Biomedical subjects

N Tsakalakos

Publications and source records attributed to N Tsakalakos.

16 recordsLinked to original sources

PubMed2000

Body composition in dancers: the bioelectrical impedance method.

PURPOSE: The aim of this study was to generate and validate a prediction equation for estimating the body composition in dancers using the bioelectrical impedance analysis (BIA) as a method of assessment. METHODS: The fat-free mass (FFM) of 42 young female professional dance students was estimated by four different methods: dual x-ray absorptiometry (DXA), BIA, simple anthropometry, and skinfold thickness; DXA was used as a criterion method. RESULTS: The dancers' FFM was 42.6 kg (SD: 3.3) and, on the average, body fat represented the 19.4% (SD: 4.3) of their body weight. Two dancer-specific BIA equations for the prediction of FFM (E(BIA)) were developed by multiple regression analysis using weight, height, resistance index, and triceps as predictor variables (E(BIA) and E(BIA-TRICEPS)). The validity of these equations as well as of those previously reported was assessed in two randomly selected subgroups of the initial study group, as described by the Bland-Altman analysis. The bias and the limits of agreement of the equations developed in the present study were lower than those resulting from the application of the previously used equations of Segal et al. and Hergenroeder et al. It was also found that, when validated against DXA, skinfolds measurements did not accurately predict body fatness in this group of young females. CONCLUSION: The new equations allow for an accurate routine assessment of body composition in young female dancers by using the method of BIA. Further studies are needed for the cross-validation of the equations in various groups of dancers.

Absorptiometry, Photon↗

PubMed1997

The effect of a modified etidronate cyclical regimen on postmenopausal osteoporosis: a four-year study.

To develop an improved treatment schedule for osteoporosis, a study was undertaken in 100 postmenopausal women using a modified ADFR 90-day cyclical regimen with etidronate. After one year of treatment, the etidronate-treated group showed a significant increase in bone density of the spine, which continued over the following 2 years of treatment and remained stable during the fourth year. In contrast, in the non-etidronate group, bone density decreased significantly after four years. In addition, the fracture rate was significantly lower in the etidronate group than in the non-etidronate group. Side effects were minimal in both groups and no serious adverse reactions were reported. In conclusion, it appears that a cyclical regimen using 1,25-dihydroxyvitamin D3, etidronate and calcium increases bone mass and reduces fractures with no significant side effects, thus making a useful contribution in the treatment of postmenopausal osteoporosis.

Aged↗

PubMed1995

Prevention of bone loss in early nonsurgical and nonosteoporotic high turnover patients with salmon calcitonin: the role of biochemical bone markers in monitoring high turnover patients under calcitonin treatment.

Annual bone loss rate was estimated in a group of randomly selected 150 nonsurgical and nonosteoporotic early postmenopausal women, 42-56 years, with the use of the mathematical equation proposed by Christiansen et al. (OSTEOTREND-R) [1]. Fifty-six women were characterized as high turnover patients (estimated annual bone loss more than 2.7%). These high turnover patients were included in a double-blind, placebo-controlled clinical study. Patients were divided into two groups of 28 women each. The first group of patients received 100 IU of salmon calcitonin intranasally daily for 1 year and the second group intranasal spray of placebo daily. Blood and urine biochemical parameters as well as bone mineral content of the spine and proximal forearm were determined initially and at the end of 6 and 12 months. No other side effects were noted apart from discomfort of nasal mucosa in two patients (one in each group). The group of calcitonin-treated patients showed a dramatic decrease in bone loss rate as estimated with the use of biochemical bone markers at the end of 6 and 12 months (3.7% versus 0.8% and 0.0% at the end of 6 and 12 months, respectively, P < 0.001) whereas in the placebo group, bone loss rate remained unchanged (4.2% versus 4.1% and 4.3% at the end of 6 and 12 months, respectively). The calcitonin-treated patients showed a significant increase in bone mineral content of spine and proximal forearm (P < 0.001 at the end of 6 and 12 months, respectively). On the other hand, a significant decrease in all measurement sites appeared in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Effect of nandrolone decanoate and 1-alpha-hydroxy-calciferol on patients with vertebral osteoporotic collapse. A double-blind clinical trial.

Eighty-eight postmenopausal women with at least one vertebral collapse were randomly assigned to two groups of 44 patients each. All patients were treated for a period of 12 months with 50 mg of nandrolone decanoate every 3 weeks or 1 microgram of 1-alpha-hydroxy-calciferol daily. Both groups received an identical placebo of the inactive drug. Pain intensity was significantly decreased in the nandrolone group and mobility was improved. Patients treated with vitamin D metabolite had also a beneficial but less obvious clinical result. Bone mineral measurements showed an increase of 5% in the nandrolone decanoate group, but a 2.5% decrease in the vitamin D metabolite group. Biochemical results showed a significant hypercalciuric effect of vitamin D metabolite, while nandrolone decanoate caused a reduction in calcium/creatinine excretion. No difference in serum lipids was found during the annual treatment in both groups. It is concluded that nandrolone decanoate has a beneficial effect in clinical symptoms, bone mineral density and biochemical parameters in patients with established osteoporotic vertebral fractures.

