Factitious thyrotoxicosis is the presence of excess circulating thyroid hormone from an exogenous source. It can be iatrogenic or it can occur due to intentional thyroid hormone misuse or abuse. It can also occur due to accidental ingestion, pharmacy error, or inadvertent exposure to unlabeled thyroid hormone in supplements or contaminated hamburger meat. Consequences range from mild thyrotoxic symptoms to more serious or life-threatening sequelae including thyrotoxic periodic paralysis, seizure, coma, arrhythmias, myocardial infarction, and thyroid storm. If unclear from the history, differentiating factitious thyrotoxicosis from other etiologies of thyroid hormone excess is challenging, and may require radioactive iodine uptake and serum thyroglobulin testing. In most cases, treatment simply consists of stopping the exogenous thyroid hormone exposure with subsequent monitoring. However, in cases of massive acute poisoning with thyroid hormone, gastric decontamination strategies and inpatient care in a monitored setting with measures to reduce circulating T3 levels may be needed.

First-trimester ultrasound, performed between 11 and 14 weeks' gestation, has become a cornerstone of modern prenatal care, supporting early risk assessment and guiding subsequent pregnancy management. This review summarises current principles, clinical applications, and practical considerations in first-trimester ultrasound, including confirmation of viability, accurate pregnancy dating, determination of chorionicity in multiple pregnancies, and early anatomical assessment. The scan also enables screening for chromosomal abnormalities through measurement of nuchal translucency and evaluation of additional sonographic markers, while complementing non-invasive prenatal screening by providing essential structural information. Systematic assessment further allows early detection of major fetal anomalies, evaluation of placental location and placenta accreta spectrum risk, screening for pre-eclampsia, and identification of uterine or adnexal pathology. Emphasis is placed on standardised protocols, operator training, appropriate equipment, and optimisation of imaging techniques to maximise diagnostic accuracy. As technology and expertise continue to advance, first-trimester ultrasound plays an increasingly central role in improving maternal and fetal outcomes through early, integrated prenatal evaluation.

Clinical and research imaging have been instrumental in shifting our understanding of osteoarthritis from a structural, cartilage-focused disorder to a whole-joint complex disease with biomechanical and inflammatory components. Initially, the only osteoarthritis imaging modality was x-ray; therefore, the focal point of diagnosis was the bone: osteophytes, sclerosis, but most importantly, the joint space narrowing. Soft-tissue visualization, dynamic imaging, and advanced image analysis techniques have shown that numerous other joint tissues and features are associated with osteoarthritis progression and symptom severity, and many of them appear before joint space narrowing is detectable. Inflammatory features like bone marrow lesions and effusion-synovitis have emerged as promising targets for intervention. The exact pathogenesis of and structure-modifying treatments for osteoarthritis remain elusive. Clinical and research imaging modalities are essential tools for monitoring the initiation and progression of the disease, identifying targets for intervention, and quantifying the impact of new treatments.

Major guidelines recommend exercise for hip and knee osteoarthritis (OA), yet few provide guidance on how to prescribe it. This narrative review synthesizes high-quality and clinically relevant evidence on exercise therapy for hip or knee OA, prioritizing systematic reviews and randomized controlled trials. Findings were summarized across nine topics, with a focus on translating the evidence into specific guidance for clinicians. Clinicians should consider measuring pain, physical function, quality of life, and global assessment for most patients with hip or knee OA. When educating about OA, clinicians should focus on what patients can do and avoid impairment-based language. Exercise therapy is safe and provides small to moderate improvements in pain and function, although effects appear smaller for hip OA than for knee OA. No exercise type has proven superior, nor has a dose-response relationship been established. Patients with higher baseline pain and poorer function may benefit somewhat more, but effects differ little across other patient characteristics, including comorbidity burden and radiographic severity. Whether increasing adherence leads to greater improvements in pain and function remains unclear, but helping patients start and sustain exercise remains a priority, given its wide-ranging health benefits. In-person, telehealth, and self-directed delivery can all improve pain and function, and they appear to offer benefits of similar magnitude. Overall, exercise is safe, with the most common adverse event being temporary muscle or joint soreness. Clinicians do not need to search for an optimal program but can instead build one around the patient's priorities, preferences, and needs.

Osteoarthritis (OA) is a common condition affecting nearly 600 million people worldwide, resulting in significant morbidity and disability. This paper reviews the latest updates on the systemic and local risk factors associated with development and progression of this disease. Some systemic risk factors, such as increasing age and obesity for example, have been well-established as strong risk factors for decades. Other potential risk factors such as smoking, nutritional deficiencies, and various medication exposures are less well-understood currently and require further investigation. The review of local risk factors focuses on congenital and acquired abnormalities that contribute to OA development such as joint malalignment, leg length discrepancy, and prior injury among others. This overview of OA risk factors highlights the importance of identifying modifiable risk factors as targets for treatment and progression-prevention in patients with OA as well as for the purpose of risk stratification and prevention in unaffected individuals.

