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Biomedical subjects

P Lapatsanis

Publications and source records attributed to P Lapatsanis.

At least 19 recordsLinked to original sources

Treatment of complicated pulmonary echinococcosis with albendazole in childhood.

The case of an 11-year-old boy suffering from pulmonary hydatid disease with rupture and bacterial superinfection is presented. After 3 courses of chemotherapy with albendazole the boy recovered fully, uneventfully and without relapse. Conservative management should always be considered before surgical intervention in children with echinococcosis, even when complications have occurred.

Albendazole↗

Bone minerals in beta-thalassemia minor.

Homozygous beta-thalassemia is a severe hereditary disorder associated with osteopenia. Recently it was suggested that thalassemia minor may be a risk factor for osteoporosis. The purpose of the present study was to investigate this suggestion. Bone mineral status was assessed in 22 premenopausal women and 21 men with beta-thalassemia minor. In vivo neutron activation analysis was applied to measure hand-bone phosphorus (HBP), single-photon absorptiometry to measure forearm bone mineral content (BMC), and dual-energy X-ray absorptiometry to measure spinal bone mineral density (BMD). Comparison of the HBP, BMC, and BMD values with those of sex- and age-matched healthy subjects without the beta-thalassemia trait failed to indicate a statistically significant difference for either sex group. Concerning the biochemical markers of bone metabolism that were studied (serum calcium, phosphate, alkaline phosphatase, osteocalcin, and parathyroid hormone, and 3-h fasting urine calcium-to-urine creatinine ratio) no difference was observed between the study subjects and matched controls. In conclusion, the present study showed that subjects with beta-thalassemia minor are not at risk for osteoporosis.

Absorptiometry, Photon↗

Flow rate and chemistry of parotid saliva related to dental caries and gingivitis in patients with thalassaemia major.

Twenty-one child patients with thalassaemic major (TM) and 83 healthy control children were examined for dental caries and gingivitis. Stimulated parotid gland secretions were collected from each child. Parotid saliva flow rate was measured and the saliva samples were tested for calcium, phosphorus, potassium, sodium, urea, lysozyme and immunoglobulin levels (IgA, IgG, IgM). The results showed that dental caries experience was significantly higher in the TM group. Parotid saliva flow rates in TM patients were not significantly different from those in the healthy controls. However, the median saliva concentrations of phosphorus and IgA were significantly lower in the patients than in the controls. The concentration of lysozyme was also lower in the TM group, but the difference was not statistically significant. The findings could provide an explanation for the higher dental caries experience and gingivitis observed in the TM group.

Adolescent↗

Red cell phosphate metabolism in full-term neonates.

The effects of hypoxia and feeding on red cell inorganic phosphate (Pi) concentrations were studied in neonates. Although hypoxia caused a rise in extracellular Pi, the intracellular concentration of this ion did not change in comparison to control infants of the same age (first 24 h). As a result of these changes, the distribution of phosphate ions across the erythrocyte membrane was significantly lower in the hypoxic infants than in the controls. In the hypoxic infants, adenosine triphosphate (ATP) levels in the red cells were found significantly lower than in controls, while the 2,3-diphosphoglycerate (2,3-DPG) levels were raised. In breast-fed 2 or 3-day-old neonates, both plasma and red cell Pi were found to be increased but to different degrees, affecting therefore the molar Pi distribution, which was lower than in the controls of the first day. In these infants, ATP was lower and 2,3-DPG higher than in the controls of the first day of life. These findings suggest that intracellular phosphate metabolism in neonates does not follow extracellular phosphate changes. Further investigation is needed to elucidate the controlling factors.

2,3-Diphosphoglycerate↗

Calcium and phosphorus disturbances in children.

Calcium and phosphorus disturbances in childhood are discussed in vitamin D deficiency rickets, neonatal tetany and beta-homozygous thalassaemia. The nutritional, epidemiological, hereditary and other factors facilitating the development of the disease in these three groups of children are illustrated. The level of culture and sociability of the community must be taken into consideration for the success of the preventive medicine services, especially with regard to vitamin D deficiency rickets. The administration of phosphorus and vitamin D or metabolites of vitamin D to thalassaemic children would probably produce beneficial effects on bone and muscle changes.

Adolescent↗

Bone growth in thalassaemic children.

X-ray measurements were made of the length and width of the 3 middle metacarpal bones of both hands, in 61 thalassaemic and 35 control children of both sexes aged 5--13 years. Growth in length of the bone was normal until age 11 years but after this it was smaller in thalassaemic children. The growth of total width in thalassaemic children was greater than that of the controls until age 11 years and then became equal. The proportion of children with bone age retardation was greater after 7 years.

Adolescent↗

Serum 25-hydroxyvitamin D levels in thalassaemia.

Serum 25-hydroxyvitamin D levels were measured in 36 thalassaemic children and 27 controls aged 5-15 years. Blood specimens were collected from the beginning of April until the end of October 1976. We considered as the winter period the first 3 months and the summer period the last 4 months. We found that (a) thalassaemic children had lower levels of serum 25-hydroxyvitamin D than controls: (b) there was a seasonal variation of serum 25-hydroxyvitamin D in both groups; and (c) the thalassaemic children had malabsorption of vitamin D. We suggest that the bone lesions in thalassaemic children are related to vitamin D deficiency.

Adolescent↗

Bone density in thalassemic children during the course of the disease.

The study was carried out on 50 thalassemic children and 20 control subjects aged 5--15 years. The cortical thickness in thalassemic children was less than in control subjects. The bone loss was more obvious in girls (P less than 0.0005) than in boys (P less than 0.05). The greater bone loss in girls could not be explained by the level of blood hemoglobin because in both sexes the mean value was the same (7.3 +/- 0.5 g/dl). Of the 12 thalassemic children observed for 9--24 months, 9 showed no signficant bone change, 2 showed an improvement of cortical thickness and only 1 showed bone loss. Of the 11 thalassemic children observed for 25--48 months, 4 showed significant bone loss and 7 no change of the bone density. In both groups the mean value of pretransfusion blood Hb was 7.3 g/dl and the sex distribution was equal. A relationship was found in both control and thalassemic children between bone density and urine phosphorus to urine creatinine ratio.

Adolescent↗

Two types of nutritional rickets in infants.

In 100 infants with nutritional rickets, i.e., responsive to vitamin D therapy, we found a close inverse relationship between serum phosphorus, on the one hand, and serum alkaline phosphatase and the presence of radiological signs of rickets, on the other. There was no correlation between serum calcium and the severity of bone lesions. It is concluded that hypophosphatemia but not hypocalcemia is typical of rickets. Since hypophosphatemia and rickets can be produced experimentally by phosphate deficiency alone, we suggest our infants can be divided into two groups, one with true vitamin D deficiency that leads to hypocalcemia and no or mild bone lesions, and one with primary phosphate deficiency, resulting perhaps from a defect in phosphate transport, which leads to rickets and hypophosphatemia.

Age Factors↗

Genetic aspects of nutritional rickets.

Amino acid excretion was investigated in 21 rachitic infants and in 22 of their parents. There was (a) increased alpha-amino acid excretion in one-third of the infants a long time after the rickets had healed, (b) an abnormally high excretion of alpha-amino nitrogen and of phosphorus in many of the parents (c) an abnormal pattern of amino acid excretion in all 9 infants tested, and (d) a good correlation between the excretion of individual amino acids by an infant and by its parents. Our findings suggest that in at least some cases of nutritional rickets there is a genetic element which may manifest itself only under adverse environmental conditions.

Adult↗