Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diphosphonates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,261 records · Page 70Linked to original sources

The effect of anti-rheumatic drugs on factors from porcine synovium inducing chondrocyte mediated cartilage degradation.

A selection of NSAID's and diphosphonates were studied in a tissue culture model of cartilage degradation utilising porcine synovium and bovine nasal cartilage. All the NSAID's significantly reduced cartilage degradation when incorporated into the synovial culture medium. Lesser reductions were recorded when preformed chondrocyte stimulating factors were used and NSAID's added at the cartilage assay stage. These findings suggested that the principle site of action of NSAID's is upon the production of chondrocyte stimulating factors. None of the NSAID's tested affected inherent cartilage degradation. Diphosphonates had the opposite effects, they increased inherent cartilage degradation but had no effect on chondrocyte mediated cartilage degradation. The relationship of these results to previous known effects of NSAID's and diphosphonates upon cartilage is discussed. In addition, correlations between chondrocyte stimulating factors, catabolin and interleukin 1 are made.

Animals↗

Comparative study of available medical therapy for hypercalcemia of malignancy.

The relative efficacy of five drugs in the treatment of hypercalcemia of malignancy was assessed in a randomized study. The drugs were oral phosphate, mithramycin, glucocorticoids, indomethacin, and ethane-1-hydroxy-1, 1-diphosphonate (EHDP). No single agent was universally effective. Oral phosphate and mithramycin were the most efficacious, each producing a decrease in serum calcium concentrations in four of five patients, although there were serious disadvantages with the use of each. Glucocorticoids were effective in only two of five patients who received randomized treatment. A further five patients received nonrandomized treatment with glucocorticoids, and only three of these showed response. Indomethacin was effective in only one of five patients to whom it was given, and EHDP was effective also in only one of five patients. The new diphosphonate, 3-amino-1-hydroxypropane-1, 1-diphosphonate (APD) was evaluated in the treatment of hypercalcemia in 13 patients with malignant disease and two with primary hyperparathyroidism. APD caused a significant decrease in serum calcium concentration in nine of 12 patients within 72 hours. These results indicate that there is no currently available pharmacologic agent that is entirely satisfactory in the treatment of hypercalcemia. The most effective agents were mithramycin, oral phosphate, and APD. Glucocorticoids and orally administered EHDP showed limited effectiveness, and indomethacin was ineffective in the majority of patients.

Administration, Oral↗

Endocrine and pharmacological suppressors of bone turnover protect against osteopenia in ovariectomized rats.

This study was designed to test the hypothesis that endocrine and pharmacological suppressors of bone turnover prevent the development of osteopenia during estrogen deficiency. Sham-operated control and ovariectomized (OVX) rats were treated intermittently with vehicle alone, estrogen, or the diphosphonate compounds etidronate disodium (EHDP) and NE-58095 [2-(3-pyridinyl)2-hydroxyethylidene-1,1-bisphosphonate disodium] for 35 or 70 days after surgery. Their proximal tibiae were processed undecalcified for quantitative bone histomorphometry. Vehicle-treated OVX rats were characterized by decreased cancellous bone volume and 3- to 4-fold increases in osteoblast surface, osteoclast surface, bone formation rate, and bone resorption rate. Treatment of OVX rats with estrogen and NE-58095 provided complete protection against bone loss and significantly depressed all of the above indices of bone turnover. OVX rats treated with EHDP exhibited at least partial protection against bone loss and decreased bone turnover. EHDP induced a mild mineralization defect, as indicated by a prolonged mineralization lag time at the tibial endocortical surface. The new diphosphonate compound NE-58095 did not impair bone mineralization. Our results indicate that endocrine and pharmacological suppressors of bone turnover prevent the development of osteopenia during the early stages of estrogen deficiency. If confirmed by clinical trials in humans, diphosphonate compounds may prove to be an alternative to estrogen for the prevention of postmenopausal bone loss.

Animals↗

99mTc-DPD uptake in juvenile hemarthrosis. Scintimetry and autoradiography of the knee in dogs.