Artificial intelligence (AI) is increasingly influencing clinical care and research in osteoarthritis and osteoporosis. For patients, AI can broaden access to health information, including understanding of disease and treatment options. For clinicians, AI-based systems may assist risk stratification and decision-making, including identifying individuals most likely to benefit from specific therapies. In medical imaging, AI approaches can grade osteoarthritis severity, identify occult pathology (including atypical femoral fractures), and estimate low bone mineral density from non-dedicated examinations. In research, AI can facilitate analysis of complex, high-dimensional datasets (e.g., multi-omics and cell-cell communication) supporting the discovery of biomarkers, candidate therapeutic targets and disease endotypes. Emerging directions include agentic AI systems for end-to-end workflows, adaptation of foundation models pre-trained on large, diverse datasets, and carefully evaluated synthetic data for augmentation and validation/quality-control pipelines. This review examines current and emerging AI applications across osteoarthritis and osteoporosis, and pathways for safe, equitable and effective deployment.

Osteoporosis is increasingly recognized as a heterogeneous syndrome rather than a single disease, driven by diverse pathophysiological mechanisms. Subtypes-including postmenopausal estrogen deficiency, age-related bone loss, anorexia nervosa, and GLP-1 receptor agonist-associated weight loss-exhibit distinct bone turnover, fracture patterns, and therapeutic responses. Recent studies have established bone marrow adipose tissue (BMAT) as a critical regulator of the marrow microenvironment in postmenopausal and age-related bone loss. Weight loss of various origins-anorexia, GLP-1 agonists, caloric restriction, and intermittent fasting-impairs bone through reduced mechanical loading, hormonal alterations, IGF-1 resistance, adipokine dysregulation, and mesenchymal stem cell lineage shifts. Parathyroid hormone (PTH) shows bidirectional effects, with continuous exposure promoting resorption and intermittent stimulation enhancing formation, providing a rationale for subtype-guided therapy. Exercise exerts skeletal benefits via mechanical loading, myokines, autophagy, non-coding RNAs, and epigenetics, with effects varying by type and combination. This review synthesizes these mechanistic advances, differentiates the skeletal consequences of weight loss by etiology, and discusses the clinical application of PTH analogs, sclerostin antibodies, and tailored exercise prescriptions in personalized osteoporosis care.

Sarcopenia is a progressive skeletal muscle disorder characterised by reduced muscle strength, impaired muscle quantity or quality, and declining physical performance, with important consequences for falls, fractures, disability, and loss of independence. Whether sarcopenia prevalence itself is rising remains difficult to quantify because diagnostic frameworks and surveillance methods vary, yet a growing burden is plausible. Population ageing, increasing multimorbidity, obesity, hospitalisation, surgery, and incomplete recovery after musculoskeletal events are likely to increase the absolute number of people living with low musculoskeletal reserve. Osteoarthritis (OA) and osteoporosis (OP) are central to this problem because they amplify the functional consequences of weakness and reduced loading. OA may lead to strength loss through pain, inflammation, altered movement, and activity restriction, while OP increases the likelihood that falls or loading errors will result in fracture and subsequent deconditioning. Shared mechanisms for sarcopenia include mechanical unloading, adiposity-related metabolic dysfunction, inflammageing, mitochondrial stress, endocrine change, and nutritional insufficiency, although the strength of evidence differs across pathways. New weight-loss approaches using glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may substantially affect sarcopenia risk and therefore require careful consideration. Current diagnostic frameworks increasingly prioritise muscle strength and performance over lean mass alone, supporting pragmatic case-finding in older adults with severe OA, fragility fracture, recurrent falls, poor postoperative recovery, or weight loss. Current management should focus on progressive resistance and balance training, adequate energy and protein intake, guideline-based OP care, optimised OA treatment, and protection of mobility during transitions of care. The most immediate clinical gains are likely to come from integrating existing rheumatology, orthopaedic, fracture-prevention, rehabilitation, and nutritional services rather than from any osteosarcopenia-specific drug therapy.

Osteoporosis therapeutics have advanced from antiresorptive drugs that slow bone loss to osteoanabolic and dual-action agents that can rapidly rebuild skeletal integrity and reduce fracture risk. Yet the current anabolic era leaves important clinical questions unresolved: why responses vary among older adults, why gains are transient, how best to sequence therapy, and how to sustain skeletal resilience in the biologically aged bone microenvironment. Cellular senescence has emerged as a plausible mechanistic bridge linking skeletal aging, chronic inflammation, impaired osteoblastogenesis, increased osteoclastogenesis, marrow adiposity, diabetes-associated fragility, and delayed repair. Preclinical studies show that senescent-cell clearance can prevent or partially reverse age-related bone loss, while early human senolytic data suggest that skeletal response may depend on baseline senescent-cell burden. This review discusses current anabolic therapies, the rationale for senescence-targeted approaches, and future biomarker-informed strategies to integrate anabolic induction, antiresorptive consolidation, and experimental modulation of skeletal aging biology.

