Due to the lack of specific Western medicine therapies for post-coronavirus disease 2019 (COVID-19) syndrome in clinical practice, this study aimed to investigate the efficacy of traditional Chinese medicine (TCM) for post-COVID-19 syndrome using a cohort study design and to explore its clinical value in alleviating patients’ symptoms and improving clinical outcomes.

In this cohort study, patients were divided into two groups according to clinical treatment. The control group received conventional Western medicine, and the treatment group received additional TCM syndrome differentiation–based treatment. Propensity score matching methods were used to reduce selection bias by equating groups based on observed covariates. Clinical data, including TCM symptom scores, the Short Form 36 Health Survey, clinical efficacy, and adverse events at Day 7, were collected. The primary outcome was the efficacy rate, defined by improvement at Day 7 compared with the Day 0 score. Data were processed and analyzed using SPSS 23.0 and R 4.5.0 software.

A total of 434 patients were enrolled in the cohort, including 306 patients in the control group and 128 in the treatment group. After 1:1 matching, 94 matched pairs were analyzed. For the primary outcome, the effective rate in the treatment group was higher than that in the control group (30.8% vs. 17.2%; odds ratio (OR) = 2.17, 95% confidence interval (CI): 1.09–4.35, P = 0.003). After seven days of treatment, the TCM syndrome score improved more in the treatment group than in the control group (median difference (MD) = 2.00, 95% CI: 0.50–3.50, P = 0.009). Subgroup analyses showed generally favorable efficacy in the treatment group across subgroups, though not all reached statistical significance.

TCM syndrome differentiation–based therapy effectively relieves clinical symptoms in patients with post-COVID-19 syndrome.

Antimitochondrial antibody (AMA)-negative primary biliary cholangitis (PBC) is a rare presentation of PBC that comprises 5%–10% of all PBC patients. The pathogenesis of AMA-negative PBC appears to be similar to that of AMA-positive PBC. AMA-negative PBC presents similarly to AMA-positive PBC, with symptoms of cholestasis, fatigue, and pruritus most commonly reported. Defective bicarbonate production, resulting in acidification of bile and bile acids, has been proposed as the primary mechanism of damage to bile ducts and hepatocytes and is reflected in elevations of alkaline phosphatase and aminotransferases. Chronic damage can lead to the development of cirrhosis. The diagnosis is made by the finding of AMA negativity by ELISA or assays of similar sensitivity and a positive PBC-specific antinuclear antibody (ANA; anti-glycoprotein 210 and anti-speckled 100 kDa protein) test. In cases in which anti-glycoprotein 210 and anti-speckled 100 kDa protein assays are also negative, a liver biopsy is required to make the diagnosis after exclusion of other causes of cholestasis by magnetic resonance cholangiopancreatography or endoscopic retrograde cholangiopancreatography. Treatment for AMA-negative PBC is the same as for AMA-positive cases, with ursodeoxycholic acid as the first-line treatment. Current treatment is most effective in early stages, where it slows but does not eliminate progression. Risk stratification by validated tools such as the GLOBE and UK-PBC scores remains useful in AMA-negative PBC.

Autoimmune pancreatitis (AIP) is a rare immune-mediated form of chronic pancreatitis. It may affect multiple organs, and its heterogeneous clinical manifestations complicate diagnosis and management. Based on the Chinese Guidelines for the Diagnosis and Management of Autoimmune Pancreatitis (Shanghai 2012 Draft), together with the latest domestic and international guidelines and research advances, the present guideline provides 20 recommendations covering four aspects: diagnosis, treatment, follow-up, and prognosis. The aim is to improve the diagnosis and management of AIP in China and ultimately improve patient outcomes.

Medullary thyroid carcinoma (MTC) is a neuroendocrine malignancy arising from parafollicular C-cells with known variations in cytomorphologic and immunophenotypic features. New neuroendocrine markers pituitary homeobox 2 (PITX2), paired-like homeobox 2B (PHOX2B), and heart and neural crest derivatives expressed 2 (HAND2) have recently been introduced, but studies using these markers in MTC are limited. The aim of this study was to evaluate the expression and potential diagnostic utility of PITX2, PHOX2B, and HAND2 in primary and secondary MTCs and to compare their expression with chromogranin A, synaptophysin, insulinoma-associated protein 1 (INSM1), and calcitonin.

A total of 34 histologically confirmed cases of MTC with available cell blocks were included. Sixteen MTC samples were fine-needle aspirates from primary thyroid lesions, and eighteen were from secondary metastatic lesions. Twelve samples from thyroid carcinomas of follicular origin were included as controls.

PITX2 positivity was observed in 17 (50.0%) MTC samples and in 4 (33.3%) control samples (P = 0.502). PITX2 positivity was found in 43.8% of primary thyroid MTC lesions and in 55.6% of secondary MTC lesions (P = 0.366). Co-expression of PITX2 with chromogranin A, synaptophysin, INSM1, and calcitonin was observed. PHOX2B and HAND2 were negative in all MTC and control samples.

