Methanol is a widely used industrial and household alcohol that poses significant health risks upon exposure. Despite its extensive use, methanol poisoning remains a critical public health concern globally, often resulting from accidental or intentional ingestion and outbreaks linked to contaminated beverages. Methanol toxicity stems from its metabolic conversion to formaldehyde and formic acid, leading to severe metabolic acidosis and multiorgan damage, including profound CNS effects and visual impairments. Epidemiological data underscore the widespread impact of methanol poisoning, with alarming case fatality rates reported in various countries. Comprehensive prevention and effective management strategies are urgently needed to address the significant morbidity and mortality associated with methanol poisoning. The clinical manifestations of methanol toxicity vary between adult and pediatric populations and between acute and chronic exposure. Adults typically present with gastrointestinal and neurological symptoms, whereas pediatric patients often exhibit more severe outcomes due to differences in metabolism and body weight. The diagnosis of methanol poisoning involves a combination of clinical evaluation, laboratory testing, and advanced diagnostic techniques. The identification of metabolic acidosis, elevated anion and osmolal gaps, and confirmation through methanol and formate levels are critical for accurate diagnosis. Timely intervention is crucial, and the management of methanol poisoning includes securing the airway, breathing, and circulation; addressing metabolic acidosis with sodium bicarbonate; administering antidotes such as fomepizole or ethanol; and administering hemodialysis, which plays a pivotal role in eliminating methanol and its toxic metabolites, especially in severe cases. The complexity of methanol poisoning necessitates a comprehensive approach encompassing early recognition, prompt intervention, and coordinated care among healthcare providers. Increased awareness, effective prevention strategies, and timely treatment protocols are essential to mitigate severe health consequences and improve patient survival and recovery.

Background: Vasopressin (VP) and hydrocortisone (HC) have been shown to improve outcomes in patients with septic shock. However, there is very little literature addressing the impact of the timing of the combination. Objective: This study was conducted to evaluate the impact of early versus late initiation of both VP and HC on time to shock reversal in septic shock patients. Methods: This was a retrospective study conducted at a tertiary academic medical center. Data were collected from system-generated reports, which were used to identify patients with septic shock who were admitted to an intensive care unit (ICU) and received both VP and HC. The primary endpoint was time to shock reversal. Patients were divided into the “early” group if both VP and HC were initiated within 12 hours of vasopressor initiation or into the “late” group if either VP or HC (or both agents) were initiated after 12 hours of vasopressor initiation. Results: A total of 122 patients were included in the analysis. Early initiation was associated with a shorter time to shock reversal (34 hours vs 65 hours; P = 0.012) compared to late initiation. There were no differences in ICU length of stay, mortality, the number patients requiring renal replacement therapy, or the duration of mechanical ventilation in either group. Conclusion and relevance: Our study addressed a major gap in the literature and suggests that adding the combination of VP and HC within 12 hours of septic shock may be associated with improved patient outcomes.

Background: Antiphospholipid Syndrome (APS) is an autoimmune condition that increases thrombosis risk. Although Vitamin K antagonists (VKA) are standard treatment, interest in direct oral anticoagulants (DOAC) has grown. Recent studies evaluated DOAC across all APS subgroups. This review updates our understanding of DOAC's efficacy and safety compared to VKA in preventing thrombotic complications, integrating new findings into the literature. Methods: A systematic review across PubMed/Medline, Embase, and Cochrane was conducted in accordance with PRISMA guidelines. The quality of randomized controlled trials (RCTs) and cohort studies was assessed using the Cochrane Risk of Bias tool and the Newcastle-Ottawa Scale, respectively. Meta-analysis calculated odds ratios (OR) using the random effect model for arterial and venous thrombotic and bleeding outcomes Results: Of a total of 2385 records identified, the meta-analysis included 11 studies, comprising 5 RCTs and 7 observational studies, with a combined total of 1813 participants. The analysis revealed no significant difference in the odds of venous thromboembolism (VTE) between DOAC and VKA (OR = 0.80; 95% CI 0.41-1.56). However, a significant increase in thromboembolism recurrence was noted in triple-positive APS patients using DOAC compared to VKA (OR = 3.62; 95% CI 1.10-11.98). The risk of major bleeding was similar between DOAC and VKA (OR = 1.02; 95% CI 0.62-1.68). Additionally, the pooled analysis indicated a higher risk of arterial thrombosis with DOAC (OR = 6.21; 95% CI 2.06-18.76). Conclusion: Overall, findings suggest DOAC are comparably safe but increase the risk of arterial thrombosis and VTE in triple-positive APS, favoring warfarin for prophylaxis.

