Introduction and Objective: Women with T1D have increased risk of CVD. Whether CVD risk factors worsen during the menopausal transition is unclear. Methods: We conducted a secondary analysis of women who had undergone natural menopause (n=243) in the Epidemiology of Diabetes Interventions and Complications Study (EDIC), a prospective observational study of persons with T1D originally enrolled in the Diabetes Control and Complications Trial. Risk factors were assessed annually or biannually. We examined risk factors relation to the final menstrual period and fit linear models, consistent with chronologic aging, as well as piecewise models that would capture ovarian aging. Covariates included age at menopause, race, body mass index (BMI) at EDIC baseline, smoking, anti-hypertensives and lipid lowering medications, randomization group, complications at DCCT baseline (primary vs. secondary cohort), and exogenous estrogen use. Results: Although several CVD risk factors worsened during the menopausal transition, patterns of change were consistent with chronological aging and medication use. Despite suboptimal glycemic control, insulin dosing was lower postmenopause than premenopause. Conclusion: Women with T1D have worsening CVD risk factors during menopause consistent with chronologic aging. The high risk of CVD in women with T1D is unlikely due to adverse CVD risk factor changes during menopause. Disclosure C. Kim: None. D. Appiah: None. Z. Yin: None. J. Snell-Bergeon: None. E. Codner: None. Funding National Institutes of Health (R56HL169167)

Objective:To determine the degree of diabetes-specific distress in children with type 1 diabetes mellitus (T1DM) and its association with demographic characteristics, family and educational situation indicators, glycemic control, complications, and disease duration. Study design:A cross-sectional study (Jan-Mar 2025) in Argentina and Chile included 143 T1DM patients (8-17 years, ≥1-year duration). Diabetes distress was measured using the Problem Areas in Diabetes (PAID) questionnaire (0-80; high distress ≥40). Results:One hundred forty-three children (53.8%; 77 females), median age 13.4 years (IQR 11.5-15.8 years), T1DM duration 4.4 y (IQR 3.3-6.6 years), hemoglobin A1c (HbA1c) 8.5%, 69.8 mmol/mol (IQR 7.4%-9.4%), were included. The median PAID score was 25 (IQR 15-42), with 28% (95% CI: 20.6-35.3) experiencing high distress (PAID ≥ 40). HbA1c was higher in children with high distress 9.00% (IQR: 8.1%-10.4%) than in moderate 8.5% (IQR: 7.5%-9.7%) or low distress 7.8% (IQR: 7.0%-8.9%). There was a higher prevalence of children living with only one parent among those with high or moderate distress (33.3%, 95% CI: 24%-34%) compared to those with low distress (9.8%, 95% CI: 2%-18%). Multiple logistic regression analysis revealed that higher HbA1c values were significantly associated with being in the high distress group (OR = 1.48; 95% CI: 1.12-1.96 per % point HbA1c), adjusted for confounding variables. Conclusions:Diabetes distress was linked to higher HbA1c in Latin American children with T1DM. This suggests that addressing diabetes distress may contribute to improved glycemic control.

