A mass event of paraquat poisoning via inhalation.

Objective: In January 2023, a rare event of collective inhalation paraquat poisoning occurred in Shandong, China. To analyze the clinical characteristics of an event of respiratory tract paraquat poisoning through inhalation. Methods: Clinical data from eight patients with paraquat inhalation poisoning were retrospectively analyzed. Results: The patients were mainly exposed to paraquat via the respiratory tract. The main clinical manifestations were ocular and respiratory irritation. Lung computed tomography (CT) showed that all eight patients had varying degrees of lung injury, mainly manifesting as exudative lesions. Laboratory tests revealed arterial blood gas hypoxemia, abnormal white blood cell count, and increased neutrophil ratio. Sufficient glucocorticoid impact therapy was effective, and all eight patients survived. Conclusion: Eight patients experienced chest tightness, shortness of breath, and varying degrees of lung injury due to inhalation of paraquat through the respiratory tract. The early use of glucocorticoids and other comprehensive treatment measures, active prevention and treatment of lung infections, and protection of organ function have beneficial effects in such cases.

Case report: Analysis of a case of hydrogen sulfide poisoning in a waste treatment plant.

This paper summarizes and analyzes the clinical data of a patient with Occupational hydrogen sulfide poisoning admitted to our hospital on March 4, 2023. On the morning of March 2, 2023, the patient worked at an environmental energy company (waste treatment plant) in Shandong Province for the first time, The job was to flush the sludge from the walls of the sludge treatment tank (anaerobic tank) with a water gun, which can release hydrogen sulfide gas. When the patient was about to start work after entering the tank for about 1 min, he suddenly smelled a harsh and pungent odor, felt dizzy and weak, and then the patient suddenly fainted. After hearing the sound of the patient fainting, the workman waiting at the entrance of the tank immediately called someone to go into the tank and quickly pull the patient out, and sent to the local hospital. In the local hospital, the patient was confused, accompanied by irritability, convulsion and other manifestations, and was treated with sedation and nutritional support. Two days later, the patient's condition did not improve. For further diagnosis and treatment, the patient was transferred to the Department of Poisoning and Occupational Diseases in our hospital. After comprehensive treatment in our hospital, the patient got better and was discharged. Subsequent reexamination and follow-up showed that the patient recovered well. The work unit of the patient did not provide any personal protective equipment. According to the field investigation after the accident, the pipeline around the sludge treatment tank was blocked by sludge, resulting in a large amount of high concentration of H2S accumulated in the tank, causing the patient to faint soon after entering the tank, and his worker should be in the tank for a short time, and no health abnormalities were found. Hydrogen sulfide has a strong irritation to the human body, which can lead to asphyxia or even death in severe cases. The safety prevention and prevention knowledge of hydrogen sulfide poisoning should be popularized among enterprises and workers to reduce the occurrence of such incidents.

Tim-3 facilitates immune escape in benzene-induced acute myeloid leukemia mouse model by promoting macrophage M2 polarization.

Benzene poisoning can cause acute myeloid leukemia (AML) through a variety of passways. Tim-3 has gained prominence as a potential candidate in mediating immunosuppression in tumor microenvironments. The macrophage polarization is also related to immune escape. Herein, we reported that Tim-3 and macrophage M2 polarization play a vital role in benzene-induced AML. First, the benzene-induced AML C3H/He mouse model was constructed by subcutaneously injecting 250 mg/kg of benzene. After six months, macrophage phenotype, cytokines, and Tim-3 expression levels were investigated. Flow cytometry assay revealed that the T-cell inhibitory receptor Tim-3 was significantly upregulated in both bone marrow and spleen of the benzene-induced AML mouse model. Elisa's results displayed a decreased serum level of IL-12 while increased TGF-ß1. Mechanistically, changes in cytokine secretion promote the growth of M2-type macrophages in the bone marrow and spleen, as determined by immunofluorescence assay. The increased levels of PI3K, AKT, and mTOR in the benzene-exposure group further proved the crucial role of Tim-3 in regulating the functional status of macrophages in the AML microenvironment. These results demonstrate that Tim-3 and macrophage polarization may play a vital role during the immune escape of the benzene-induced AML. This study provides a new potential intervention site for immune checkpoint-based AML therapeutic strategy.

Case report: Reversible splenial lesion syndrome caused by diquat poisoning.

