Background. Adipokines are reported to participate in many common pathologic processes of glucose dysregulation, such as insulin resistance, β-cell dysfunction, and chronic inflammation. Objective. To detect the concentrations of plasma asprosin in subjects with impaired glucose regulation (IGR) and newly diagnosed type 2 diabetes (nT2DM) and its relationship to parameters of glucose and lipid metabolism, insulin resistance, and pancreatic β-cell function. Methods. 143 eligible participants were included and were divided into three groups including normal glucose regulation (NGR, n=52), IGR (n=40), and nT2DM group (n=51). The intravenous glucose tolerance test (IVGTT) and clinical and biochemical parameters were measured in all participants. Results. Plasma asprosin levels were higher in IGR (82.40 ± 91.06 ng/mL, P<0.001) and nT2DM (73.25 ± 91.69 ng/mL, P<0.001) groups compared with those in the NGR (16.22 ± 9.27 ng/mL) group, especially in IGR subjects. Correlation analysis showed that plasma asprosin levels were positively correlated with waist circumference (Wc), fasting plasma glucose (FPG), postchallenge plasma glucose (2hPG), HbA1c, triglyceride (TG), and homeostasis model assessment for insulin resistance (HOMA-IR) and negatively correlated with homeostasis model assessment for β-cell function (HOMA-β), area under the curve of the first-phase (0–10 min) insulin secretion (AUC), acute insulin response (AIR), and glucose disposition index (GDI) (all P<0.05). Multiple logistical regression analyses revealed that plasma asprosin concentrations were significantly correlated with IGR and nT2DM after controlling for age, sex, BMI, and WHR. Conclusions. Circulating asprosin might be a predictor of early diagnosis in DM and might be a potential therapeutic target for prediabetes and T2DM.

Rationale: Budd-Chiari syndrome (BCS) complicated by ruptured hepatocellular carcinoma (HCC) is relatively uncommon. This case underscores the critical role of multimodal imaging and interdisciplinary collaboration. Patient concerns: A 46-year-old female presented with abdominal pain for 10 + days, aggravated for 5 hours. the emergency abdominal enhanced computed tomography: malignant space occupying in the left inner lobe of liver (HCC is possible) and hematocele in abdominal cavity. Magnetic resonance imaging enhancement of the upper abdomen was performed: malignant mass of the left lobe of the liver with hemorrhage and necrosis, compensatory enlargement of the right lobe of the liver, unclear display of hepatic veins, and stenosis of the hepatic segment of the inferior vena cava, which was consistent with Budd-Chiari syndrome. Diagnoses: Budd-Chiari syndrome with hepatocellular carcinoma rupture and bleeding. Interventions: Interventional therapy, surgical treatment. Outcomes: Hepatic venous outflow obstruction was successfully relieved by interventional therapy combined with surgery and tumor resection was performed. After 39 days of intensive care, the patient improved and was discharged smoothly. Lessons: For patients with Budd-Chiari syndrome and hepatocellular carcinoma, the Multidisciplinary diagnosis and treatment (MDT) model should be implemented throughout the entire treatment process. Through the MDT model, personalized treatment plans can be developed, combining various methods to relieve liver vein outflow obstruction and remove tumors, while also establishing appropriate treatment measures and processes, thereby improving treatment outcomes and reducing the risk of complications and disease progression. However, within the MDT model, different physicians must propose treatment plans based on their professional knowledge and the specific circumstances of each patient. In the process of personalized treatment, issues such as how to balance pros and cons and select the optimal solution also present challenges to clinical practitioners.

Rationale: Sepsis can trigger life-threatening atypical hemolytic uremic syndrome (aHUS) through dysregulated complement activation. Diagnosis is challenging due to overlapping features with septic shock, often leading to delayed recognition and high mortality. Patient concerns: A 23-year-old female with chronic kidney disease presented with a 3-day history of productive cough, fever, and progressive dyspnea, which rapidly escalated to respiratory failure, anuria, and coma within 24 hours. Diagnoses: Laboratory findings confirmed thrombotic microangiopathy (hemoglobin 57 g/L, platelets 69 × 10 ⁹ /L, schistocytes 0.3%, lactate dehydrogenase [LDH] 469 U/L) and acute kidney injury (creatinine 535 µmol/L). The diagnosis of complement-mediated aHUS was established by markedly elevated soluble C5b-9 (sC5b-9) (578 ng/mL) with preserved a disintegrin and metalloproteinase with thrombospondin motifs 13 activity (89%). Interventions: Critical care included mechanical ventilation and continuous renal replacement therapy. Specific aHUS therapy comprised plasma exchange (10 sessions) and complement blockade with eculizumab (900 mg weekly for 4 weeks, then 1200 mg every 2 weeks), accompanied by meningococcal prophylaxis. Outcomes: By day 31, hematologic and renal parameters improved (platelets 72 × 10 ⁹ /L, LDH 273 U/L, creatinine 151 µmol/L). By day 51, complement activity normalized (sC5b-9 261 ng/mL, a 54.8% reduction), with full hematologic recovery (platelets 198 × 10 ⁹ /L, LDH 171 U/L), renal function near baseline (creatinine 96 µmol/L), and resolution of hemolysis. Lessons: In sepsis with persistent thrombocytopenia despite infection control, urgent sC5b-9 testing is critical to diagnose aHUS. Eculizumab, combined with supportive continuous renal replacement therapy and plasma exchange, can effectively reverse multi-organ failure even during active bacteremia, with serial sC5b-9 monitoring serving as a key biomarker for guiding therapy.