ContextThe prevalence of type 2 diabetes (T2D) and gestational diabetes (GD)among women of reproductive age has increased in recent decades, making it the most common pregnancy complication. Many studies have examined pregnancy complications in women with diabetes; however, the impact of diabetes on the intrauterine environment, specifically ovarian markers and metabolic profiles in very preterm infants at birth, has not been studied. This study aimed to investigate AMH, sex steroid levels, and the metabolic profile in venous cord blood (VCB) in gestations affected by type 2 diabetes (T2D) and gestational diabetes (GD).Material and methodsHormonal profile was evaluated in VCB of pregnancies with T2D (n=24), GD (n=26), and pregnancies without diabetes (C, n=25). Only pregnancies carrying a female offspring were included. AMH, sex steroids, and metabolic function biomarkers, including glucose, insulin, IGF-1, and adiponectin (APN) were measured. Clinical and anthropometric data were assessed in the mothers and offspring.ResultsAMH VCB levels were significantly higher in T2D than in GD and C pregnancies (P<0.01 and P<0.005, respectively). Dehydroepiandrosterone sulfate (DHEAS) and sex hormone-binding globulin (SHBG) VCB levels were lower in T2D pregnancies than in GD and C (P < 0.01, P < 0.0001, respectively). APN levels were lower in T2D pregnancies than in C (P < 0.05). Additionally, higher insulin and IGF-1 VCB levels and HOMA-IR index were observed in T2D than in C and GD (P < 0.001, P<0.05, and P<0.05, respectively). No significant correlations were observed between maternal and AMH, insulin, IGF-1, and androgen VCB levels.DiscussionT2D disrupts the intrauterine environment, leading to increased insulin, IGF-1, HOMA-IR, and AMH concentrations and decreased adiponectin levels in VCB. These findings describe the impact that maternal T2D may have on the health and development of their offspring.

The International Society for Pediatric and Adolescent Diabetes (ISPAD) guidelines represent a rich repository that serves as the only comprehensive set of clinical recommendations for children, adolescents, and young adults living with diabetes worldwide. This chapter builds on the 2022 ISPAD guidelines, and updates recommendations on the principles of intensive insulin regimens, including more intensive forms of multiple daily injections with new-generation faster-acting and ultra-long-acting insulins; a summary of adjunctive medications used alongside insulin treatment that includes details on pramlintide, metformin, glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1RA) and sodium-glucose cotransporter inhibitors; and key considerations with regard to access to insulin and affordability to ensure that all persons with diabetes who need insulin can obtain it without financial hardship.

Abstract Context Adolescents and young women (AYA) with type 1 diabetes (T1D) may require hormonal contraception for an extended period. However, it is unclear what effect hormonal contraception has on telomere length, a marker of the risk for complications. Objectives To investigate the relative telomere length (RTL) in AYA with T1D (AYA-T1D) and healthy young women (AYA-C) after 18 months of combined oral contraception use (COC) with ethinyl estradiol/desogestrel, or a subdermal etonogestrel implant (IM). Methods A non-randomized prospective study was performed. Thirty-nine AYA-T1D and forty AYA-C chose the COC or the IM. RTL was measured by monochrome multiplex quantitative PCR in DNA from peripheral blood mononuclear cells (PBMC). The impact of contraceptives and clinical variables on RTL was assessed using lineal regression analysis. Results Longer RTL compared to baseline was observed in AYA-T1D (P&lt; 0.05) and AYA-C (P&lt;0 .01) after using the IM. However, the total of AYA and the AYA-C group treated with COC decreased RTL after 18 months of treatment compared to baseline (P&lt; 0.05). The type of contraceptive used was determinant for the changes in RTL compared to baseline in all subjects and controls (P≤ .006). For AYA-T1D, HbA1c levels were not associated with RTL, but the high-sensitivity C-reactive protein was negatively related with the changes in RTL at eighteen months compared to baseline (standardized R2: .230, P=.003). Conclusion IM was associated with longer RTL in AYA-T1D and AYA-C. In contrast, a shortening of telomere length in PMNC was observed after using COC.