There were no significant differences in PITX2 expression between primary and secondary MTC samples. PITX2 did not show reliable utility in distinguishing MTC from thyroid carcinomas of follicular origin. PHOX2B and HAND2 were negative in all samples. These results suggest that these new markers do not offer diagnostic value for MTC as stand-alone markers or as additions to the diagnostic workup panel.

Myelodysplastic syndromes (MDS) are a group of hematopoietic disorders characterized by ineffective hematopoiesis, with manifestations of cytopenias in one, two, or three lineages. CD34+ micromegakaryocytes and giant platelets are very rarely seen in MDS patients but may lead to unnecessary treatments. Therefore, we report and follow up on an MDS case with such an unusual finding.

A 57-year-old male veteran with a history of MDS, alcoholic cirrhosis, and portal hypertension presented to the Emergency Department in 2020 for evaluation after a blackout, at which time peripheral blood samples and bone marrow biopsies were obtained. Flow cytometry analysis of his peripheral blood detected 8% CD34+ cells. This finding raised the possibility of acute leukemic transformation from MDS. Further studies revealed that these CD34+ cells represented dysplastic micromegakaryocytes and giant platelets rather than blasts. During his 4-year follow-up, the patient was alive and complained only of easy fatigability, lasting several weeks. His laboratory results showed pancytopenia and persistent iron-deficiency anemia.

The distinction between micromegakaryocytes and giant platelets versus megakaryoblasts is extremely important in patients with MDS. This distinction may prevent misdiagnosis of acute leukemia and unnecessary treatments such as chemotherapy.

Metabolic dysfunction–associated steatotic liver disease (MASLD) is increasing rapidly, yet regional differences in burden and care quality remain unclear. This study aimed to compare regional incidence, mortality, and disability; evaluate care quality; identify key determinants; and project future incidence.

We analyzed the Global Burden of Disease 2023 estimates of MASLD incidence, deaths, and disability-adjusted life years from 1990 to 2023 by age, sex, country, and region. Age-standardized rates were assessed using joinpoint regression. A composite Quality of Care Index (QCI) was derived through principal component analysis. Gradient boosting models with SHapley Additive exPlanations interpretation identified key predictors, and Bayesian age–period–cohort models generated incidence projections.

In 2023, South and East Asia had the largest numbers of new cases, while North Africa and the Middle East and Andean Latin America recorded the highest age-standardized incidence, mortality, and disability rates. Eastern Europe and Andean Latin America showed sustained increases in mortality and disability despite moderate incidence growth. QCI values were lowest in South Asia, Western Sub-Saharan Africa, and Eastern Europe. High body mass index and fasting plasma glucose were prominent contributors in comparative risk attribution analyses, and machine learning models identified age and calendar year as the strongest predictors of modeled burden patterns. Incidence is projected to continue increasing through 2050, particularly in India and China.

MASLD burden and care quality vary widely across regions. Low-QCI regions show higher mortality and disability, unfavorable metabolic risk profiles, and delayed detection patterns. Strengthening prevention, early case finding, fibrosis assessment, and treatment access may slow MASLD progression.

The gut microbiota engages in a complex, bidirectional dialogue with the liver via the gut–liver axis, and its dysbiosis plays a central role in the initiation and progression of various liver diseases. This review comprehensively integrates recent advances in the common features and etiology-specific patterns of gut microbial dysbiosis in liver diseases, signal decoding of key microbial metabolite axes, gut–liver immune crosstalk mechanisms, the accelerating role of gut barrier disruption, and recent progress in the use of the microbiome as diagnostic and prognostic biomarkers. We focus on analyzing the common patterns of reduced diversity, depletion of beneficial bacteria, and enrichment of pathogenic bacteria associated with gut flora dysbiosis across different liver diseases, ranging from nonalcoholic fatty liver disease and alcoholic liver disease to cirrhosis and hepatocellular carcinoma, as well as their unique etiology-related characteristics. Core findings reveal that microbial metabolites act as key chemical messengers that precisely drive liver disease progression by modulating host metabolic, immune, and inflammatory pathways. Meanwhile, the translocation of microbes and their products resulting from disruption of gut barrier integrity serves as a key accelerator, exacerbating liver injury and related complications. Based on these mechanisms, this review further explores ecological niche remodeling strategies targeting the gut microbiota, including the existing evidence and limitations of fecal microbiota transplantation and probiotics/prebiotics, as well as the prospects of emerging precision interventions such as phage therapy, microbial enzyme inhibitors, and engineered bacteria. Finally, we emphasize the potential and personalized implementation pathways of synergistically integrating microbiota modulation with existing therapies such as antivirals, antifibrotics, immunotherapy, and metabolic surgery. Future research must focus on promoting the translation of microbiome research from association studies to clinical applications through multi-omics integration and prospective clinical trials, ultimately achieving precise prevention and treatment of liver diseases based on gut–liver axis regulation.