Vibration-controlled transient elastography (VCTE)-based liver stiffness measurement (LSM) is widely used for non-invasive assessment of liver fibrosis and portal hypertension in chronic liver disease. In daily practice, LSM values are often interpreted using etiology-specific fibrosis cut-offs embedded in device software. However, an increasing proportion of patients now present with mixed liver disease etiologies, particularly combinations of metabolic-associated steatotic liver disease (MASLD) with viral or alcohol-related liver disease. In such patients, applying singleetiology cut-offs may lead to misclassification of fibrosis stage and portal hypertension risk. We highlight the limitations of this approach and argue that LSM should be interpreted within a broader clinical context, integrating platelet count, biochemical markers, and validated risk-stratification algorithms rather than relying solely on fibrosis staging tables.

Variceal hemorrhage is a severe and often fatal consequence of portal hypertension from liver cirrhosis. Although endoscopic and radiographic interventions have largely replaced balloon tamponade, the Sengstaken-Blakemore tube (SBT) remains a critical salvage therapy. However, declining use has led to limited provider experience and familiarity with SBT placement and management.

Polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes (POEMS) syndrome is a rare paraneoplastic disorder associated with plasma cell dyscrasia and multisystem involvement. This report describes a case of splanchnic venous thrombosis presenting as the initial clinical manifestation. A 38-year-old woman presented with acute abdominal pain associated with progressive polyneuropathy. Imaging studies revealed extensive thrombosis of the superior mesenteric vein with extension into the portal vein, moderate ascites, hepatosplenomegaly, and diffuse osteosclerotic bone lesions. Laboratory investigations demonstrated an immunoglobulin A (IgA) lambda monoclonal gammopathy. Positron emission tomography-computed tomography showed widespread hypermetabolic osteosclerotic lesions, hypermetabolic axillary lymphadenopathy, and increased cardiac uptake. Transthoracic echocardiography revealed right ventricular dilation with an intermediate probability of pulmonary hypertension. The overall clinical, radiological, and laboratory findings were consistent with disseminated POEMS syndrome. This case illustrates a rare initial presentation of POEMS syndrome manifesting as splanchnic venous thrombosis. It emphasizes the importance of considering POEMS syndrome in patients with unexplained portal hypertension or atypical venous thrombosis in the presence of systemic manifestations.

Background. This rat study reveals a new point: the considerable impact of unilateral adrenalectomy, severe vascular and multiorgan failure, occlusion/occlusion-like syndrome, and the stable gastric pentadecapeptide BPC 157 therapy. Based on the recent Fourier transform infrared (FTIR) spectroscopy vascular disturbance studies, particularly those after unilateral adrenalectomy in rats, the noted cytoprotective vascular recovery effect of the BPC 157 therapy may be useful. Methods. In rats, unilateral adrenalectomy (at 15 min, 5 h, 24 h) leads to integrated gross and morphological changes, vascular alterations, oxidative stress parameters, molecular markers and occlusion/occlusion-like syndrome and BPC 157 as useful therapy (/kg ig) (10 µg, 10 ng). Results. Peripherally and centrally, counteraction includes the lesions (adrenal, brain, heart, lung, liver, kidney, gastrointestinal tract), organ hemorrhage, and thrombosis. Attenuated/eliminated were arrhythmias, intracranial (superior sagittal sinus), portal, caval hypertension, and aortic hypotension. Significant resolution occurred via activation of collateral pathways, the azygos vein (direct blood flow delivery), and the recovered peduncle of the inferior suprarenal artery and superior suprarenal vein. Virchow's triad circumstances were reversed. Occlusion/occlusion-like syndrome was counteracted as a whole. Also, BPC 157 counteracted adrenal lesions (lipid depletion, congestion). There were higher cortisol values, but still very low, and a shift toward the left of the adrenal compensatory weight increase. For the indicative conclusion along with previous studies, mechanistically, BPC 157 therapy exhibits the NO-system modulation/oxidative stress balance, increases NO-level, counteracts oxidative stress (malondialdehyde (MDA)), upregulates NOS1-3, and VEGF-A expression. Conclusions. These effects of BPC 157 therapy and its easy applicability deserve further consideration.

