The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Sateesh Kumar Somisetty - One of the best experts on this subject based on the ideXlab platform.
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subcutaneous fat necrosis in newborn an unusual case and review of literature
European Journal of Pediatrics, 2011Co-Authors: Subhabrata Mitra, Jennifer Dove, Sateesh Kumar SomisettyAbstract:Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon, self-limiting panniculitis mostly occurring within the first few weeks after birth. SCFN has been described mostly in term or post-term newborn infants in literature. We report a preterm infant developing extensive subcutaneous fat necrosis within the first week of life after significant perinatal hypoxic injury. The infant was conservatively managed for subcutaneous fat necrosis but developed Hypercalcaemia and required prolonged medical treatment. Hypercalcaemia is a rare but serious complication of subcutaneous fat necrosis and needs prolonged follow-up. The etiopathogenesis of both subcutaneous fat necrosis in newborn and the resultant Hypercalcaemia are poorly understood. Conclusion: Significant subcutaneous fat necrosis can develop in both preterm and term infants, and preterm infants also develop significant complications including Hypercalcaemia.
Scott A Rivkees - One of the best experts on this subject based on the ideXlab platform.
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etidronate therapy for hypercalcemia in subcutaneous fat necrosis of the newborn
The Journal of Pediatrics, 1999Co-Authors: Alan M Rice, Scott A RivkeesAbstract:Subcutaneous fat necrosis of the newborn (SCFN) is characterized by indurated violet skin nodules and, occasionally, life-threatening hypercalcemia. Current treatments of patients with SCFN-related hypercalcemia are often only partially successful and may be associated with prolonged hypercalcemia. We now report the use of etidronate, a bisphosphonate, to control hypercalcemia in an infant with SCFN.
Robert W Elder - One of the best experts on this subject based on the ideXlab platform.
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hypercalcemia in patients with williams beuren syndrome
The Journal of Pediatrics, 2016Co-Authors: Sampat Sindhar, Michael Lugo, Mark D Levin, Joshua R Danback, Benjamin D Brink, Dennis J Dietzen, Amy L Clark, Carolyn A Purgert, Jessica L Waxler, Robert W ElderAbstract:Objective To evaluate the timing, trajectory, and implications of hypercalcemia in Williams-Beuren syndrome (WBS) through a multicenter retrospective study. Study design Data on plasma calcium levels from 232 subjects with WBS aged 0-67.1 years were compared with that in controls and also with available normative data. Association testing was used to identify relevant comorbidities. Results On average, individuals with WBS had higher plasma calcium levels than controls, but 86.7% of values were normal. Nonpediatric laboratories overreport hypercalcemia in small children. When pediatric reference intervals were applied, the occurrence of hypercalcemia dropped by 51% in infants and by 38% in toddlers. Across all ages, 6.1% of the subjects had actionable hypercalcemia. In children, actionable hypercalcemia was seen in those aged 5-25 months. In older individuals, actionable hypercalcemia was often secondary to another disease process. Evidence of dehydration, hypercalciuria, and nephrocalcinosis were common in both groups. Future hypercalcemia could not be reliably predicted by screening calcium levels. A subgroup analysis of 91 subjects found no associations between hypercalcemia and cardiovascular disease, gastrointestinal complaints, or renal anomalies. Analyses of electrogradiography data showed an inverse correlation of calcium concentration with corrected QT interval, but no acute life-threatening events were reported. Conclusions Actionable hypercalcemia in patients with WBS occurs infrequently. Although irritability and lethargy were commonly reported, no mortality or acute life-threatening events were associated with hypercalcemia and the only statistically associated morbidities were dehydration, hypercalciuria, and nephrocalcinosis.
Subhabrata Mitra - One of the best experts on this subject based on the ideXlab platform.
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subcutaneous fat necrosis in newborn an unusual case and review of literature
European Journal of Pediatrics, 2011Co-Authors: Subhabrata Mitra, Jennifer Dove, Sateesh Kumar SomisettyAbstract:Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon, self-limiting panniculitis mostly occurring within the first few weeks after birth. SCFN has been described mostly in term or post-term newborn infants in literature. We report a preterm infant developing extensive subcutaneous fat necrosis within the first week of life after significant perinatal hypoxic injury. The infant was conservatively managed for subcutaneous fat necrosis but developed Hypercalcaemia and required prolonged medical treatment. Hypercalcaemia is a rare but serious complication of subcutaneous fat necrosis and needs prolonged follow-up. The etiopathogenesis of both subcutaneous fat necrosis in newborn and the resultant Hypercalcaemia are poorly understood. Conclusion: Significant subcutaneous fat necrosis can develop in both preterm and term infants, and preterm infants also develop significant complications including Hypercalcaemia.
Ogo I Egbuna - One of the best experts on this subject based on the ideXlab platform.
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hypercalcaemic and hypocalcaemic conditions due to calcium sensing receptor mutations
Best Practice & Research: Clinical Rheumatology, 2008Co-Authors: Ogo I Egbuna, Edward M BrownAbstract:The extracellular calcium (Ca 2+ o )-sensing receptor (CaSR) enables the parathyroid glands and other CaSR-expressing cells involved in calcium homeostasis, such as the kidney and bone, to sense alterations in the level of Ca 2+ o and to respond with changes in function that are directed at normalizing the blood calcium concentration. Several disorders of Ca 2+ o sensing arise from inherited or acquired abnormalities that ‘reset' the serum calcium concentration upwards or downwards. Heterozygous inactivating mutations of the CaSR produce a benign form of Hypercalcaemia, termed ‘familial hypocalciuric Hypercalcaemia', while homozygous mutations produce a much more severe hypercalcaemic disorder resulting from marked hyperparathyroidism, called ‘neonatal severe hyperparathyroidism'. Activating mutations cause a hypocalcaemic syndrome of varying severity, termed ‘autosomal-dominant hypocalcaemia or hypoparathyroidism' as well as Bartter's syndrome type V. Calcimimetic CaSR activators and calcilytic CaSR antagonists have also been developed with potential for use in the treatment of these disorders.