Treatment and histological healing of aluminum-related osteomalacia.
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Adult↗
Biomedical subjects
B F Boyce
Publications and source records attributed to B F Boyce.
Effects of a synthetic peptide of a parathyroid hormone-related protein on calcium homeostasis, renal tubular calcium reabsorption, and bone metabolism in vivo and in vitro in rodents.
A synthetic peptide corresponding to the first 34 amino acids of the parathyroid hormone-related protein (PTH-rP) produced by a human tumor associated with hypercalcemia was examined for skeletal and renal effects on calcium metabolism in vivo and in vitro. These effects were compared with those of human parathyroid hormone (1-34), hPTH (1-34). Equal doses of PTH-rP(1-34) and hPTH(1-34) produced equivalent stimulation of adenylate cyclase in vitro in bone cells and kidney cells and tubules. Subcutaneous injection of PTH-rP(1-34) in mice caused a significant dose-related increase in blood ionized calcium similar to that seen with hPTH(1-34) at equivalent doses. Repeated injections of equal doses of both peptides caused sustained hypercalcemia which was significantly greater in PTH-rP(1-34)-treated mice, although each induced comparable increases in histomorphometric indices of osteoclastic bone resorption. PTH-rP(1-34) and hPTH(1-34) also caused similar increases in bone resorption when incubated with fetal rat long bones in organ culture. Infusion of either peptide into thyroparathyroidectomized rats suppressed urinary calcium excretion and increased urinary excretion of cyclic AMP. PTH-rP appears to have similar effects to those of PTH on the skeleton, the kidney, and overall calcium homeostasis.
Adenylyl Cyclases↗
Aluminium bone disease in patients receiving plasma exchange with contaminated albumin.
Aluminium balance studies were carried out on eight patients with various immunological disorders who were receiving plasma exchange with albumin solutions known to be contaminated with aluminium. Four patients with impaired renal function (creatinine clearance less than 50 ml/min) retained between 60% and 74% of the aluminium infused during a single plasma exchange. Transiliac bone biopsy specimens from three patients in this group had a high content of aluminium and showed histological evidence of current or previous bone disease related to aluminium. Two of these patients suffered intermittent bone pain. The main route of excretion of injected aluminium was in urine, only a small proportion of the total input being removed in the "plasma bag" during plasma exchange. The extent of aluminium retention and bone deposition was not reflected by the plasma aluminium concentration before or after plasma exchange. Treatment of five patients with intravenous desferrioxamine increased the plasma aluminium concentration and urinary output of aluminium in those with evidence of aluminium retention. These studies show that patients with poor renal function receiving treatment with albumin contaminated with aluminium retain the metal and deposit it in bone, where it may eventually cause aluminium bone disease. Plasma exchange should be used with caution in patients with renal impairment.
Adult↗
The effect of 1 alpha-hydroxyvitamin D3 on the mineralization defect in disodium etidronate-treated Paget's disease--a double-blind randomized clinical study.
A double-blind randomized study of 29 patients with symptomatic Paget's disease was conducted comparing the clinical, biochemical, and histomorphometric responses to 3-month treatment with placebo (10 patients), low-dose disodium etidronate (EHDP) (5-7 mg/kg/day) (10 patients), and low-dose EHDP plus 1 alpha-hydroxyvitamin D3 (1 alpha D3) 0.5 mcg daily (9 patients). In placebo-treated patients no significant changes were observed in symptoms, biochemistry, or bone histomorphometry. Histologically apparent mineralization defects developed after 3 months of therapy in 90% of patients in the EHDP group, compared with 45% of patients in the EHDP/1 alpha D3 group. In 19% of the patients treated with active medication, the mineralization defects in pagetic bone were accompanied by histological evidence of continued osteoclastic resorption. The development of mineralization defects was not related to serum levels of vitamin D metabolites, alkaline phosphatase, or intestinal calcium absorption but did correlate with the occurrence of hyperphosphatemia during treatment, which was most marked in patients treated with EHDP alone. Although mineralization defects were less frequent in the EHDP/1 alpha D3 group, these patients also responded less well symptomatically, thus limiting the potential usefulness of this drug combination in Paget's disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Alkaline Phosphatase↗
An outbreak of 'slapped cheek' parvovirus infection (erythema infectiosum) in a Scottish street.
One adult and six children living in a small Scottish street developed erythema infectiosum (fifth disease) during the summer of 1985. The rash was attributed to infection with the human parvovirus. Leg pain and arthralgia occurred in five of the children.
Adult↗
Does osteomalacia contribute to development of oral complications of oxalosis?
