Anti-glutamic acid decarboxylase (anti-GAD) autoimmunity possess a poorly understood diversity in the development of neurological manifestations with or without diabetes mellitus (DM) association. A possible genetic contribution might further expand the complexity of anti-GAD pathogenesis and demand further exploration and research. We report three siblings in the same family (two sisters and one brother) who were tested positive for anti-GAD antibodies (anti-GAD-Abs) and presented with different clinical disorders, associated with DM in one of them. Although scarce data are available in the literature concerning the influence of possible genetic predisposition on the development of anti-GAD autoimmunity, yet there is cumulative evidence to support this association which is further elucidated in this report. Whether to recommend family screening tests for patients with positive anti-GAD autoimmunity is still undetermined and further studies are required to solve the unanswered queries pertinent to this potentially treatable autoimmune disorder.

To assess whether initiation of glucagon-like peptide-1 receptor agonists (GLP-1RAs) rather than sulfonylureas is associated with all cause acute pancreatitis and cause specific acute pancreatitis and to characterise temporal risk patterns of the various causes of acute pancreatitis associated with GLP-1RA use.

Target trial using the electronic healthcare databases of the US Department of Veterans Affairs healthcare system.

US Department of Veterans Affairs.

333 687 users of the Veterans Affairs healthcare system with type 2 diabetes initiating GLP-1RA (n=132 551) or sulfonylureas (n=201 136) between 1 January 2017 and 31 December 2023.

Initiation of GLP-1RA or sulfonylureas, and separately, continued use of GLP-1RA or sulfonylureas during follow-up.

Risks of acute pancreatitis during 12 months' follow-up including all cause acute pancreatitis and cause specific acute pancreatitis (eg, pancreatitis that is suspected drug induced, alcohol induced, hypertriglyceridaemia associated, biliary, and idiopathic or other cause). The risks were measured through discrete time survival models after application of inverse probability weighting.

In intention-to-treat analyses, participants who initiated GLP-1RAs had similar rates of all cause pancreatitis at one year compared with participants who initiated sulfonylureas (rate difference -3.64, 95% confidence interval (CI) -30.76 to 23.48 per 100 000 persons at one year). However, the overall null finding was the net result of countervailing effects across various causes of acute pancreatitis. GLP-1RA was associated with an increased risk of suspected drug induced acute pancreatitis (23.45 (14.27 to 33.85)) and decreased risks of hypertriglyceridaemia associated (-16.96 (-27.41 to -7.34)) and alcohol induced pancreatitis (-10.32 (-18.12 to -3.17)). Similar rates of biliary and idiopathic or other causes of acute pancreatitis were observed in the two groups. In per protocol analyses, drug induced acute pancreatitis attributable to GLP-1RA clustered early (42% of GLP-1RA attributable events over one year of follow-up occurred in the first three months), whereas reductions in alcohol related acute pancreatitis concentrated between months four and six and hypertriglyceridaemia associated acute pancreatitis concentrated between months 10 and 12. Cumulatively, these divergent temporal trends resulted in a net increase in risk of all cause pancreatitis during the first two months of treatment, with similar monthly risk observed for the remainder of follow-up.

In this nationwide cohort, similar rates of all cause acute pancreatitis in GLP-1RA and sulfonylurea users were observed at one year. Increased risk of suspected drug induced pancreatitis during the early period was offset by later reductions in alcohol induced and hypertriglyceridaemia associated acute pancreatitis. Clinicians should counsel patients on early risk while recognising the overall neutral long term effect.

Septic arthritis is an uncommon but severe complication of intra-articular procedures and is associated with significant morbidity and mortality when diagnosis or source control is delayed. Large cohort data have demonstrated adverse joint and systemic outcomes even when surgical washout is performed.

We report the case of a 64-year-old woman with Type 2 diabetes mellitus who developed septic arthritis of the knee 2 days after intra-articular hyaluronic acid injection, a procedure generally considered safe but known to carry a small risk of infection. Synovial fluid cultures identified Streptococcus anginosus and subsequently Streptococcus gordonii, organisms recognised for their propensity to cause invasive and disseminated infections. Despite prolonged hospitalisation and exposure to multiple sequential broad-spectrum antibiotic regimens, the infected joint was not surgically drained. During treatment, the patient developed persistent diarrhoea, abdominal pain and systemic inflammatory features. Repeated testing for Clostridioides difficile was negative, despite recognised associations between antibiotic exposure, acid-suppressive therapy and enteric complications. Computed tomography later demonstrated intestinal dilatation and ultimately pneumoperitoneum. Emergency bowel resection was performed, but the patient died shortly thereafter from multiple organ failure. Histopathological examination revealed extensive inflammatory ulceration of the colon.

