, which explains the participation of the endocrine glands in the etiopathogenesis of lumbar osteochondritis and its neurological manifestations.
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PMID:[Role of various endocrine glands in the pathogenesis of the neurologic symptoms of lumbar osteochondrosis]. 389 Apr 27

The pathophysiology, clinical presentation, prevention, and treatment of aluminum-related osteomalacia in renal-failure patients are reviewed. Aluminum-related osteomalacia can develop in patients exposed to high concentrations of aluminum either in dialysis solutions or through gastrointestinal aluminum absorption from aluminum-containing antacids used to treat hyperphosphatemia. Although the exact etiology of aluminum-related osteomalacia is unknown, aluminum is believed to inhibit bone mineralization by forming an inhibitory complex with citric acid at physiologic concentrations. The complex is deposited along bone mineralization fronts and in bone marrow. The major symptoms of aluminum-related osteomalacia include skeletal pain, fractures, and vertebral collapse. The disease is difficult to diagnose because patients may have normal or slightly elevated serum concentrations of calcium, phosphate, alkaline phosphatase, and parathyroid hormone. Direct measurement of bone aluminum content (using biopsy) is often needed to confirm diagnosis. The aluminum-chelating agent deferoxamine mesylate can be used to measure bone aluminum content indirectly. Aluminum intoxication can be managed either by preventing exposure to aluminum or by removing deposited aluminum from bone. New standards restrict aluminum content in dialysis solutions, and prevention now focuses on the use of aluminum-free phosphate binders for treatment of hyperphosphatemia. Calcium carbonate may be as effective as aluminum-containing antacids in controlling serum phosphate concentrations, but it should be used cautiously in patients who are hypercalcemic or at risk of developing metastatic calcification. Chelation therapy with deferoxamine has improved the symptoms and bone histology in a small number of patients. Clinical improvements have been seen in patients receiving intravenous deferoxamine 2-6 g per week for 20 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aluminum-related osteomalacia in renal-failure patients. 389 71

Dialysis osteomalacia is characterized by distinctive, although not pathognomonic, clinical and biochemical features. Symptoms and signs may include musculoskeletal pain, arthralgias, proximal muscle weakness, and spontaneous fractures. Biochemical characteristics may be hypercalcemia and normal serum alkaline phosphatase activities. Vitamin D administration may induce early severe hypercalcemia. Plasma phosphate and immunoreactive parathyroid hormone concentrations may be at any level. Only bone histology allows to establish the diagnosis of dialysis osteomalacia with certainty. Diphosphonate bone scan, however, enables to distinguish between severe osteitis fibrosa and dialysis osteomalacia. The diagnostic value of desferrioxamine administration with subsequent measurement of plasma aluminium remains to be determined. The complex interactions existing between parathyroid hormone and aluminium are not yet fully understood.
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PMID:Dialysis osteomalacia: clinical aspects and physiopathological mechanisms. 391 57

An association between chronic renal failure and skeletal deformities in the adolescent patient was first documented by Lucas in 1883. Since then it has been established that the kidneys play a major role in the regulation of calcium, phosphate, and parathyroid hormone, and that chronic renal failure is characterized by profound alterations in the normal metabolic homeostasis of the human body. With the hyperphosphatemia of uremia, compensatory hyperparathyroidism is also a well known complication. Due to these factors, loss of normal renal function ultimately leads to derangement in mineral and bone metabolism resulting in severe skeletal deformities. Reports in the English literature suggest that the changes of renal osteodystrophy are much more pronounced in the pediatric patient, as compared to those in the adult. In the last two decades, renal transplantation has come to be recognized as a satisfactory modality for controlling renal failure and its complications. This procedure is often not available as an option, however, in small patients, especially those under three years of age. The pediatric nephrologist is often forced to manage these patients for long periods with conservative therapy, in an attempt to control the ravages of renal osteodystrophy. The problem becomes unmanageable when the compensatory hyperparathyroidism proceeds to autonomy. When this occurs, despite maintenance of normal serum calcium levels, the renal osteodystrophy progresses rapidly, producing pain, deformities and growth retardation. At this point, the condition is often refractory to medical management and resection of parathyroid tissue remains the only satisfactory modality for control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total parathyroidectomy and autotransplantation for tertiary hyperparathyroidism in children with chronic renal failure. 648 83

