The prevalence of gestational diabetes mellitus (GDM) continues to rise and is estimated to affect 14% of women worldwide. It is well established that early identification and treatment of GDM can improve maternal and fetal outcomes. While hyperglycemia typically resolves after delivery, metabolic risks to mother and offspring persist postpartum and continued surveillance is essential to prevent long-term complications. Women with prior GDM have increased risk of future type 2 diabetes (T2D), cardiovascular disease (CVD), and recurrence of GDM. There is evidence-based support for the prevention of diabetes following GDM, with both intensive lifestyle modification and metformin. Although specific data on how to decrease CVD risk in women with GDM are not currently available, it is prudent to apply general CVD recommendations to these women. Women with a history of GDM should have long-term monitoring and continued counseling, including family planning, with proactive approaches to reduce future risk of progression to diabetes and cardiovascular disease.

Lipoprotein(a) [Lp(a)] is a common, genetically determined lipoprotein that is independently associated with myocardial infarction, stroke, peripheral artery disease, and calcific aortic stenosis. Because Lp(a) levels are stable over time and minimally influenced by lifestyle, the 2026 ACC/AHA/Multisociety Dyslipidemia Guideline now recommends one-time measurement in all adults and cascade screening in high-risk families; as a result, endocrinologists can expect to encounter and manage elevated Lp(a) frequently in routine clinical practice. Despite its clinical importance, no approved drug therapies specifically targeting Lp(a) yet exist, therefore management should currently focus on aggressive optimization of traditional risk factors, particularly LDL-C lowering with statins and selective use of adjunctive therapies such as PCSK9 inhibitors and lipid apheresis. Emerging evidence suggests potential benefit of selective aspirin use, while novel therapeutics - anti-sense oligonucleotides and small interfering RNAs - which robustly lower Lp(a) are currently being tested in phase 3 clinical trials. We present case-based examples to highlight practical approaches to risk assessment and management of elevated Lp(a).

Inequities in diabetes diagnosis, management, and outcomes are deeply rooted in social determinants of health and structural racism. Historical policies such as redlining and concentrated poverty in low-income neighborhoods have shaped environments characterized by limited access to healthy food and proper healthcare, which ultimately led to a disproportionate burden of diabetes in these populations. The consequences of these disparities for racial and ethnic minoritized groups include a lower ability to achieve glycemic targets, receive novel glucose-lowering agents, and/or have access to diabetes technology. The downstream effect is that this population experiences worse health outcomes from complications (i.e., amputation, blindness, end-stage renal disease) and mortality. This narrative review synthesizes current literature on racial/ethnic inequities in diabetes care, highlighting differences in screening, glycemic control, complication rates, and mortality in people living with diabetes from diverse racial and ethnic backgrounds, but also identifies opportunities for intervention to ensure equitable access to evidence-based care.

Autoimmune polyendocrine syndrome type 1 (APS-1), also known as Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), is a monogenic disorder of impaired central immune tolerance classically inherited in an autosomal recessive manner and caused by biallelic deleterious variants in the autoimmune regulator (AIRE) gene, leading to chronic mucocutaneous candidiasis (CMC) and multiorgan autoimmunity. Although hypoparathyroidism and adrenal insufficiency are among the most common and clinically consequential manifestations, it is increasingly recognized that several non-endocrine features - including autoimmune enteritis, urticarial eruption (termed APECED rash), enamel hypoplasia, autoimmune pneumonitis, and autoimmune hepatitis - often precede classical endocrinopathies, contributing to delayed diagnosis. Endocrinologists are often among the first specialists to encounter these patients and play a central role in early recognition and longitudinal care. Here we present five cases that illustrate the expanding clinical spectrum of APS-1, novel genetic mechanisms, key diagnostic challenges, and emerging therapeutic approaches. These cases highlight the importance of applying expanded clinical criteria and recognizing the limitations of standard genetic testing, including the need to consider deep intronic and dominant-negative AIRE variants. Finally, evolving mechanistic insights have established APS-1 as an interferon-γ (IFN-γ)-driven disease, providing a rationale for emerging targeted immunomodulatory therapies such as Janus kinase (JAK) inhibition with ruxolitinib. Early diagnosis enables proactive surveillance and may allow timely initiation of disease-modifying treatment.

Identifying imminent fracture risk is a critical opportunity to manage osteoporosis. This term refers to the sharply elevated probability of sustaining a subsequent fragility fracture within a determined period-typically 12 to 24 months-after an initial sentinel fracture. While a prior fracture is widely recognised as a primary predictor of future events, epidemiological data show that this risk is not uniform; rather, it peaks significantly within the first 3 to 6 months after injury. This review discusses a significant clinical gap: traditional assessment tools often focus on long-term, 10-year risk projections, which may delay treatment during this high-vulnerability period. Recognising imminent risk highlights clinical urgency, indicating the need for early use of therapeutic interventions to rapidly reduce the risk of further fractures. Identifying patients at imminent risk offers an opportunity for secondary prevention, promoting immediate pharmacological action to interrupt the 'fracture cascade' and enhance long-term skeletal health.