Osteoarthritis is a degenerative disorder of the whole joint and the leading cause of chronic disability in older adults, yet no disease-modifying therapy exists. Here we review what the gut microbiome teaches us about how osteoarthritis develops and progresses. We outline a biologically plausible gut-joint axis in which an altered intestinal community, a more permeable gut barrier, translocated microbial products, and low-grade systemic inflammation converge on the joint, together with the recently described bile acid and incretin changes. Animal experiments supply the strongest causal evidence, as removing, perturbing, or transplanting the microbiome alters joint damage. Human studies remain observational and often discordant, reflecting differences in the joint studied, in population, and in method; functional measures such as circulating endotoxin reproduce more reliably than taxonomic ones. We appraise therapeutic opportunities, including dietary fiber, prebiotics, weight loss, and incretin-based agents, and define the research agenda required before microbiome-directed therapy enters practice.

Congenital malformations of the central nervous system (CNS) are among the most common congenital anomalies, with neural tube defects being the most prevalent, comprising approximately 40% of CNS malformations. The estimated prevalence of CNS anomalies varies, but many cases remain undiagnosed at birth, potentially leading to underestimation. These conditions significantly impact neurodevelopmental outcomes and contribute to a high societal burden due to the need for specialized medical care and support. Prenatal imaging plays a crucial role in the early detection of CNS anomalies. Routine mid-trimester ultrasound, performed between 18 and 24 weeks of gestation, is the primary screening method, with detection rates ranging from 68% to 92%. Standardized guidelines by the International Society of Ultrasound in Obstetrics and Gynecology (ISUOG) recommend acquiring three axial planes-transventricular, transthalamic, and transcerebellar-to improve diagnostic accuracy. The addition of mid-sagittal plane evaluation may further enhance detection rates. When abnormalities are suspected, targeted fetal neurosonography (with transvaginal probes), incorporating coronal and sagittal planes, is necessary for detailed assessment and diagnosis. Accurate prenatal assessment of CNS anomalies is critical for diagnosis, prognosis, and management planning. Standardized approaches and advanced imaging techniques contribute to improved detection and better-informed clinical decision-making, ultimately enhancing outcomes for affected fetuses.

Visual symptoms are commonly reported by patients in the endocrine clinic. Separating the benign and reversible from sight-threatening disease relies heavily on examination. In this review, we offer a practical framework for ophthalmic assessment in endocrine disease, aimed at the non-ophthalmologist working without specialist equipment. We discuss visual acuity, intraocular pressure, colour vision, pupillary response, visual fields, eye movement assessment. We also discuss some of the specific external and fundal signs that are important not to miss, including optic disc swelling and relative afferent pupillary defect (RAPD). Emphasis throughout is on the small number of bedside tests that may identify those patients needing urgent ophthalmic and neuro-ophthalmic review.

Von Hippel-Lindau disease (VHL) is a rare autosomal dominant hereditary tumour predisposition syndrome affecting multiple organ systems, including the retina, central nervous system, kidneys, pancreas, adrenal glands, and inner ear. It is caused by pathogenic variants in the VHL gene, resulting in loss of functional pVHL, abnormal stabilization of hypoxia-inducible factor (HIF)-α subunits, and activation of downstream transcriptional programmes involved in angiogenesis, metabolism, cell survival, and tumour growth. Clinically, VHL is characterized by a spectrum of benign and malignant neoplasms that require lifelong surveillance and multidisciplinary management. Retinal hemangioblastomas are among the earliest manifestations and may provide the first clue to diagnosis of this multisystem disorder. Historically, management has relied on screening, surveillance, and local treatment according to lesion size, location, symptoms, and malignant potential. The emergence of HIF-2α-targeted therapy, particularly belzutifan, has begun to change this paradigm by offering a mechanism-based systemic treatment option for selected VHL-associated tumours. In this review, we summarize the ocular and systemic manifestations of VHL, its genetic and molecular basis, genotype-phenotype correlations, contemporary surveillance strategies, current local therapies, and the emerging role of HIF-2α inhibition in reshaping management.

Neuroendocrine neoplasms (NENs) comprise a diverse group of malignancies arising across multiple anatomical sites and displaying remarkable biological and clinical heterogeneity. While advances in sequencing have identified recurrent genetic alterations in several NEN subtypes, these tumors remain largely characterized by a relatively low mutational burden and lack of dominant oncogenic drivers. Consequently, emerging evidence suggests that the molecular basis of neuroendocrine tumorigenesis extends beyond individual mutations and involves broader processes such as chromatin remodeling, telomere maintenance, epigenetic dysregulation and cellular plasticity. This review aims to summarize the current molecular landscape of pulmonary, gastro-enteropancreatic and thymic NENs, focusing on the biological pathways and cellular programs disrupted by recurrent genetic alterations unrelated to syndromes. We discuss how multi-omic studies have refined molecular classification and revealed common principles underlying neuroendocrine tumor development. Collectively, recent literature supports a shift from mutation-centered models toward a more integrated understanding of the complex biology and evolution of NENs.