Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

7 cases of pruritus in pregnancy are reported and their laboratory findings compared with a group of normal pregnant women; then pruritus is reviewed with respect to diagnosis, pathogenesis, therapy, and prognosis. The 7 women developed pruritus in 28-38 weeks of typically the 2nd pregnancy, although during oral contraception in 1 woman. The frequency was about 2/1000 pregnancies. Lab findings suggestive of cholestasis included normal prothrombin, elevated transaminaes, alkaline phosphatase, total bilirubin, total cholesterol, and slowed BSP clearance. None of these women had any history of hepatitis, medication, or positive Australia antigen. It is important in diagnosis to rule out infections, toxic or iatrogenic hepatitis, and especially herpes gestationis, which is teratogenic. Pruritus of pregnancy is identical to that seen during oral contraception, i.e., it is a less severe form of cholestatsis than jaundice. It can be treated with cholestyramine, or will regress spontaneously after delivery, but may cause prematurity.
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PMID:[Significance of pruritus during pregnancy. Relations with the hepatic disorders of gestation]. 113 31

During pregnancy, calcium is continuously transferred directly from the maternal intestine to the fetal bone, a transfer that is mainly induced by the interrelated actions of the calcium-regulating hormones parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D) and calcitonin. It has recently been demonstrated in animals that PTH-related protein (PTHrP) is the fetal equivalent of PTH. Human PTHrP, originally described as a product of a human lung cancer cell line and implicated in the pathogenesis of humoral hypercalcemia of malignancy, is a protein with 141 amino acids, and it has biochemical actions similar to PTH. It is believed that fetal PTHrP is mainly derived from the placenta during early gestation and from the fetal parathyroid glands during further development and that this protein has the role of maintaining the maternal-fetal calcium gradient either alone or in concert with 1,25(OH)2D. With birth, the placental supply of calcium ceases abruptly, stimulating the increase of PTH and 1,25(OH)2D, which are the main regulators of postnatal calcium metabolism. Alterations in the placental calcium (and phosphate) gradient may be caused by maternal hypo- or hypercalcemia and placental insufficiency and may be followed by transient disorders of calcium metabolism in the newborn. Due to abrupt cessation of the calcium and phosphate supply after delivery at a time when mineral demands are the highest, preterm infants are especially prone to hypocalcemia and osteopathy. If bone disease of prematurity is to be prevented, the amounts of calcium and phosphate must be adequate, as demonstrated by laboratory tests, the most important being calcium and phosphate in urine and alkaline phosphatase activity in serum.
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PMID:[Perinatal calcium metabolism. Physiology and pathophysiology]. 143 20

During the last trimester of pregnancy, there is a sixfold increase in fetal calcium and phosphorus accumulation. Unsupplemented human breast milk may not provide sufficient calcium and phosphorus for the rapidly growing preterm infant to match the accumulation that should have taken place in utero and to permit normal bone mineralization. Rickets of prematurity may present clinically between the 6th and 12th postnatal week. The clinical diagnosis may be confirmed using simple biochemical tests. Inadequate mineral substrate intake, particularly of phosphorus, is the most common cause, although a delay in the maturation of the renal enzyme, 1-alpha hydroxylase, with low plasma concentrations of 1,25-dihydroxyvitamin D, may also occur. The biochemical response to treatment can be determined by documenting a fall in plasma alkaline phosphatase activity and a rise in plasma phosphate concentration and urinary phosphate excretion.
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PMID:Calcium and phosphorus metabolism in the premature infant. 177 18

To assess the effects of increasing the mineral content of parenteral nutrition solutions on the biochemical and radiological indicators of metabolic bone disease of prematurity 27 neonates who required parenteral nutrition were sequentially allocated to receive either a standard solution (group 1) or one with an increased mineral content (group 2). The 13 patients in group 1 received 0.68 mmol/kg/day of calcium and 0.61 mmol/kg/day of phosphorus, and the 14 in group 2 received 1.25 and 1.20 mmol/kg/day, respectively. The two groups did not differ significantly in the severity of their illness measured by birth weight, gestational age, duration of parenteral nutrition or ventilation, or the amount of supplementary oxygen required. In patients in group 2 the median plasma phosphate concentration was higher, the plasma alkaline phosphatase activity was lower, and there was less radiological evidence of rickets. There were no complications caused by excess calcium and phosphorus, and the rate of growth was similar in both groups. We conclude that an increased mineral content in parenteral nutrition solutions reduces the severity of metabolic bone disease in sick infants who require this form of nutrition.
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PMID:Association of mineral composition of neonatal intravenous feeding solutions and metabolic bone disease of prematurity. 249 71

The bone mineral status of very low birthweight (VLBW) infants fed exclusively their own mother's milk (group I) was compared with that of VLBW infants fed mother's milk in the initial 4 weeks followed by a 1:1 mixture of mother's milk and preterm formula containing high phosphorus (P) and calcium (Ca) (group II). In both groups, most infants showed a biochemical picture characteristic of phosphorus deficiency syndrome by the fourth week. Thereafter, serum alkaline phosphatase activity (ALP) decreased and serum P increased in all group II infants. Conversely, serum ALP rose and hypophosphatemia persisted in most group I infants. Group II had a significantly higher serum P at weeks 8 and 12 and a significantly lower ALP at week 12 than group I. Furthermore, group II had a lower incidence of severe radiographic abnormalities than group I at week 12. We confirmed previous observations that VLBW infants fed exclusively human milk require P and Ca supplementation to prevent metabolic bone disease of prematurity.
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PMID:Improved bone mineral status in very low birthweight infants fed human milk mixed with preterm formula. 250 28