Diquat (DQ), chemically known as 1,1 '-ethylene-2,2' -bipyridine, is a non-selective herbicide for leaf removal and drying. It has toxic effects on central nervous system cells, and toxic neurological lesions include axonal degeneration and pontine myelolysis. At the same time, DQ can also affect the activity of dopaminergic nerve cells through oxidative stress, causing degeneration and reducing dopamine uptake. With the increasing application of DQ in agricultural production, the clinical reports of neurotoxicity caused by acute DQ poisoning are also increasing. At present, DQ rapid-phase-related toxic encephalopathy mainly involves the pons, midbrain, basal ganglia, thalamus and other brain regions. However, this case is unusual in that the lesion mainly involved the splenium of the corpus callosum. It is also the first time to be reported.

Case report: Occupational poisoning incident from a leak of chloroacetyl chloride in Jinan, Shandong, China.

Chloroacetyl chloride is a potent acylation agent that decomposes violently in water to produce chloroacetic acid and irritant hydrogen chloride. It and its decomposition products are corrosive to the eyes, skin, and respiratory system and can cause multiple organ failure. Herein, we report cases of poisoning by chloroacetyl chloride and its decomposition products in the skin and respiratory system. After exposure, one patient developed vomiting, irritability, coma, hypoxemia, hypotension, acidosis, and hypokalemia. Another patient developed bronchiolitis, pneumonia, and decreased vision. One patient died and two recovered. Chloroacetyl chloride and its decomposition products are corrosive and can damage multiple organs after absorption through the skin and respiratory tract, leading to severe heart failure. Cardiogenic shock may be the primary cause of early mortality.

Study on the therapeutic effect of glucocorticoids on acute kidney injury in rats exposed to diquat.

AIMS: To preliminarily explore, whether glucocorticoids have a therapeutic effect on diquat-induced acute kidney injury in rats. METHOD: 150 Wistar rats were randomly divided into six groups: exposure model group (DQ group), dexamethasone control group (GC group), blank control group (Ctrl group), dexamethasone 2.1 mg/kg dose group (DQ+L-GC group), dexamethasone 4.2 mg/kg dose group (DQ+M-GC group), and dexamethasone 8.4 mg/kg dose group (DQ+H-GC group), with 25 rats in each group. Each group was further divided into five subgroups, 24 h, 3 d, 7 d, 14 d, and 21 d after exposure, according to the feeding time and the course of treatment, with five animals in each subgroup. The rats in DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups were administered 115.5 mg/kg diquat by gavage, respectively. Moreover, 30 min after gavage, rats in DQ+L-GC group, DQ+M-GC group, DQ+H-GC group and GC group were intragastric administered dexamethasone 2.1 mg/kg, 4.2 mg/kg, 8.4 mg/kg and 8.4 mg/kg, respectively. After 7 days, the intraperitoneal injection of dexamethasone was changed to 6.3 mg/kg prednisone by intragastric administration. Subsequently, 7 days later, it was changed to 3.15 mg/kg prednisone by intragastric administration until the end of the experiment on 21 days. After the start of the experiment, changes in the conditions of the rats in each group were observed at a fixed time every day, changes in the body weight of the rats were monitored at the same time, and the death of the rats was recorded at 24 h, 3 d, 7 d, 14 d, and 21 d after exposure. The rats were sacrificed by an intraperitoneal injection of 100 mg/kg sodium pentobarbital overdose. Blood was collected by puncture of the inferior vena cava, used to determine Cr and BUN. The upper segment of the left kidney was collected for histopathological examination. Elisa was used to detect neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in the lower segment of left kidney. TLR4, Myd88, and NF-κB were detected in the right kidney. RESULTS: (1) After exposure, most rats in DQ group, DQ+L-GC group, DQ+M-GC group and DQ+H-GC group showed shortness of breath, oliguria, diarrhea, yellow hair and other symptoms. No symptoms and related signs were observed in Ctrl group and GC group. (2) The weight of rats in the Ctrl group and the GC group increased slowly during the test. the body weight of the rats in the DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups continued to decrease after self-infection. Body weight dropped to the lowest point at approximately 7 d, and gradually increased from 7 d to 21 d. (3) A small amount of capillary congestion in the medulla was observed after 7 days in the GC group. The DQ group showed tubular atrophy, edema of the epithelial cells, and over time, the tubules were seen dilated and became irregular in shape; large amount of capillary congestion was also observed in the renal cortex and medulla. The renal injury in the DQ+L-GC group was less than that in the DQ group. DQ+H-GC group had no obvious injury before 7 d, but more renal tubules were seen in the DQ+H-GC group from 7 d to 14 d. (4) Compared with the DQ group, there was no difference before 14 d, and at 14 d-21 d, DQ+L-GC group, DQ+M-GC group, DQ+H-GC group all had different degrees of decline. NGAL content: Compared with the DQ group, the content of NGAL and KIM-1 in kidney tissue of the DQ+L-GC, DQ+M-GC, and DQ+H-GC groups decreased compared with the DQ group at each time node. (5) Compared with the Ctrl group, the expression of TNF-α, TLR4, MyD88, NF-κB in the DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups at each time node increased in the renal tissue. The content of TNF-α, TLR4, MyD88, NF-κB in kidney tissue of the DQ+L-GC, DQ+M-GC, and DQ+H-GC groups at each time node was lower than that in the DQ group. CONCLUSION: (1) Diquat can cause kidney damage in rats, mainly manifested as renal tubular atrophy, epithelial cell edema, capillary congestion and dilation, and the renal function damage indicators have been improved to varying degrees. (2) Glucocorticoids have therapeutic effects on acute kidney injury in rats exposed to diquat. During the treatment, the efficacy of glucocorticoids did not increase with increasing doses after reaching a dose of 4.2 mg/kg. (3) TLR4 receptor-mediated TLR4/Myd88/NF-κB signaling pathway is involved in the inflammatory response of acute kidney injury in diquat poisoning rats. Glucocorticoids can inhibit the inflammatory response, thereby affecting the expression of TLR4/Myd88/NF-κB signaling pathway-related proteins.

