Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the clinical usefulness of the calcitonin test in predicting the hyperparathyroid bone disease severity in uremia. 200 IU of synthetic salmon calcitonin was given intranasally to 77 hemodialysed patients with end-stage renal failure. Before the test, serum calcium, PTH and serum alkaline phosphatase had been sampled; serum calcium was determined also in 2 to 4 hours after. The subjects were divided into 3 groups according to their serum PTH levels. Group I consisted of 24 patients with at least 10-fold serum PTH elevation, group II of 34 patients with intermediate values, and group III of 19 patients with serum PTH within normal range. In the group I the mean serum calcium fall was 0.32 +/- 0.16 mmol/l (1.28 +/- 0.64 mg/dl) (p < 0.001) and 0.27 +/- 0.15 mmol/l (1.08 +/- 0.60 mg/dl) (p < 0.001), after 2 to 4 hours respectively. In the group II serum calcium decreased by 0.16 +/- 0.12 mmol/l (0.64 +/- 0.48 mg/dl) after 2 hours and by 0.14 +/- 0.09 mmol/l (0.56 +/- 0.36 mg/dl) after 4 hours; the differences were statistically insignificant. In the group III no reduction in serum calcium was observed. In the whole 77 patients population significant linear correlations between the hypocalcemic response and iPTH as well as serum alkaline phosphatase were found. Our results confirm that the calcitonin-induced hypocalcemia a test can be, in addition to serum alkaline phosphatase and PTH evaluation, a simple and useful index of advanced hyperparathyroid bone disease in hemodialysed patients with chronic renal failure.
Pol Arch Med Wewn 1993 Feb
PMID:[Test with calcitonin as an index of parathyroid function in chronic renal failure]. 850 92

The study was performed in 17 children with chronic renal failure, 7 were on hemodialysis, 6 on continuous ambulatory peritoneal dialysis, 4 were treated conservatively. In all, serum levels of alkaline phosphatase, PTH intact and osteocalcin were measured and bone biopsy was performed. We analyzed correlations between biochemical markers of bone metabolism and histomorphometric parameters. The lowest mean serum osteocalcin levels were found in children with adynamic bone disease, the highest with osteitis fibrosa. The serum osteocalcin level was significantly correlated with the dynamic parameter of bone formation rate (BFR), which suggests that this biochemical marker can be of use in discriminating between renal osteopathy with low and high bone turnover. Lack of correlation between serum osteocalcin level and mineralizing surface confirms it significance as a good marker of osteoblastic activity in bone formation but not in bone mineralization.
Pediatr Pol 1995 Dec
PMID:[Correlation between osteocalcin and bone histomorphometry in children with chronic renal failure]. 864 39

In the present paper a 67 years old female with chronic renal failure is reported, who developed at least three episodes of live-threatening hypercalcemia during long-term therapy with calcium carbonate. Results of biochemical and hormonal parameters and of dual x-ray photon absorptiometry (DEXA) were indicative for the presence of adynamic bone disease. Results obtained in this patient and published in the literature suggest, that presence of subnormal plasma concentrations of intact parathyroid hormone seems to be a valuable predictor of hypercalcemia in uremic patients treated with calcium carbonate.
Pol Arch Med Wewn 1996 May
PMID:[Life threatening hypercalcemia in a patient with chronic renal failure. Case report]. 884 14

