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Biomedical subjects

S Adami

Publications and source records attributed to S Adami.

At least 109 records · Page 6Linked to original sources
PubMed1993

[Microbiological validation of a film system for monitoring total aerobic bacteria on surfaces and laboratory garments in controlled areas].

The microbiological control of the environment is a real issue inside the pharmaceutical production plants. Actually the most used methods are the Contact Plates and the Swabs. The purpose of this study is to evaluate the performance of a new "ready to use" method called Petrifilm SM (produced by 3M Laboratories). Petrifilm consists of a dry-rehydratable growth medium coated on a flexible film. Petrifilm is tested in comparison with Swabs and Contact Plates to monitor the microbiological pollution on labs surfaces and operator's overalls. The results obtained are comparable with the above mentioned methods, but with important advantages being less bulky, considerably time saving and highly reproducible. Hence, we think that Petrifilm S, can be successfully used instead of the other two more traditional methods.

Bacteria, Anaerobic↗
PubMed1992

The effects of menopause and estrogen replacement therapy on the renal handling of calcium.

Mineral metabolism was studied in 99 premenopausal and 80 postmenopausal women both before and after 9-14 months of treatment with 50 micrograms/day transdermal estradiol. In estrogen-repleted subjects (premenopausal women and postmenopausal women on estrogen replacement therapy) total serum calcium was significantly lower (0.065 mmol/l; p less than 0.001) than in those who were estrogen-depleted (untreated postmenopausal women). This difference was smaller but still significant for calculated ultrafiltrable calcium (UFCa: 0.02-0.03 mmol/l; p less than 0.001). However, ionized calcium (both calculated and measured) was not different in the two groups of women. This finding explains why estrogen repletion does not induce changes in the serum level of intact parathyroid hormone (PTH), despite lower total or ultrafiltrable serum calcium. In a parallel study we have shown that intravenous administration of aminobutane bisphosphonate, a powerful inhibitor of bone resorption, produces similar decreases in serum calcium which were associated with significant increases in intact PTH. Estrogen-depleted women had, on the one hand, significantly higher serum levels of bicarbonate, anion gap, complexed calcium, pH, phosphate and alkaline phosphatase, and higher rates of tubular reabsorption of phosphate and urinary excretion of calcium and hydroxyproline. On the other hand they had lower serum chloride levels and lower rates of tubular reabsorption of calcium. Altogether these findings might indicate that estrogen deficiency decreases renal sensitivity to PTH. This is responsible for the higher serum phosphate and bicarbonate levels, the resulting mild metabolic alkalosis leading to higher serum levels of complexed ultrafiltrable calcium and higher rates of urinary excretion of calcium, but unchanged serum levels of ionized calcium and PTH.

Adult↗
PubMed1992

Effects of ipriflavone on bone mass and calcium metabolism in postmenopausal osteoporosis.

Recently it has been demonstrated that ipriflavone (IP), an isoflavone derivative, is able to increase bone mass in patients with established postmenopausal osteoporosis (PMO). Here we present a preliminary report of a 2-year multicenter, double-blind, placebo-controlled clinical study performed in order to evaluate the efficacy and tolerability of IP in PMO. A large number of patients with PMO, referred to 12 Italian centers, was randomly divided into 2 groups and treated with oral IP (600 mg/day) or placebo (Pl). All patients received an oral Ca supplement (1 g/day). One hundred and twenty six patients completed 1 year of the study. Bone mineral density (BMD) of the distal radius, measured by DPA, serum osteocalcin (BGP), and urinary hydroxyproline excretion (HOP/Cr), were measured before and after 12 months. After 12 months, a significant increase in BMD was observed in the IP-treated group (P < 0.05). IP determined a reduction of HOP/Cr, while in Pl-treated patients a significant increase of this index, as well as of BGP, was observed. After 12 months the difference between the two groups resulted significant (P < 0.05) for BGP. The drug was well tolerated and the patients' compliance to the oral treatment resulted excellent. The results of this study indicate that IP is able to increase bone mass in patients with PMO.

Aged↗
PubMed1992

The radiological assessment of vertebral osteoporosis.