Calcitonin obtained from eels (ell-CT) was given to 14 patients who had developed bony pains due to bone metastases of malignant tumors and who did not respond to 12 various analgesics. The patients consisted of 12 males and 2 females, with a mean age of sixty-five. Eel-CT (Elcitonin) was injected intramuscularly to each patient at a dose of 40 units twice daily. Other analgesics were assessed to be ineffective at the time of CT administration and they were not given consideration in the evaluation. For the assessment of drug effect, a pain score was prepared. Eel-CT was markedly effective in 3 patients, effective in 8 patients, and ineffective in 2 patients. Eel-CT had a better effect on prostatic cancer than any other cancer. The analgesic effect was observed in the first week of drug administration at around a total dose of 1,000 units. Although the pain tended to appear at regions on which the body weight was liable to rest, the analgesic effect was seen irrespective of the side of pain. Since serum calcium, phosphate, parathyroid hormone (PTH), CT levels and bone scintigrams between pre-and post-CT administration did not differ, the analgesic mode of action of CT is not supposed to be related to inhibition of bone absorption nor bone formation. The therapeutic effect hardly suggests any direct action of CT on the tumor.
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PMID:[Effect of calcitonin on body pains caused by bone metastases of urogenital cancer]. 667 46

Results presented in this paper indicate that intracerebroventricular injection of parathyroid hormone reduces pain threshold in male rats. This effect is induced by whole molecule (84 amino acids) or by fragments 1-34 and 44-68 of PTH. The fragment 65-84 of PTH does not induce any change in pain threshold.
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PMID:Hyperalgesic activity of parathyroid hormone and its fragments in male rats. 671 98

Painful bone disease, characterized by patchy osteomalacia and inactive bone, can develop in patients treated with total parenteral nutrition for more than 3 months. Serum levels of 1 alpha,25-dihydroxyvitamin D (1 alpha, 25(OH)2D), 24,25-dihydroxyvitamin D and 25-hydroxyvitamin D were measured in seven adults and five children treated with parenteral nutrition for 9 to 60 months. Serum levels of 1 alpha, 25(OH)2D were markedly reduced, while levels of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D were normal. Serum calcium and phosphorus levels were normal or slightly increased, and immunoreactive parathyroid hormone levels were normal or low. Renal function was normal or minimally reduced. Skeletal symptoms disappeared and serum 1 alpha, 25(OH)2D levels rose to normal in one patient when nutrient infusions were discontinued for 6 weeks. Removal of calcium from the nutrient solution for 2 to 4 days was associated with no change in serum 1 alpha, 25(OH)2D in two patients. The cause of the reduction in serum levels of 1 alpha, 25(OH)2D and its role in the pathogenesis of bone disease in these patients remain uncertain.
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PMID:Reduced serum levels of 1 alpha,25-dihydroxyvitamin D during long-term total parenteral nutrition. 678 51

Osteosclerosis, an increased volume of trabecular bone, is a common but often misinterpreted feature of uremic osteodystrophy. Despite the apparent radiographic density of osteosclerotic bone, pain and fracture may be associated. If accumulated osteoid and woven bone exceed the volume of lamellar bone removed in chronic renal insufficiency, bone density may be reduced despite increased trabecular volume. Concomitant histomorphometric and photon absorption determinations of transileal bone biopsies were done to investigate the relationship between quantity and quality of bone in uremic and non-uremic osteopenic patients. In osteopenic patients with uremia, bone core density had no significant relationship to trabecular bone volume or mineralized bone volume whereas in non-uremic osteopenic patients, these parameters were directly related (r = 0.867 and r = 0.921, respectively, p less than 0.001). The bone core density in the uremic patients was negatively correlated with the total osteoid volume (r = -0.764, p less than 0.05) and positively related to the serum phosphorus concentration (r = 0.739, p less than 0.05). Serum levels of immunoreactive parathyroid hormone (iPTH) and alkaline phosphatase activity were higher in the patients with radiographic osteosclerosis than in the other uremic patients. The lack of correlation between bone volume and density indicates a qualitative defect in uremic bone. It appears that in uremia, elevated iPTH and serum phosphorus levels may augment bone formation, albeit poorly mineralized with woven architecture. While radiographic density paradoxically increases, the amount of normally mineralized bone may be reduced.
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PMID:Qualitative bone defect in uremic osteosclerosis. 709 50


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