Multiorgan failure caused by Chinese herbal medicine Xanthii Fructus poisoning: a case report.

BACKGROUND: Xanthii Fructus was used in the treatment of rhinitis and related nasal disease. It is the most commonly used chemically active component in compounds formulated for the treatment of rhinitis. However, poisoning, resulting in serious consequences, can easily occur owing to cocklebur overdose, improper processing, or usage without processing. CASE PRESENTATION: We reported on a 55-year-old man who experienced allergic rhinitis for 2.5 years. He ingested unprocessed Xanthii Fructus for 2 months as treatment. However, he developed anorexia; nausea; abdominal pain; general weakness; hiccups; oliguria and anuria; significantly elevated serum alanine aminotransferase, aspartate aminotransferase, and creatinine levels; and abnormalities in blood coagulation series. Nutritional support; daily drugs for liver protection, gastric protection, inflammation reduction; fresh plasma; and cryoprecipitate infusion were administered. Continuous venovenous hemodialysis (Prismaflex ST100) was also administered. However, the patient's multiple organ failure gradually worsened, ultimately leading to death. CONCLUSION: Xanthii Fructus poisoning affects multiple systems, and its clinical manifestations are complex. Therefore, it is easily misdiagnosed and missed. Along with careful inquiry of medical and medication history, early diagnosis and intervention are vital for a successful treatment. It is also important to educate people and create awareness about this poisoning. Therefore, this intractable case has great clinical significance.

Current situation and influencing factors for suicidal intent in patients with intentional acute pesticide poisoning.

Introduction: Since pesticides have been widely used in agricultural production, acute pesticide poisoning (APP) has gradually become a worldwide public health problem. Recently, the number of APP cases has been high in China, and the intentional self-administration of pesticides is the main cause of APP. However, there is a lack of relevant studies on the factors influencing suicidal intent in patients with intentional APP. This study aimed to explore the current situation and influencing factors for suicidal intent among patients with intentional APP. Methods: In this cross-sectional study, we enrolled a total of 225 patients with intentional APP admitted to the emergency department of our Grade A comprehensive hospital in Shandong Province between June 2019 and January 2021. Patients were investigated using a health status interview questionnaire, Beck Suicidal Intent Scale, Duke Social Support Index, psychological stress scale, Dickman Impulsivity Inventory, Trait Anxiety Inventory, Center for Epidemiologic Studies Depression Scale, and Beck Hopelessness Scale. Descriptive statistics, single-factor analysis, and multiple linear regression were used for data analysis. Results: Suicidal intent scores were collected and averaged (14.23 ± 6.22). Multiple linear regression analysis revealed that marital status, residential area, impulsivity, hopelessness, depression, psychological strain, and social support impact suicidal intent. Conclusion: Patients with intentional APP have high suicidal intent. Therefore, different interventions should be tailored to different patients.

