This update, written by authors designated by multiple pediatric endocrinology societies (see List of Participating Societies) from around the globe, concisely addresses topics related to changes in GnRHa usage in children and adolescents over the last decade. Topics related to the use of GnRHa in precocious puberty include diagnostic criteria, globally available formulations, considerations of benefit of treatment, monitoring of therapy, adverse events, and long-term outcome data. Additional sections review use in transgender individuals and other pediatric endocrine related conditions. Although there have been many significant changes in GnRHa usage, there is a definite paucity of evidence-based publications to support them. Therefore, this paper is explicitly not intended to evaluate what is recommended in terms of the best use of GnRHa, based on evidence and expert opinion, but rather to describe how these drugs are used, irrespective of any qualitative evaluation. Thus, this paper should be considered a narrative review on GnRHa utilization in precocious puberty and other clinical situations. These changes are reviewed not only to point out deficiencies in the literature but also to stimulate future studies and publications in this area.
In obesity, adipose tissue (AT) and liver are infiltrated with Th‐1 polarized immune cells, which are proposed to play an important role in the pathogenesis of the metabolic abnormalities of obesity. Aging is also associated with increased adiposity, but the effects of this increase on inflammation and associated metabolic dysfunction are poorly understood. To address this issue, we assessed insulin resistance (IR) and AT and liver immunophenotype in aged, lean (AL) and aged, obese (AO) mice, all of whom were maintained on a standard chow diet (11% fat diet) throughout their lives. For comparison, these variables were also assessed in young, lean (YL) and young diet‐induced obese mice (41% fat diet, YO). Despite similar body weight and fat accumulation, YO mice were substantially more IR and had greater liver steatosis compared to AO mice. YO also had elevated infiltration of macrophages/dendritic cells in AT and liver, but these increases were absent in AO. Furthermore, liver immune cells of YO were more Th‐1 polarized then AO. Notably, aging was associated with accumulation of T cells, but this occurred independent of obesity. Together, the data suggest that reduced inflammation in AO underlies the improved insulin sensitivity and lowered steatosis compared to YO.
The majority of patients with Type 1 Diabetes Mellitus (T1D) present with similar symptoms including polyuria, polydipsia, weight loss and fatigue. Unfortunately, some patients progress to diabetic ketoacidosis (DKA) at the time of diagnosis of T1D 1 . Children diagnosed in DKA have increased risk of morbidity, mortality, poor glycaemic control, higher medical costs and healthcare resource utilization including ICU level care 1,2 . Previous research has identified the predictors for children to present in DKA, which include younger children (under 5 years of age), Hispanic or African American race, low socioeconomic status, misdiagnosis at an initial clinical encounter and lack of private health insurance 3 . Thus far, there are limited data on the impact of the COVID-19 pandemic on the rate and severity of DKA in children at initial diagnosis of T1D. Interestingly, some geographic locations noted an increase in DKA frequency during the
Noonan syndrome (NS) is associated with short stature. Growth hormone treatment has been FDA approved for use in these patients. Children with NS are at a higher risk of developing benign and malignant proliferative disorders, primary brain tumors being one of them. Since growth hormone therapy can worsen the tumor burden, screening with a brain MRI prior to growth hormone initiation in NS patients is strongly recommended. Here we present two NS patients who developed different primary brain tumors while being on growth hormone therapy.
Background Self-management of type 1 diabetes (T1D) requires numerous decisions and actions by people with T1D and their caregivers and poses many daily challenges. For those with T1D and a developmental disorder such as autism spectrum disorder (ASD), more complex challenges arise, though these remain largely unstudied. Objective This study aimed to better understand the barriers and facilitators of raising a child with T1D and ASD. Secondary analysis of web-based content (phase 1) and telephone interviews (phase 2) were conducted to further expand the existing knowledge on the challenges and successes faced by these families. Methods Phase 1 involved a qualitative analysis of publicly available online forums and blog posts by caregivers of children with both T1D and ASD. Themes from phase 1 were used to create an interview guide for further in-depth exploration via interviews. In phase 2, caregivers of children with both T1D and ASD were recruited from Penn State Health endocrinology clinics and through the web from social media posts to T1D-focused groups and sites. Interested respondents were directed to a secure web-based eligibility assessment. Information related to T1D and ASD diagnosis, contact information, and demographics were collected. On the basis of survey responses, participants were selected for a follow-up telephone interview and were asked to complete the adaptive behavior assessment system, third edition parent form to assess autism severity and upload a copy of their child’s most recent hemoglobin A1c (HbA1c) result. Interviews were transcribed, imported into NVivo qualitative data management software, and analyzed to determine common themes related to barriers and facilitators of raising a child with both ASD and T1D. Results For phase 1, 398 forum posts and blog posts between 2009 and 2016 were analyzed. Common themes related to a lack of understanding by the separate ASD and T1D caregiver communities, advice on coping techniques, rules and routines, and descriptions of the health care experience. For phase 2, 12 eligible respondents were interviewed. For interviewees, the average age of the child at diagnosis with T1D and ASD was 7.92 years and 5.55 years, respectively. Average self-reported and documented HbA1c levels for children with T1D and ASD were 8.6% (70 mmol/mol) and 8.7% (72 mmol/mol), respectively. Common themes from the interviews related to increased emotional burden, frustration surrounding the amount of information they are expected to learn, and challenges in the school setting. Conclusions Caregivers of children with both T1D and ASD face unique challenges, distinct from those faced by caregivers of individuals who have either disorder alone. Understanding these challenges may help health care providers in caring for this unique population. Referral to the diabetes online community may be a potential resource to supplement the care received by the medical community.
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