Study Objective: To determine the metabolic effects of the subcutaneous etonogestrel implant compared with an oral contraceptive in adolescents and young adults (AYAs) with type 1 diabetes (T1D) on body weight, body composition, glucose, lipids, and C-reactive protein levels. Methods: This was a non-randomized, interventional, prospective study. Thirty-nine AYAs with T1D participated; 20 used the implant (Implant-T1D), and 19 used an oral combined contraceptive (OC-T1D). Body composition, HbA1c, intermittent continuous glucose monitoring, lipids, and high-sensitivity C-reactive protein (hsCRP) levels were evaluated. Results: All participants were followed for at least 12 months, and 26 completed the 24-month follow-up. No women discontinued the intervention due to adverse effects. Body weight increased by 0.8 +/- 3.5 and 1 +/- 2.9 kg in the OC-T1D and the Implant-T1D group at 12 months and by 2.6 +/- 3.9 and 3.3 +/- 3.6 kg at 24 months, respectively. OC-T1D and Implant-T1D had similar HbA1c, mean interstitial glucose levels, and time in range throughout the study; no significant difference over time was observed. hsCRP levels increased in both groups and were associated with BMI and HbA1c (P < .001 for both variables). Women in the OC-T1D group had higher total cholesterol, HDL-C, and triglyceride levels compared with the Implant-T1D. Conclusion: Glucose levels were similar in youth using the subdermal progestin implant and an OC. However, both AYA groups showed increased BMI, fat mass, and subclinical inflammation. Changes in lipid levels were associated with the OC method. These data highlight the importance of weight gain prevention in young women with T1D using hormonal contraception.

Context: Adolescents and young women (AYA) with type 1 diabetes (T1D) may require hormonal contraception for an extended period. However, it is unclear what effect hormonal contraception has on telomere length, a marker of the risk for complications. Objective: To investigate the relative telomere length (RTL) in AYA with T1D (AYA-T1D) and healthy young women (AYA-C) after 18 months of combined oral contraception use (COC) with ethinyl estradiol/desogestrel, or a subdermal etonogestrel implant (IM). Methods: A nonrandomized prospective study was performed in which 39 AYA-T1D and 40 AYA-C chose the COC or the IM. RTL was measured by monochrome multiplex-quantitative PCR in DNA from peripheral blood mononuclear cells (PBMC). The impact of contraceptives and clinical variables on RTL was assessed using lineal regression analysis. Results: Longer RTL compared to baseline was observed in AYA-T1D (P < .05) and AYA-C (P < .01) after using the IM. However, the total of AYA and the AYA-C group treated with COC decreased RTL after 18 months of treatment compared to baseline (P < .05). The type of contraceptive used was determinant for the changes in RTL compared to baseline in all subjects and controls (P <= .006). For AYA-T1D, HbA1c levels were not associated with RTL, but the high-sensitivity C-reactive protein was negatively related with the changes in RTL at 18 months compared to baseline (standardized R-2: 0.230, P = .003). Conclusion: IM was associated with longer RTL in AYA-T1D and AYA-C. In contrast, a shortening of telomere length in PBMC was observed after using COC.

Section of Pediatric and Adult Endocrinology, Diabetes and Metabolism, Kovler Diabetes Center and Comer Children's Hospital, University of Chicago Medicine, Chicago, Illinois, USA Hôpital Universitaire Necker-Enfants Malades, Université de Paris Cité, INSERM U1016, Institut IMAGINE, Paris, France Department of Clinical Science, University of Bergen, and Children and Youth Clinic, Hauk eland University Hospital, Bergen, Norway Clinical Laboratory Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy National Severe Insulin Resistance Service, Cambridge University Hospitals NHS Trust, Cambridge, UK Endocrinology and Diabetes Research Group, Biocruces Bizkaia Health Research Institute, Cruces University Hospital, CIBERDEM, CIBERER, Endo-ERN, UPV/EHU, Barakaldo, Spain Department of Paediatric Endocrinology and Diabetology, Charité – Universitätsmedizin, Berlin, Germany Center for Endocrinology, Metabolism, Genetics and Molecular Therapy, Departement of Pediatric Endocrinology and Diabetes, Vietnam National Children's Hospital, Hanoi, Vietnam Department of Pediatrics and Department of Biology and Medical Genetics, Hanoi Medical University, Hanoi, Vietnam Department of Pediatrics, Prince Mohamed bin Abdulaziz Hopsital, National Guard Health Affairs, Madinah, Saudi Arabia Institute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, UK Institute of Maternal and Child Research, School of Medicine, University of Chile, Santiago, Chile