Construction of a clinical nursing pathway for acute paraquat poisoning: Evidence-based research.

Aim: This study used the Delphi method and clinical expert discussions to develop an acute paraquat poisoning clinical nursing pathway to standardize acute paraquat poisoning nursing care. Background: In clinical practice, especially in basic-level hospitals, there is no unified standard pattern of treatment and nursing care for patients with paraquat poisoning. Methods: An extensive literature search was used to gather current clinical guidelines for treating paraquat poisoning which were then compiled into a Delphi expert letter of inquiry questionnaire which was sent to a panel of 12 experts. Results: A preliminary draft of the clinical nursing pathway table for acute paraquat poisoning with a standard hospitalization period of 21 days was established, with 6, 23, and 152 classes and I, II, and III indicators determined. The clinical nursing pathway table reduced the randomness of work, avoided nursing interruptions or omissions caused by negligence, and simplified the writing of nursing documents. Conclusions: The clinical nursing pathway can promote and improve the nursing care quality and management efficiency and has good clinical application value.

Case report: Methemoglobinemia caused by nitrobenzene poisoning.

Nitrobenzene poisoning is uncommon, with most cases occurring in the dye, paint, and other chemical industries. Nitrobenzene enters the body mainly through the skin, respiratory tract, and oral cavity. Nitrobenzene poisoning symptoms include hypermethemoglobinemia, hemolytic anemia, liver and kidney dysfunction, cardiogenic pulmonary edema, and toxic encephalopathy, which endanger people's lives. Therefore, we present a case of nitrobenzene poisoning caused by skin absorption, focusing on its clinical characteristics and treatment outcomes. A 58 years-old man presented to our department with confusion and cyanosis. He has a history of hypertension and cerebral infarction. The patient was diagnosed with moderate occupational acute benzene poisoning with nitro compounds. Symptomatic support, methylene blue, and other antioxidant treatments were commenced after diagnosis. After treatment, the patient's condition gradually improved, and he was discharged.

Case report: Death caused by 1, 3-dichloropropene, a novel fumigant used in China.

As an efficient and broad-spectrum soil fumigant, 1, 3-dichloropropene is widely used in the control of nematodes, soil pests, and plant pathogens. However, as a volatile chlorine-containing organic compound, 1, 3-dichloropropene is harmful to human health, although no deaths caused by inhalation of 1, 3-dichloropropene have been reported. This article describes the case of a 50-year-old man who died of acute renal failure and brain edema after inhaling 1, 3-dichloropropene at work. This case demonstrates that 1, 3-dichloropropene can be absorbed through the respiratory tract and that exposure to 1, 3-dichloropropene in a confined environment without any protective measures can cause death in humans.

Case Report: Acute Intoxication from Phosphine Inhalation.

Aluminum phosphide is a highly effective insecticide for fumigation in granaries and is often used in rural grain storage. However, people's awareness of its toxicity is not strong. A case of acute inhalation toxicity of phosphine caused by the use of aluminum phosphide to fumigate a granary is reported here. The case presented with aspiration pneumonia and acute left heart failure. The patient was cured using comprehensive life support treatment, including respiratory support, antiarrhythmic treatment, and blood pressure maintenance with vasoactive drugs. There is no specific antidote for phosphine poisoning at present, and the comprehensive application of restricted fluid resuscitation, high-dose glucocorticoid shock, vasoactive drugs and bedside hemofiltration is significant in improving the prognosis of patients. It is also important to remind people to pay attention to their own protection in the process of using aluminum phosphide.

Therapeutic potential of amitriptyline for paraquat-induced pulmonary fibrosis: Involvement of caveolin-1-mediated anti-epithelial-mesenchymal transition and inhibition of apoptosis.

