Publications by authors named "Serge Prop"

3 Publications

  • Page 1 of 1

[A practical algorithm for polydipsia in children].

Ned Tijdschr Geneeskd 2014 ;158:A7595

Tergooi, afd. Kindergeneeskunde, Blaricum.

There is a lack of consent on a clinical diagnostic work-up for children with polydipsia. This can result in a delay in diagnosis in some children and unnecessary investigations in others. We describe three children who presented with polydipsia. Two of them were diagnosed with psychogenic polydipsia and one with central diabetes insipidus. We discuss the differential diagnosis and relevant clinical signs before going on to propose a clinical diagnostic algorithm that can be used in children with polydipsia. A systematic diagnostic work up for children with polydipsia helps to differentiate between those in whom polydipsia is unlikely to have a somatic cause and those where a water deprivation-test is indicated. A water deprivation test in children is an invasive procedure and should be performed by a paediatric endocrinologist or nephrologist.
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April 2015

[A boy with cervical focal myositis].

Ned Tijdschr Geneeskd 2014 ;158:A6935

Tergooiziekenhuizen, afd. Kindergeneeskunde, Blaricum.

Background: Focal myositis is a rare idiopathic pseudotumour that mostly occurs in the extremities in adults.

Case Description: An 8-year-old boy presented with a few months history of swelling in the neck and fever. Ultrasound investigation revealed an inhomogenous mass consistent with lymphadenitis. After nine days of antibiotic therapy, the clinical picture of fever and swelling was unchanged. MRI imaging revealed continuity of the swelling in the sternocleidomastoid muscle and a malignant process was suspected. Microscopy showed no malignant cells, however, but a lymphoplasmocytic infiltration with fibrosis and degeneration of muscle fibres, consistent with focal myositis. No intervention was undertaken and one year after presentation the tumour had regressed almost entirely.

Conclusion: Focal myositis can present as a cervical tumour. On ultrasound, the condition is hard to distinguish from lymphadenopathy or malignancy. In cases of insufficient response to empirical antibiotic therapy, focal myositis should be considered.
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November 2014

Natural killer T cells in adipose tissue prevent insulin resistance.

J Clin Invest 2012 Sep 6;122(9):3343-54. Epub 2012 Aug 6.

Department of Metabolic Diseases, University Medical Center Utrecht, Utrecht, the Netherlands.

Lipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT cell-deficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissue-resident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissue-resident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.
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http://dx.doi.org/10.1172/JCI62739DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428087PMC
September 2012