Biomedical subjects
Elizabeth A C Sellers
Publications and source records attributed to Elizabeth A C Sellers.
Is luteinizing hormone-releasing hormone agonist justified in short adolescents?
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Adaptation of Inuit children to a low-calcium diet.
For Inuit children, a traditional diet contains 20 mg of elemental calcium per day, well below the recommended daily intake. To identify alterations in intestinal or renal calcium absorption, 10 healthy Inuit children (5 to 17 years of age) were given a standardized calcium load (Pak test). Five had hypercalciuria (hyperabsorptive in 3 and renal leak in 2), a frequency markedly different from that for white children (p < 0.004) and not explained by calcitropic hormone and serum calcium levels, which were normal. There was a preponderance of the bb vitamin D receptor genotype (8 of 10 subjects; p < 0.01 for comparison with white populations). Dietary calcium absorption appeared to be more efficient in these Inuit children, with an increased frequency of hypercalciuria associated with the bb genotype. This may represent a genetic adaptation to dietary constraints and may predispose to nephrolithiasis or nephrocalcinosis if standard nutritional guidelines are followed.
Type 2 diabetes mellitus in children: prenatal and early infancy risk factors among native canadians.
BACKGROUND: Type 2 diabetes mellitus is increasingly being observed among children and youth, including the Native population of Canada. Only one study has investigated prenatal and early infancy risk factors for the disease. METHODS: A case-control study was conducted; 46 patients younger than 18 years were recruited from the only clinical center for the treatment of diabetes serving the province of Manitoba, and 92 age- and sex-matched controls were recruited from a pediatric ambulatory clinic serving a large Native population in Winnipeg, Manitoba. Information on exposure to prenatal and early infancy risk factors was obtained through questionnaires administered by a Native nurse-interviewer. RESULTS: Multiple logistic regression modeling identified preexisting diabetes (odds ratio [OR], 14.4; 95% confidence interval [CI], 2.86-72.5), gestational diabetes (OR, 4.40; 95% CI, 1.38-14.1), and breastfeeding longer than 12 months (OR, 0.24; 95% CI, 0.13-0.99) as significant independent predictors of diabetic status. Other factors, such as low (<2500 g) and high (>4000 g) birth weight and maternal obesity, were also associated with diabetes in our population, but the elevated risks were not statistically significant. CONCLUSION: Breastfeeding reduces the risk of type 2 diabetes among Native Canadian children and should be promoted as a potential intervention to control the disease.
Indicators of adult height outcome in classical 21-hydroxylase deficiency congenital adrenal hyperplasia.
OBJECTIVE: To obtain objective information on the relationship between adult height (AH), glucocorticoid (GC) dose, and degree of hormonal suppression in a population of patients with 21-hydroxylase deficiency congenital adrenal hyperplasia (21-OHD CAH) to optimize treatment regimes. STUDY DESIGN: Multicenter retrospective chart review of patients with salt wasting 21-OHD CAH diagnosed in the first 6 months of life, and who had reached AH (n = 54). The data were compiled into a single database. RESULTS: Mean adult height standard deviation score - midparental height standard deviation score was -1.1 for both sexes. Growth velocity was normal during childhood but compromised during infancy and puberty. Onset and tempo of puberty were normal-to-delayed. Bone age was closely correlated with chronologic age (r = 0.93). AH was negatively correlated with androstenedione in infancy (r -0.68; P =.03) and childhood (-0.66; P <.01) and with testosterone in childhood (r -0.44; P =.01), but not with dehydroepiandrosterone or 17-hydroxyprogesterone. GC dose was not associated with AH. CONCLUSIONS: Mean AH was in the lower range of genetic potential in this group of persons with 21-OHD CAH. Androgen levels should be used in conjunction with growth velocity measurements to optimize GC dosing in persons with 21-OHD CAH.
The prevalence of the HNF-1alpha G319S mutation in Canadian aboriginal youth with type 2 diabetes.
OBJECTIVE: To investigate the prevalence of the unique HNF-1alpha G319S mutation in a population of aboriginal youth with type 2 diabetes and to describe the relationship between clinical and historical characteristics and the presence or absence of the HNF-1alpha G319S mutation. RESEARCH DESIGN AND METHODS: Participating youth were genotyped for the G319S mutation of the HNF-1alpha gene. Clinical, laboratory, and historical data were collected via chart review (blinded to genotype results). Comparison data were derived from another study involving young nondiabetic pregnant aboriginal women. RESULTS: A total of 51 youth seen sequentially in a type 2 diabetes clinic participated in this study. Of these, 21 (41.2%) had at least one copy of the mutant allele. The allele frequency in the study population was 0.29 (95% CI 0.20-0.38), which was significantly different from the allele frequency of 0.13 in the comparison population (chi(2) = 6.78, P = 0.009). The frequency of the homozygous mutation (S319/S319) was 0.18. Mean BMI was significantly lower (P = 0.002), mean HbA(1c) was significantly higher (P = 0.02), and acanthosis nigricans was significantly less frequent (P = 0.004) in those with the mutation compared with the wild type. Mean insulin levels were lower and insulin sensitivity (assessed by homeostasis model assessment [HOMA]) was greater in the homozygote group compared with the wild-type group (P = 0.002 and P = 0.0007, respectively). A dose-dependent gradient was observed for these characteristics. CONCLUSIONS: These data support the association between the HNF-1alpha G319S mutation and early-onset type 2 diabetes in this population. Those with the mutation lacked clinical characteristics of insulin resistance (e.g., obesity and acanthosis nigricans) and had lower insulin levels, suggesting that an insulin-secretory and/or -production defect plays an important role in the development of diabetes in this group. Further investigation of the pathophysiology of the S319 homo- and heterozygote is needed because it may impact treatment and/or prevention of this disease.