The pathogenesis of subchondral bone lesions and growth plate affection in hemophilic arthropathy was studied in puppies by means of repeated regional 99mTc-diphosphonate scintimetry and contact autoradiography. Unilateral hemarthrosis of the knee was induced by biweekly intraarticular injections of autologous blood for 12 weeks. Hemarthrosis caused an early (2 to 4 weeks) decrease in uptake of 99mTc-diphosphonate in the juxtaarticular growth plates (ratio 0.7) and a delayed (8 to 10 weeks) increase in epiphyseal uptake (ratio 1.5). In a recovery phase after hemarthrosis, growth plate uptake returned to normal, while the epiphyseal uptake remained elevated for 8 to 10 weeks. By contact autoradiography, the growth plate uptake was localized to the calcification layer at the metaphyseal aspect of the growth plates, while the epiphyseal uptake mainly was seen in the thin subchondral and subsynovial bone layer and around osteophytes. The changes in uptake of 99mTc-diphosphonate following hemarthrosis for 3 months were reversible and could be ascribed to the presence of synovial inflammation.

Animals↗

Paget's disease of bone--current thinking and management.

OBJECTIVES: The objective of this article was to critically review the current knowledge on Paget's disease of bone, focusing primarily on possible etiologies and trends in management. Current courses of treatment are described, including calcitonin, diphosphonate and mithramycin therapy and the efficacy of each drug regime is analyzed. Finally, newer, more experimental pharmaceutical agents, such as gallium nitrate, are described. DATA SOURCES: Information was obtained from English language medical and scientific journals and medical/physiology text books. Index Medicus (1983-1989) and MEDLINE computerized data base were used. Paget's disease of bone, paramyxovirus, osteoclast, calcitonin and diphosphonate were the terms indexed directly. Key authors indexed included Rebel, Baste and Paget. Further information was obtained from the National Association for the Relief of Paget's Disease (England). CONCLUSIONS: Current research focuses primarily on histological and hybridization studies over the past 15 yr in favor of a slow virus as the causative agent in the disease, and the evidence supporting this is analyzed in some detail. In particular, the discovery of nuclear and cytoplasmic inclusion bodies within the osteoclasts of patients with Paget's disease and their similarity to respiratory syncytial virus and measles virus are discussed. Some form of environmental or physiological trigger may be involved, but the exact mechanism remains obscure. The current treatment of Paget's disease is based around the prevention of bone resorption using various diphosphonates and calcitonins, but many of these are associated with severe side effects. Newer pharmaceutical agents to control bone turnover, including gallium nitrate, have given promising results in preliminary medical trials.

Calcitonin↗

[In vitro decrease of the cytolytic effect of E. histolytica by inhibition of its phosphofructokinase].

The C14 radioactive label of PPi analogues was incorporated to E. histolytica after 24 hours of incubation at 37 degrees C; more than 90% of trophozoites remained viable. The PPi dependent phosphofructokinase was isolated in order to determine its kinetic parameters. With PPi, the Km was 18.06 +/- 0.91 micromol/mL-1. Using three different PPi analogues (tetrasodium salts) of (I) 1,1 hydroxy-methyl diphosphonate; (II) 1,1 hydroxy ethylene diphosphonate; (III) 1,1 hydroxy-nonano diphosphonate, KiI was 35.19 +/- 1.74; KiII was 42.65 +/- 0.65, and KiIII 2as 62.81 +/- 0.27 micromol/mL-1. The graphic expression of these results shows that the enzyme was competitively inhibited by the three analogues. When trophozoites were incubated with each one of the three inhibitors, a correlation was observed between the concentration and the cytolytic inhibition with an r = 0.98. Nevertheless, the slope obtained was different for each one of them. The smallest concentration of inhibitor to achieve a 50% lysis inhibition of trophozoites was that of inhibitor III. In addition, it was demonstrated that the incubation of the trophozoites with this inhibitor increased the time needed to destroy CHO cells. We conclude that enzymatic inhibition of the PPi dependent phosphofructokinase caused by the PPi analogues was responsible for the modification of the lytic capacity of trophozoites, possibly by altering the metabolic pathway of carbohydrates.

Animals↗

[Effect of 2 phosphonates on the osteolysis induced by tumor extracts].

An in-vitro model is proposed to test the potential effect of diphosphonates in treatment or preventing bone metastases. This model involves culturing of neonatal mice calvaria in sterile conditions in an appropriate medium and measuring 45Ca release from bone to medium, the mice being injected with 45Ca on the day of birth. Tumour extracts added to the medium usually increase the bone lysis; this effect is significantly decreased when the mice have been treated with either ethane-hydroxy-diphosphonate (EHDP) or dichloromethylene-diphosphonate (Cl2MDP). These experiments represent a first step in a group of experiments with a view to clinical trials in cases of bone metastases.