The traditional skeletal X-ray is of little help in quantifying osteopenia in the spine, and indirect criteria, such as increased lucency, loss of horizontal trabeculae and reduction in end-plate thickness with relatively increased opaqueness, can be misleading. However, the clinical expression of osteoporosis is fracture, which can be identified by radiography. Any reduction in the anterior, middle, or total height of the vertebral body should be classified as vertebral fracture. In mild cases, such fractures are not easily detectable, particularly when previous radiographs are not available for comparison. Thus several objective methods for fracture identification have been developed. Most of these methods are based on the ratio between posterior and anterior or middle height (wedge or biconcave deformity, respectively) and on the ratio between posterior height of adjacent vertebrae or with a single vertebral reference (T4). Some of these indices are referred to normal ranges in order to take into account intervertebral and interindividual variability. In 36 women with postmenopausal osteoporosis we have compared the lateral radiographs of lumbar and thoracic spine to similar X-ray pictures taken by chance at least five years before menopause. By defining a fracture as any decrease in vertical height above 1 mm, we found 77 deforming events in 29 out of 36 patients. We then applied some of the methods to identify objectively fractures in our postmenopausal radiographs: the sensitivity of the various systems ranged from 50 to 100%; however there was a large overlap between false positives and false negatives and the methods with the highest sensitivity lack specificity and vice versa.

Body Height↗
PubMed1992

Hypercalcemia of malignancy: pathophysiology and treatment.

Hypercalcemia is a relatively common terminal complication of malignancy. In the majority of the patients it is due to excessive bone resorption, secondary either to local destruction by metastases or by the activity of several paracrine and/or endocrine factors. Increased renal tubular reabsorption of calcium plays a role in the aetiology and maintenance of hypercalcemia. It is due both to factors which stimulate the renal transport of calcium and to volume depletion that is frequently present in hypercalcemic patients. This explains why the administration of large amounts of fluids intravenously is often a necessary first step in the management of malignant hypercalcemia, followed by specific inhibitors of bone resorption such as the bisphosphonates.

Bone Resorption↗
PubMed1992

Effect of deflazacort on growth hormone response to insulin tolerance test.

Deflazacort (DF) has been claimed to be provided with a reduced distribution into the central nervous system, therefore it is conceivable that this glucocorticoid holds a lower inhibitory effect on GH secretion. To test this hypothesis we studied the GH response to insulin tolerance test (ITT) in two matched groups of patients given equivalent doses of DF and prednisone (PN). The serum glucose changes induced by ITT were similar in the two groups and in control subjects; the mean increase in plasma GH, in particular the peak and the area under the curve (delta AUC), were not different in control subjects and DF-treated patients (25 +/- 12.5 ng/ml and 1790 +/- 904 ng/ml/min versus 27.7 +/- 21.5 ng/ml and 1578 +/- 1242 ng/ml/min) but were significantly reduced in PN-treated patients (8.8 +/- 9.7 ng/ml and 431.6 +/- 451 ng/ml/min). Our study demonstrates that DF does not interfere with the GH response to ITT as PN does.

Adult↗
PubMed1991

The prevention of corticosteroid-induced osteoporosis with nandrolone decanoate.

The effects of nandrolone decanoate (ND; 50 mg IM every three weeks) on calcium metabolism and forearm bone density were studied in a randomized trial in 35 women receiving long-term therapy with corticosteroids (CST) for rheumatic disease. The 17 patients who served as controls were on CST therapy for less years and their bone density was higher. Thus a second control group, pair-matched with the active treatment group for age, duration of CST therapy and bone density, was selected retrospectively. At the end of the 18 months' treatment course with ND, forearm bone density was increased by 5.1% (P less than 0.01) but fell by 11.3% (P less than 0.01) and 6.7% respectively in the first and second control group. The patients on ND differed significantly from both control groups in the changes at 6, 12 and 18 months (P less than 0.01). Urinary excretion of hydroxyproline fell significantly in patients receiving ND, whereas the biochemical indices of bone formation did not change (alkaline phosphatase) or increased (osteocalcin; P less than 0.01). In conclusion, nandrolone decanoate therapy may be used in the prevention of CST-induced osteoporosis. It also seems to exert mild inhibition of bone resorption without affecting or even stimulating bone formation.

Absorptiometry, Photon↗
PubMed1991

Effects of vitamin D metabolites and bisphosphonates on fibronectin release from monocyte-derived macrophages.