OBJECTIVE: Treatment of pulmonary fibrosis caused by paraquat (PQ) poisoning remains problematic. Amitriptyline (AMT) has multiple pharmacological effects. Here we investigated the anti-fibrotic effect of AMT on PQ-induced pulmonary fibrosis and its possible mechanism. METHODS: C57BL/6 mice were randomly divided into control, PQ, PQ + AMT and AMT groups. Histopathology of the lungs, blood gas analysis, and levels of hydroxyproline (HYP), transforming growth factor ß1 (TGF-ß1) and interleukin 17 (IL-17) were measured. The siRNA transfection inhibited caveolin-1 in A549 cells, which induced epithelial-mesenchymal transition (EMT) by PQ and followed intervention with AMT. E-cadherin, N-cadherin, α-smooth muscle actin (α-SMA) and caveolin-1 were studied by immunohistochemistry and western blot analysis. The apoptosis rate was measured by flow cytometry. RESULTS: Compared with the PQ group, the PQ + AMT group displayed mild pathological changes in pulmonary fibrosis, lower HYP, IL-17 and TGF- ß1 levels in lung, but high TGF- ß1 in serum. Levels of N-cadherin and α-SMA in the lungs were significantly decreased, but caveolin-1 was increased, while SaO2 and PaO2 levels were higher. Compared with the PQ group, the apoptosis rate, N-cadherin and α-SMA levels in A549 cells were significantly decreased after PQ treatment and high dose AMT intervention (p < 0.01). The expressions of E-cadherin, N-cadherin and α-SMA in the PQ-induced cells transfected with caveolin-1 siRNA or siControl RNA were significantly different (p < 0.01), but the apoptosis rate was unaltered. CONCLUSION: AMT inhibited PQ-induced EMT in A549 cells and improved lung histopathology and oxygenation in mice by up-regulating caveolin-1.

Comparing the application of three thrombosis risk assessment models in patients with acute poisoning: A cross-sectional survey.

Background: Patients with acute toxic hemoperfusion are prone to deep vein thrombosis. However, there is no risk assessment model for thrombosis in patients with acute toxic hemoperfusion. Therefore, we compared three commonly used risk assessment models for deep vein thrombosis to determine the model most suitable for assessment of deep vein thrombosis in patients with acute toxic hemoperfusion. Methods: Caprini, Autar, and Padua thrombosis risk assessment models were used to assess the risk of deep vein thrombosis in patients with acute poisoning and hemoperfusion admitted to a grade A hospital in Shandong province from October 2017 to February 2019. The predictive values of the three models were compared using receiver operating characteristic (ROC) curve analysis. Results: The risk assessment model scores of Caprini, Autar, and Padua were 7.55 ± 1.76, 8.63 ± 2.36, and 3.92 ± 0.55, respectively. The Caprini risk assessment model was significantly different (p < 0.05) in high-risk patients in the thrombus and non-thrombotic groups; the difference between the other two models was not significant (p > 0.05). The areas under the ROC curve of the Caprini, Autar, and Padua risk assessment models were 0.673, 0.585, and 0.535, respectively. The difference in areas under the ROC curve between the Caprini risk assessment model and the Autar risk assessment model as well as the Padua risk assessment model was significant (p < 0.05), but the areas under the ROC curve of the Autar risk assessment model and the Padua risk assessment model were not statistically significant (p > 0.05). The Caprini risk assessment model had a sensitivity of 91.9%, specificity of 33.1%, and a Youden index of 0.249. The sensitivity and specificity of Autar's risk assessment model were 37.0 and 77.2%, respectively, and the Youden index was 0.141. The Padua risk assessment model had a sensitivity of 91.3%, specificity of 15.0%, and a Youden index of 0.063. Conclusion: The three thrombosis risk assessment models were not suitable for patients with acute poisoning and hemoperfusion.

Case series: Diquat poisoning with acute kidney failure, myocardial damage, and rhabdomyolysis.

Diquat is a herbicide that can have deleterious effects on the kidneys, liver, heart, lungs, and central nervous system on ingestion. Diquat poisoning-associated rhabdomyolysis has rarely been reported. We describe two cases of diquat poisoning with acute renal failure, myocardial damage, and rhabdomyolysis. Case 1: A 17-year-old man experienced anuria after ingesting ~200 mL of diquat 16 h prior. On admission, his creatinine (400 µmol/L), urea (11.7 mmol/L), creatine kinase (2,534 IU/L), and myohemoglobin (4,425 ng/mL) concentrations were elevated. Case 2: An 18-year-old woman who ingested ~200 mL of diquat 5.5 h prior to admission had normal creatinine, urea, and creatine kinase concentrations. Eleven hours after ingestion, she developed anuria with elevated creatinine (169 µmol/L) concentration; her creatine kinase (13,617 IU/L) and myohemoglobin (>3,811 ng/mL) concentrations were remarkably elevated 24 h after ingestion. Both patients also had elevated aminotransferase and myocardial enzyme concentrations. After undergoing hemoperfusion and hemofiltration, blood diquat concentrations in cases 1 and 2 on admission (16/6 h after ingestion), after hemoperfusion (20/11 h after ingestion), and after 8 h of hemofiltration/8 h of hemofiltration and 2 h of hemoperfusion (29/21 h after ingestion) were 4.9/9.1, 3.4/5.4, and 1.5/1.2 µg/mL, respectively. Severe diquat poisoning can cause acute kidney failure and rhabdomyolysis. Rhabdomyolysis may induce myocardial injury, aggravating kidney damage, and also increase transaminase concentration. Hemoperfusion and hemofiltration could be effective treatments for eliminating diquat in the blood.

