Severe acute pancreatitis (SAP) lacks a definitive treatment option. Although ulinastatin has demonstrated anti-inflammatory and organ-preserving properties, its role in SAP remains unclear due to divergent findings. Hence, we evaluated the efficacy and role of ulinastatin in patients with SAP. A systematic review and meta-analysis were performed according to the 2020 PRISMA guidelines. An extensive search was performed in databases including PubMed, ClinicalTrials.gov, WHO International Clinical Trials Registry Platform, Embase, IndMED, Cochrane Library, Cochrane Methodology Register, and Cochrane Database of Systematic Reviews to obtain relevant data. Prospective and retrospective studies evaluating patients aged ≥ 18 years with SAP were included. Factors including mortality rate, hospitalisation duration, acute physiology and chronic health evaluation (APACHE-II) score, white blood cell (WBC) count, c-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and time to abdominal pain disappearance were assessed. The pooled analysis of seven studies revealed a significant reduction in mortality risk, [risk ratio, (95% CI: 0.20, 0.65); i2 = 53%]. No significant reductions in the hospitalization duration [mean difference, 4.18 days (95% CI: -9.03, 0.68); i2 = 98%] and APACHE-II score [mean difference, -0.11 (95% CI: -1.48, 1.26); i2 = 97%] were noted. Treatment with ulinastatin demonstrated significant improvements in WBC count, CRP levels, time to abdominal pain disappearance, TNF-α levels, and IL-6 levels. Ulinastatin, administered either alone or in combination with other therapeutic agents, was associated with significant improvements in clinical outcomes and reduced mortality rates in patients with severe acute pancreatitis.

Budd-Chiari syndrome (BCS) is the constellation of clinical signs and symptoms resulting from occlusion of two or more hepatic veins, often due to an underlying thrombophilic disorder. Acute myeloid leukemia has been rarely reported to be associated with hepatic vein thrombosis due to hyperleukocytosis, hyperfibrinolysis and disseminated intravascular coagulation. We report a case of acute promyelocytic leukemia where the clinical onset of the hematological disease was with acute BCS.

Metabolic-associated fatty liver disease (MAFLD) or metabolic dysfunction-associated steatohepatitis (MASH) in lean individuals represents a distinctive subset of MASH. Current pharmacotherapies, for MASH as demonstrated in in clinical trials, predominantly target obese patients with limited consideration for lean MASH. We aimed to systematically review the literature on the pharmacotherapy of lean MASH. We searched standard medical databases, such as PubMed, Embase, Scopus, Cochrane CENTRAL, and ClinicalTrials.gov to identify eligible studies published in English up to 31 December 2023 regarding the effect of pharmacological interventions in individuals with lean MASH. We have summarized the role of various drug classes including peroxisome proliferator-activated receptor agonists, glucagon-like peptide-1 receptor agonists, sodium-glucose cotransporter 2 inhibitors, vitamin E, farnesoid X receptor agonists, selective thyroid hormone receptor-β agonists, and selective cholesterol absorption inhibitors. Consequently, lifestyle interventions, encompassing dietary modifications, exercise, and weight loss particularly directed at visceral obesity or achieving a reduction in body weight are recommended for all non-obese individuals with MASH. A highlight on the only available treatment recommendation for lean MASH is also presented. The available evidence regarding the efficacy of various drugs for the treatment of lean MASH is limited. Conclusive evidence is warranted from clinical trials exclusively involving lean individuals with MASH.