Isr Med Assoc J
February 2007
Background: Leptin, a pleiotropic hormone, has been suggested to be part of an acute-phase response during an inflammatory stimulus. Its correlation with other acute-phase reactants during minor infection in children has not been investigated.
Objectives: To study the correlation between levels of serum leptin and those of C-reactive protein, a well-documented acute-phase reactant, in a series of pediatric patients with acute minor infections.
J Pediatr Endocrinol Metab
July 2005
Background: Intrauterine growth retardation (IUGR) is a major cause of short stature in childhood. Most but not all children experience catch-up growth by 2 years of age.
Methods: We investigated the endocrine profile (thyroid function, prolactin, cortisol, C-peptide and insulin-like growth factor-I [IGF-IJ levels) of 57 children with IUGR, aged 2-10 years, and compared it with 30 controls whose birth weight was appropriate-for-gestational-age.
Objective: To investigate the prevalence of autoimmune diseases in young patients (probands) with type 1 diabetes and their first-degree relatives, and to determine the spectrum of extrapancreatic manifestations in these subjects.
Research Design And Methods: The study population included 109 probands age 13 +/- 4.9 years and 412 first-degree relatives age 28.
J Pediatr Endocrinol Metab
June 2002
The growth and maturation of the gastrointestinal tract during development is influenced by diverse genetic and growth factors. Since prolactin is abundant in amniotic fluid and breast milk, we hypothesized that it may also affect gut development. The effect of prolactin on thymidine incorporation and tissue alkaline phosphatase, maltase and lactase activity was studied on jejunal explants from fetal, newborn and 2 week-old rats.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
February 2002
During GnRH agonist therapy of patients with central precocious puberty (CPP), growth is sometimes suppressed to subnormal velocity. The working hypotheses were that estrogen levels are suppressed by GnRH agonist therapy below normal prepubertal levels, that such suppression is responsible for the slow growth of girls with CPP during GnRH agonist therapy, and that a mini-dose of estrogen replacement will normalize growth. The present pilot study examined growth and bone maturation over 2 yr in 13 patients with CPP and compared therapy with a combination of GnRH agonist and 8 microg conjugated equine estrogen (group 1) to therapy with GnRH agonist alone (group 2).
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