Animals↗

[Comparative evaluation of the accumulation of 99mTc-labeled phosphate compounds in the bones].

Distribution of osteotropic radiopharmaceuticals was studied in bone, different organs and tissues of rats. 99mTc-pyrophosphate (USSR and France) and 99mTc-diphosphonate (GDR and Hungary) were investigated. Differences in their behaviour were demonstrated. According to a degree of accumulation in the bone tissue, the preparations may be arranged as follows: 99mTc-diphosphonate (GDR), 99mTc-diphosphonate (Hungary), 99mTc-pyrophosphate (USSR and France).

Animals↗

In vitro stability of 99Tcm bone scan preparations from different manufacturers measured by various radiopharmaceutical parameters.

We have investigated the stability of 99Tcm-labelled kit preparations of the bone seeking agents methylene diphosphonate (MDP), hydroxymethylene diphosphonate (HDP) and dicarboxypropane diphosphonate (DPD). This was done by determining amounts of free 99Tcm pertechnetate under various experimental parameters. The radiopharmaceuticals were made with 100 and 300 mCi 99Tcm eluents and kept under the moderate condition of occasional inverting (1) or continuous rolling (2). Analysis took place 5 min, 2 h, 4 h and 6 h after preparation. In general free 99Tcm pertechnetate concentrations were less when 100 mCi 99Tcm eluent was used than with 300 mCi amounts. The level of impurity was also lower in vials kept under condition (1) than in vials kept under condition (2). Unexpected concentrations of free 99Tcm pertechnetate (maximum about 30%) were found in some commercial preparations. Only in one MDP and one HDP preparation did the average free 99Tcm pertechnetate concentration stay within tolerable limits under all experimental parameters. This study demonstrates that careful quality control is needed and that only freshly prepared bone-seeking radiopharmaceuticals should be applied, especially when 99Tcm eluents of about 300 mCi are used for kit preparation.

Bone and Bones↗

Therapeutic progress--review VII. The medical treatment of Paget's disease.

The presentation of Paget's disease varies from a painful or deforming skeletal affliction to an asymptomatic disorder diagnosed on routine biochemical or radiological assessment. When involvement of the peripheral skeleton by Paget's disease is extensive, the clinical diagnosis is usually clear. Affected bones are thickened and deformed and the overlying skin is warm. Bone pain is sometimes severe and malignant change rarely occurs. The new bone formed is structurally abnormal and is consequently liable to deformity and fractures. Serum alkaline phosphatase concentrations and urinary hydroxyproline excretion are raised. Characteristic X-ray changes are seen. Paget's disease should be treated when it causes skeletal pain and tenderness, or when there are neurological symptoms, fractures, marked deformities, or other complications. New therapeutic agents offer both symptomatic relief and some control of the basic disease process. Simple analgesics should be tried before proceeding to the anti-osteoclastic agents, calcitonin, diphosphonates and mithramycin. All are effective in relieving bone pain and improving biochemical indices. The major advantage of the diphosphonates lies in their oral usage and thus, the number of patients who nowadays require calcitonin is small. The majority of patients should be commenced on a course of diphosphonate therapy (EHDP in most instances), but if clinical response is unsatisfactory calcitonin should be tried. Mithramycin should be reserved for special indications e.g. an elderly patient with severe disabling pain.

Calcitonin↗

Isotope retention for assessment of bone turnover in involutional osteoporosis.