Polycystic ovary syndrome (PCOS) is one of the most common endocrine conditions in women. PCOS may be more challenging to diagnose during adolescence due to an overlap with the physiological events of puberty, which are part of the diagnostic criteria in adult women. This review focuses on the evidence available in relation to PCOS diagnostic criteria for adolescents. Adolescent PCOS should be diagnosed using two main criteria irregular -menstrual cycles (relative to number of years post-menarche) and hyperandrogenism (clinical and/or biochemical); after excluding other conditions that mimic PCOS. Accurate definitions of the two main criteria will decrease challenges/controversies with the diagnosis and provide timely diagnosis during adolescence to establish early management. Despite the attempts to create accurate diagnostic criteria and definitions, this review highlights the limited research in this area, especially in the follow up of adolescents presenting with one diagnostic feature that are called “at risk of PCOS”. Studies in adolescents continue to use the Rotterdam diagnostic criteria that uses pelvic ultrasound. This is inappropriate, because previous and emerging data that show many healthy adolescents have polycystic ovarian morphology in the early years post-menarche. In the future, anti-Müllerian hormone levels might help support PCOS diagnosis if adolescents meet two main criteria.

Department of Clinical Science and Education, Södersjukhuset, Karolinska Institute, Stockholm, Sweden Sachs' Children and Youths Hospital, Södersjukhuset, Stockholm, Sverige Parent and Advocate of Child with Type One Diabetes, Toronto, Ontario, Canada London Diabetes Centre, London Medical, London, UK Department of Health and Caring Sciences, Western Norway University of Applied Sciences, Bergen, Norway Medical Psychology Unit, Hannover Medical School, Hannover, Germany Department of Paediatrics and child health, Muhimbili National Hospital, Dar es Salaam, Tanzania Departement of peadiatrics and child health, Kilimanjaro Christian Medical University College, Moshi, Tanzania Department of Endocrinology, Hospital for Sick Children, Toronto, Ontario, Canada Pediatric Diabetology Unit, San Camilo Hospital, Medicine School, Universidad de Valparaiso, San Felipe, Chile Childhood, Adolescence & Diabetes, Toulouse Hospital, Toulouse, France Children with Diabetes and Department of Pediatric Endocrinology, Stanford University, California, USA Division of Endocrinology, Department of Pediatrics, Hospital for Sick Children, University of Toronto, Ontario, Canada

Department of Paediatrics, University of Otago, Christchurch, New Zealand Institute of Maternal and Child Research (IDMI), School of Medicine, Universidad de Chile, Santiago, Chile Institute of Endocrinology and Diabetes, Children's Hospital at Westmead, Sydney, Australia Discipline of Child and Adolescent Health, University of Sydney, Sydney, Australia Discipline of Paediatrics & Child Health, School of Clinical Medicine, University of New South Wales Medicine & Health, Sydney, Australia Department of Endocrinology & Diabetes, Queensland Children's Hospital, South Brisbane, Queensland, Australia Department of Chemical Pathology, Mater Pathology, South Brisbane, Queensland, Australia School of Clinical Medicine, Faculty of Medicine, The University of Queensland, Brisbane, Queensland, Australia Department of Pediatrics, Division of Endocrinology, Lucile Salter Packard Children's Hospital, Stanford University, Stanford, California, USA Stanford Diabetes Research Center, Stanford University, Stanford, California, USA Department of Epidemiology, Stanford University, Stanford, California, USA Division of Endocrinology, Department of Pediatrics, Hospital for Sick Children, University of Toronto, Toronto, Canada Department of Paediatrics, University of Cambridge and Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK Department of Pediatrics, Division of Pediatric Endocrinology and Diabetology, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana, USA

None of the authors has any conflicts of interest relevant to the subject matter of the article. The peer review history for this article is available at https://publons.com/publon/10.1111/pedi.13406. This article is an invited review/consensus statement. Data sharing is not applicable.