Two renal dialysis patients with oral manifestations of oxalosis had undecalcified sections of iliac and alveolar bone and teeth examined histologically in an attempt to explain the development of tooth mobility and tooth loss. Osteomalacia was detected in all bone specimens and attributed to aluminum toxicity after the histochemical localization of aluminum at the calcification front between osteoid and calcified matrix. Aluminum was also detected histochemically in the cementum of teeth. Calcium oxalate crystals were present in bone marrow, teeth, and gingiva. It is proposed that tooth mobility and tooth loss in oxalosis result from the combined effects of osteomalacia and oxalate crystal deposition within the periodontium. To prevent avoidable tooth loss it is suggested that patients with oxalosis who develop tooth mobility should have aluminum toxicity and osteomalacia excluded as causal factors.
Adolescent↗
Malignant histiocytosis complicating rheumatoid arthritis: report of four cases.
Four patients with rheumatoid arthritis developed a similar type of lymphoreticular tumour. The morphology and immunocytochemical findings suggested that this was a form of malignant histiocytosis: there may be an important correlation between this tumour and rheumatoid arthritis.
Aged↗
Humoral hypercalcaemia of malignancy: metabolic and histomorphometric studies during surgical management of the primary tumour.
Several aspects of calcium metabolism were studied in five patients during the surgical exploration of malignant tumours associated with humorally-mediated hypercalcaemia. Before operation in all patients the renal tubular threshold for calcium reabsorption was raised and the threshold for renal tubular phosphate reabsorption depressed. On removal of the primary tumour in three cases, serum calcium returned to normal, renal calcium threshold fell, renal phosphate threshold rose, but urinary hydroxyproline excretion did not change. In two patients where the tumour proved inoperable, serum calcium remained elevated and no changes in renal calcium threshold or phosphate threshold occurred. Histomorphometry carried out on biopsy specimens from four patients showed normal bone resorption in three, and slightly increased resorption in one, without depression of osteoblastic bone formation. It is suggested that hypercalcaemia in these patients resulted mainly from an alteration in renal calcium threshold caused by a humoral substance released by tumour cells. Correction of hypercalcaemia on removal of the primary tumour was achieved rapidly and could be explained principally by a reduction in renal calcium threshold with increased loss of calcium into the urine. These data contrast with those of many previous studies which have emphasised the predominant role of accelerated osteoclastic bone resorption as the principal cause of hypercalcaemia in malignancy and suggest that a renal effect of the putative humoral agent may predominate in some cases.
Adenoma, Bile Duct↗
Focal osteomalacia due to low-dose diphosphonate therapy in Paget's disease.
Transiliac bone biopsies carried out on 13 patients with Paget's disease to evaluate the effects of low-dose diphosphonate (disodium etidronate) therapy showed focal osteomalacia in the 9 patients in whom post-therapy specimens were taken through pagetic bone. Active bone resorption persisted in 5 of these. A mineralisation defect not amounting to osteomalacia--ie, osteoid of increased thickness but of normal extent--was present in the 4 specimens taken through non-pagetic bone. Although 9 patients experienced symptomatic improvement, 2 suffered fissure fractures in affected lower limbs. In Paget's disease, the combination of osteomalacia and continuing active resorption within a lytic lesion may increase the risk of fracture in a weight-bearing bone. It is suggested that although disodium etidronate often provides effective pain relief it should be administered with caution until the optimum dose and duration of therapy are further evaluated.
Aged↗
Correlation of skeletal uptake of 99mTc-diphosphonate and alkaline phosphatase before and after oral diphosphonate therapy in Paget's disease.
In Paget's disease of bone, quantitation of skeletal uptake of radiolabeled diphosphonate has been proposed as a means of monitoring response to therapy. However, the validity of such techniques has been questioned during oral diphosphonate therapy because of possible interaction between oral and radiolabeled diphosphonate. In the present study 18 patients with Paget's disease received a 6 month course of oral diphosphonate therapy. Measurements of 24 h whole body retention (WBR) of 99mTc-labeled hydroxyethylidene diphosphonate (HEDP), serum alkaline phosphatase (SAP), and urinary hydroxyproline excretion were obtained before, during, and after treatment. WBR correlated well with SAP and urinary hydroxyproline throughout the course of therapy. In addition, the relationship between WBR and SAP was maintained after cessation of oral diphosphonate. It would thus appear that in Paget's disease 24 h WBR of HEDP, a quantitative measure of skeletal uptake of diphosphonate, will reflect disease activity even in the presence of an oral diphosphonate load.
Administration, Oral↗
Bone scan appearances following biopsy of bone and bone marrow.