Aged↗

PubMed1993

The effect of short-term calcitonin administration on biochemical bone markers in patients with acute immobilization following hip fracture.

The effect of salmon calcitonin on changes in mineral metabolism was studied in 40 elderly patients with recent hip fracture. All patients underwent surgery (internal fixation) 1 week after admission and were randomly divided into two equal groups: group A, which received no treatment, and group B, which received 100 IU/day salmon calcitonin intramuscularly for 2 weeks starting on admission. Blood and 24-h urine parameters of mineral metabolism were measured on admission and at the end of weeks 1 and 2. No intra- or intergroup changes in serum calcium, phosphorus or alkaline phosphatase were observed. At the end of week 2 biochemical markers of bone resorption (urinary calcium and hydroxyproline) had significantly increased in group A and significantly decreased in group B, indicating a reduction in bone resorption in group B. Urinary phosphorus had also increased in group B, possibly due to the phosphaturic effect of calcitonin. It is concluded that immobilization resulting from a hip fracture, and possibly surgery itself, causes significant changes in biochemical markers of bone resorption. Calcitonin successfully reverses these changes and may also be effective in preventing subsequent bone loss, particularly in patients who cannot be remobilized immediately.

Aged↗

PubMed1991

Analgesic effect of salmon calcitonin in osteoporotic vertebral fractures: a double-blind placebo-controlled clinical study.

Back pain due to vertebral collapse is the main symptom of postmenopausal osteoporosis. The clinical picture in these crush fractures varies, depending on the type and the location of fracture, but in general, a new vertebral crush fracture gives rise to severe pain that immobilizes the patient and necessitates bedrest. In this double-blind controlled clinical trial, 56 patients who had recently (within the last 3 days) suffered an osteoporotic vertebral fracture were hospitalized for a period of 14 days. Salmon calcitonin (100 IU) or placebo injections were given daily. Pain was rated daily on a 10-point scale by the same observers. Blood and urinary parameters were also evaluated. The results showed a significant (P less than 0.001) difference in pain intensity between the calcitonin group and the placebo group. This beneficial effect was generally apparent from the second day of treatment onward, and over the following 2 weeks, the patients were able to sit and stand, and gradually started to walk again. A significant decrease in urinary hydroxyproline and urinary calcium was also noted in the calcitonin group. It is concluded that calcitonin exerts a beneficial effect on back pain following a vertebral crush fracture.

Aged↗

PubMed1989

The natural history of the osteoporotic vertebral fracture.

The clinical picture of the osteoporotic fractures of the spine presents an heterogeneity in their intensity and duration. In 210 cases of osteoporotics with acute pain and radiological evidence of spinal fracture we separate their clinical picture in two groups. In Type I (121 cases) pain is acute and severe, improving gradually; the vertebral wedging is obvious from the beginning and remain unchanged. The duration of this event exceeds 4-8 weeks. In Type II (89 cases) pain is less and of shorter duration, but after 6-16 weeks a new attack of acute pain presents. This picture can be repeated for 6-18 months. Radiologically the fracture is not clear during the first attack but wedging gradually developed during the next months. Bone density of the lumbar spine (DPA) was measured in all cases. Type I had a significantly lower BMC than Type II. We suggest that patients with unclear vertebral fractures, minor symptoms and relatively high bone mass must classified in Group II and deterioration can occur during the next months. Long term treatment and additional orthopaedic prevention is needed. In Group I a short term calcitonin treatment helps early relief and mobilization.

Aged↗

PubMed1988

The extended Pedersen hypothesis.

The Pedersen hypothesis of fetal macrosomia in neonates born to diabetic mothers has been extended. In neonates born to gestational diabetic mothers, it is suggested that an intrinsic fetal pancreatic beta-cell hyperplasia 'pulls' glucose across the placenta, i.e. assists in glycemic control of the mother. The initial increase in fetal size due to fetal hyperinsulinism gives rise to developing hypoxemia, and the limitation in fetal oxygen availability alters differential tissue utilization of glucose, increases alpha-glycerophosphate synthesis in fetal adipocytes, and gives rise to a further increase in fetal adiposity.

Female↗

PubMed1987

Value of acetylated haemoglobin assay in fetal assessment.

Acetylation of fetal haemoglobin, probably a post-translational, intracellular, enzyme-mediated reaction, depends upon an adequate supply of glucose and oxygen to the fetus and the nature of the diabetes (if present) in the mother. These complicating factors limit the general usefulness of acetylated fetal haemoglobin assay in fetal assessment.

Acetylation↗

PubMed1986

A previously undescribed ectodermal dysplasia of the tricho-odonto-onychial subgroup in a family.