Toxic Encephalopathy and Methemoglobinemia after 5-Amino-2-(trifluoromethyl)pyridine Poisoning.

The aromatic amino compound 5-amino-2-(trifluoromethyl)pyridine acts as an intermediate in the synthesis of pharmaceutical products. However, the toxicity profile of this compound is sparse and no related poisoning events have been reported. Here, we report the case of a 35-year-old man who inhaled 5-amino-2-(trifluoromethyl)pyridine at work. After inhalation, the patient rapidly developed symptoms such as dizziness, fatigue, nausea, vomiting, chest tightness, and loss of consciousness. After admission, methemoglobinemia, hemolytic anemia, acute renal failure, and toxic encephalopathy occurred. Symptoms improved significantly after intravenous treatment with a low dose of methylene blue. This revealed that 5-amino-2-(trifluoromethyl)pyridine is toxic to the human body and can be absorbed through the respiratory tract, resulting in methemoglobinemia and toxic encephalopathy; thus, caution should be taken in industrial production.

Reversible Splenial Lesion Syndrome (RESLES) after Nitrous Oxide Abuse: A Case Report.

BACKGROUND: Reversible splenial-lesion syndrome (RESLES) is a relatively rare and underrecognized clinical-imaging syndrome involving the splenium of the corpus callosum (SCC). RESLES can be caused by various etiologies. CASE DESCRIPTION: An 18-year-old man with no previous history of neurological or psychiatric disorders presented to our hospital with headache, intermittent blurred vision, and limb weakness after 150 days of recreational nitrous-oxide abuse. The patient's serum vitamin B12 concentration was normal, and magnetic-resonance imaging (MRI) examination revealed isointensity on T1-weighted imaging (T1WI) of the corpus callosum and high signal intensity on T2WI, T2FLAIR, and diffusion-weighted MRI (DWI); thus, a diagnosis of RESLES was established. The patient received 0.5 mg of mecobalamin daily and nitrous oxide was discontinued. After 4 weeks, the patient's symptoms disappeared and the imaging examination revealed normal findings. CONCLUSION: We report for the first time a case of headache, blurred vision, and hallucination caused by RESLES associated with nitrous-oxide abuse. In cases of headaches and hallucinations of unknown etiology, the possibility of RESLES caused by nitrous oxide abuse should be considered.

Diagnosis and treatment of acquired factor VIII deficiency: a case report and literature review.

Acquired haemophilia A (AHA) is a rare haemorrhagic disease characterized by spontaneous extensive subcutaneous haemorrhage and soft tissue haematoma. The activated partial thromboplastin time is significantly prolonged and cannot be corrected by normal plasma. Approximately 50% of AHA patients lack a specific aetiology, so this can easily result in a misdiagnosis. This current case report describes a 27-year-old male that presented with gingival bleeding, haematuria and haematochezia with no obvious cause. At first, it was thought that he might have experienced anticoagulant rodenticide poisoning, but the subsequent anticoagulant rodenticide test was negative. At the same time, the patient was screened for mutations associated with bleeding and coagulation diseases. Two mutations were identified: a p.Y471H mutation the plasminogen activator, tissue type (PLAT) gene; and a p.Y244Y mutation the serpin family E member 1 (SERPINE1) gene. It should be noted that patient had no previous history of thrombosis or haemorrhagic disease, which confused the diagnosis. A professional haemophilia research centre provided clarification of the diagnosis when anti-factor VIII antibodies were detected. The patient was treated with 30 mg/day prednisone orally. Multiple follow-up examinations showed continuous complete remission. No factor VIII antibodies were detected in his blood and coagulation factor VIII increased significantly.