Jamie R. Wood has research grants unrelated to the current manuscript from the following: AstraZeneca, Novo Nordisk, Boehringer Ingelheim, and MannKind. Sabine E. Hofer has received lecturing honoraria from Eli Lilly, Sanofi, Medtronic, Pfizer, Insulet and Vertex. Ragnar Hanas has consulting activities unrelated to the current manuscript with Abbott, AstraZeneca and NovoNordisk. Warren Lee has consulted for NovoNordisk previously, and received speaking honoraria from Eli Lilly, Sanofi, Medtronic, Merck. None of these activities have conflicts with the current manuscript. The other authors have declared no conflicts of interest. The peer review history for this article is available at https://publons.com/publon/10.1111/pedi.13415. Data sharing is not applicable to this article as no new data were created or analyzed in this study.

Context First-degree relatives of women with polycystic ovary syndrome (PCOS) present hormonal and metabolic alterations compared to girls unrelated to PCOS. It is unknown whether glucose intolerance in the PCOS proband confers a more severe metabolic predisposition on their first-degree relatives. Objective To determine whether glucose tolerance status in women with PCOS is associated with worsened glucose metabolism and sex hormone levels in their peripubertal daughters or sisters. Design Cross-sectional study. Setting Seven academic centers in North America, South America, and Europe. Patients Sixty-four pairs of women with PCOS and their daughters or younger sisters aged between 8 and 14 years were recruited. Twenty-five mothers or older sisters with PCOS were glucose intolerant (GI) and 39 were normal glucose tolerant (NGT). Main Outcome Measures Beta-cell function estimated by the insulin secretion-sensitivity index-2 (ISSI-2) during an oral glucose tolerance test and by the disposition index during a frequently sampled IV glucose tolerance test. Free testosterone and 17-hydroxyprogesterone (17-OHP) levels. Results Being related to a GI PCOS proband was associated with a lower ISSI-2 (P-value = 0.032) after adjusting for ethnicity, body mass index z-score, and pubertal stage. They also had higher free testosterone (P-value = 0.011) and 17-OHP levels compared to girls with an NGT proband, the latter becoming significant after adjusting for confounders (P-value = 0.040). Conclusions Compared to first-degree female relatives of women with PCOS and NGT, first-degree relatives of women with PCOS and GI display lower beta-cell function and hyperandrogenemia, putting them at higher risk of GI and PCOS development.