Pulmonary arterial hypertension (PAH) is a progressive, fatal disease of the pulmonary vasculature characterized by obliterative remodeling of small pulmonary arteries, leading to sustained elevation of pulmonary vascular resistance, right ventricular failure, and premature death. The diagnostic gold standard remains right heart catheterization, requiring a mean pulmonary artery pressure greater than 20 mmHg at rest, a pulmonary arterial wedge pressure of 15 mmHg or below, and a pulmonary vascular resistance exceeding 2 Wood units. PAH is an autosomal dominant disorder with markedly incomplete penetrance of approximately 20-30%, indicating that germline mutations alone are insufficient to cause disease. Disease manifestation requires additional "second hits", including chronic hypoxia, systemic inflammation, hemodynamic stress, hormonal influences, and common genetic modifiers such as single-nucleotide polymorphisms (SNPs). This genetic and environmental complexity underpins the broad clinical heterogeneity observed across PAH subtypes, which include idiopathic PAH, heritable PAH, and disease associated with connective tissue disorders, HIV infection, portal hypertension, congenital heart disease, schistosomiasis, and drug or toxin exposure. This review provides a comprehensive and critical appraisal of the molecular-genetic architecture of PAH. Thirty genes have now been implicated in disease pathogenesis, spanning seven functional categories: receptors of the TGF-β/BMP signaling family (BMPR2, ACVRL1, ENG, BMPR1B); circulating BMP ligands (GDF2, BMP10); transcription factors (TBX4, SOX17, KLF4, FOXF1, SMAD1, SMAD4, SMAD9); membrane and polyamine transporters (ATP13A3, AQP1); potassium channel regulators (KCNA5, KCNK3, ABCC8); metabolic and mitochondrial genes (EIF2AK4, NFU1, GGCX); signaling receptors and structural proteins (NOTCH3, KDR, CAV1, PLEKHH2); vasoactive and extracellular matrix regulators (KLK1, CBLN2, CD248); and epigenetic regulators (TET2, TOPBP1). Among these, BMPR2 is the dominant contributor, accounting for 53-86% of heritable PAH and 14-35% of idiopathic cases. The remaining genes each account for fewer than 5% of cases individually, collectively reflecting a broad landscape of rare and ultra-rare genetic contributions. For each gene, we critically evaluate the strength of genetic evidence, pathogenic mechanisms, degree of mechanistic resolution, and clinical relevance. We further discuss the contribution of emerging technologies, including whole-genome sequencing, single-cell and spatial transcriptomics, multi-omics integration, iPSC-derived vascular models, and artificial intelligence, to expanding the PAH genetic architecture beyond single-gene discovery. A key theme across this landscape is convergence: despite mechanistic diversity at the gene level, most PAH-associated variants ultimately impair endothelial quiescence, promote smooth muscle proliferation, and drive apoptosis resistance through disruption of BMP signaling amplitude, transcriptional stability, ion channel homeostasis, metabolic integrity, or epigenetic regulation. This convergence supports both a unified therapeutic rationale and a precision medicine framework for genotype-stratified intervention in PAH.

Pembrolizumab is standard adjuvant therapy for high-risk clear cell renal cell carcinoma, but serositis is an uncommon immune-related adverse event that may mimic recurrence or infection. We report a 55-year-old man who achieved no evidence of disease after nephrectomy and metastasectomy and developed anasarca, large bilateral pleural effusions, mild ascites, peripheral eosinophilia, and a small pericardial effusion after six cycles of adjuvant pembrolizumab. Pleural fluid was exudative and contained 20% eosinophils. Cytology showed inflammatory cells without evidence of malignancy; bacterial, mycobacterial, and fungal studies were negative; and mildly elevated adenosine deaminase did not support tuberculosis. Cardiac function and natriuretic peptides were preserved. Pembrolizumab was discontinued, thoracentesis and corticosteroids were administered, and symptoms, eosinophilia, renal function, and albumin improved rapidly. Follow-up through March 2026 showed no oncologic progression, although some residual pleural and abdominal fluid persisted alongside imaging findings suggestive of portal-hypertension physiology, which may have contributed to residual fluid but did not explain the eosinophilic pleural syndrome. In a targeted literature review, effusion eosinophil data were infrequently reported. This case highlights a likely underrecognized eosinophilic pleural-fluid phenotype within pembrolizumab-associated polyserositis and supports routine differential cell counts in drained serosal fluid when immune-related serositis is suspected.

Transjugular intrahepatic portosystemic shunt (TIPS) is a mainstay treatment for complications of portal hypertension. Despite advances in covered stents, hepatic encephalopathy (HE) remains a common complication, affecting 21%-53% of patients within one year. Refractory HE, often resistant to medical therapy, poses significant management challenges. We present a case of refractory post-TIPS HE successfully managed with selective splenic artery embolization (SSAE), underscoring its therapeutic potential.

Background In Tanzania, hepatosplenic schistosomiasis (HSS) is a common cause of morbidity and mortality among adult patients. However, capacity to manage HSS is very low. Here we report learning experience, capacity building, and collaborative partnership in establishing a functional gastrointestinal (GI) endoscopy unit. Methods A need assessment for a GI endoscopy unit at Nansio District Hospital was conducted. The findings highlighted a clear need for establishing the endoscopy unit, given the burden of HSS, its associated mortality, and the lack of skilled human resources. Key priorities included capacity building for human resources, renovation of the building, provision of scholarships for residents in internal medicine, establishment of an HSS patient registry and clinic, and strengthening of ultrasound services. Results The GI endoscopy unit commenced operations in August 2023. To date, a total of 666 patients have been attended (442 [66.4%] male and 224 [33.6%] female). Abdominal distension (66%), hematemesis (41%), and melena (41%) were common symptoms. Ultrasound examination revealed periportal fibrosis (PPF) in 71.5% of patients and liver image patterns C-F in 80.4%, both correlating with the severity of PPF. Of the 666 patients, 560 underwent endoscopic examination and the most common diagnosis was grade IV esophageal varices (52.1%). Among these, 84% underwent variceal ligation. On follow-up, 90% of patients achieved variceal eradication. Conclusion The establishment of the GI endoscopy unit at the district hospital in rural Tanzania was possible through the support of different stakeholders.

Gastric varices represent a challenging clinical scenario due to the severity of consequences when bleeding occurs, the cohort of patients in which it occurs and a paucity of high-quality prospective data to guide treatment decisions. Whilst a range of endoscopic and radiologic management strategies are now available, ambiguity exists about when to utilize each of these therapies.