A continuous bone remodelling takes place throughout life at different turnover speed according to age, physiological and pathological conditions. The evaluation of bone turnover may be of value for a prognostic and therapeutical assessment. Calcium bone exchange may be considered a suitable marker of bone turnover; for this reason 47Ca or 45Ca kinetics may be used; these methods have been employed in the past. Labelled diphosphonates, and in particular 99Technetium-methylene-diphosphonate (99TcmDP) are simpler and safer, because these substances are strongly and almost completely stored in bone and not absorbed by the soft tissue; for this reason they are used at the present time. The evaluation of blood levels and 24 hrs urinary elimination of 99TcmDP is used to measure whole bone diphosphonate retention (WBR). This parameter is positively correlated with other markers of bone turnover such as alkaline phosphatase (AP), osteocalcin (OC), urinary hydroxyproline (HOP). A bicompartmental analysis schedule of 99TcmDP distribution has been proposed some years ago and therefore applied by our group, based on the mathematical evaluation of serum concentration at different times and urinary elimination of the label given intravenously. This method provides the possibility to calculate not only WBR but also total body retention (TBR) and a constant (Kbh) which reflects the influx speed of the tracer in the bone. Kbh probably represents a more sensitive index of bone turnover than WBR. It presents a better correlation with AP and OC values and also shows some (statistically less significant correlations with some indices of bone remodelling obtained by histomorphometry on bone biopsies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Aggregation of hydroxyapatite crystals.

A system to study the aggregation of hydroxyapatite crystals was developed. The effect of several factors (Ca2+ x Pi product, Ca2+/Pi ratio, pH, and various substances) were tested. Pb2+, Zn2+, Mg2+ and methyleneblue had only small effects; citrate inhibited aggregation. Pyrophosphate was a strong inhibitor and the diphosphonates disodium ethane-1-hydroxy-1,1-diphosphonate and disodium dichloromethylene diphosphonate were even more potent. The monophosphonate pentanemonophosphonate had no effect. Potent inhibition also occurred with glycosaminoglycans: heparin greater than hyaluronic acid greater than dermatan sulfate greater than chondroitin 4-sulfate greater than chondroitin 6-sulfate. Urine also showed high inhibitory activity. The inhibition of heparin but not that of hyaluronic acid, PPi or urine was abolished by egg white lysozyme. The effects described might be relevant in the normal mineralization process as well as in the mechanisms leading to pathological calcification, such as urinary stone formation.

Binding Sites↗

Radionuclide imaging in metabolic and systemic skeletal diseases.

Radionuclide imaging with Tc-99m diphosphonates is not an effective method for detecting or ruling out most osteoporotic diseases including senile osteoporosis or accelerated postmenopausal osteoporosis, and the slow loss of bone tissue generally remains undetected by this modality. Nonetheless, it frequently surpasses or supplements radiographic findings in evaluating the focal complications of metabolic bone disease, including fractures, microfractures, stress fractures, vertebral compressions, Milkman-Looser zones, aseptic necrosis, and acute infarction. In contrast to its secondary role in osteoporosis, bone imaging is of prime importance in investigating hypercalcemia, because the major cause of this abnormality is skeletal metastatic malignancy. In defective bone mineralization due to hyperparathyroidism or osteomalacia, a general increase in diphosphonate skeletal uptake is detected more frequently than radiographic abnormalities. However, normal skeletal images do not rule out metabolic bone disease. Biochemical testing is more reliable in detecting primary hyperparathyroidism. On the other hand, in renal osteodystrophy, biochemical abnormalities are variable and bone imaging is helpful in assessing the severity of skeletal involvement, but not its etiology. Many methods of quantitating the kinetics of Tc-99m diphosphonates have been explored, such as plasma clearance, bone-to-soft-tissue ratios, 24-hour total body retention and 24-hour urinary excretion. None of these have been widely accepted. The value of bone imaging is established in other systemic diseases, most notably in Paget's disease, hypertrophic pulmonary osteoarthropathy, sickle cell disease, fibrous dysplasia, and sympathetic dystrophy.

Bone Diseases↗

Disodium etidronate in the prevention of heterotopic ossification following spinal cord injury (preliminary report).

Heterotopic ossification is a frequent complication following spinal cord injury with 16 per cent to 53 per cent of patients developing varying degrees of pathologic ossification. The diphosphonates are known to block the transformation of amorphous calcium phosphate into crystalline hydroxyapatite. Therefore, one of the diphosphonates, disodium etidronate (generic name of disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) was selected fro clinical trials to study the effectiveness of EHDP in preventing heterotopic ossification following spinal cord injury. In a double-blind, clinical study of 149 spinal cord injury patients, disodium etidronate has proven its effectiveness in the prevention of heterotopic ossification. The extent of heterotopic ossification development as measured by the total heterotopic ossification X-ray grade was significantly less in EHDP-treated patients compared to placebo-treated patients (P less than 0-05). For maximal effectiveness, EHDP treatment must be started before the onset of the pathological process initiating the development of heterotopicossification. Further studies are necessary to determine the optimal time to institute EHDP treatment, length of treatment, and minimal effective dose. EHDP is the first hterapeutic agent known to alter the formation of heterotopic ossification after spinal injury and may prove useful in other conditions where heterotopic ossification prevention is clinically indicated.