Background: Diabetic ketoacidosis (DKA) is a life-threatening acute complication of diabetes mellitus, most commonly precipitated by infection. Patients with diabetes are at a significantly elevated risk for severe infections and sepsis. Odontogenic infections represent a prevalent but potentially overlooked source of sepsis in this population, given the established bidirectional relationship between diabetes and periodontitis. Case presentation: A 57-year-old female with poorly controlled type 2 diabetes presented with a one-week history of left jaw pain and one day of severe dyspnea and lethargy. Examination revealed left submandibular swelling, Kussmaul respirations, and lethargy. Laboratory findings confirmed severe DKA (pH 7.04, β-hydroxybutyrate 7.19 mmol/L) and sepsis (leukopenia, procalcitonin 2.34 ng/mL). Echocardiography demonstrated severe left ventricular systolic dysfunction (ejection fraction 36%) with normal cardiac biomarkers, consistent with sepsis-induced cardiomyopathy (SICM). Imaging identified a left submandibular abscess. Management involved prompt sepsis bundle implementation, including early empiric antibiotics (amoxicillin-clavulanate and tinidazole), aggressive fluid resuscitation, and concurrent intravenous insulin infusion for DKA, alongside proactive electrolyte repletion. Multidisciplinary source control was achieved. Outcomes: The patient showed rapid clinical improvement. Metabolic acidosis and ketosis resolved. Infection markers normalized. Remarkably, follow-up echocardiography on day 14 demonstrated complete recovery of cardiac function (ejection fraction 72%). She was discharged after 15 days and remained well at one-month follow-up. Conclusions: This case underscores that odontogenic infection can be a potent trigger for life-threatening DKA and septic shock with multi-organ dysfunction in diabetic patients. It highlights the critical importance of thorough physical examination, including oral cavity inspection, in the evaluation of sepsis or DKA. The presentation and complete reversibility of SICM reinforce that treatment must focus on correcting the underlying septic and metabolic insults. Early multidisciplinary management is essential for optimal outcomes.

Background: Hyperkalemia is a common and potentially lethal electrolyte disorder in the emergency department (ED). We aim to explore the real-world effectiveness of hyperkalemia treatment, and the patterns of hyperkalemia management in the ED in China. Methods: POETRY-E (ChiCTR2100053100) was a multicenter, prospective, observational study. Adult patients with serum potassium (sK ⁺ ) ≥ 5.5 mmol/L admitted to the ED were enrolled from 15 centers across China and followed until discharge from the ED. The primary endpoint was the change in sK ⁺ from baseline to 6 h after treatment initiation. Secondary and exploratory endpoints included the clinical burden of hyperkalemia (e.g., severity, complications, survival, etc.), and the real-world management strategies of hyperkalemia in the ED. Results: Between October 2021 and March 2023, 577 patients were enrolled. The median (Q1, Q3) baseline sK ⁺ was 6.25 (5.82, 6.83) mmol/L. At 6 h, after treatment initiation, the median (Q1, Q3) change in sK ⁺ from baseline was − 1.30 (− 1.96, − 0.72) mmol/L ( P < 0.001), with 46.4% ( n = 268) achieving sK ⁺ < 5.5 mmol/L. Most patients ( n = 457, 79.2%) received combination therapies, among which 36.1% ( n = 165) received oral potassium binders, predominantly sodium zirconium cyclosilicate (SZC) ( n = 152). The SZC-containing therapies were associated with a lower median (Q1, Q3) sK ⁺ at 4 h compared with non-SZC-containing regimens (5.20 [4.90, 5.70] vs. 5.81 [4.99, 6.10] mmol/L, P = 0.019) and a trend towards lower sK ⁺ at 6 h (4.98 [4.60, 5.50] vs. 5.20 [4.67, 5.70] mmol/L, P = 0.140). Moreover, the SZC-containing therapies were associated with numerically favorable median (Q1, Q3) change in sK ⁺ from baseline compared with non-SZC-containing regimens at 4 and 6 h (4 h: − 1.23 [− 1.65, − 0.70] vs. − 0.94 [− 1.42, − 0.55] mmol/L; 6 h: − 1.42 [− 1.98, − 0.90] vs. − 1.30 [− 1.90, − 0.73]). Death in the ED occurred in 24 (4.2%) patients. Conclusions: In Chinese patients with hyperkalemia presented to the ED, hyperkalemia management was effective in rapidly reducing sK ⁺ . SZC-containing therapies may be more effective treatment options. Trial registration Chinese Clinical Trial Register (ChiCTR2100053100), registered on November 10, 2021.