This case illustrates a complex and fatal clinical course occurring in the context of persistent septic arthritis managed without joint drainage and prolonged antimicrobial exposure. Although causality cannot be established from a single report, the case reinforces the importance of timely source control in native joint septic arthritis, highlights the consequences of prolonged empirical antimicrobial therapy in the absence of adequate surgical debridement and underscores the need for early multidisciplinary reassessment when gastrointestinal symptoms arise during prolonged hospitalisation.

Short-form videos are an increasingly important source of health information for individuals with type 1 diabetes mellitus (T1DM), yet their quality is unverified.

This study aimed to evaluate and compare the quality, reliability, and engagement of T1DM-related videos on Bilibili and TikTok.

We conducted a cross-sectional analysis of the top 100 T1DM-related videos from Bilibili and TikTok (N=200). Videos were systematically evaluated using four validated instruments: the Global Quality Scale (GQS), Journal of the American Medical Association (JAMA) criteria, Video Information and Quality Index (VIQI), and modified DISCERN (mDISCERN). Engagement metrics were extracted, and Spearman correlations and a multivariable negative binomial regression were performed to identify predictors of video 'likes'. A comprehensive sensitivity analysis, including Principal Component Analysis (PCA), was conducted to ensure robustness.

TikTok videos achieved significantly higher user engagement than those on Bilibili (median views: 88,089 vs. 3,418). In terms of quality, TikTok scored higher on the VIQI (median: 12.0 vs. 9.0, P < 0.001), while Bilibili scored higher on the JAMA criteria (median: 2.0 vs. 0.0, P < 0.001). No significant platform differences were found for GQS or mDISCERN. In the adjusted regression model, VIQI score was a strong positive predictor of likes (RR=1.66, 95% CI 1.32-2.13), whereas a higher GQS score was a negative predictor (RR=0.24, 95% CI 0.13-0.45). These findings were robust across all sensitivity analyses.

T1DM-related short videos on Bilibili and TikTok exhibit substantial variability in quality and reliability. TikTok demonstrates stronger audiovisual quality, whereas Bilibili shows better transparency (JAMA). Engagement was driven more by production quality than informational accuracy. These findings suggest that optimizing content strategies and strengthening professional participation may be beneficial for digital diabetes education.

Diabetic peripheral neuropathy (DPN) is the most common chronic complication of diabetes mellitus and is frequently assumed to be the sole cause of neuropathic symptoms in patients with diabetes. This diagnostic simplification may lead to misdiagnosis, delayed treatment of alternative etiologies, and preventable neurological disability. Accurate differentiation between DPN and non-diabetic neuropathies remains a major clinical challenge.

This narrative review examines the principal differential diagnoses of generalized DPN, integrating clinical presentation, disease tempo, electrophysiological patterns, and targeted laboratory evaluation. A structured literature search of PubMed, Scopus, and Web of Science (2015 2025) was conducted, focusing on inflammatory, nutritional, toxic, hereditary, amyloid, autoimmune, and systemic causes of peripheral neuropathy. Emerging diagnostic tools, including biomarkers and advanced neurophysiological techniques, are also discussed, and a practical diagnostic algorithm is proposed to support real-world clinical decision-making.

DPN should be regarded as a diagnosis of exclusion rather than a default explanation in patients with diabetes. A phenotype-driven and structured diagnostic approach is essential to reduce diagnostic anchoring, prevent iatrogenic harm, and enable early identification of treatable neuropathies, ultimately improving neurological outcomes and precision medicine strategies.

Diabetes mellitus, a highly prevalent metabolic disorder worldwide, poses a severe threat to patient health primarily through its debilitating vascular complications. The cerebral microvasculature, essential for maintaining brain homeostasis and function, is particularly vulnerable to diabetic injury. However, diabetic cerebral microvascular disorder-a key contributor of neurological diseases like stroke, dementia, and cerebral small vessel disease-remains insufficiently characterized, and its pathophysiological mechanisms and therapeutic implications are not yet fully integrated.

This review comprehensively summarizes the structural and functional abnormalities of cerebral microcirculation in diabetes, encompassing pathological neovascularization, pathological remodeling, blood-brain barrier disruption, cerebrovascular reactivity impairment, capillary stalling, impaired autoregulation, and neurovascular uncoupling. These microvascular alterations are then examined in relation to major neurological diseases, such as stroke, cerebral small vessel disease, cognitive impairment, Parkinson's disease, and depression. Current and emerging interventions, ranging from lifestyle modification and glucose-lowering therapies to mechanism-targeted strategies, are also discussed. While this review covers cerebral microvascular alterations across diabetes subtypes, it should be noted that the majority of currently available evidence derives from studies in type 2 diabetes.

