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)

Biochemical and bone morphometric measurements were evaluated in 12 patients who were on long-term anticonvulsant therapy with barbiturates. Half of the patients had no symptomatic bone disease, and half presented with bone disease and pain. Serum biochemical values were normal except for a few patients who had an elevated serum level of parathyroid hormone; the concentration of serum 25-hydroxy vitamin D was decreased in the majority of patients in whom it was measured. Bone absorptiometric values were normal but proved to be misleading: the Singh Index and videodensitometric measurements indicated that bone mass was below normal in all patients. Bone morphometric data indicated that bone resorption was 3 times greater than normal, and there was no evidence of osteomalacia. Vitamin D and possibly calcium have been suggested as potentially useful agents in the treatment of the bone disease associated with chronic anticonvulsant therapy.
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PMID:The frequency of bone abnormality in patients on anticonvulsant therapy. 7 73

In an adult with sporadic idiopathic osteomalacia an increased phosphate clearance, hypophosphataemia, normocalcaemia, normal serum-25-hydroxycalciferol and an only slightly increased immunoreactive parathormone were found. Intestinal 47Ca absorption was clearly decreased. Radiologically and histologically there was a clear-cut defect of skeletal mineralisation. Under treatment with daily doses of 1-1.25 mg of vitamin D3 the 25-hydroxycalciferol level increased markedly, the immunoreactive parathormone decreased slightly. Serum calcium and hypophosphataemia remained unchanged and intestinal 47Ca absorption was improved. Already 4 weeks after commencing treatment pain and defective gait of the patient disappeared. Radiologically skeletal changes were improved after 7 months. However, histologically no significant bone healing had occurred. The biochemical findings of this disease correspond to those of familial hypophosphataemic (vitamin-D-resistant) rickets. The therapeutic effects of pharmacological doses of vitamin D resemble those in pseudo-vitamin-D-deficient rickets. The pathogenesis of idiopathic osteomalacia of the adult remains unclear. Vitamin D metabolism is unchanged as far as the stage of 25-hydroxycholecalciferol. It is unknown if a disorder of the renal synthesis of 1,25-dihydroxycholecalciferol or a peripheral resistance to the effects of this metabolite exists. In addition a defect of the tubular phosphate reabsorption independent of parathormone and vitamin D is assumed.
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PMID:[Idiopathic hypophosphataemic osteomalacia (author's transl)]. 18 46

Treatment for osteoporosis cannot yet be prescribed in a perfectly rational manner, as the total picture of the pathogenesis of this disease remains uncertain. Furthermore, lack of significant criteria makes it difficult to evaluate the different therapeutic methods proposed, and none of them appears to be entirely satisfactory. By acting methodically, however, one can obtain good relief of pain, quiescent osteoporotic activity over long periods, and bone remineralization. At the present time, preference has to be given to standard medications such as calcium, phosphorus, and anabolic proteins which are nearly always given in association. Calcium inhibits osteolysis by slowing down parathyroid secretion. Phosphorus accelerates calcium fixation in bone and appears to stimulate the formation of osteoblasts. Anabolic compounds protect the bone-forming framework and assist the deposition of mineral salts in the bones. The prescription of vitamin D is of value when there is a deficiency. Among recent medications which have been tried, only calcitonin appears to be of some practical value, by assisting inhibition of certain flare-ups and lytic episodes of the osteoporosis when associated with standard therapy.
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PMID:[The treatment of osteoporosis (author's transl)]. 43 27

Radiological sacroiliac (SI) changes were found in 3 patients, 2 with primary hyperparathyroidism (1 also with associated chondrocalcinosis) and 1 with osteomalacia. Osteomalacia was due to celiac disease. None of the 3 patients, all females, had a history of psoriasis, urethritis, iritis or chronic colitis. There was no renal function impairment. Peripheral joints were affected in the patient with associated condrocalcinosis. HLA B 27 was negative in all cases. Low back pain and vertebral stiffness were present in the patient with osteomalacia. A dramatic improvement in pain and stiffness ensued after vitamin D injections. These SI lesions, which may simulate ankylosing spondylitis, were attributable to subchondral bone changes related to the metabolic bone diseases. In the case of osteomalacia the SI lesions were predominantly on the right side, where there was a Looser's zone on the ischial ramus suggesting that pseudofractures could be a cause of SI changes. Metabolic osseous diseases such as osteomalacia or primary hyperparathyroidism should be investigated in cases of HLA B 27 negative radiological "sacroiliitis".
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PMID:[Sacroiliac changes, HLA-B27 negative, in primary hyperparathyroidism and osteomalacia]. 46 71

A case of adult onset hypophosphatemic vitamin D resistant osteomalacia is described. A 40-year-old female who complained of thorax and lumbar pain and gait disturbance was admitted to our hospital on 7 November, 1988. The patient had hypophosphatemia with normal plasma calcium, parathyroid hormone and 25-hydroxy vitamin D3 concentrations, but had decreased tubular reabsorption of phosphate and decreased plasma 1, 25-dihydroxy vitamin D3 concentrations. The iliac crest bone biopsy showed osteomalacic changes. The 99mTc-MDP bone scintigram showed evidence of increased bone turnover with raised plasma alkaline phosphatase concentrations. After treatment with oral 1 alpha-hydroxy vitamin D3 (3-6 micrograms/day) and intravenous or oral phosphate supplement (0.47-1.74g/day), the subjective and clinical findings improved.
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PMID:[A case of adult onset hypophosphatemic vitamin D resistant osteomalacia]. 144 82

