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

The authors report five cases of an association between osteomalacia and chronic calcifying pancreatitis. The pancreatic involvement, which was pain-free in four patients, resulted in all cases in enzyme insufficiency with steatorrhoea. The deficiency-type osteopathy was highly vitamin sensitive. Aetiological study of these cases of osteomalacia revealed the constant presence of factors aggravating the vitamin deficiency, playing a role by increasing deficient intake or malabsorption, or by increasing Vitamin D requirements. It thus appears that hypovitaminosis D alone, of particular severity, was sufficient to result in the appearance of clinically evident osteomalacia. Such a vitamin deficiency, necessary when the intestinal mucosa is intact, is only rarely encountered, which accounts for the extreme rarity of osteomalacia in association with chronic pancreatic disorders.
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PMID:[Osteomalcaia and chronic pancreatis. 5 cases]. 121 65

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

To investigate whether progesterone metabolites' antinociceptive effects correlate with their previously established binding efficacies at the GABA receptor complex (GBR), seven progestin metabolites were administered to ovariectomized Long-Evans rats s.c. (Expt. 1), via i.c.v. implantation (Expt. 2) and then i.c.v. infusion (Expt. 3). Progestins, listed from most to least efficacious at the GBR, were THP [5 alpha-pregnan-3 alpha-ol-20-one], THDOC [5 alpha-pregnan-3 alpha,21-diol-20-one], P [4-pregnen-3,20-dione], DHP [5 alpha-pregnan-3,20-dione],17-OH-P [17-hydroxyprogesterone], DHEAS [5-androsten-3 beta-ol-17-one sulfate] and PS [5-pregnen-3 beta-ol-20-one sulfate]. Pain sensitivity was measured via the radiant heat tailflick method 0, 5, 20, 40, 60, 80, 100 and 120 min after weekly progestin administration. Peripheral administration of 0.0, 0.1, 0.4, 1.6, 3.2 or 6.4 mg/kg of potent to moderate agonists of the GBR (THP, THDOC, P and DHP) tended to elevate tailflick latencies above baseline, whereas administration of the non-5 alpha-reduced metabolite (17-OH-P) and GBR antagonists (DHEAS and PS) did not. Intracerebroventricular implantation and infusion (0.0, 0.5, 1.0, 2.0 micrograms/rat) of THP, THDOC, P and DHP all significantly increased tailflick latencies above baseline and vehicle control, consistent with their GBR efficacies. Central 17-OH-P, DHEAS and PS did not elevate tailflick latencies. These rapid differences were unlikely confounded by stress given that corticosterone levels were not elevated (Expt. 4). As pain sensitivity was attenuated rapidly (0-5 min post-i.c.v.) and consistent with GBR efficacies, this suggests that progestins' modulation of pain may occur via GBR action.
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PMID:Progesterone metabolites, effective at the GABAA receptor complex, attenuate pain sensitivity in rats. 803 14

Progesterone (P), its metabolites, and other neuroactive steroids alter pain thresholds consistent with their efficacies at modulating gamma-aminobutyric acid (GABAA) receptor complexes. We investigated whether estradiol benzoate (EB) potentiates low dosages of neuroactive steroids' effects on pain. Subcutaneous EB (10 micrograms) or sesame oil vehicle was administered to ovariectomized Long-Evans rats (n = 40) 48 h before intracerebroventricular (ICV) infusion of a neuroactive steroid (0.0, 0.1, 0.3, or 0.5 micrograms) in cyclodextrin vehicle. Neuroactive steroids (listed from greatest to least efficacious at GABAA receptor complexes) were THP [5 alpha-pregnan-3 alpha-ol-20-one], THDOC [5 alpha-pregnan-3 alpha, 21-diol-20-one], DHP [5 alpha-pregnan-3,20-dione], P [4-pregnen-3,20-dione], and DHEAS [5-androsten-3 beta-ol-17-one sulfate]. Pain sensitivity was assessed using the radiant heat tail-flick method before and 20 and 60 min following infusion. Estradiol benzoate interacted with the neuroactive steroids to alter tail-flick latencies. In particular, EB potentiated the antinociceptive effect of THP and DHP by significantly increasing tail-flick latencies above those of non-EB-treated animals. A similar pattern of increased tail-flick latencies occurred in EB-primed animals that received THDOC. Estradiol benzoate less consistently altered the pain threshold of animals administered P, which is less effective at modulating GABAergic activity. Conversely, EB increased the nociceptive effect of the neurosteroid DHEAS, an allosteric antagonist of GABAA receptor complexes, by significantly decreasing tail-flick latencies of EB-compared to vehicle-primed rats. Thus, EB priming potentiated neuroactive steroids' effects on pain threshold.
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PMID:Estradiol benzoate potentiates neuroactive steroids' effects on pain sensitivity. 884 56