The influence of sternal marrow aspiration, iliac crest marrow aspiration, and iliac crest bone biopsy on bone scan appearances was examined. Eighteen patients were scanned a mean of 9.9 days after sternal marrow aspiration with a Salah needle (diameter 1.2 mm). Only one patient had an abnormality at the biopsy site. Bone scans obtained in 9 patients a mean of 10 days after iliac crest trephine marrow biopsy with a Jamshidi needle (diameter 3.5 mm) showed no abnormality at the biopsy site. In 18 patients with metabolic bone disease who had undergone iliac crest bone biopsy with an 8-mm needle, a scan abnormality due to the biopsy was usually present when the interval between the biopsy and the scan was 5 days to 2 months. Patients who were scanned within 3 days of iliac crest bone biopsy or more than 2 months after biopsy had normal scan appearance at the biopsy site.
Biopsy↗
Pre-operative localisation of parathyroid tumours using neck vein catheterisation and radioimmunoassay for parathyroid hormone: the Glasgow experience.
Reliable pre-operative localisation of parathyroid tumours can be of value in surgery for primary hyperparathyroidism, and particularly so where re-exploration of the neck is required. Neck vein catheterisation and parathyroid hormone radioimmunoassay have been suggested as a sensitive means of tumour localisation, and we report our experience of the technique over the last five years. A total of 46 patients with primary hyperparathyroidism had 50 studies performed with positive localisation and a pre-operative prediction made on 38 occasions (76%). Forty-two operations were carried out and a parathyroid tumour confirmed in 39 cases for a localisation efficiency of 69 per cent. No negative neck exploration followed a positive localisation. Twelve studies were performed in patients with renal osteodystrophy and localisation to a single site was achieved on only three occasions. It is concluded that neck vein catheterisation and parathyroid hormone assay can correctly localise parathyroid tumours in most cases of primary hyperparathyroidism, but it is suggested that its use be restricted to selected cases such as those subjects with previous negative neck exploration or patients for whom prolonged or repeated surgery may be a particular hazard.
Adenoma↗
Hypercalcaemic osteomalacia due to aluminium toxicity.
In 16 patients with chronic renal failure and osteomalacia resistant to vitamin-D therapy, aluminium was demonstrated in bone biopsy specimens at the interface between thickened osteoid and calcified bone by means of both X-ray microanalysis and a specific histochemical stain. 14 patients also had hypercalcemia. It is suggested that this is due to the blocking by aluminium of additional calcium uptake into bone coupled with the availability of additional calcium from dialysis fluid and vitamin-D therapy. This study provides more aetiological evidence linking aluminium and the development of osteomalacia in chronic renal failure. Further, if hypercalcaemia develops in such patients it is important that aluminium toxicity be excluded as the cause to prevent unnecessary parathyroidectomy.
Adolescent↗
Diphosphonates and inhibition of bone mineralisation.
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Bone and Bones↗
Hyperplastic parathyroiditis--a new autoimmune disease?
A case of parathyroiditis with epithelial hyperplasia is reported in which the histological features suggest an autoimmune process analogous to Hashimoto's disease.
Autoimmune Diseases↗
Do anticonvulsant drugs commonly induce osteomalacia?
Twenty adult epileptic out-patients who had received anticonvulsant therapy for a mean duration of 15 years were assessed for clinical, biochemical, radioisotopic and bone biopsy evidence of osteomalacia. Occasional biochemical abnormalities were demonstrated but no individual subject was found to have osteomalacia. There is increasing evidence to cast doubt on the existence of a strong relationship between anticonvulsant drugs and osteomalacia. This evidence is reviewed and it is concluded that in the presence of adequate sunlight exposure anticonvulsant therapy alone is most unlikely to lead to osteomalacia in adults.
Adult↗
Quantitation and localisation of aluminum in human cancellous bone in renal osteodystrophy.
There is increasing evidence that aluminium toxicity may be responsible for a type of vitamin D-resistant osteomalacia and an unusually severe form of dementia ("dialysis dementia") occurring in some patients with chronic renal failure on regular haemodialysis. High concentrations of Al have been found in blood, bone and brain tissue from these patients. The A1 comes either from the water used during dialysis (added in some public water supplies during purification to precipitate contaminants) or from aluminium salts taken orally to bind phosphates and so restrict their dietary adsorption. Recent X-ray microanalytical studies have demonstrated Al in lysosomes of cerebral cells and at the calcification front in bone of patients dying of dialysis dementia but its concentration at this site in bone has not been measured using this technique. We have examined transiliac bone biopsies from 3 patients with dialysis dementia and 6 non-demented patients on regular haemodialysis, Atomic absorption spectrometry (AAS) reveals high Al content in bone from the 3 demented and 2 of the non-demented patients. All had vitamin D-resistant osteomalacia. Using X-ray microanalysis Al was located in the bone of these five patients only. The Al had a highly focal distribution and was measured at up to 40 times higher concentration than by AAS but only in mineralisation nuclei of the calcification front or less than 2 micrometer into the mineralized bone. The study was done retrospectively on biopsies fixed in 10% buffered formalin, which almost certainly eluted some of the Al. In life, Al levels may have been higher than those we have detected.
Adolescent↗