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Pediatric Reports
Volume 10
Issue 2
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Pediatric Reports is published by MDPI from Volume 12 Issue 3 (2020). Previous articles were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence, and they are hosted by MDPI on mdpi.com as a courtesy and upon agreement with PAGEPress.

Pediatr. Rep., Volume 10, Issue 2 (May 2018) – 4 articles

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485 KiB  
Case Report
Takayasu Arteritis with an Initial Presentation of Chronic Monoarthritis Mimicking Oligoarticular Juvenile Idiopathic Arthritis
by Maynart Sukharomana, Sorawit Viravan, Nuntawan Piyaphanee and Sirirat Charuvanij
Pediatr. Rep. 2018, 10(2), 7648; https://doi.org/10.4081/pr.2018.7648 - 09 Jul 2018
Viewed by 513
Abstract
Patients with Takayasu arteritis (TA) generally present with non-specific symptoms that, if unrecognized and untreated, may develop vessel stenosis and/or aneurysm. There is limited data regarding chronic monoarthritis as the initial presentation in children with TA. We report a 6-yearold girl diagnosed and [...] Read more.
Patients with Takayasu arteritis (TA) generally present with non-specific symptoms that, if unrecognized and untreated, may develop vessel stenosis and/or aneurysm. There is limited data regarding chronic monoarthritis as the initial presentation in children with TA. We report a 6-yearold girl diagnosed and treated as oligoarticular juvenile idiopathic arthritis (JIA). She later developed stroke with malignant hypertension and was definitively diagnosed with TA. She additionally developed proteinuria secondary to focal segmental glomerulosclerosis. This is the report of a patient with chronic monoarthritis mimicking oligoarticular JIA which chronic monoarthritis was the presentation of TA. Since JIA is a diagnosis of exclusion, any atypical features of oligoarticular JIA should illuminate the possibility of an alternative diagnosis. Our literature review focused on musculoskeletal presentations of children with TA. Full article
504 KiB  
Case Report
A Case of Atypical Systemic Primary Carnitine Deficiency in Saudi Arabia
by Abdulrahman Alghamdi, Hani Almalki, Aiman Shawli, Rahaf Waggass and Fahad Hakami
Pediatr. Rep. 2018, 10(2), 7705; https://doi.org/10.4081/pr.2018.7705 - 27 Jun 2018
Cited by 1 | Viewed by 535
Abstract
Systemic primary carnitine deficiency (SPCD) is an autosomal recessive inborn error of fatty acid metabolism caused by a defect in the transporter responsible for moving carnitine across plasma membrane. The clinical features of SPCD vary widely based on the age of onset and [...] Read more.
Systemic primary carnitine deficiency (SPCD) is an autosomal recessive inborn error of fatty acid metabolism caused by a defect in the transporter responsible for moving carnitine across plasma membrane. The clinical features of SPCD vary widely based on the age of onset and organs involved. During infancy, patients might show episodes of hypoketotic hypoglycemia, hepatomegaly, elevated transaminases, and hyperammonemia. Skeletal myopathy, elevated creatine kinase, and cardiomyopathy are the main manifestations in children with SPCD, while in adults, the disorder is usually manifested as cardiomyopathy, arrhythmias, or fatigability. Here, we report a 5-year-old boy with SPCD that presented as dilated cardiomyopathy with atypical features, such as anemia, respiratory distress, and proximal muscle weakness. This report supports considering carnitine deficiency treatment in the work-up of unexplained pediatric dilated cardiomyopathy. Full article
367 KiB  
Case Report
Rapunzel Syndrome: How to Orient the Diagnosis
by Enrico Finale, Piergiorgio Franceschini, Cesare Danesino, Michelangelo Barbaglia and Andrea Guala
Pediatr. Rep. 2018, 10(2), 7689; https://doi.org/10.4081/pr.2018.7689 - 27 Jun 2018
Cited by 8 | Viewed by 666
Abstract
Rapunzel syndrome is a rare form of tricobezoar with a tail extending from the stomach into the small bowel; surgical removal is generally required. About 60 cases have been reported and described in the literature since 1968. We present the case of an [...] Read more.
Rapunzel syndrome is a rare form of tricobezoar with a tail extending from the stomach into the small bowel; surgical removal is generally required. About 60 cases have been reported and described in the literature since 1968. We present the case of an 8-year-old girl who, during the course of a genetic consultation, was initially assigned with a clinical suspicion of ectodermal dysplasia. Surgical intervention, which resulted in the extraction of a tricobezoar of enormous size and extension, led us to the diagnosis of Rapunzel syndrome. The possibility of a tricobezoar should be considered in all cases of adolescent patients who present signs of intestinal occlusion or sub-occlusion, suffer from psychiatric disorders, and have a history of trichotillomania. Endoscopic methodology, medical imaging and clinical diagnostics are fundamental for a differential diagnosis. Psychiatric follow-up is advised to prevent recurrence. Full article
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Case Report
Waardenburg Syndrome with Isolated Deficiency of Myenteric Ganglion Cells at the Sigmoid Colon and Rectum
by Shun Watanabe, Shotaro Matsudera, Takeshi Yamaguchi, Yukiko Tani, Kei Ogino, Masanobu Nakajima, Satoru Yamaguchi, Kinro Sasaki, Hiroshi Suzumura and Takashi Tsuchioka
Pediatr. Rep. 2018, 10(2), 7500; https://doi.org/10.4081/pr.2018.7500 - 24 May 2018
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Abstract
Waardenburg syndrome (WS) has the characteristic clinical features caused by the embryologic abnormality of neural crest cells. WS patients sometimes suffer from functional intestinal obstruction. When it is Hirschsprung disease (HD), the WS is diagnosed as type 4 WS. We report a case [...] Read more.
Waardenburg syndrome (WS) has the characteristic clinical features caused by the embryologic abnormality of neural crest cells. WS patients sometimes suffer from functional intestinal obstruction. When it is Hirschsprung disease (HD), the WS is diagnosed as type 4 WS. We report a case of WS which did not have myenteric ganglion cells in the sigmoid colon and rectum. Whether to diagnosis this case as type 1 or 4 WS is controversial. Moreover, this is the third report which has peristalsis failure caused by abnormal myenteric plexus. In all three cases, the eosinophils had aggregated in the myenteric layer of the transition zone. During embryonic life, enteric ganglion cells migrate to the myenteric layer from the proximal to the distal side sequentially and, subsequently, to the submucosal layer through the circular muscle. Therefore, we hypothesize that myenteric ganglion cells that had already migrated were eliminated by an eosinophil-mediated mechanism in these three cases. We believe this report may be helpful to elucidate the pathogenesis of some types of HD. Full article
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