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1.
Pediatr Diabetes ; 10(8): 554-62, 2009 Dec.
Article in English | MEDLINE | ID: mdl-19496963

ABSTRACT

Children and adolescents with type 1 diabetes mellitus (T1DM) are at risk for a variety of problems at school. Well-controlled studies using data collected in schools, however, are limited. The purposes of this study are to determine whether selected school problems are associated with T1DM and to investigate an association between these problems and medical variables. Teachers rated 95 diabetic students (M = 11.8; SD = 3.0 yr old) and 95 of their siblings (M = 12.1; SD = 3.0 yr old) regarding academic skills, work completion, day-to-day variability, and classroom attention. Medical and school records also were accessed. The T1DM group had lower academic skills ratings overall (p < 0.02), especially in writing (p < 0.01), a trend toward poorer classroom attention (p < 0.08), and many more missed school days (p < 0.001). Diabetics on intensive therapy protocols had better academic ratings overall (p < 0.02), including in math (p < 0.03) and fewer missed school days (p < 0.03), but they unexpectedly were rated as having more classroom behaviors that jeopardize work completion (p < 0.05) than counterparts on conventional therapy. Among all diabetics, glycated hemoglobin (HbA(lc)) levels were moderately related to each academic skill rating (r = -0.34 to -0.37; p < 0.01) and strongly related to classroom attention (r = 0.53; p = 0.000). T1DM itself appears to be a relatively minor influence to several important aspects of school. Furthermore, although intensive therapy alone may well promote school success, meticulous glycemic control, however achieved, appears more important in mitigating prospective classroom attention and academic problems.


Subject(s)
Diabetes Mellitus, Type 1 , Students/statistics & numerical data , Absenteeism , Adolescent , Attention , Child , Cognition , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/physiopathology , Diabetes Mellitus, Type 1/psychology , Educational Status , Female , Humans , Male , Risk Factors , Siblings , Surveys and Questionnaires
2.
Endocr Pract ; 13(7): 716-20, 2007.
Article in English | MEDLINE | ID: mdl-18194927

ABSTRACT

OBJECTIVE: To investigate taste, a component of flavor perception, using electrogustometry (EG) in patients with congenital anosmia associated with Kallmann syndrome (KS). METHODS: Four patients with KS and 4 control subjects participated in this study. During the first phase of the investigation, the study subjects were administered the University of Pennsylvania Smell Identification Test. During the second phase of the study, EG testing of 2 regions on the anterior tongue tip was performed through an electrode. RESULTS: Patients with KS, as expected, scored in the anosmic range on the University of Pennsylvania Smell Identification Test, whereas the control group had a normal sense of smell. The difference in the olfaction scores was significant between the 2 study groups (P<0.015). The result of taste assessment of patients with KS and control subjects with use of EG was not significantly different between the 2 study groups (P = 0.874). CONCLUSION: The current study demonstrates that patients with KS have a normal sense of taste, as determined by EG. This finding is consistent with the fact that the deficit in KS is purely olfactory. Because flavor perception is not a common complaint in patients with this condition, it may be postulated that persons with KS compensate for the absent sense of smell. Further studies need to be undertaken to explore how patients with KS compensate for the olfactory dysfunction, information that should contribute to the understanding of the interplay of the various components of flavor perception.


Subject(s)
Kallmann Syndrome/complications , Kallmann Syndrome/physiopathology , Olfaction Disorders/congenital , Olfaction Disorders/etiology , Taste/physiology , Electric Stimulation , Estradiol/blood , Female , Follicle Stimulating Hormone/blood , Humans , Luteinizing Hormone/blood , Male , Models, Biological , Smell , Testosterone/blood
3.
Endocr Pract ; 11(2): 104-7, 2005.
Article in English | MEDLINE | ID: mdl-15901525

ABSTRACT

OBJECTIVE: To describe a patient with aldosterone synthase deficiency, who presented with failure to thrive, hypovolemic hyponatremia, and the unexpected finding of hypertension. METHODS: We present a case report, review the related literature, and outline a possible mechanism for the concomitant occurrence of high blood pressure and hyponatremia in this patient. RESULTS: A 5-month-old infant with unambiguous female genitalia was admitted to our hospital with failure to thrive and hyponatremia. Her blood pressure was 115/88 mm Hg (>95% for age). The serum sodium concentration was 123 mEq/L (normal for age, >130), and the potassium level was 5.3 mEq/L (normal, 3.5 to 5.3). A direct renin measurement by immunochemiluminescence assay was 11,400 microU/mL (normal, <5), and the aldosterone level was 4 ng/dL (normal, 2 to 70). These findings indicated a diagnosis of aldosterone synthase deficiency. Treatment with fludrocortisone and sodium chloride was begun, but the hypertension worsened. Therapy with an angiotensin-converting enzyme inhibitor was transiently required. CONCLUSION: Angiotensin II, a potent vasoconstrictor, is an intermediate in the renin-angiotensin system. We believe that this protein was the cause of the hypertension in the setting of aldosterone deficiency in our patient.


Subject(s)
Hypertension/etiology , Hypoaldosteronism/complications , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/therapeutic use , Blood Pressure/drug effects , Cytochrome P-450 CYP11B2/deficiency , Drug Therapy, Combination , Failure to Thrive , Female , Fludrocortisone/adverse effects , Fludrocortisone/therapeutic use , Humans , Hypertension/drug therapy , Hypertension/physiopathology , Hypoaldosteronism/etiology , Hypoaldosteronism/physiopathology , Hyponatremia/etiology , Infant , Sodium Chloride/adverse effects , Sodium Chloride/therapeutic use , Steroid Metabolism, Inborn Errors/complications
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