Active vitamin D3 pulse therapy effectively suppresses parathormone (PTH) synthesis in uremic hyperparathyroidism but high serum levels of calcitriol achieved can induce direct osteoclastic resorption and block bone formation. Therefore we found it interesting to examine whether an addition of the osteoclast inhibitor, calcitonin (CT), could reduce those unwanted effects. 75 hemodialysis patients with at least 5-fold 1-84 PTH serum level elevation were divided into 4 treatment groups: I (n = 19)-CT and 1 alpha-OH-D3; II (n = 20)-CT; III (n = 19)-1 alpha-OH-D3 (n = 10) or 1.25 (OH)2D3 (n = 9) alone; IV (n = 17)-none of these drugs. CT (200 IU) and 1 alpha-OH-D3/1.25(OH)2D3 (up to 5 micrograms) were given 3 times a week. Dialysate Ca was 1.40-1.45 (Group I, III) or 1.95-2.00 mmol/l (Group II, IV). Within 8 months serum 1-84 PTH fell by 75% (p < 0.001) in Group I and by 77% (p < 0.001) in Group II, serum Ca increased by 0.22 +/- 0.05 mmol/l in Group I (p < 0.005) and by 0.25 +/- 0.05 mmol/l in Group III (p < 0.005), alkaline phosphatase activity decreased by 35% in Group I (p < 0.01) and 31% in Group III (p < 0.005) whereas in Groups II and IV no significant changes were noted. In Group III no differences between patients taking 1 alpha-OH-D3 or 1.25 (OH)2D3 were observed. The significant reduction of serum hydroxyproline (37%; p < 0.001) was seen only in Group 1. The increase in bone mineral density (BMD) measured by dual-energy X-ray absorptiometry was greater in Group I than in Group III (p < 0.05). In Group II the effect was mostly insignificant, whereas in Group IV a substantial decrease (p < 0.001) in BMD was observed. These data suggest that combined therapy with CT and oral 1 alpha-OH-D3 pulses is more effective than pulses alone in inhibiting bone resorption and in increasing BMD in hemodialysis patients with uremic hyperparathyroid bone disease.
Pol Arch Med Wewn 1996 Jul
PMID:[Combined therapy with calcitonin and high doses of active vitamin D3 metabolites in uremic hyperparathyroidism]. 896 42

The purpose of the study was to evaluate the effectiveness of the oral pulse therapy with high doses of alphacalcidol (1 alpha(OH)D3) in secondary hyperparathyroidism. 16 hemodialysis patients with 4 to 9-fold iPTH serum elevation were given ones in week oral 1 alpha(OH)D3 in doses from 5.0 to 7.0 micrograms (0.1 microgram/b.m.) according to serum levels of calcium, phosphate, activity of alkaline phosphatase with its bone fraction. Serum iPTH levels were measured every 3rd month of the treatment. The dialysate calcium was reduced to 1.25 mmol/l. CaCO3 was used as a main phosphate binder in doses from 3.0 to 9.0 g/day. After first three months of treatment the serum iPTH levels decreased from 486.0 +/- 200 pg/ml to 218.0 +/- 117 pg/ml (p = 0.0001). Calcium levels increased from 2.39 +/- 0.2 mmol/l to 2.52 +/- 0.29 mmol/l (p > 0.05). Phosphate levels increased from 2.15 +/- 0.67 mmol/l to 2.17 +/- 0.62 mmol/l (p > 0.05). Alkaline phosphatase levels decreased from 35.2 +/- 17.3 IU/l to 31.1 +/- 7.78 IU/l (p > 0.05). Bone isoenzyme of alkaline phosphatase decreased from 19.2 +/- 13.4 IU/l to 15.5 +/- 7.51 IU/l (p > 0.05). Because of early serum hypercalcemia, doses of 1 alpha(OH)D3 had to be reduced in 2 patients. In 8 patients (50%) demonstrating decrease of serum iPTH levels (below 200 pg/ml) after first 3 months of treatment doses of 1 alpha(OH)D3 were reduced in the following months. We conclude that oral 1 alpha (OH)D3 pulse therapy is effective for parathyroid activity suppression in patients with severe hyperparathyroidism. To avoid dangerous hypercalcemia and adynamic bone disease serum iPTH and calcium levels should be strictly monitored.
Pol Arch Med Wewn 1997 Oct
PMID:[Evaluation of the treatment efficacy of secondary hyperparathyroidism with oral pulse doses of alphacalcidol]. 955 90