A sample of 871.3 patients/year was conformed by 205 postmenopausal women, aged 64.8 +/- 18.2 years (mean +/- SD), followed up during 51 +/- 12 months. All have osteoporosis, diagnosis assessed through radiological findings of at least one atraumatic fracture or vertebral crush ("severe osteoporosis" according to the new WHO classification). Each woman received 100 mg/day oral pamidronate (enteric coated soft gelatin capsules), half an hour before breakfast. Additional calcium and vitamin D were supplemented as follows: Total daily calcium = 1 g provided by diet and/or calcium carbonate. Vitamin D equivalent to 400-1200 IU/day. All patients were recommended to improve their physical activity, at least by walking exercise. Clinical examination radiological, bone mineral density (BMD) and biochemical studies were periodically performed. But, fracture indicence was the end-point of the study. Same was related to the 1,673 fall episodes recorded in the sample. In addition, height loss, lumbar BMD, proximal femur BMD, are also reported. Data has been cross-sectional collected in March 1995. All patients improved the symptomatology, specifically pain. This, and the good tolerability of the treatments proved to be considerably favorable for their compliance. Within the observation period, only 12 patients decreased their height (5.85%; mean = 0.85 cm; range = 0.5-2.0 cm). Lumbar spine BMD increased in 90% of 48 women. Mean gain after 2 years was 5.3 +/- 1.0% (p < 0.001). Proximal femur increased in 78% of other 32 women. Mean gain 6.3 +/- 0.7% (p < 0.001) after 2 years. A total of 78 new fractures were recorded, 47 vertebral crush, 29 forearm fractures and 2 hip fractures. Its incidence related to the fall episodes was of 2.8; 1.7 and 0.12% respectively. When compared with a historical estimated data, from an untreated population (Cummings SR et al, 1994), both, the total number of new fractures and the new hip fractures were significantly lower (p < 0.01) in our treated population than the reference data. Pamidronate, in oral doses of 100 mg/day, adequately supplemented with calcium and vitamin D, proved to be effective and a well tolerated therapy. The low rate of height's loss, BMD significant increases in subgroups of patients and the low rate of new fractures, strongly support the use of the compound to treat severe osteoporotic women. To our knowledge, this is the first time, that the new fracture incidence is related to the fall frequency reported in a bisphosphonate treated sample.
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PMID:[New spine and non-spine fractures in 871 women/year treated with oral pamidronate plus calcium and vitamin D supplements]. 956 52

Stress fractures of the sacrum during pregnancy or the postpartum seem uncommon. We report a new case of nontrauma-related postpartal sacral fracture. Only four similar cases have been reported to date. The patient was 36 years of age and her fracture was diagnosed four weeks after her first delivery. Vitamin D levels were low, but there was no osteomalacia. Other standard laboratory tests were normal, as were absorptiometry measurements at the lumbar spine and femur. Rheumatologists should consider sacral fracture in pregnant or nursing patients with buttock pain. Magnetic resonance imaging is the diagnostic investigation of choice.
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PMID:Postpartal sacral fracture without osteoporosis. 1123 85

Severe Vitamin D(dihydrotachysterol)-intoxication with temporary anemia and hypercalcemia responsive to bisphosphonates. HISTORY AND FINDINGS: A 31-year old female patient presented with pain of her skeletal system. 6 months prior to her presentation, she underwent thyroid surgery for Graves disease. She also suffered from endocrine orbitopathy. Afterwards, she expirienced surgical hypoparathyroidism and received dihydrotachy-sterol (A.T.10 (R)) in a dose of up to 4 mg per day. The physical examination was unremarkable except for the presence of Graves' ophthalmopathy and a swelling at the left ancle. INVESTIGATIONS: Upon admittance, she had severe hypercalcemia (serum calcium: 4.1 mmol/l) with plasma intact PTH levels below the limit of detection, renal failure (serum creatinine: 5.5 mg/dl) and normocytic anemia (initial hemoglobin: 8.3 g/dl, upon rehydration: 6.6 g/dl). TREATMENT AND COURSE: Upon rehydration and induced diuresis, the renal function improved and the serum calcium came down rapidly in the early treatment phase. However, serum calcium remained elevated at around 3.0 mmol/l after 4 weeks. Only after the use of the bisphosphonate pamidronate (15 mg), serum calcium returned into the normal range and remained there. Treatment for hypoparathyroidism had to be reinstituted only 20 weeks after dihydrotachysterol had been discontinued. The anemia had resolved without any treatment at that time. CONCLUSIONS: Treatment with dihydrotachysterol and other long-acting Vitamin D preparations has to be monitored closely because of the risk of severe hypercalcemia, which may be difficult to treat. In our case, dihydrotachysterol was still active until week 20 after the drug was discontinued. Anemia should be considered as a side effect of dihydrotachysterol intoxication and does not warrant elaborate differential diagnosis in this context. A single administration of a bisphosphonate turned out to be of major therapeutic benefit and resulted in a lasting correction of hypercalcemia. Therefore, bisphosphonates should become part of the treatment regimen for vitamin D intoxication.
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PMID:[Severe Vitamin D(dihydrotachysterol)-intoxication with temporary anemia and hypercalcemia responsive to bisphosphonates] 1275 Oct 20

Vitamin D deficiency is a problem of considerable magnitude that has reemerged as a major public health issue in the United States and several other developed countries. Vitamin D plays a crucial role in calcium homeostasis in the body. Hypovitaminosis D leads to osteomalacia and increased risk of fractures, especially in the elderly. Preliminary research suggests that vitamin D can prevent certain types of cancer and autoimmune diseases. A recent large study has shown the association between severe hypovitaminosis D and persistent, non-specific musculoskeletal pain, further suggesting that patients with no apparent cause of pain should be assessed and possibly treated for vitamin D deficiency.
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PMID:Hypovitaminosis D-induced pain. 1549 69


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