INTRODUCTION:Opioid-induced adrenal insufficiency (OIAI) is a known, but often overlooked complication associated with chronic opioid use. It is important to recognize OIAI as, if untreated, can lead to increased morbidity and mortality. AREAS COVERED:This narrative review discusses the prevalence, pathophysiology, diagnosis, and management of OIAI, with special emphasis on the current challenges. While investigations and treatment of OIAI is similar to other causes of adrenal insufficiency, it is important to recognize and test for other opioid-induced endocrinopathies. Furthermore, unlike some causes of adrenal insufficiency, OIAI has demonstrated reversibility following the discontinuation of opioids; therefore, cessation of opioids should be considered as a part of a multidisciplinary collaboration. EXPERT OPINION:Identification and appropriate treatment of patients with OIAI is important. Although recognition of this condition is increasing, further investigation is needed to identify additional risk factors to allow close follow-up of those at risk of OIAI or minimize the development OIAI.
INTRODUCTION:Chronic kidney disease (CKD) affects ~30-40% of people living with type-1 diabetes (T1D) and remains a major driver of cardiovascular morbidity, kidney-failure, and premature mortality. Despite advances in diabetes-technologies, kidney-protective pharmacotherapy in T1D has remained largely unchanged since the introduction of renin-angiotensin-system (RAS)-inhibition >30 years ago. In contrast, CKD-treatment in type-2 diabetes (T2D) has been transformed by sodium-glucose co-transporter (SGLT)-inhibitors, glucagon-like peptide (GLP)-1-based therapies, and nonsteroidal mineralocorticoid receptor antagonists. Exclusion of people with T1D from these pivotal trials created a critical evidence-gap. AREAS COVERED:We synthesizes mechanistic-/clinical evidence supporting a paradigm shift in kidney-protection for T1D. Literature searches of PubMed/MEDLINE, Embase, Web of Science, and ClinicalTrials.gov identified relevant English-language publications and ongoing studies through March 2026. We describe how the evolving T1D-phenotype, characterized by rising obesity and cardiometabolic dysfunction, strengthening the rationale for therapeutic translation. We critically evaluate current standards-of-care, unmet needs, and the renoprotective potential and safety of SGLT-inhibitors, GLP-1-based therapies, and finerenone in T1D, highlighting the pivotal FINE-ONE trial and albuminuria as a bridging biomarker for regulatory translation. EXPERT OPINION:CKD-management in T1D is entering a long-overdue phase of therapeutic renewal. Ongoing trials, 'pillar'-strategies, validated surrogate endpoints, precision-medicine, and multidisciplinary care may finally enable meaningful modification of CKD-trajectories.
INTRODUCTION:Resmetirom and semaglutide are the first drugs to be approved for the pharmacological treatment of metabolic-associated steatohepatitis (MASH) and moderate-to-severe liver fibrosis. However, approval was based on histological endpoints obtained during a relatively short trial period, leaving some important questions unanswered. AREAS COVERED:Resmetirom acts directly on the liver by activating thyroid hormone receptor β. Semaglutide acts systemically, reducing weight and improving metabolism. Both drugs induce resolution of MASH and improve liver fibrosis in a significant proportion of patients. The drugs are generally well tolerated, but significant gastrointestinal side effects can occur. Patient selection for treatment and efficacy evaluation should be based on noninvasive tests (NITs), but a substantial unresolved issue remains. Further issues include monitoring and the duration of treatment, as well as the impact of treatment on hepatic and systemic disease outcomes. Ensuring fair access to treatment for all is a challenge facing the global health community. EXPERT OPINION:This review explores the current approach to issues and challenges associated with using resmetirom and semaglutide in patients with MASH, proposing reference points to assist physicians in their clinical practice. Furthermore, we emphasize the importance of implementing interventions within the healthcare system to ensure equitable access to therapies.
INTRODUCTION:Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a rare genetic endocrine disorder characterized by impaired cortisol synthesis, excessive adrenal androgen production, and elevated adrenocorticotropic hormone (ACTH) concentrations. The current standard of care involves supraphysiologic doses of glucocorticoids to suppress ACTH and manage androgen excess, often leading to long-term complications. AREAS COVERED:A literature search of PubMed was conducted. This review critically examines the pharmacology, clinical efficacy, and potential role of crinecerfont in redefining CAH management. EXPERT OPINION:Crinecerfont, a selective corticotropin-releasing factor type 1 receptor (CRF1) antagonist, offers a novel therapeutic approach by targeting ACTH secretion at its hypothalamic origin. Recent Phase 2 and Phase 3 trials have demonstrated promising efficacy and safety across adult, adolescent, and pediatric populations. Crinecerfont may represent a promising adjunctive therapy in CAH management, addressing both biochemical control as well as quality of life and potentially long-term outcomes.