The aim of the study was to estimate predisposing factors which can cause adynamic bone disease (ABD) and biochemical markers, bone densitometry results, bone histomorphometry in 17 children with this from of the renal osteodystrophy. Half of these of patients were treated with alphacalcidol pulses. In 47% of patients hypercalcemic episodes were noted, 76% had PTH level < 50 pg/ml. Four patients with osteoporosis (low bone volume at histological analysis) were distinguished. Two of them were treated with corticosteroids, 1 was immobilized for a long time.
Pol Merkur Lekarski 2000 Apr
PMID:[Risk factors of adynamic bone disease in children with end-stage renal failure: personal experience]. 1089 41

Osteogenesis imperfecta (OI), commonly known as "brittle bone disease", is a dominant autosomal disorder characterized by bone fragility and abnormalities of connective tissue. Biochemical and molecular genetic studies have shown that the vast majority of affected individuals have mutations in either the COL1A1 or COL1A2 genes that encode the chains of type I procollagen. OI is associated with a wide spectrum of phenotypes varying from mild to severe and lethal conditions. The mild forms are usually caused by mutations which inactivate one allele of COL1A1 gene and result in a reduced amount of normal type I collagen, while the severe and lethal forms result from dominant negative mutations in COL1A1 or COL1A2 which produce structural defects in the collagen molecule. The most common mutations are substitutions of glycine residues, which are crucial to formation and function of the collagen triple helix, by larger amino acids. Although type I collagen is the major structural protein of both bone and skin, the mutations in type I collagen genes cause a bone disease. Some reports showed that the mutant collagen can be expressed differently in bone and in skin. Since most mutations identified in OI are dominant negative, the gene therapy requires a fundamentally different approach from that used for genetic-recessive disorders. The antisense therapy, by reducing the expression of mutant genes, is able to change a structural mutation into a null mutation, and thus convert severe forms of the disease into mild OI type I.
Acta Biochim Pol 2002
PMID:Mutations in type I collagen genes resulting in osteogenesis imperfecta in humans. 1236 85

Osteolytic bone destruction, caused by the aberrant production and activation of osteoclasts, results in significant morbidity for patients with multiple myeloma (MM). Pamidronate [(3-amino-1-hydroxypropylidene)-1,1-bis-phosphonate] inhibits osteoclastic activity and reduces bone resorption. A potency of zoledronic acid (2-[imidazol-1-yl]-1-hydroxyethylidene-1,1-bisphosphonic acid, a new third generation bisphosphonate, as inhibitor of resorption was 850-fold greater than pamidronate, as was shown in preclinical models of bone resorption. Randomized, double-blind study was conducted to compare the efficacy and safety of zoledronic acid and pamidronate for treating myeloma bone disease. Since March 1999 the efficacy and safety of pamidronate and zoledronic acid is evaluated in MM patients all receiving anti-myeloma chemotherapy acc. to VMCP/VBAP alternating regimen. Nine patients with stage III myeloma and osteolytic lesions (3 female, 6 male, median age 57 years, range 52-67, with monoclonal protein: IgG-7, IgA-2) were randomly assigned (1:1:1 ratio) to treatment with either 4 or 8 mg of zoledronic acid via 15-minute intravenous infusion or 90 mg of pamidronate via 2-hour intravenous infusion every 3 to 4 weeks for 12 months. All patients have received 500 mg of calcium supplements and 500 IU of vit.D, orally, once daily, for the duration of administration of study medication. In extension phase of the study (June 2000-April 2002) patients did not received bisphosphonates. In 7 patients 18 cycles of assessed treatment was administered to each of them and one patient received 16 cycles. One patient died after receiving of 12 pamidronate therapy cycles at 11 month of the trial duration (and at 49 month since MM diagnosis and anti-tumour treatment). The patient's death occurred during the progression of plasma cell proliferation due to acute left ventricle cardiac failure. During the 12-month-period of bisphosphonate treatment skeletal related events (SRE) and progression of osteolysis occurred with the same frequency in 3 treatment groups. One patient experienced spinal cord compression and received radiation to bone and 2 patients experienced vertebral fracture. Time from study entry to the first SRE was 304 days in pamidronate and 366 and 392 days in 4 and 8 mg zoledronic acid group, respectively. The skeletal morbidity rate was identical in all treatment groups. Single hypocalcemic events occurred in 2 patients, mild hypertransaminasemia was observed in 3, worsening of renal function parameters in 2 patients (transient in one of them). Muscular pain and fever up to 39 degrees C (transient and self-limiting "flu-like" symptoms) occurred in 6 patients after several or some dozens of hours from study drug administration. Adverse events were similar in nature and frequency with zoledronic acid and pamidronate and were experienced by a similar proportion of patients in each treatment group. Median time of patient's observation duration after completing of administered treatment with zoledronic acid and pamidronate amounts to 20 months. At present actual median survival time of analysed patients since MM diagnosis is 42 months, since the beginning of treatment with pamidronate and zoledronic acid--33 months, and since completing treatment--20 months and is similar in 3 treatment groups. As was shown in our single center study in MM patients the safety and efficacy of pamidronate 90 mg and zoledronic acid 4 mg and 8 mg in monthly i.v. infusion are comparable. Thus the recommended dosage of zoledronic acid is 4 mg administered as a 15 minute i.v. infusion at intervals of 3 to 4 weeks.
Acta Pol Pharm
PMID:Comparative evaluation of safety and efficacy of pamidronate and zoledronic acid in multiple myeloma patients (single center experience). 1266 77