Adolescent↗

Re-186 HEDP conditioning therapy in patients with advanced acute lymphoblastic leukemia before allogeneic bone marrow transplantation.

The authors present their experience with dose calculation of Retin1,1-hydroxyethylidene-186-diphosphonate (Re-186 HEDP) therapy used as part of an intensified conditioning regimen before allogeneic stem cell transplantation in 2 patients with advanced acute lymphoblastic leukemia during the second partial or third complete remission. Kidneys were shielded during total-body irradiation (TBI) to limit the TBI-mediated renal radiation dose to 7 Gy. The aim of this dose calculation of Re-186 HEDP therapy was to deliver additional radiotherapy to the red bone marrow without exposing more than an additional 5 Gy to the kidneys in addition to the TBI standard dose of 12.6 Gy. Pretherapeutic kidney scintigraphy (Tc-99m mercaptoacetyltriglycine) showed normal results. Thus, dynamic Tc-99m methylene diphosphonate bone scintigraphy was used to calculate the expected bone marrow and kidney doses. A total amount of 8.8 GBq (238 mCi) Re-186 HEDP was given to patient no. 1 and 14.3 GBq (387 mCi) Re-186 HEDP was given to patient no. 2. Re-186 HEDP activity was monitored based on its gamma radiation measurement daily for 5 days in patient no. 1 and 7 days in patient no. 2. Therapeutic Re-186 isotope distribution and biologic half-life correlated well with the prediction by a pretherapeutic Tc-99m methylene diphosphonate scan. The calculated effective Re-186 bone marrow dose was 3.3 Gy for patient no. 1 and 5.6 Gy for patient no. 2. Effective kidney doses were 1.6 Gy and 2.1 Gy respectively. No unexpected complications occurred after completing conditioning and allogeneic stem cell transplantation. Posttransplant kidney function remained normal. Patient no. 1 remains in a second complete remission of his advanced acute lymphoblastic leukemia 18 months after HEDP therapy. Patient no. 2 relapsed 5 months after transplantation and eventually died as a result of progressive disease. The authors conclude that Re-186 HEDP will be able to increase the total additional bone marrow dose. In patients in whom the kidney dose is limited to 5 Gy in addition to TBI, doses near 10 Gy can be achieved on the bone marrow.

Adult↗

Aminomethylenediphosphonate: A Potent Type-Specific Inhibitor of Both Plant and Phototrophic Bacterial H+-Pyrophosphatases.

The suitability of different pyrophosphate (PPi) analogs as inhibitors of the vacuolar H+-translocating inorganic pyrophosphatase (V-PPase; EC 3.6.1.1) of tonoplast vesicles isolated from etiolated hypocotyls of Vigna radiata was investigated. Five 1,1-diphosphonates and imidodiphosphate were tested for their effects on substrate hydrolysis by the V-PPase at a substrate concentration corresponding to the Km of the enzyme. The order of inhibitory potency (apparent inhibition constants, Kiapp values, [mu]M, in parentheses) of the compounds examined was aminomethylenediphosphonate (1.8) > hydroxymethylenediphosphonate (5.7) [almost equal to] ethane-1-hydroxy-1,1-diphosphonate (6.5) > imidodiphosphate (12) > methylenediphosphonate (68) >> dichloromethylenediphosphonate (>500). The specificity of three of these compounds, aminomethylenediphosphonate, imidodiphosphate, and methylenediphosphonate, was determined by comparing their effects on the V-PPase and vacuolar H+-ATPase from Vigna, plasma membrane H+-ATPase from Beta vulgaris, H+-PPi synthase of chromatophores prepared from Rhodospirillum rubrum, soluble PPase from Saccharomyces cerevisiae, alkaline phosphatase from bovine intestinal mucosa, and nonspecific monophosphoesterase from Vigna at a PPi concentration equivalent to 10 times the Km of the V-PPase. Although all three PPi analogs inhibited the plant V-PPase and bacterial H+-PPi synthase with qualitatively similar kinetics, whether substrate hydrolysis or PPi-dependent H+-translocation was measured, neither the vacuolar H+-ATPase nor plasma membrane H+-ATPase nor any of the non-V-PPase-related PPi hydrolases were markedly inhibited under these conditions. It is concluded that 1, 1-diphosphonates, in general, and aminomethylenediphosphonate, in particular, are potent type-specific inhibitors of the V-PPase and its putative bacterial homolog, the H+-PPi synthase of Rhodospirillum.

