Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial calcification has been rarely described in premature infants after myocardial infarction and myocarditis with coxsackievirus B1. In adults and older children, metastatic myocardial calcification has been reported in chronic renal failure. We report a case of myocardial calcification in a 680-gm preterm infant after a prolonged course of renal failure complicated by secondary hyperparathyroidism. Subclinical myocardial injury was evidenced by a high serum creatine phosphokinase MB band concentration, which probably provided a susceptible substrate for the deposition of calcium crystals, because the multiplication product of serum calcium and inorganic phosphorus levels transiently exceeded 75 mg x mg/100 ml, indicating serum saturation during the course of secondary hyperparathyroidism. We report this case as an unusual complication of renal immaturity in extremely low birth weight infants and an indication of a relatively intact parathyroid glandular function in them. Hypoxia, myocardial dysfunction, and renal failure are common complications in such infants, and in the presence of renal failure, the serum levels of calcium and inorganic phosphorus should be maintained below the pathologic level to avoid ectopic calcification of the tissues, including the myocardium.
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PMID:Myocardial calcification in an extremely low birth weight infant with chronic renal failure and secondary hyperparathyroidism. 851 2

Morphological and virological studies were carried out in 26 cases of perinatal and neonatal deaths in a group at a high risk of vertical transmission of Coxsackie viruses. Antigens of Coxsackie viruses A and B were identified in 73.1% of autopsy materials, including the thymus. Adenovirus and rubella virus antigens were detected much more rarely: in 26.9 and 30.8% of cases. The incidence of Coxsackie viruses was minimal (50%) in cases when thymic abnormalities were confined to the initial signs of preterm involution and reliably increased if the involution was more expressed in the presence of underdeveloped thymus, reaching 100% in cases with the terminal stage of preterm involution in the presence of marked immaturity. The data confirm the hypothesis about the principal role of Coxsackie virus in the etiology of secondary congenital immunodeficiencies detected in children at a high risk of vertical transmission of these viruses.
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PMID:[Study of vertical transmission of coxsackie group enteroviruses in the etiology of congenital immunodeficiencies]. 930 99

Enteroviruses generally cause mild disease; however, neonates are at higher risk for severe illness because of the immaturity of their immune systems. Neonatal systemic enterovirus disease, characterized by multiorgan involvement, is among the most serious, potentially fatal conditions associated with enterovirus infection. Typical clinical presentations include encephalomyocarditis (characteristic of group B coxsackieviruses) and hemorrhage-hepatitis syndrome (typical of echovirus 11). To describe the severity of neonatal illness associated with coxsackievirus B1 (CVB1) infection, CDC analyzed case reports and preliminary data from the National Enterovirus Surveillance System (NESS) for 2007. This report describes the results of that analysis, which indicated that, in 2007, CVB1 for the first time was the predominant enterovirus in the United States, accounting for 113 (25%) of 444 enterovirus infections with known serotypes. In addition, phylogenetic analysis of the 2007 CVB1 strains suggested that the cases resulted from widespread circulation of a single genetic lineage. Health-care providers and public health departments should be vigilant to the possibility of neonatal disease caused by CVB1. Testing for enteroviruses in clinically compatible cases and reporting of identified enteroviruses to NESS should be encouraged.
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PMID:Increased detections and severe neonatal disease associated with coxsackievirus B1 infection--United States, 2007. 1849 4