Acute liver failure as initial presentation in a Chinese patient with Budd-Chiari syndrome due to protein C deficiency: A case report and literature review.

Acute liver failure is an uncommon presentation in the clinic. Common causes for acute liver failure include viral hepatitis and drug-related hepatotoxicity. However, acute liver failure due to Budd-Chiari syndrome is rare. This case highlights the importance of necessary constrast-enhanced imaging studies to rule out vascular etiologies of acute liver failure, in addition to common causes like viral or drug-induced hepatic failure. We present a case of a male Chinese patient who presented with nausea, vomiting, fatigue, and fever after eating a large amount of fatty food. Six days after hospitalization, the patient developed acute liver failure and hepatic encephalopathy. Contrast-enhanced computerized tomography and ultrasound examinations revealed thromboses in the hepatic veins and inferior vena cava. Further testing also showed decreased protein C activity. Therefore, a diagnosis of Budd-Chiari syndrome secondary to protein C deficiency was made. He received supportive care and a transjugular intrahepatic portal shunt. Hepatic function, coagulation panel results, and clinical presentations gradually returned to normal. Budd-Chiari syndrome from protein C deficiency could be a rare but valid cause of acute liver failure in Chinese patients.

Hemorrhagic Fever with Renal Syndrome Complicated by Acute Pancreatitis, High Intraocular Pressure, and Pulmonary Involvement: a Case Report.

Hemorrhagic fever with renal syndrome (HFRS), a naturally occurring epidemic disease, is primarily caused by hantaviruses. It frequently involves the lungs and is characterized by symptoms such as fever, hemorrhage, and renal failure. However, the occurrence of acute pancreatitis (AP) in HFRS patients can be neglected, and high intraocular pressure (IOP) is exceedingly uncommon. In this report, we discuss the case of a 30-year-old male who presented with fever, nausea, vomiting, and abdominal pain. Physical examination revealed extremity petechiae rashes and elevated IOP. Laboratory tests indicated coagulopathy and renal failure. A computed tomography scan confirmed AP. Further testing revealed a positive anti-hantavirus IgM antibody. The patient received supportive care, fluid hydration, hemofiltration, mannitol, brinzolamide, and brimonidine to reduce IOP. Three days post-admission, the patient developed shortness of breath and chest pain. Subsequent chest computed tomography revealed pulmonary edema and bilateral pleural effusion. Treatment included oxygen supply, respiratory support, and thoracentesis, with continued hemofiltration. The patient recovered, regaining normal pulmonary and renal functions and normalized IOP. This case underscores the importance of comprehensive evaluations and vigilant monitoring in HFRS patients, particularly measuring IOP in those with visual complaints, to save lives and reduce morbidity.

Multiorgan dysfunction syndrome due to high-dose cantharidin poisoning: A case report.

BACKGROUND: This report delves into the diagnostic and therapeutic journey undertaken by a patient with high-dose cantharidin poisoning and multiorgan dysfunction syndrome (MODS). Particular emphasis is placed on the comprehensive elucidation of the clinical manifestations of high-dose cantharidin poisoning, the intricate path to diagnosis, and the exploration of potential underlying mechanisms. CASE SUMMARY: A patient taking 10 g of cantharidin powder orally subsequently developed MODS. The patient was treated with supportive care, fluid hydration and antibiotics, and hemoperfusion and hemofiltration therapy for 24 h and successfully recovered 8 d after hospital admission. Cantharidin poisoning can cause life-threatening MODS and is rare clinically. This case underscores the challenge in diagnosis and highlights the need for early clinical differentiation to facilitate accurate assessment and prompt intervention. CONCLUSION: This article has reported and analyzed the clinical data, diagnosis, treatment, and prognosis of a case of high-dose cantharidin poisoning resulting in MODS and reviewed the relevant literature to improve the clinical understanding of this rare condition.

Lethal diquat poisoning manifesting as central pontine myelinolysis and acute kidney injury: A case report and literature review.

Diquat is a nonselective herbicide that is used as a contact and preharvest desiccant to control terrestrial and aquatic vegetation. Increasing numbers of cases of diquat poisoning have recently been reported. Organs commonly affected by diquat poisoning include the kidney, liver, and lung. Neurological involvement of diquat poisoning is relatively rare. A 21-year-old man ingested 100 mL of diquat (20 g/100 mL) 5 hours before admission. Fifteen minutes after ingestion, he developed nausea and vomiting. The patient was sent to the emergency intensive care unit, and gastric lavage was performed. Continuous renal replacement therapy and continuous venovenous hemodiafiltration with hemoperfusion were performed, and methylprednisolone was administered. Five days after admission, the patient developed disturbance of consciousness and positive bilateral Babinski signs. Head computed tomography demonstrated hypodensity in the pons. At 11 days after admission, brain magnetic resonance imaging showed acute pontine demyelination. At 15 days after admission, the patient died of multiple organ dysfunction syndrome. We encountered a case of diquat poisoning with central pontine myelinolysis and acute kidney injury. This case highlights the clinical value of neuroimaging examination for early diagnosis of central pontine myelinolysis.

Characteristics of CD4+CD25+Foxp3+ regulatory T cells in patients with multiple organ dysfunction syndrome.

