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      PAEDIATRIC ENDOCRINE DISORDERS AT THE UNIVERSITY COLLEGE HOSPITAL, IBADAN: 2002 – 2009

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          Abstract

          Background:

          Until recently, most published research focus more on infectious diseases and malnutrition giving the impression that endocrine disorders are uncommon. Reports on endocrine disorders in children in developing countries are few compared to developed countries reflecting the different level of prevalence in the different geographical locations and or level of awareness and availability of facilities for proper diagnosis.

          Objective:

          This study aims at defining the burden of paediatric endocrine disorders in Ibadan.

          Subjects/Methods:

          A review of records of children who presented at University College Hospital, Ibadan with paediatric endocrine disorders from 2002 to 2009 was carried out.

          Results:

          During the eight-year period, a total of 110 children presented with various endocrine disorders but only 94 had complete data for this study. There were 47(50%) males and 37(39.4%) females, and in 10(10.6%) of them, had genital ambiguity at presentation. Patients’ ages ranged from 2 weeks to 15 years with a median of 3 years. Many (35%) patients were malnourished with weight less than 80% of the expected weight for age and only 9% were overweight. Yearly distribution of cases showed a steady increase in number of cases from 2005. Rickets and metabolic disorders constituted 56.4% of patients; Diabetes mellitus was diagnosed in 12.8%, adrenal disoders in 10.6%, pubertal disorders in 5.3% and growth disorders in 4.3% of the patients. Thyroid disorders were present in 6.4%, obesity in 3.2% while the least common disorder was Diabetes insipidus (1%). About 58% of the children had parents in the low socioeconomic status and the management of the cases were severely hampered by lack of funds. About 60.6% of these patients were lost to follow up, during the period.

          Conclusions:

          Paediatric endocrine disorders are associated with a high incidence of malnutrition. Most patients presented with rickets which is a preventable condition.

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          Most cited references11

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          Maternal and fetal hypothalamic-pituitary-adrenal axes during pregnancy and postpartum.

          Ioannis Ilias, George Mastorakos (2003)
          The principal modulators of the hypothalamic-pituitary-adrenal (HPA) axis are corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP). Corticotropin-releasing hormone is not exclusively produced in the hypothalamus. Its presence has been demonstrated at peripheral inflammatory sites. Ovulation and luteolysis bear characteristics of an aseptic inflammation. CRH was found in the theca and stromal cells as well as in cells of the corpora lutea of human and rat ovaries. The cytoplasm of the glandular epithelial cells of the endometrium has been shown to contain CRH and the myometrium contains specific CRH receptors. It has been suggested that CRH of fetal and maternal origin regulates FasL production, thus affecting the invasion (implantation) process through a local auto-paracrine regulatory loop involving the cytotrophoblast cells. Thus, the latter may regulate their own apoptosis. During pregnancy, the plasma level of circulating maternal immunoreactive CRH increases exponentially from the first trimester of gestation due to the CRH production in the placenta, decidua, and fetal membranes. The presence in plasma and amniotic fluid of a CRH-binding protein (CRHbp) that reduces the bioactivity of circulating CRH by binding is unique to humans. Maternal pituitary ACTH secretion and plasma ACTH levels rise during pregnancy-though remaining within normal limits-paralleling the rise of plasma cortisol levels. The maternal adrenal glands during pregnancy gradually become hypertrophic. Pregnancy is a transient, but physiologic, period of hypercortisolism. The diurnal variation of plasma cortisol levels is maintained in pregnancy, probably due to the secretion of AVP from the parvicellular paraventricular nuclei. CRH is detected in the fetal hypothalamus as early as the 12th week of gestation. CRH levels in fetal plasma are 50% less than in maternal plasma. The circulating fetal CRH is almost exclusively of placental origin. The placenta secretes CRH at a slower rate in the fetal compartment. AVP is detected in some neurons of the fetal hypothalamus together with CRH. AVP is usually detectable in the human fetal neurohypophysis at 11 to 12 weeks gestation and increases over 1000-fold over the next 12 to 16 weeks. The role of fetal AVP is unclear. Labor appears to be a stimulus for AVP release by the fetus. The processing of POMC differs in the anterior and intermediate lobes of the fetal pituitary gland. Corticotropin (ACTH) is detectable by radioimmunoassay in fetal plasma at 12 weeks gestation. Concentrations are higher before 34 weeks gestation, with a significant fall in late gestation. The human fetal adrenal is enormous relative to that of the adult organ. Adrenal steroid synthesis is increased in the fetus. The major steroid produced by the fetal adrenal zone is sulfoconjugated dehydroepiandrosterone (DHEAS). The majority of cortisol present in the fetal circulation appears to be of maternal origin, at least in the nonhuman primate. The fetal adrenal uses the large amounts of progesterone supplied by the placenta to make cortisol. Another source of cortisol for the fetus is the amniotic fluid where cortisol converted from cortisone by the choriodecidua, is found. In humans, maternal plasma CRH, ACTH, and cortisol levels increase during normal labor and drop at about four days postpartum; however, maternal ACTH and cortisol levels at this stage are not correlated. In sheep, placental CRH stimulates the fetal production of ACTH, which in turn leads to a surge of fetal cortisol secretion that precipitates parturition. The 10-day-long intravenous administration of antalarmin, a CRH receptor antagonist, significantly prolonged gestation compared to the control group of animals. Thus, CRH receptor antagonism in the fetus can also delay parturition. The HPA axis during the postpartum period gradually recovers from its activated state during pregnancy. The adrenals are mildly suppressed in a way analogous to postcure Cushing's syndrome. Provocation testing has shown that hypothalamic CRH secretion is transiently suppriently suppressed at three and six weeks postpartum, normalizing at 12 weeks.
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            Prevalence of the metabolic syndrome among U.S. adolescents using the definition from the International Diabetes Federation.