Fibronectin release from cultured macrophages, derived from human blood monocytes, was measured during incubation of the cells with increasing concentrations of vitamin D3 metabolites or of aminobutane bisphosphonate (AHButBP) or dichloromethylene bisphosphonate (Cl2MBP), two powerful inhibitors of bone resorption. The bisphosphonates significantly inhibited fibronectin release at 10(-8) M concentration and this inhibition was almost complete at 10(-5) M concentration. Opposite results were observed when the cells were incubated with vitamin D3 metabolites: the stimulation of fibronectin release was specific for 1,25-dihydroxyvitamin D3 relative to other vitamin D3 metabolites (1,25-dihydroxyvitamin D3 greater than 25-hydroxyvitamin D3 greater than 24,25-dihydroxyvitamin D3).

24,25-Dihydroxyvitamin D 3↗
PubMed1990

Bone loss in response to long-term glucocorticoid therapy.

A number of studies have shown that an excess of glucocorticoids induces osteoporosis, but the mechanism(s) and the time course of the reduction of bone mass remain uncertain. In order to clarify this issue we carried out a longitudinal clinical and histomorphometric study of patients requiring long-term glucocorticoid treatment. In 23 patients (9 men, 10 post- and 4 premenopausal women) biochemical and bone histomorphometric investigations were carried out before and during treatment with 10-25 mg/day of prednisone. Histomorphometric analysis of bone biopsies of the iliac crest showed that the decrease of TBV (up to -27%, P less than 0.001) occurs predominantly within the first 5-7 months of treatment; during the subsequent stages, which include observations after 12 months of treatment, only minor changes were observed. Therefore trabecular bone loss can be satisfactorily described by a negative exponential function. None of the other histomorphometric parameters (osteoid surfaces, resorption surfaces, etc.) showed significant changes. However, the histological features of the bone biopsies during steroid therapy, showing a virtual lack of osteoblastic activity, ruled out an increase of bone resorption. Moreover, the dynamic study of the bone formation by double tetracycline labelling showed, in a small subgroup of patients, a decrease of the apposition rates (from 0.763 +/- 0.053 to 0.305 +/- 0.074 microns/day (mean +/- SE) after treatment). No significant changes, at any time during steroid treatment, were observed in serum alkaline phosphatase, 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone or urinary calcium excretion. Serum calcium increased significantly within the first 1-2 months of therapy and then it returned to baseline. Urinary hydroxyproline excretion decreased significantly within the first 1-2 months and continued to fall throughout the treatment. Thus, both biochemical and histological findings suggest that long-term glucocorticoid therapy causes a reduction of bone turnover, that the bone loss occurs predominantly within the first 6 months of treatment and that patients with lower bone mass have a lower rate of bone loss.

Adult↗
PubMed1990

Response of renal transplanted patients to oral calcium load.

In a previous study we demonstrated that cyclosporin-treated renal transplanted patients have a reduced 1,25(OH)2D3 synthesis in comparison with azathioprine-treated transplanted patients. To assess the impact of this defect on intestinal calcium transport we compared the plasma calcium variation and the urinary calcium excretion in 14 cyclosporin-treated and in 12 azathioprine-treated patients, in fasting conditions and 4 hours after an oral calcium load (1 g). In ten cyclosporin patients we also correlated cyclosporin plasma values with plasma 1,25(OH)2D3 values before and after a 25(OH)D3 oral load. After the oral calcium load, plasma and urinary calcium increased significantly in the azathioprine group, while remaining unchanged in the cyclosporin group. A negative correlation between plasma concentrations of cyclosporin and the increment in 1,25(OH)2D3 after 25(OH)D3 oral load was also observed. Thus, our data suggest that cyclosporin impairs 1-alpha hydroxylase activity and alters the response to an oral calcium load.

Adult↗
PubMed1990

Regulation of calcium-parathyroid hormone feedback in primary hyperparathyroidism: effects of bisphosphonate treatment.

Dichloromethylene bisphosphonate (C12MBP), a powerful inhibitor of bone resorption, was administered to 27 patients with primary hyperparathyroidism. It was given by either intravenous infusion (six patients, 500-100 mg day), or by intramuscular injection (six patients, 100-200 mg/day) or by mouth (15 patients, 1600-2400 mg/day) for 20-180 days. Sustained suppression of bone resorption was observed in all patients, as judged by a fall in the urinary hydroxyproline excretion. In contrast, the hypocalcaemic effect was inconsistent and short-lived, particularly in the patients without overt bone disease. The fall in serum calcium seemed largely to be due to a transient dissociation between bone resorption and bone formation and was associated with increases in circulating parathyroid hormone (PTH). In ten patients given the bisphosphonate orally for 6 months, serum calcium was unchanged but serum PTH was significantly raised. These results suggest that C12MBP may be of use for short-term correction of severe hypercalcaemia due to hyperparathyroidism, particularly in the patients with overt bone disease. However, its long-term use should not be recommended because of increased PTH secretion.