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

An unusual pain occurred in five patients in the presence of compromised vitamin D status and resolved 5 to 7 days after supplementation with vitamin D in the form of ergocalciferol. The pain had a hyperesthetic quality and did not respond to the use of analgesics, including opiate derivatives. Treatment with therapeutic levels of a tricyclic antidepressant did not bring relief of symptoms. In one case, months after treatment and subsequent improvement of vitamin D status and pain, the vitamin D status again declined and the pain recurred. The pain again resolved with vitamin D replacement and improvement of levels. There may be a pain syndrome associated with vitamin D depletion that appears as hyperesthesia worsened by light, superficial pressure or even small increments of movement. This pain restricts mobility and function and may lead to further complications, such as pressure sores.
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PMID:Can vitamin D deficiency produce an unusual pain syndrome? 149 6

We report clinical and bone morphometric findings in 18 osteoporotic patients who experienced stress fractures during fluoride therapy. Patients were treated with either sodium fluoride (n = 15), or sodium monofluorophosphate (n = 3). Oral calcium supplementation was given in 11 patients, and vitamin D in 13. Stress fractures occurred after 17.1 +/- 10.3 months of therapy (range: 5-41 months). Atraumatic sudden pain in a lower limb bone extremity, normal initial roentgenogram, high 99technetium uptake on early bone scan, and a 3 to 4 week delay in linear bone condensation area at the same site were characteristics of stress fracture. The most frequent sites were the tibial metaphysis (n = 13), femoral neck (n = 10), and calcaneus (n = 4). Biochemical data showed increased plasma alkaline phosphatase levels in 11 patients, and mild renal failure in 2. Bone histomorphometry was performed on an iliac crest specimen in 10 patients at the time of the stress fracture. Trabecular bone volume was normal, and formation parameters were increased. Features of osteomalacia were encountered in only 2 patients with decreased renal function. Trabecular resorption was increased, as assessed by the osteoclastic surface (1.01 +/- 1.15% bone surface), and the number of osteoclasts (0.44 +/- 0.49 per mm2 bone section). The clinical course was favorable in all patients who stopped fluoride, although 5 patients who continued the treatment had either completion of femoral neck stress fractures to hip fractures (n = 2), or recurrent stress fractures (n = 2), or both (n = 1). Fluoride appears to be a key factor in the pathogenesis of stress fractures, and may be associated with increased trabecular resorption in some treated patients.
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PMID:Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. 233 28

The possible effects of fluoride in inducing fractures were studied in 61 patients treated with sodium fluoride (NaF), 40-60 mg daily in combination with calcium and vitamin D. Nine patients developed the fluoride-(F) related lower extremity pain syndrome. Four other patients had stress fractures associated with trauma. Seven of the 61 patients had 10 upper femur fractures of which 5 were stress fractures. The bone mineral mass of the central skeleton including the hips was measured by neutron activation and the results expressed as a calcium bone index (CaBI) which normalizes the results to that of young adults of the same body size (normal range 0.75-1.2). At the time of hip fracture, 4 patients with a minimal increase in bone mass (mean delta CaBI 0.01) had 4 femur fractures and 3 patients with a marked increase (mean delta CaBI 0.24) had 6. The 7 patients with upper femur fractures at 4 years had a significantly higher bone fluoride retention, 30 mg/g Ca compared with 23.9 mg/g Ca for the other 54 (p less than 0.02) and were older, 73.1 versus 64.2 years (p less than 0.01). Using all 61 fluoride-treated patients, femur fractures/patient were significantly correlated to bone fluoride (p less than 0.05) and to age (p less than 0.05). By partial correlation, only the correlation between hip fractures/patient and bone fluoride remained significant after controlling for the effect of age (p less than 0.05). These results suggest that fluoride therapy may be implicated in the pathogenesis of hip fractures which may occur in treated patients despite a rapid, marked increase in bone mass. The lower extremity pain syndrome is not frequently associated with stress fractures in this study.
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PMID:Fluoride-induced fractures: relation to osteogenic effect. 233 32

Hypercalcemia and leukocytosis of malignancy have been highlighted over a decade. We report a case of a gallbladder cancer with marked hypercalcemia and leukocytosis. A 54-year-old woman was admitted to the hospital because of remittent fever and left hypochondric pain. The computed tomographic scan of the abdomen revealed the cancer of the gallbladder with liver metastases. The patient's medical condition deteriorated as the tumor was rapidly growing up. Her medical course was marked by hypercalcemia and an increase in mature neutrophils. Medical therapy with normal saline, furosemide, indomethacin, prednisolone, and calcitonin failed to ameliorate hypercalcemia. On the twenty-ninth hospital day the serum calcium was elevated to 17.6 mg/dl which responded to 1000 micrograms of mithramycin while leucocytosis continued. Despite the chemotherapy with doxorubicin and tegafur, the tumor continued to grow. Leukocytosis was attributed to the elevated colony-stimulating factor activity which was two-fold of control. The parathyroid hormone and nephrogeneous cyclic AMP levels were normal with low vitamin D levels. Hypercalcemia was attributed to a parathyroid hormone-like substance because of a decrease in %TRP in the presence of normal renal function and the normal parathyroid hormone level. Autopsy revealed an undifferentiated adenocarcinoma of the gallbladder with multiple liver metastases, and bone resorption in the vertebral column and sternum without evident bone metastasis.
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PMID:A case of a gallbladder cancer with marked hypercalcemia and leukocytosis. 253 86


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