            Ali Mokdad, Earl S. Ford, Terry W. Pearson … (2008)
            Our objective was to estimate the prevalence of the metabolic syndrome using the 2007 pediatric International Diabetes Federation (IDF) definition among adolescents in the U.S. We used data from 2,014 participants aged 12-17 years of the National Health and Nutrition Examination Survey 1999-2004. The prevalence of the metabolic syndrome for the period 1999-2004 was approximately 4.5% ( approximately 1.1 million adolescents aged 12-17 years in 2006). It increased with age, was higher among males (6.7%) than females (2.1%) (P = 0.006), and was highest among Mexican-American adolescents (7.1%). The prevalence of the metabolic syndrome was relatively stable across the 6-year period: 4.5% for 1999-2000, 4.4-4.5% for 2001-2002, and 3.7-3.9% for 2003-2004 (P for linear trend >0.050). Our results provide the first estimates of the prevalence of the metabolic syndrome using the pediatric IDF definition among adolescents in the U.S.
            Article 0 comments Cited 60 times – based on 0 reviews     Review now
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              A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children.

              T. D. Thacher, Christian Fischer, J. Lawson … (1999)
              Nutritional rickets remains prevalent in many tropical countries despite the fact that such countries have ample sunlight. Some postulate that a deficiency of dietary calcium, rather than vitamin D, is often responsible for rickets after infancy. We enrolled 123 Nigerian children (median age, 46 months) with rickets in a randomized, double-blind, controlled trial of 24 weeks of treatment with vitamin D (600,000 U intramuscularly at enrollment and at 12 weeks), calcium (1000 mg daily), or a combination of vitamin D and calcium. We compared the calcium intake of the children at enrollment with that of control children without rickets who were matched for sex, age, and weight. We measured serum calcium and alkaline phosphatase and used a 10-point radiographic score to assess the response to treatment at 24 weeks. The daily dietary calcium intake was low in the children with rickets and the control children (median, 203 mg and 196 mg, respectively; P=0.64). Treatment produced a smaller increase in the mean (+/-SD) serum calcium concentration in the vitamin D group (from 7.8+/-0.8 mg per deciliter [2.0+/-0.2 mmol per liter] at base line to 8.3+/-0.7 mg per deciliter [2.1+/-0.2 mmol per liter] at 24 weeks) than in the calcium group (from 7.5+/-0.8 [1.9+/-0.2 mmol per liter] to 9.0+/-0.6 mg per deciliter [2.2+/-0.2 mmol per liter], P<0.001) or the combination-therapy group (from 7.7+/-1.0 [1.9+/-0.25 mmol per liter] to 9.1+/-0.6 mg per deciliter [2.3+/-0.2 mmol per liter], P<0.001). A greater proportion of children in the calcium and combination-therapy groups than in the vitamin D group reached the combined end point of a serum alkaline phosphatase concentration of 350 U per liter or less and radiographic evidence of nearly complete healing of rickets (61 percent, 58 percent, and 19 percent, respectively; P<0.001). Nigerian children with rickets have a low intake of calcium and have a better response to treatment with calcium alone or in combination with vitamin D than to treatment with vitamin D alone.
              Article 0 comments Cited 54 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Ib Postgrad Med
                Journal ID (iso-abbrev): Ann Ib Postgrad Med
                Journal ID (publisher-id): AIPM
                Title: Annals of Ibadan Postgraduate Medicine
                Publisher: Association of Resident Doctors (ARD), University College Hospital, Ibadan
                ISSN (Print): 1597-1627
                Publication date (Print): December 2013
                Volume: 11
                Issue: 2
                Pages: 96-101
                Affiliations
                [1 ]Department of Paediatrics, University College Hospital, Ibadan, Nigeria.
                [2 ]Endocrine Science Research Group, University of Manchester, Royal Manchester Children’s Hospital, Manchester, UK.
                Author notes
                Correspondence: Dr. Omolola Ayoola Endocrine Science Research Group, 5th Floor (Research), Royal Manchester Children’s Hospital, Oxford Road Manchester M13 9WL Tel: +441617016949 E-mail: ooayoola@ 123456yahoo.com
                Article
                Publisher ID: AIPM-11-96
                PMC ID: 4111065
                SO-VID: c3a1f9f3-2abb-40de-9b9f-25b4a1db362d
                Copyright © © Association of Resident Doctors, UCH, Ibadan
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

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                Categories
                Subject: Article

                Keywords: endocrine disorders,awareness,rickets,malnutrition,financial constraints.
                Data availability:
                Keywords: endocrine disorders, awareness, rickets, malnutrition, financial constraints.

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