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Background With the onset of the COVID-19 pandemic and state-mandated school closures in the spring of 2020, the management of type 1 diabetes in children underwent significant changes. The aim of our study was to assess the effect of stay-at-home orders on glycemic control in children. Methods We conducted a retrospective review of 238 children with type 1 and type 2 diabetes who were seen in the Pediatric Endocrinology Clinic at the University of South Alabama. Average Hemoglobin A1c (A1c) levels in the year prior to stay-at home orders (May 2019–April 2020) were compared with A1c values during the quarantine period (May 2020–July 2020) using a paired t-test. We also analyzed the change of A1c level with respect to sex, race, type of diabetes, type of insurance, and mode of insulin administration, using a 2-sample t-test. Results The average A1c significantly increased from 9.2% during the previous year to 9.5% during the quarantine period (p = 0.0097). The increase of A1c was significantly higher in public insurance patients (0.49% increase) compared to private insurance patients (0.03% increase), (p = 0.0137). We also observed a significant association between the direction of change and type of insurance. Forty-eight percent of public insurance patients had an A1c increase of > 0.5% while 54% of private insurance patients had no change or decrease in A1c (p = 0.0079). Conclusions The COVID-19 pandemic resulted in worsening glycemic control in children with type 1 diabetes, with those on public insurance affected in greater proportion than those with private insurance.

Background: Acrodyostosis type 1 (ACRDYS1) is a rare skeletal dysplasia, and sometimes it can be misdiagnosed as pseudohypoparathyroidism type 1A (PHP1A), a subtype of Albright hereditary osteodystrophy (AHO), due to overlapping features. Growth hormone releasing hormone (GHRH) resistance with severe short stature is common in both ACRDYS1 and PHP1A (Emily L. Germain-Lee, et al. J Clin Endocrinol Metab, 88:4059-4069, 2003). Whereas growth hormone (GH) treatment has been studied in patients with PHP1a, the same is not true for the rarer ACRDYS1. Here in we report an adverse orthopedic outcome in a patient with ACRDYS1 with severe short stature treated with growth hormone. Our experience could have implications for the treatment of other patients with this disorder. Case presentation: We report a case of Legg-Calve-Perthes Disease (LCPD) in an 8-year old female with ACRDYS1 treated with GH. She initially presented with marked short stature (height Z-score − 3.46) with a low normal insulin like growth factor-1 (IGF1) level, and had biochemical evidence of thyrotropin and parathyroid hormone resistance. GH therapy was initiated at 0.35 mg/kg/week leading to increased growth velocity. After 7 months on GH, she developed right knee pain. Radiographic images revealed flattening of her right femoral head consistent with LCPD. GH was discontinued. Six weeks later, radiographs revealed further collapse of the entire femoral head. Her lesion stabilized after 8 months with conservative management and she never resumed GH. Her final adult height is 4′2″ (128 cm). Conclusion: Patients with ACRDYS1 on GH therapy may be at increased risk of LCPD. This has not been reported in patients with PHP1A treated with GH. Clinicians and families need to be aware of this potential complication when counseling about GH treatment.

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Objective: To describe new and unusual endocrinopathies in children with de novo 18q deletion (18q-) syndrome. Methods: We describe 2 patients who have atypical thyroid conditions and 1 who also developed symptomatic hypocalcemia. Results: The first patient developed hyperthyroidism at the age of 3 years, with a free thyroxine level of 3.9 (range, 0.8-1.8) ng/dL. Thyroid peroxidase antibodies were 262 (range, 0-32) IU/mL, and thyroidstimulating immunoglobulin antibodies were 384% (range, 0-139%). On low-dose methimazole treatment, she developed hypothyroidism. Thyroid-stimulating hormone (TSH) level was 163 (range, 0.4-4.5) mIU/mL. Moreover, she later developed growth hormone deficiency. The second patient developed hypothyroidism at the age of 4 years, with a TSH level of 46 mIU/mL. However, TSH remained elevated at levels of 10 to 24 mIU/mL for 3 years, despite appropriate treatment, suggesting TSH resistance. She then developed hypocalcemic seizures and was diagnosed with pseudohypoparathyroidism. Her total calcium level was 6.6 (range, 8.5-10.5) mg/dL and parathyroid hormone level was 432 (range, 15-65) pg/dL. Conclusion:The first patient had a mixed picture of autoimmune hypothyroidism and hyperthyroidism, requiring a combination of methimazole and levothyroxine to achieve a euthyroid state. For the second patient, the mild TSH resistance was possibly the early suggestion of a parathyroid hormone resistant state. Although growth hormone deficiency and hypothyroidism are common in patients with 18qsyndrome, the occurrence of hyperthyroidism due to Graves' disease with the coexistence of Hashimoto's hypothyroidism is rare. Pseudohypoparathyroidism has not yet been reported in patients with 18qsyndrome.