Adult↗
PubMed1989

Clodronate therapy of metastatic bone disease in patients with prostatic carcinoma.

Metastatic bone disease represents the most disabling complication in patients with prostatic carcinoma. In an open multicenter trial 80 out of 92 patients with bone metastasis due to prostatic carcinoma experienced a dramatic improvement of bone pain after treatment with 300 mg clodronate infused intravenously daily for 10 days. Further to this, 56 patients were randomly allocated to four single-blind controlled therapeutic trials, assessing bone pain by daily consumption of analgesic drugs and by visual analogue scale. In the first protocol the effects of 2 weeks' treatment with intravenous infusion of either 300 mg clodronate dissolved in 500 ml saline (7 patients) or 500 ml saline (6 patients) were compared. The differences in both pain score and analgesic consumption were so striking that the trial was not extended for ethical reasons and all patients on placebo were given clodronate intravenously. Oral administration of 1200 mg clodronate for 2 weeks was completely ineffective in 11 patients. Intramuscular administration of 100 mg clodronate for 2 weeks induced in 12 patients a significant fall in analgesic consumption but not in the pain score. In most of the 13 patients given clodronate intravenously for 2 weeks bone pain relapsed fairly soon. However, in 18 patients a maintenance therapy with 1200 mg clodronate/day for at least 6 weeks after a 2-week intravenous treatment course did prevent the relapse of bone pain. In all patients given clodronate routine biochemical examination was carried out during and after treatment. For an overall follow-up of 42 patient-years hematologic toxicity was never observed. These results confirm that clodronate represents the most effective and convenient conservative treatment of patients with painful bone metastasis from prostatic carcinoma.

Administration, Oral↗
PubMed1989

Transdermal estradiol in the treatment of postmenopausal bone loss.

The effects on calcium metabolism and forearm bone mineral density of sequential transdermal estradiol (ESTRADERM TTS-50), 50 micrograms/day and medroxyprogesterone (10 mg/day for 12 days) was studied in a randomised controlled trial in 34 healthy females 2-4 years after the menopause. At the end of the 18 months' treatment course with transdermal estradiol, bone density was increased by 4.31% (P less than 0.01) but was decreased by 3.5% (P less than 0.01) in the control group. In the treated group, serum calcium, calcium excretion and hydroxyproline excretion significantly fell during the first 2 months with no significant changes thereafter. Serum alkaline phosphatase significantly decreased only after 4 months, it continued to fall until the fourteenth month when a plateau became apparent. Serum phosphate and tubular maximum for urinary phosphate progressively fell until the tenth month of therapy but thereafter they rose up to initial values. Serum intact parathyroid hormone did not show any significant change. In conclusion, small doses of transdermal estradiol are as effective as oral estrogens. This suggests that the bone sparing effects of estrogens may be due only to low circulating estradiol concentrations, but not to supraphysiological estrone levels. It seems also that estrogens exert both a straight inhibition of bone resorption and a partial inhibition of parathyroid responsiveness.

Administration, Cutaneous↗
PubMed1988

Intramuscular administration of salmon calcitonin impairs delayed cutaneous hypersensitivity.

The delayed cutaneous hypersensitivity to seven ubiquitous antigens (Multitest CMI, Istitute Mĕrieux) was evaluated in normal healthy volunteers before and at the time of intramuscular administration of 50 (12 subjects) or 50 + 50 (nine subjects) units of salmon calcitonin or 2 ml of saline (eight subjects). The delayed cutaneous hypersensitivity, in terms of number of positive tests or sum of positive tests, significantly fell in both groups given salmon calcitonin, but no changes were observed in the control group. These results indicate that salmon calcitonin, as well as inhibiting osteoclastic bone resorption, has important immunological effects.

Adult↗
PubMed1987

The acute-phase response after bisphosphonate administration.