This review provides a comprehensive synthesis of current knowledge on diabetic cerebral microvascular disorder, providing a framework for mechanistic research and supporting the clinical translation of microcirculation-targeted strategies for managing diabetes-related neurological complications.

Diabetic ulcers, a serious complication associated with diabetes, present a significant therapeutic challenge due to their recurrent and persistent chronic inflammation. A crucial factor contributing to this sustained inflammation is mast cell degranulation. This study examined the effects of the traditional Chinese herbal formula Zizhu ointment (ZZO) on mast cell degranulation in diabetic ulcers, as well as its underlying mechanisms in promoting wound healing. Analysis of clinical specimens revealed that ZZO significantly inhibited mast cell degranulation in diabetic ulcer wounds. In a diabetic mouse wound model, ZZO was observed to suppress mast cell degranulation, decrease the expression of TNF-α and MMP-9, and facilitate wound healing. Cellular experiments demonstrated that ZZO inhibited IgE/DNP cross-linking-mediated degranulation, calcium (Ca²⁺) influx, and the release of β-hexosaminidase, histamine (HIS), and TNF-α in both human HMC-1 and murine P815 mast cells. Furthermore, ZZO was found to block the IgE/DNP cross-linking-mediated activation of FcεRI-proximal signaling pathways (LYN/SYK/PLCγ) and inflammatory cascades (IKK/NFκB and MAPKs). We hypothesize that ZZO facilitates the healing of diabetic ulcers by stabilizing mast cells and inhibiting their degranulation, thereby reducing the release of inflammatory mediators and promoting wound repair.

Diabetic peripheral neuropathy (DPN) is a severe complication of diabetes mellitus (DM). Measurement of plantar fascia thickness (PFT) by ultrasound has been proposed as an alternative index of tissue glycation and a marker for diabetes complications such as DPN.

A cross-sectional study was conducted in 290 patients with type 1 DM (age 54 [20-87] years and diabetes duration 28 [1-79] years) and 41 healthy volunteers (age 49 [26-73] years). PFT was measured during outpatient clinical evaluation by means of ultrasound. Values were compared with sex, age, anthropometric parameters, advanced glycation end products (AGEs) measured by skin autofluorescence, and parameters derived from clinical evaluation of DPN.

Patients with type 1 DM had significantly thicker plantar fascia than controls (2.9 ± 0.6 mm vs. 2.4 ± 0.2 mm; P < 0.001); 199/290 (68.6%) patients with type 1 DM had altered PFT. In this population, male patients and those with worse glycemic control and longer duration of disease had a higher risk of having altered PFT. Higher PFT was significantly associated with reduced vibration sensitivity, higher levels of HbA1c and AGEs, presence of retinopathy and reduced renal function, and a worse diabetic foot risk classification. The use of AHCL integrated systems appeared to be associated with better plantar fascia outcomes.

Our findings indicate that PFT showed a relationship with diabetes microvascular complications, glucometabolic compensation, and with the use of automated insulin delivery systems. PFT might be a useful tool in the assessment of patients with T1DM.

In the year 2000 the first once daily long-acting bioengineered insulin analogue (LAIA), insulin glargine ('glargine'), a true basal insulin (BI), became available for clinical use. This led to the decline in the 50-year-old era and prominence of the intermediate-acting insulins, neutral protamine Hagedorn (NPH) and lente, requiring twice daily administration to control the basal metabolism of people with type 1 diabetes (T1DM) and type 2 diabetes (T2DM). This milestone bridged the gap between regimens involving unmodified human insulins of the previous century to those referred to as using 'designer insulins', with the introduction 4 years previously of the meal-time analogue, insulin lispro. The rapid gain in popularity of glargine is explained by its clinical benefits (once-daily dosing, titration to achieve improved pre-breakfast plasma glucose, with a lower risk of nocturnal hypoglycaemia compared to NPH, and less frequent blood glucose monitoring). These benefits correlate with the pharmacokinetic/pharmacodynamic characteristics of insulin glargine being closer to physiological BI supply. In T2DM glargine changed the paradigm of insulin substitution by embedding the concept of 'treating-to-target', by starting BI 'early', with focus on near-normal fasting plasma glucose prior to the introduction of prandial insulin, and more recently in combination with GLP-1 receptor agonists. These practices/principles have continued with the introduction of additional innovative LAIAs for once-daily or indeed weekly use. Today glargine remains in widespread worldwide use in people with T1DM and T2DM, is often the initial BI used, while it serves as a reference against which other LAIAs are tested in clinical trials.