Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dexamethasone is used commonly in the treatment of chronic lung disease of prematurity, but there are concerns about possible deleterious effects on growth and bone. Our aim in this study was to examine the effects of dexamethasone treatment on bone and collagen turnover in preterm infants. Bone-specific alkaline phosphatase, the C-terminal propeptide of type I collagen (PICP, reflecting whole-body type I collagen synthesis), and the N-terminal propeptide of type III procollagen (P3NP, reflecting soft tissue collagen turnover), together with the C-terminal telopeptide of type I collagen (ICTP), urinary pyridinoline (Pyd), and deoxypyridinoline (all markers of collagen breakdown) were measured at weekly intervals over the first 12 wk of life in 14 preterm infants with chronic lung disease treated with dexamethasone. Results were expressed as SD scores relative to preterm control infants not treated with dexamethasone. PICP, P3NP, ICTP, and Pyd all showed marked decreases (-2.1 to -3.7 SD scores) during the first week of treatment (p < 0.001), returning to pretreatment levels after stopping dexamethasone. In the group as a whole, these collagen markers were negatively correlated with dexamethasone dose (p < 0.0001); negative correlations were also seen in most individual babies, although the slopes of individual regression lines varied by a factor of 2. Weight gain at 12 wk was correlated with PICP, expressed as the mean SD score over 12 wk for each baby, (r = 0.69, p < 0.01) but not with other markers or cumulative dose of dexamethasone. We conclude that dexamethasone markedly suppressed collagen turnover in preterm infants in a dose-dependent fashion, although some babies were more affected than others. The degree of suppression of type I collagen synthesis was a strong independent predictor of overall weight gain over the first 12 wk of life.
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PMID:Effects of dexamethasone treatment on bone and collagen turnover in preterm infants with chronic lung disease. 1092 89

Neonatal sepsis is very common in preterm infants, and severe morbidity during the neonatal period is a major cause of osteopenia of prematurity. We examined the effect of neonatal sepsis on bone turnover markers in premature infants. Twenty-four premature infants participated in the study. Ten of the premature infants developed sepsis during their hospitalization in the neonatal intensive care unit (mean gestational age [GA] 27.3 +/- 0.4 weeks; mean birth weight [BW] 898 +/- 82 g). Fourteen infants who did not develop sepsis served as controls (GA: 26.8 +/- 0.8 weeks, BW: 892 +/- 66 g). Blood samples for bone turnover markers were collected during the initial sepsis workup, and at the end of the first week of treatment, and were compared to the corresponding weekly changes in bone markers in the controls. In addition, samples were collected at the end of the 10th week of life to determine long-term effects of sepsis on bone turnover. Bone osteoblastic activity was assessed by measurements of circulating osteocalcin, bone-specific alkaline phosphatase (BSAP) and the C-terminal procollagen peptide (PICP) levels. Bone resorption was assessed by measurements of circulating carboxy terminal cross-links telopeptide of type I collagen (ICTP). There were no significant differences in the weekly changes of all bone turnover markers in premature infants who developed or did not develop sepsis. No significant differences were found in bone turnover markers at the age of 10 weeks between the groups. Neonatal sepsis in premature infants was not associated with biochemical evidence of reduced bone turnover.
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PMID:The effect of neonatal sepsis on bone turnover in very-low birth weight premature infants. 1270 67

The hypertrophic chondrocytes lack the ability to proliferate, thus permitting matrix mineralization as well as vascular invasion from the bone in both the mandibular condyle and the epiphyseal cartilage. This study attempted to verify whether the histological appearance of the hypertrophic chondrocytes is in a steady state during postnatal development of the mouse mandibular condyle. Type X collagen immunohistochemistry apparently distinguished the fibrous layer described previously as the "articular zone," "articular layer," and "resting zone" from the hypertrophic zone. Interestingly, the ratio of the type X collagen-positive hypertrophic zone in the entire condyle seemed higher in the early stages but decreased in the later stages. Some apparently compacted cells in the hypertrophic zone showed proliferating cell nuclear antigen (PCNA) immunoreaction, indicating the potential for cell proliferation at the early stages. As the mice matured, in contrast, they further enlarged and assumed typical features of hypertrophic chondrocytes. Apoptotic cells were also discernible in the hypertrophic zone at the early but not later stages. Consistent with morphological configurations of hypertrophic chondrocytes, immunoreactions for alkaline phosphatase, osteopontin, and type I collagen were prominent at the later stage, but not the early stage. Cartilaginous matrices demonstrated scattered patches of mineralization at the early stage, but increased in their volume and connectivity at the later stage. Thus, the spatial and temporal occurrence of these immunoreactions as well as apoptosis likely reflect the prematurity of hypertrophying cells at the early stage, and imply a physiological relevance during the early development of the mandibular condyles.
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PMID:Histochemical evidences on the chronological alterations of the hypertrophic zone of mandibular condylar cartilage. 1617 89