Journal Article↗

Serum levels of type I and III procollagen fragments in Paget's disease of bone.

Patients with Paget's disease of bone were found to have elevated serum levels of type I procollagen carboxyterminal peptide (pColl-I-C) which correlated with other measurements of disease activity. The elevated levels of pColl-I-C decreased within hours after the injection of salmon calcitonin and within weeks after oral dichloromethylene diphosphonate treatment. The decrease in serum pColl-I-C after a single injection of salmon calcitonin was associated with a decrease in urinary hydroxyproline excretion, both of which rose toward pretreatment values within 7 h. The pColl-I-C levels remained normal for months after dichloromethylene diphosphonate therapy was discontinued. Using a RIA for the type III procollagen amino-terminal peptide (pColl-III-N), it was found that serum levels were also elevated in patients with Paget's disease. The levels of pColl-III-N also decreased after the injection of salmon calcitonin, but not to the same extent as those of pColl-I-C. After chronic therapy with dichloromethylene diphosphonate, serum levels of pColl-III-N decreased, but not into the normal range. We postulate that whereas pColl-I-C is derived from synthesis of mineralized bone collagen, pColl-III-N is derived from the loose fibrous stroma replacing marrow in areas closely associated with active Pagetic bone disease.

Antibody Specificity↗

Adverse reactions and drug interactions with radiopharmaceuticals.

Adverse reactions to radiopharmaceuticals are comparatively few in number. Various estimates quote an incident rate of 1 to 6 reactions per 100,000 injections. Other figures quoted are 1 in 800 for the bone-seeking radiopharmaceutical methylene diphosphonate, and 1 in 400 for the lung visualisation agent macroaggregated albumin. The very low numbers of reported adverse effects probably reflect the tiny amounts of material which are used in the formulation of radiopharmaceuticals. Adverse reactions to radiopharmaceuticals are usually mild and transient and require little or no medical treatment. A few reactions involve respiratory or circulatory collapse or loss of consciousness. Several fatalities have been reported with the liver scanning agent 99mTc (technetium 99m)-albumin colloid. Clinical manifestations may be categorised under the headings of vasomotor effects i.e. faintness, pallor, diaphoresis or hypotension, and anaphylactoid effects such as nausea, dermographism, wheezing, bronchospasm, erythema and pruritus. The most prominent group of radiopharmaceuticals that have been reported to produce adverse events are the diphosphonates, which are used for scanning the skeleton. Typical diphosphonate reactions include erythema (especially over the extremities), nausea, vomiting and malaise. The onset of reaction is usually 2 to 3 hours after injection. The second group of radiopharmaceuticals which give rise to adverse events are the colloids, which are used for liver and spleen scintigraphy. Typical colloid reactions include pallor, nausea, flush and pulse changes. Adverse events may also occur as a result of the patient's medication interfering with the disposition of the radiopharmaceutical. Although not usually hazardous or dangerous, such events may be so pronounced that a marked deviation in the expected pharmacokinetics may occur. Drug interactions can be conveniently categorised under the headings of unusual handling of the radiopharmaceutical because of pharmacological action, genuine in vivo interaction between the medication and radiopharmaceutical, drug-induced disease and interaction between the radiopharmaceutical and catheters or syringes. The most serious drug interactions are those where the patient is taking cortisone or cytotoxic agents prior to tumour scintigraphy. Other important effects occur in patients undergoing bone scanning who are receiving iron preparations. Nifedipine has been reported to produce quite severe problems in scanning, including difficulties in the radiolabelling of red cells (for cardiac scintigraphy), and other effects where the drug appears to prevent the transport of bone-seeking materials into the skeleton. Many drugs alter hormonal status and these effects may produce marked deviations from the expected biodistribution. Diethylstilbestrol (stilboestrol), digitalis, gonadotrophins, phenothiazines and cimetidine all increase estrogen levels in high doses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