In patients who have never previously received bisphosphonate therapy, the intravenous administration of 4-amino-1-hydroxybuthilidene-1,1-bisphosphonate (AHButBP), 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (AHPrBP), or 6-amino-1-hydroxyhexylidene-1,1-bisphosphonate (AHHexBP) induced an acute-phase response (APR) irrespective of the underlying disease, manifested by a fall in circulating lymphocyte number and serum zinc concentration and in a rise in C-reactive protein (CRP); a febrile reaction occurred in 30% of the patients. The APR was maximally expressed within 28-36 hours of i.v. administration of the bisphosphonates and disappeared 2-3 days later despite continuous treatment. These effects were dose dependent and the lowest doses necessary for an APR were 10 mg of AHButBP and AHPrBP and 75 mg of AHHexBP. Doses up to 1,000 mg/day i.v. of dichloromethanebisphosphonate (Cl2MBP) were devoid of these side effects. In patients treated with either a single i.v. dose of amino-bisphosphonates which resulted in an APR or with a suboptimal dose, a subsequent challenge 12-160 days later of the high dose failed to cause a rise in CRP or a fall in the lymphocyte count. The desensitization to AHButBP or AHPrBP was also seen following pretreatment with Cl2MBP. These findings suggest that bisphosphonates interact with macrophage-like cells resident in the skeleton and stimulate interleukin-1 release which is responsible for the appearance of the APR. At the same time, however, the bisphosphonates render these cells insensitive to further stimulation for several months.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗
PubMed1987

Extrarenal synthesis of 1,25-dihydroxyvitamin D: sensitivity to glucocorticoid treatment.

The response of circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D] to challenge with vitamin D treatment both before and after 7-10 days of prednisone therapy (25 mg/day) was investigated in five anephric subjects, six patients with chronic renal failure (CRF), two patients with vitamin D intoxication and four patients with hypoparathyroidism. In anephric subjects serum 25-hydroxyvitamin D [25-(OH)D] rose from 58 +/- 48 (SD) to 377 +/- 221 (SD) nmol/l after administration of 150 micrograms of 25-(OH)D3 for 1 month. Serum 1,25-(OH)2D, which was barely detectable in only two out of five patients under basal conditions, rose to 30 +/- 21 pmol/l after 2 weeks of therapy with 25-(OH)D3, but fell to 10 +/- 5 pmol/l during prednisone treatment. In CRF patients circulating 1,25-(OH)2D rose from 37 +/- 24 to 58 +/- 24 pmol/l during 25-(OH)D3 therapy, but fell to 41 +/- 31 pmol/l during prednisone treatment. In two patients with rheumatoid arthritis, hypercalcaemia due to vitamin D intoxication was associated with raised levels of 1,25-(OH)2D (288 and 317 pmol/l). Administration of prednisone resulted in suppression of 1,25-(OH)2D levels (132 and 96 pmol/l respectively) and reduction of serum calcium to within the normal range. In the hypoparathyroid patients prednisone therapy did not affect circulating 25-(OH)D levels but serum 1,25-(OH)2D fell from 192 +/- 42 to 117 +/- 23 pmol/l and serum calcium from 2.41 +/- 0.21 to 2.20 +/- 0.05 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcifediol↗
PubMed1987

The use of dichloromethylene bisphosphonate and aminobutane bisphosphonate in hypercalcemia of malignancy.

54 patients with malignant hypercalcemia were treated with either dichloromethylene bisphosphonate (Cl2MBP) or aminobutane bisphosphonate (AHButBP). Both compounds infused intravenously (i.v.) were rapidly effective in lowering serum calcium to normal range and a potency ratio between Cl2MBP and AHButBP could be roughly estimated as 1:100-250. 600 mg of Cl2MBP infused in one day over 9 h in nine patients were only slightly less effective (serum calcium from 12.3 +/- 1.7 to 10.1 +/- 1.1 SE, mg/dl) than 3300 mg infused in 11 consecutive days (13.4 +/- 1.9 to 9.3 +/- 1.2 SE, mg/dl). Thus the effectiveness of treatment with Cl2MBP was related better to the overall time of infusion than to the cumulative dose administered. This could not be demonstrated in a similar trial using AHButBP. 1600 mg Cl2MBP daily p.o. was unable to prevent the relapse of hypercalcemia in four patients after a treatment course with i.v. bisphosphonates. 100 mg of Cl2MBP intramuscularly maintained serum calcium within the normal range in two out of eight patients; however, weekly infusions of either Cl2MBP or AHButBP prevented the relapse of hypercalcemia in eight similarly treated patients for several weeks. Providing that adequate dosages are adopted, parenteral Cl2MBP and AHButBP may be a useful measure for controlling hypercalcemia in patients with carcinoma.

Administration, Oral↗