Pediatric DiabetesVolume 23, Issue 8 p. 1277-1296 ISPAD GUIDELINES ISPAD Clinical Practice Consensus Guidelines 2022: Insulin treatment in children and adolescents with diabetes Eda Cengiz, Corresponding Author Eda Cengiz eda.cengiz@ucsf.edu University of California San Francisco (UCSF) Pediatric Diabetes Program, UCSF School of Medicine, San Francisco, California, USA Correspondence Eda Cengiz, Pediatric Diabetes Program, University of California San Francisco School of Medicine, 1500 Owens St. Suite 300, San Francisco, CA 94158, USA. Email: eda.cengiz@ucsf.eduSearch for more papers by this authorThomas Danne, Thomas Danne Auf Der Bult, Diabetes Center for Children and Adolescents, Hannover, GermanySearch for more papers by this authorTariq Ahmad, Tariq Ahmad Pediatric Endocrinology, UCSF Benioff Children's Hospital Oakland, Oakland, California, USASearch for more papers by this authorAhila Ayyavoo, Ahila Ayyavoo Department of Pediatrics, G. Kuppuswamy Naidu Memorial Hospital, Coimbatore, IndiaSearch for more papers by this authorDavid Beran, David Beran Division of Tropical and Humanitarian Medicine, Faculty of Medicine University of Geneva and Geneva University Hospitals, Faculty of Medicine Diabetes Centre, Geneva, SwitzerlandSearch for more papers by this authorSarah Ehtisham, Sarah Ehtisham Division of Pediatric Endocrinology, Mediclinic City Hospital, Dubai, UAESearch for more papers by this authorJan Fairchild, Jan Fairchild Department of Endocrinology and Diabetes, Women's and Children's Hospital, North Adelaide, AustraliaSearch for more papers by this authorPrzemyslawa Jarosz-Chobot, Przemyslawa Jarosz-Chobot Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, PolandSearch for more papers by this authorSze May Ng, Sze May Ng Paediatric Department, Southport and Ormskirk NHS Trust, Southport, UK Department of Women's and Children's Health, University of Liverpool, Liverpool, UKSearch for more papers by this authorMegan Paterson, Megan Paterson John Hunter Children's Hospital, HRMC, New South Wales, AustraliaSearch for more papers by this authorEthel Codner, Ethel Codner Institute of Maternal and Child Research (IDIMI), School of Medicine, University of Chile, Santiago, ChileSearch for more papers by this author Eda Cengiz, Corresponding Author Eda Cengiz eda.cengiz@ucsf.edu University of California San Francisco (UCSF) Pediatric Diabetes Program, UCSF School of Medicine, San Francisco, California, USA Correspondence Eda Cengiz, Pediatric Diabetes Program, University of California San Francisco School of Medicine, 1500 Owens St. Suite 300, San Francisco, CA 94158, USA. Email: eda.cengiz@ucsf.eduSearch for more papers by this authorThomas Danne, Thomas Danne Auf Der Bult, Diabetes Center for Children and Adolescents, Hannover, GermanySearch for more papers by this authorTariq Ahmad, Tariq Ahmad Pediatric Endocrinology, UCSF Benioff Children's Hospital Oakland, Oakland, California, USASearch for more papers by this authorAhila Ayyavoo, Ahila Ayyavoo Department of Pediatrics, G. Kuppuswamy Naidu Memorial Hospital, Coimbatore, IndiaSearch for more papers by this authorDavid Beran, David Beran Division of Tropical and Humanitarian Medicine, Faculty of Medicine University of Geneva and Geneva University Hospitals, Faculty of Medicine Diabetes Centre, Geneva, SwitzerlandSearch for more papers by this authorSarah Ehtisham, Sarah Ehtisham Division of Pediatric Endocrinology, Mediclinic City Hospital, Dubai, UAESearch for more papers by this authorJan Fairchild, Jan Fairchild Department of Endocrinology and Diabetes, Women's and Children's Hospital, North Adelaide, AustraliaSearch for more papers by this authorPrzemyslawa Jarosz-Chobot, Przemyslawa Jarosz-Chobot Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, PolandSearch for more papers by this authorSze May Ng, Sze May Ng Paediatric Department, Southport and Ormskirk NHS Trust, Southport, UK Department of Women's and Children's Health, University of Liverpool, Liverpool, UKSearch for more papers by this authorMegan Paterson, Megan Paterson John Hunter Children's Hospital, HRMC, New South Wales, AustraliaSearch for more papers by this authorEthel Codner, Ethel Codner Institute of Maternal and Child Research (IDIMI), School of Medicine, University of Chile, Santiago, ChileSearch for more papers by this author First published: 20 December 2022 https://doi.org/10.1111/pedi.13442Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat CONFLICT OF INTEREST E. Cengiz is a scientific advisor for Eli Lilly, Novo Nordisk, Adocia and Arecor. TD has received speaker's honoraria and research support from or has consulted for Astra Zeneca, Bayer, Boehringer, Dexcom, Eli Lilly, Lifescan, Medtronic, Novo Nordisk, Provention Bio, Roche, Sanofi, Ypsomed and is a shareholder of Drea Med Ltd. TA, JF, DB, SH, MP, E. Codner have no disclosures. Volume23, Issue8December 2022Pages 1277-1296 RelatedInformation