Background: Nutritional deficiency anemias—including iron, vitamin B12, and folate deficiencies—are common worldwide and are increasingly recognized as potential contributors to venous thromboembolism (VTE). Mechanistic and epidemiologic data suggest that anemia may promote thrombosis through hypoxia, endothelial activation, reactive thrombocytosis, and hyperhomocysteinemia. However, a focused synthesis of clinical and genetic evidence specifically linking nutritional deficiency anemia to VTE has been lacking. Methods: We conducted a systematic search of PubMed and the Cochrane Library from inception to 30 September 2025 to identify studies assessing nutritional deficiency anemia in relation to VTE outcomes. Eligible studies included observational designs, case reports, case series, and Mendelian randomization (MR) analyses. Quality assessment followed the Newcastle–Ottawa Scale (NOS), Joanna Briggs Institute (JBI) checklists, and ROB-MR. The review was registered in PROSPERO (CRD420251235479). Results: Seven studies met the inclusion criteria. Observational analytical studies consistently showed that anemia was associated with adverse VTE-related outcomes. Lower hemoglobin predicted higher short-term mortality in acute pulmonary embolism (HR 1.16 per 1 g/dL decrease), increased symptomatic VTE among hospitalized patients (RR 1.94), and greater long-term bleeding and mortality risk in VTE cohorts (HRs 1.41–2.89). Iron-deficiency anemia increased the odds of VTE in population-based data (OR 1.43), and case reports described unprovoked DVT in young adults with moderate to severe anemia. The MR study indicated a potential causal association between anemia traits and thrombosis at unusual anatomical sites (OR 1.446). No study demonstrated a significant association with recurrent VTE. Most analytical studies were rated as good–high quality. Conclusion: Across multiple study designs, anemia—particularly iron-deficiency anemia and low baseline hemoglobin—appears to be an underrecognized factor associated with elevated VTE risk and adverse VTE-related outcomes. However, direct evidence for vitamin B12- and folate-deficiency anemia remains limited, and further well-designed prospective studies are required to confirm causality and clarify the contribution of specific nutritional deficiency subtypes, as well as to support integration of anemia assessment into VTE risk models.

Background: Hyperuricemia has been linked to various adverse clinical outcomes. Data on the clinical outcomes and the relationship between hyperuricemia and sepsis remain limited. The aim of this study was to evaluate the impact of hyperuricemia on clinical outcomes in sepsis patients and to identify whether it can predict the mortality in this patient population. Methods: This was a retrospective cohort study of adult patients with sepsis admitted to the intensive care unit (ICU) from 1 January 2021 to 31 December 2023. The patients were divided into hyperuricemia and non-hyperuricemia groups. Hyperuricemia was defined as a serum uric acid level > 416.4 µmol/L (7.0 mg/dL) in males or >357.0 µmol/L (6.0 mg/dL) in females based on the first serum uric acid reading within 24 h of ICU admission. The primary outcome of this study was ICU mortality. Secondary outcomes included in-hospital mortality, progression to septic shock, and ICU and hospital lengths of stay (LOSs). Results: A total of 599 patients were included in the study. Among these, 303 were in hyperuricemia group, while 296 were in the non-hyperuricemia group. The incidence of ICU and in-hospital mortality was higher in the hyperuricemia group compared to the non-hyperuricemia group (26.7% vs. 18.9% (p < 0.001) and 34.7% vs. 19.3% (p < 0.001), respectively). After adjusting for cofounders, hyperuricemia was not a predictor of ICU mortality (OR 1.52, 95% CI 0.95–2.43, p = 0.083). Most secondary outcomes were similar between the groups. However, the hyperuricemia group had a higher incidence of progression to septic shock (67.3% vs. 50.7%, p < 0.001), and hospital LOS was significantly longer in the hyperuricemia group (384 vs. 264 h, p = 0.004). Conclusions: Our findings demonstrated that hyperuricemia in sepsis patients was associated with worse clinical outcomes such as higher ICU and hospital mortality. Moreover, there was a higher incidence of septic shock progression and longer hospital LOS. The other outcomes were not statistically significantly different. Further prospective research is warranted to confirm these findings.

Background: Acetazolamide is a carbonic anhydrase inhibitor that inhibits proximal sodium bicarbonate reabsorption, thus increasing urinary bicarbonate excretion. Despite its widespread distribution in the body and beneficial effects on alkaline diuresis, its efficacy and the optimal dosage and duration of acetazolamide in treating metabolic acidosis remain areas of uncertainty. This review aims to assess the effectiveness of acetazolamide in treating chloride depletion alkalosis, mainly induced by diuretics, through a systematic evaluation of clinical research data. Methods: A comprehensive search was conducted on PubMed and Embase. This review included randomized controlled trials, observational studies, and case reports. Data extraction included dose, route, frequency, indication, duration of therapy, patient demographics, and outcomes. Results: A comprehensive search strategy identified 107 studies, of which 7 met the inclusion criteria after full-text review. The reviewed studies encompassed two randomized clinical trials, one case–control study, and three case reports, collectively involving 111 patients with metabolic alkalosis. The studies revealed varied outcomes regarding the efficacy of acetazolamide in treating metabolic alkalosis induced by diuretics. While some trials demonstrated significant improvements in serum bicarbonate levels and acid–base balance, others found no statistically significant reduction in the duration of mechanical ventilation. Case reports highlighted the successful use of acetazolamide in diverse patient populations, including pediatric patients with heart disease and individuals with chronic obstructive pulmonary disease. Conclusions: Acetazolamide holds promise in addressing chloride depletion alkalosis. However, a targeted clinical trial investigating its effectiveness in diuretic-induced metabolic alkalosis must strengthen the existing knowledge base.