Serum immunoreactive parathyroid hormone (iPTH), ionized calcium, the urinary cyclic AMP/creatinine ratio (cAMP/Cr) and some indices of bone turnover (alkaline phosphatase (AP), serum osteocalcin, and the urinary total hydroxyproline/creatinine ratio (OH-P/Cr)) were measured in 26 preterm infants during the first 4 weeks of life. Despite of stimulated parathyroid gland activity cAMP/Cr, AP, osteocalcin and OH-P/Cr were low during the first week. Thereafter iPTH decreased, whereas cAMP/Cr, and the indices of bone turnover increased, reaching high-normal values (in comparison to full-term infants) during the second and third week of life. Serum iPTH was negatively correlated to cAMP/Cr in the first week (r = -0.61, p less than 0.01), whereas the relationship became positive during the second (r = 0.47, p less than 0.05) and third (r = 0.54, p less than 0.05) week of life indicating maturation of the renal response to PTH. The study supports the concept that in premature infants a transient pseudohypoparathyroid-like state is present during the first week of life reflecting an immaturity of renal and possibly bone response to PTH. This may be an etiological factor in hypocalcemia of prematurity.
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PMID:Evidence for transient peripheral resistance to parathyroid hormone in premature infants. 303 25

Bone mineral content of the forearm was measured by photon absorptiometry in 17 preterm infants at a postconceptional age of 40 weeks. Radiographs of the forearm were assessed by Koo's method and plasma alkaline phosphatase activity was also measured at this time. Bone mineral content was significantly but weakly correlated with Koo score and was not significantly correlated with alkaline phosphatase activity. Neither of these two commonly used investigations accurately predicts the presence of underlying bone disease. Compared with 15 full term infants the preterm infants had significantly lower values of bone mineral content, palpated ulnar length, and crown-heel length. After adjusting for weight and ulnar length the preterm group still had a significantly lower mean value of bone mineral content than the full term group. Accurate diagnosis of osteopenia of prematurity requires photon absorptiometry, with bone mineral content assessed relative to body weight or ulnar length.
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PMID:Osteopenia of prematurity. 376 15

Rickets, hypocalcemia, hypophosphatemia, and hyperparathyroidism were found in a low-birth-weight premature infant. The concentration of plasma calcitriol (1,25-dihydroxyvitamin D) was 145 pg/mL. With additional exogenous calcitriol (37.5 ng/kg/24 hr) given for eight weeks, the biochemical abnormalities were corrected and healing of rickets was evident. Three months later, while receiving only 400 IU of ergocalciferal daily, the patient had normal levels of serum calcium, phosphate, and alkaline phosphatase with a serum calcitriol concentration of 36 pg/mL. These observations suggest that rickets of prematurity may involve a malabsorption of calcium and phosphorus with an elevated calcitriol level needed to overcome this inadequate absorption. Additional doses of calcitriol may be of benefit in these infants, although it must be given carefully. Furthermore, the role of phosphate supplementation in these infants requires consideration.
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PMID:Rickets of prematurity. Supranormal levels of serum 1,25-dihydroxyvitamin D. 696 86

Plasma alkaline phosphatase activity was measured in 349 infants aged between 5 and 10 days to establish a normal range for different gestational ages. Significant differences were observed between term and preterm infants, the highest values being associated with the shortest lengths of gestation. Plasma calcium, phosphate, and alkaline phosphatase activity were measured sequentially in 51 preterm infants less than 1500 g at birth. A significant correlation was found between raised plasma alkaline phosphatase activity and radiological changes of osteoporosis, metaphyseal change, and periosteal reaction. Plasma alkaline phosphatase appears to be of value in screening for and monitoring rickets of prematurity.
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PMID:Plasma alkaline phosphatase activity in rickets of prematurity. 709 94

Nutritional vitamin D deficiency rickets was established in 41 Sudanese children aged from 3 months to 7 years by clinical, radiological and therapeutic response supported by biochemical investigations. There were 25 boys and 16 girls, of whom 42% were infants of less than 1 year. Forty-seven per cent of rachitic children were underweight. Six infants had early rickets with no bony swellings but had other clinical features and radiological evidence of rickets. One of them, aged 3 months, presented with hypocalcaemic convulsions. Three children had icthyosis. Serum alkaline phosphatase was raised in 75%, hypophosphataemia occurred in 68% and hypocalcaemia in 54% of patients. Anaemia, mostly hypochromic, was detected in 79%. Possible causes were poor socio-economic background, inadequate dietary intake in both mothers and children, prolonged breastfeeding, prematurity, limited sun exposure and type of residence. Nutritional vitamin D deficiency rickets should be looked for in Sudanese children, especially in preterms and in those living in flats.
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PMID:Nutritional vitamin D deficiency rickets in Sudanese children. 759 40


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