We encountered two family members with a previously undescribed pure ectodermal dysplasia. The propositus exhibited hypotrichosis, hypodontia, focal linear dermal hypoplasia on the tip of her nose, irregular hyperpigmentation on her back, bilateral amastia and athelia, and mild nerve hearing loss. Her mother displayed similar characteristics, except for present, although hypoplastic, areolae and nipples. Both mother and daughter appeared to be clinically euhidrotic. Despite a comprehensive endocrine workup, the only abnormality detected was a suboptimal cortisol response to hypoglycemia in the propositus. Five other family members seemed to be affected. The pattern of inheritance appeared to be autosomal-dominant, with variable penetrance and expressivity.

Abnormalities, Multiple↗

PubMed1985

Acetylated fetal haemoglobin in neonates born to mothers with established and gestational diabetes.

Birth weight ratios (BWRs) and cord blood C-peptide values were significantly higher in neonates born to mothers with well-controlled gestational diabetes (GD) than in those born to mothers with well-controlled established diabetes (ED) or mothers with normal results on glucose tolerance testing. The neonates born to the ED mothers had the highest cord blood acetylated fetal haemoglobin (Hb F1) values, and these values correlated with cord C-peptide values. The cord C-peptide values in the GD group correlated with BWRs, but not with Hb F1 values. These results suggest differential tissue utilization of glucose in neonates born to mothers with different types of diabetes.

Birth Weight↗

PubMed1985

Value of glycosylated haemoglobin determination in diabetic pregnancy.

A single measurement of total maternal glycosylated haemoglobin (Hb A1) in the late third trimester of a diabetic pregnancy is of limited value in assessing diabetic control. There was no significant correlation between maternal Hb A1 values and neonatal C-peptide values or birth-weight ratios. An isolated Hb A1 measurement is not sufficiently sensitive to monitor the control of diabetes during pregnancy nor is it useful in predicting perinatal outcome.

Adult↗

PubMed1985

Evidence of hypoxaemia and distribution of minor haemoglobin components in the cord blood of neonates born to diabetic mothers.

The oxygenation status of normal and diabetic (White's classification A and B) mothers and their neonates was investigated. The diabetic patients had significantly increased maternal total haemoglobin and P50 values and the percentage of fetal haemoglobin was increased in cord blood taken at delivery in this group. There was a significant positive correlation between maternal P50 values and the percentage of fetal haemoglobin in cord blood. The cord blood 2,3-diphosphoglycerate, inorganic phosphate and P50 values were also increased in neonates born to diabetic mothers and these infants had a significantly increased birth weight ratio. The results are consistent with the presence of fetal hypoxaemia in the late third trimester of diabetic pregnancy in which obvious maternal vascular disease has been excluded.

Female↗

PubMed1985

Evidence of hyperinsulinaemia and hypoxaemia in the cord blood of neonates born to mothers with gestational diabetes.

Increased cord blood C-peptide levels in neonates born to mothers with gestational diabetes (GD) were directly correlated with the increased relative birth weight ratio (BWR) of these neonates. In addition, the percentage oxygen saturation of the cord blood was inversely correlated with cord blood C-peptide levels and with the relative BWR. These correlations were absent in neonates delivered to normal mothers. The results indicate the presence of both hyperinsulinaemia and mild hypoxaemia in neonates of mothers with GD. In poorly controlled diabetic pregnancy this hypoxaemia may constitute an important fetal risk factor.

Birth Weight↗

PubMed1984

Neonatal pancreatic function in infants born to mothers with gestational and overt diabetes.

Neonatal pancreatic function was assessed in infants born to non-diabetic mothers and to mothers with well-controlled gestational diabetes (GD) and overt diabetes (OD) using cord blood C-peptide estimations and the calculation of cord C-peptide/glucose ratios. Exaggerated pancreatic function was present in infants born to mothers with GD. In these infants the increased cord C-peptide values and cord C-peptide/glucose ratios correlated with their increased birth weight ratios. These results could not be explained on the basis of maternal hyperglycaemia and a possible intrinsic difference in pancreatic response between infants born to mothers with GD and those born to mothers with OD is suggested.

Blood Glucose↗

PubMed1983

Relative fetal hypoxia as a contributing factor to fetal macrosomia in diabetic pregnancy.

Results from Ogata et al (5) have shown that the initial increase in fetal size in the macrosomic neonates of diabetic mothers occurs after approximately 26 weeks gestation, and that a further more dramatic increase occurs at approximately 34 weeks until term. It is proposed that the initial increase is caused by fetal hyperinsulinism (Pedersen Hypothesis), and that the latter increase results from an induced relative fetal hypoxia. It is suggested that the mechanism responsible for the latter increase in fetal size is an increase in the amount of fetal glucose which is metabolised through the hexose monophosphate shunt pathway.

Adolescent↗