Multiple organ dysfunction syndrome (MODS) is a systemic inflammation. The aim of the present study was to evaluate the role of CD4+CD25+Foxp3+ regulatory T cells (Treg) in patients with MODS and to determine the association between Treg cells and serum cytokine levels. The percentage of Treg in 42 MODS patients and 10 healthy subjects was evaluated using flow cytometry. Serum levels of cytokines were measured using an enzyme-linked immunosorbent assay. The percentage of Treg cells was significantly elevated in patients with MODS on Day 1 (P<0.05). At Day 7, the percentage of Treg cells in MODS patients was reduced, but remained higher in comparison with the control group (P<0.05). The CD4+/CD8+ ratio and the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10 and IL-1ß were significantly enhanced in patients with MODS by Day 1. TNF-α, IL-2, IL-4 and IL-10 levels were gradually reduced to normal by Day 7, whereas the IL-6, IL-8 and IL-1ß levels remained higher compared with the healthy subjects (P<0.001). The present results demonstrated an elevated percentage of CD4+CD25+Foxp3+ Treg cells in patients with MODS. Therefore, the proinflammatory cytokines TNF-α, IL-2, IL-6, IL-8 may promote MODS development, whereas the anti-inflammatory cytokines IL-4 and IL-10 may protect against MODS.

Effect of vasopressin on hippocampal injury in a rodent model of asphyxial cardiopulmonary arrest.

The effect of vasopressin on the neuronal injury following the restoration of spontaneous circulation (ROSC) in cardiac arrest (CA) is not yet fully understood. The present study was conducted in order to investigate the effect of vasopressin alone, or in combination with epinephrine, on the ROSC and hippocampal injury in a rat model of asphyxial CA. Asphyxial CA was induced in 144 rats by clamping the tracheal tube, and animals were allocated equally into the following three groups: Treatment with vasopressin (0.8 U/kg); epinephrine (0.2 mg/kg); or vasopressin (0.8 U/kg) plus epinephrine (0.2 mg/kg). An additional 48 rats underwent a sham surgical procedure without asphyxial CA and cardiopulmonary resuscitation. Hippocampal tissue was harvested at 1, 3, 6 and 12 h post-ROSC, and the levels of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) p65 were determined using immunohistochemistry. In comparison with rats treated with epinephrine alone, higher ROSC success rates were observed in rats treated with vasopressin, or vasopressin plus epinephrine. In addition, treatment with vasopressin attenuated hippocampal injury and reduced hippocampal p38 MAPK and NF-κB expression more efficiently compared with epinephrine alone. In conclusion, treatment with vasopressin exhibits a protective effect in patients experiencing CA, and this may be attributed to the inhibition of p38 MAPK and NF-κB expression.

Prognostic Value of Plasma Visfatin Level for Chinese Patients with Severe Carbon Monoxide Poisoning.

BACKGROUND: This prospective observatory study was designed to investigate whether plasma visfatin might serve as a marker of prognosis in patients with severe carbon monoxide (CO) poisoning. METHODS: A total of 52 consecutive patients with severe CO poisoning and 52 gender- and age- matched healthy subjects were enrolled in the study, and their plasma visfatin levels were determined using an enzyme-linked immunosorbent assay. The clinical outcomes, including in-hospital mortality, 6-month mortality, and poor outcome (Glasgow Outcome Scale score of 1 - 3), were recorded. RESULTS: Plasma visfatin levels were statistically significantly higher in patients than in healthy controls (97.4 ± 28.0 ng/mL vs. 12.1 ± 3.7 ng/mL; p < 0.001). Multivariate logistic regression analysis showed that plasma visfatin level was an independent prognostic predictor of in-hospital mortality [odds ratio (OR), 1.214; 95% confidence interval (CI), 1.103 - 1.425; p < 0.001], 6-month mortality (OR, 1.269; 95% CI, 1.085 - 1.534; p < 0.001), and 6-month poor outcome (OR, 1.302; 95% CI, 1.023 - 1.520; p < 0.001). Moreover, receiver operating characteristic curves showed that plasma visfatin level had high predictive value for in-hospital mortality [area under curve (AUC), 0.931; 95% CI, 0.832 - 1.000], 6-month mortality (AUC, 0.894; 95% CI, 0.801 - 0.987), and 6-month poor outcome (AUC, 0.886; 95% CI, 0.796 - 0.977). CONCLUSIONS: Plasma visfatin levels are significantly higher in patients with severe CO poisoning and could be a useful biomarker to predict short- and long-term clinical outcome after severe CO poisoning.

Neuroprotective effects of erythropoietin in patients with carbon monoxide poisoning.

The purpose of this study was to evaluate the efficacy of erythropoietin (EPO) for treating patients with carbon monoxide (CO) poisoning. We conducted a randomized, prospective study of 103 patients with CO poisoning in two groups: an EPO group (n = 54; patients received EPO) and a placebo group (n = 49; patients received normal saline). The study endpoints were the functional outcome at day 30 (the Barthel index and neurologic sequelae), National Institutes of Health Stroke Scale (NIHSS) score, and the levels of S-100ß. At 18 days, the NIHSS score improved significantly and S-100ß levels significantly decreased in patients in the EPO group. At 30 days, patients in the EPO group had a superior Barthel index and fewer patients had delayed neurologic sequelae (DNS). This study demonstrated that early administration of EPO to patients with CO poisoning improved neurological outcomes and reduced the incidence of DNS.