Our knowledge of the mineral metabolism disturbances and skeletal disorders in patients with chronic renal insufficiency has advanced significantly in the last years. Probably the most important what we have learned is, that apart of bone disease, hyperparathyroidism and its treatment can also lead to severe extra-skeletal complications, contributing to the progression of cardiovascular disease in this population. This fact has fundamentally changed our approach to the treatment, and - as a result - the new clinical practice guidelines on the management of mineral metabolism and bone disease in chronic renal failure have been developed. Mainstays of the new approach are lower recommended serum calcium and calcium-phosphate product. However, these targets are very difficult to achieve in clinical practice. During the last decade, some additional therapeutic agents have been welcomed. There are two effective calcium-free, aluminium-free phosphate binders, sevelamer hydrochloride, and lanthanum carbonate, four vitamin D analogues of newer generation, and--last but not least--modulators of calcium-sensing receptor, calcimimetics. Future studies will be needed to determine how these recent developments will be helpful. The optimal therapy for all end-stage renal failure complications is definitely renal transplantation.
Pol Arch Med Wewn 2004 Oct
PMID:[New aspects in the management of renal osteodystrophy]. 1566 6

This review highlights the key messages from the KDIGO (Kidney Disease: Improving Global Outcomes) clinical practice guidelines for care of kidney transplant recipients, which were written to be global guidelines irrespective of the regulatory, fiscal, cultural, socioeconomic, or geographical environment. The distillation of 3168 randomized control trials, 7543 cohort studies, and 1609 reviews led to recommendations rated by the strength of supporting evidence and the quality of the data from A to D. Despite this, the quality of the evidence is surprisingly low for the majority of decisions that are routinely taken in all transplant units throughout the world, highlighting the needs for properly designed randomized controlled trials. The principle areas covered in the guidelines include immunosuppression, management of acute rejection, monitoring of the patient and graft, chronic allograft injury, kidney biopsy, nonadherence, vaccination, infectious diseases, cardiovascular risk management, malignancy, bone disease, pediatric growth, lifestyle, fertility, and mental health. This review highlights a number of these areas for consideration focusing on the different types of evidence that we use in daily clinical practice.
Pol Arch Med Wewn 2010 Jun
PMID:The KDIGO review of the care of renal transplant recipient. 2056 8


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