Primary Adrenal Insufficiency Masked by an Eating Disorder Diagnosis in an Adolescent Male.

We describe a 14-year-old male who was followed for several years for the diagnoses of avoidant restrictive food intake disorder and generalized anxiety disorder before being diagnosed with primary adrenal insufficiency (PAI) or Addison disease. The patient presented multiple times to different facilities with worsening symptoms of anorexia, nausea, vomiting, and anxiety in the months leading up to diagnosis of PAI. Dehydration and hypotension, occurring relatively late in the course of his illness, were attributed to poor intake and vomiting. Hyponatremia was attributed to his psychotropic medication, olanzapine, and to dehydration. During his third hospitalization, he was diagnosed with PAI; treatment with stress-dose glucocorticoid therapy resulted in rapid clinical improvement. This case serves as a reminder that adrenal insufficiency must be considered in the differential diagnosis of eating disorders because signs and symptoms of adrenal insufficiency can overlap and progress insidiously. Additionally, we recognize that the diagnostic process is intertwined with a patient's medical history and use this opportunity to discuss cognitive, specifically anchoring, bias in academic medicine.

Progression from prediabetes to type 2 diabetes mellitus in adolescents: a real world experience.

Background: Obesity in pediatric patients is strongly associated with increased vascular and metabolic risk. Prediabetes is present in up to 1 in 5 adolescents, aged 12-18 years-old, though is thought to remit spontaneously in a significant portion. Pediatric patients with type 2 diabetes mellitus (T2D) have a more rapid decline of beta-cell function and progression to treatment failure than adult T2D patients. Thus, there is a strong interest in better understanding the natural history of prediabetes in these youth. We aimed to evaluate the real-world rate of progression of prediabetes to T2D in adolescent patients. Methods: This is a retrospective study of 9,275 adolescent subjects aged 12-21 years-old with at least 3 years of de-identified commercial claims data and a new diagnosis of prediabetes during the observation period. Enrollees with a T2D diagnosis and/or diabetes medication use in the 1 year prior to prediabetes diagnosis or a T2D diagnosis in the 1 month following prediabetes diagnosis were excluded. Enrollees with diagnoses of type 1 diabetes (T1D) or polycystic ovarian syndrome over the 3 years were also excluded. Progression to T2D was defined by claims data of two T2D diagnoses at least 7 days apart, HbA1c ≥ 6.5%, and/or prescription of insulin without known T1D. Enrollees were followed for 2 years after prediabetes diagnosis. Results: Overall, 232 subjects (2.5%) progressed from prediabetes to T2D. There were no differences found in T2D progression based on sex or age. Progression to T2D occurred at a median of 302 days after prediabetes diagnosis (IQR 123 to 518 days). This study was limited by the lack of laboratory/anthropometric data in administrative claims, as well as the exclusion of 23,825 enrollees for lack of continuous commercial claims data over 3 years. Conclusion: In the largest sample to date on adolescent prediabetes, we found a 2.5% progression of prediabetes to T2D over a median duration of about one year.

Tirzepatide: Does the Evidence to Date Show Potential for the Treatment of Early Stage Type 2 Diabetes?

Tirzepatide is a novel "twincretin" with glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonist activity, which was recently approved by the Food and Drug Administration for the treatment of type 2 diabetes mellitus. In this review, we discuss preclinical and mechanistic human studies, which demonstrate improvements in insulin sensitivity and beta-cell function with the use of tirzepatide, as compared to placebo and glucagon-like peptide 1 receptor agonists. We then discuss SURPASS trials 1-5, which evaluated the safety and efficacy of tirzepatide for type 2 diabetes mellitus as either monotherapy or combination therapy with other antidiabetic agents. The magnitude of tirzepatide's effects and the efficacy relative to other anti-diabetes medications on weight, glycemic control, and beta-cell function may prove beneficial for the treatment of early type 2 diabetes mellitus. Further studies, including data on cardiovascular outcomes and long-term safety, will continue to elucidate the role of tirzepatide in the treatment algorithm of type 2 diabetes mellitus.

The effects of adolescent laparoscopic adjustable gastric band and sleeve gastrectomy on markers of bone health and bone turnover.

25-hydroxy vitamin D (25 OHD) deficiency and secondary hyperparathyroidism have been seen after metabolic and bariatric surgery, but data are lacking on the bone health outcomes of adolescent sleeve gastrectomy (SG). The purpose of this study was to examine bone-related nutrition after SG, compared to laparoscopic adjustable gastric band (LAGB), and trend bone turnover markers following SG. This is an observational study of 197 adolescents who underwent LAGB (n = 98) or SG (n = 99). Bone health labs were collected at baseline and 6 and/or 12 months after LAGB or SG, with additional analysis of bone turnover markers in the SG group. Calcium and 25 OHD levels increased at 6 and 12 months after LAGB and SG, with no difference between the surgeries. Parathyroid hormone levels decreased only in the SG group. SG patients had increased osteocalcin and carboxy-terminal cross-linking telopeptide of type 1 collagen (CTX) at 6 and 12 months post-SG, although CTX decreased between 6 and 12 months. Excess weight loss at 6 months predicted the rise in CTX, but the changes in osteocalcin and CTX could not be attributed to 25 OHD deficiency, hypocalcemia or hyperparathyroidism. Patients had improved 25 OHD levels post-surgery, which may be secondary to stringent vitamin supplementation guidelines. However, there were marked increases in bone turnover markers following SG. More studies are needed to evaluate the effects of SG on adolescent bone health and to correlate the early changes in bone turnover with bone mineral density and fracture risk.

The Laboratory Features of Congenital Hypothyroidism and Approach to Therapy.

Congenital hypothyroidism (CH) is one of the most common preventable causes of intellectual disability. Thyroid hormone is required for normal brain development, but neonates with CH typically appear healthy at birth, which leads to delays in diagnosis and treatment. In developed countries, newborn screening programs have led to earlier diagnosis and treatment of CH, resulting in improved neurodevelopmental outcomes. Neonates with an abnormal newborn screen require prompt confirmatory serum thyroid function tests and treatment with thyroid hormone. Further evaluation for the etiology of CH should not delay treatment decisions.