Objective:While there is general agreement that patient education is essential for compliance, no objective tools exist to assess knowledge in children and parents of children with endocrine disorders. We aimed to design and validate a Pediatric Endocrine Knowledge Assessment Questionnaire (PEKAQ) for congenital hypothyroidism, Hashimoto’s thyroiditis, isolated growth hormone deficiency, Graves’ disease, and congenital adrenal hyperplasia. We evaluated baseline knowledge of children and parents of children with these disorders and assessed impact of educational intervention.Methods:At baseline, 77 children (12-18 years) and 162 parents of children 1-18 years participated in this prospective intervention study. Educational handouts for five targeted disorders were designed. Following one-on-one educational intervention, 55 children and 123 parents participated. Baseline and post-intervention knowledge scores were compared using McNemar’s test.Results:Adequate multi-rater Kappa measure of agreement was achieved for children’s (0.70) and parent’s (0.75) PEKAQs. Flesch Reading Ease Score for both PEKAQs (15 questions each) was 65. Post-intervention, significantly higher proportion of parents and children answered majority of questions correctly (p<0.05). Sixteen percent more parents and 22% more children knew their diagnosis correctly (p<0.05). Significant improvement was noted among all participants regarding reason for treatment, steps to take in a situation of missed dose, exercise and diet with these disorders, and long-term prognosis. Parent’s knowledge score was an independent predictor of child’s score.Conclusions:To our knowledge, this is the first validated PEKAQ that can be used widely in pediatric endocrinology clinics. We noted significant improvement in knowledge of children and parents of children with endocrine disorders.

We are reporting a case of SIADH hyponatremia and pan-hypopituitarism in an otherwise stable appearing non-functional pituitary macroadenoma on MRI that suddenly developed apoplexy. Patient is a 52-year-old hispanic male with a history of a pituitary adenoma diagnosed initially on 06/2017 during MRI head for chronic headaches. MRI Pituitary on 07/2018 showed “well-circumscribed lesion” measuring approximately 12.7 x 14.8 x 13.4 mm in AP. Hormonal work up was normal in 06/2017, 01/2018, and 07/2018. In 07/2018 labs showed: IGF-1 247 ng/mL (65–222), ACTH 28 pg/mL (7–69), random cortisol 8.58 microg/dL (3.09–22.4), TSH 2.3 mIU/mL (0.4–5.5), fT4 1.06 ng/dL (0.8–1.8), LH 4.6 mIU/mL (0.98–79.7), FSH 6.2 MIU/mL (1–18), prolactin 2.92 ng/mL (2.1–24), and testosterone 310 ng/dL (87–814). Oral glucose tolerance test was done and showed: GH was 0.34 ng/mL at baseline and 1.01 ng/mL after 75 g oral glucose (equivocal result). Repeat IgF1 was normal after that. Subsequently, patient was admitted on 09/24/2018 with severe headaches, nausea, vomiting, polyuria, and polydipsia. He was hypotensive and tachycardic and was found to be hyponatremic with a Na of 124, lowest at 119 where hypertonic saline was given at that point. Urine output was 1.5 L in 24 hours while he was on an 0.8 L fluid restriction, and then 6 L the following day while he was on 1.5 L fluid restriction, serum osmolality was 251, urine osmolality was 1003, urine specific gravity was &gt;1.030. Nephrology agreed to the diagnosis of SIADH. Blood work on 09/24 showed: random cortisol 0.67 microg/dL, TSH 0.19 mIU/mL, free T4: 0.63 ng/dL, ACTH 11 pg/mL, LH 2.4 mIU/mL, FSH 4.7 MIU/mL, testosterone 13 ng/dl. Patient was started on Levothyroxine 125 mcg and hydrocortisone stress dose. MRI brain was done and showed a pituitary macro-adenoma, measuring approximately 14 x 11 x 11 mm with no significant change in size since 6/30/2017, without optic nerve compression, no hemorrhage was mentioned. Work up for other causes of panhypopituitarism, i.e. hemochromatosis was done and was negative: Ferritin: 258 ng/mL (22–322). CT abdomen and pelvis was also done and showed normal adrenal glands. We thought about granulomatous infiltrative diseases like sarcoidosis since 1–25 (OH) vitamin D was high at 120 pg/mL (19.9–79.3). CT neck and chest was done but was negative for sarcoidosis or lymphadenopathy. Patient was seen outpatient by neurosurgery in 1/2019 and a repeat MRI was done which reported resolution of cystic and blood material from a pituitary adenoma, and per neurosurgery there is resolution of a pituitary cystic adenoma with apoplexy that now looks like a partial empty sella. Patient currently continues to be pan-hypopituitary requiring hydrocortisone, levothyroxine and testosterone replacement. SIADH has resolved. An otherwise non-functioning stable pituitary macroadenoma on MRI, can suddenly present as symptomatic apoplexy with SIADH and pan-hypopituitarism.

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Compared to multiple daily insulin injections (MDI), continuous subcutaneous insulin infusion (CSII) has proven to reach target HbA1c level with less frequent hypoglycemia, be more cost-effective, and improve quality of life. However, data on the effectiveness of CSII therapy in the African American population remain limited. The primary objective of our study was to compare the effectiveness of CSII therapy in lowering HbA1c levels in patients with type 1 diabetes (T1D) and type 2 diabetes (T2D) in a predominantly African American population. The secondary objective was to identify factors that affect the effectiveness of CSII. Participants were selected randomly from a list of patients currently receiving CSII at our institution’s diabetic clinic. Each patient’s consent was obtained over the phone or during a visit to the clinic. Primary data were collected with a questionnaire, whereas additional data, including HbA1c levels before and after starting CSII, were collected from medical records. A total of 57 participants were enrolled in the study. African Americans represented 79% of the participants; 43% of the participants were unemployed, and 56% had an annual income of less than 20,000 USD. Since commencing CSII therapy, all participants achieved a decrease in mean HbA1c level from 9.7% to 8.0% (P = 0.001), and that of African American participants decreased from 9.8% to 8.2%. Increase number of individuals at home was associated with less reduction in HbA1c levels after starting CSII therapy (P = 0.02). Overall, satisfaction with CSII therapy was high, and 63% of participants reported being very satisfied with the treatment. The mean BMI among participants while using MDI was 32.6 kg/m2 but significantly increased to 33.9 kg/m2 (P = 0.01) while using CSII. The increase in mean BMI after starting CSII therapy was significantly higher in participants with T2D than in ones with T1D (P = 0.001). While receiving MDI, female participants had a significantly higher mean BMI than their male counterparts (P = 0.02); however, that difference became nonsignificant after they began CSII therapy (P = 0.06). The level of physical activity after starting CSII therapy did not alter the risk of increased BMI. The results of our interim analysis indicate the significant effect of CSII in lowering HbA1c levels in all diabetic patients regardless of sex, race, BMI, type of diabetes, marital status, employment status, level of education, adherence to diabetic diet, physical activity, duration on CSII, and use of other antidiabetic medications. The significant increase in BMI once CSII therapy commenced may reflect the increase in insulin dose among patients who were not adherent to insulin while receiving MDI. Patients need to be aware of that side effect, and additional interventions for weight management may be considered for overweight and obese patients planning to start treatment with CSII.