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 com...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 lifethreatening 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.展开更多
BACKGROUND With the withdrawal of paraquat from the market,diquat is widely used,so the treatment of diquat poisoning has become one of the focuses of emergency poisoning diagnosis and treatment.CASE SUMMARY We studie...BACKGROUND With the withdrawal of paraquat from the market,diquat is widely used,so the treatment of diquat poisoning has become one of the focuses of emergency poisoning diagnosis and treatment.CASE SUMMARY We studied the case of a 17-year-old male patient who drank 200 mL(20 g/100 mL)of diquat solution two hours before arriving at the hospital.Despite the use of treatments such as gastric lavage,hemoperfusion,continuous hemodialysis,glucocorticoids,and organ support,the patient’s condition rapidly progressed to multiorgan failure,and he died 23.5 h after admission.CONCLUSION We summarized the clinical characteristics and treatment strategies of diquat poisoning through this case and performed a literature review to provide a basis and direction for clinical treatment.展开更多
AIM: To provoke persistent/chronic multiorgan inflammatory response and to contribute to stones formation followed by fibrosis in hepatobiliary and pancreatic tissues. METHODS: Tumor necrosis factor receptors 1 and 2(...AIM: To provoke persistent/chronic multiorgan inflammatory response and to contribute to stones formation followed by fibrosis in hepatobiliary and pancreatic tissues. METHODS: Tumor necrosis factor receptors 1 and 2(TNFR1/R2) deficient mice reared in-house were given dibutyltin dichloride(DBTC) twice within 10 d by oral gavage delivery. Sham control animals received vehicle treatment and na?ve animals remained untreated throughout the study. Animals were monitored daily for symptoms of pain and discomfort. The abdominal and hindpaw hypersensitivity were assessed with von Frey microfilaments. Exploratory behaviors were recorded at the baseline, after initiation of treatment, and before study termination. Histopathological changes were examined postmortem in tissues. Collagen accumulation and fibrosis were confirmed with Sirius Red staining. RESULTS: Animals lost weight after oral administration of DBTC and developed persistent inflammatory abdominal and hindpaw hypersensitivity compared to sham-treated controls(P < 0.0001). These pain related secondary mechanical hypersensitivity responses increased more than 2-fold in DBTC-treated animals. The drastically diminished rearing and grooming rates persisted after DBTC administration throughout the study. Gross as well as micropathology at one month confirmed that animals treated with DBTC developed chronic hepatobiliary injuries evidenced with activation of stellate cells, multifocal necrosis, fatty degeneration of hepatocytes, periportal infiltration of inflammatory cells, and prominent biliary ductal dilation. The severity of hepatitis was scored 3.7 ± 0.2(severe) in DBTC-treated animals vs score 0(normal) in shamtreated animals. Fibrotic thickening was extensive around portal ducts, in hepatic parenchyma as well as in lobular pancreatic structures and confirmed with Sirius Red histopathology. In addition, pancreatic microarchitecture was presented with distortion of islets, and parenchyma, infiltration of inflammatory cells, degeneration, vacuolization, and necrosis of acinar cells and distention of pancreatic ducts. Extent of pancreatic damage and pancreatitis were scored 3.6 ± 0.4(severe) for DBTC-treated in contrast to score 0(normal) in sham-treated animals. The gall bladder became expanded with ductal distention, and occasional bile stones were detected along with microscopic hepatic lesions. DBTC-treated animals developed splenic hypertrophy with increased weight and length(P < 0.01) along with thymic atrophy(P < 0.001). Finally, colitic lesions and colitis were prominent in DBTC-treated animals and scored 3.4 ± 0.3(moderately severe) vs 0(normal) for the sham-treated animals. CONCLUSION: This is the first report of chronic inflammatory multiorgan hepatobiliary pancreatitis, along with fibrosis and calculi formation induced reliably utilizing oral DBTC administration in TNFR1/R2 deficient mice.展开更多
This editorial describes the indications and technical aspects of the simultaneous retrieval of thoracic and abdominal organs in Maastricht III donors as well as the preservation of such organs until their implantation.
Clinical severity of scrub typhus ranges from mild to fatal. Acute pancreatitis with abscess formation is a rare complication among patients with scrub typhus. This paper reports a case of scrub typhus in a 75 years o...Clinical severity of scrub typhus ranges from mild to fatal. Acute pancreatitis with abscess formation is a rare complication among patients with scrub typhus. This paper reports a case of scrub typhus in a 75 years old man with acute pancreatitis with abscess formation and multiorgan failure. Abdominal computed tomography showed multiple infected pancreatic pseudocysts with peri-pancreatic infiltration. Multiorgan failure was successfully treated with doxycycline, ceftriaxone, and supportive management. The pancreatic abscess was successfully drained percutaneously and the sizes of pseudocysts decreased remarkably.展开更多
BACKGROUND: Chronic pancreatitis following acute fatty liver of pregnancy is rarely reported.METHODS: We treated a 34-year-old woman who developed acute fatty liver of pregnancy (AFLP) after delivery by caesarean sect...BACKGROUND: Chronic pancreatitis following acute fatty liver of pregnancy is rarely reported.METHODS: We treated a 34-year-old woman who developed acute fatty liver of pregnancy (AFLP) after delivery by caesarean section at 32 weeks of gestation. AFLP was complicated by acute pancreatitis and multiple organ failure. The management of the disease was primarily supportive. She recovered from acute fulminant liver failure and multi-organ failure, apart from the development of symptomatic chronic pancreatitis thereafter. RESULTS: Investigations failed to identify any other causes of chronic pancreatitis. The patient responded very well to pancreatic enzyme supplement for the treatment of steatorrhoea.CONCLUSION: To our knowledge, this is the first report of chronic pancreatitis as a consequence of multi-organ dysfunction caused by AFLP.展开更多
基金Supported by Jilin Province Science and Technology Agency Project,No.20210101350JCProject of Jilin Provincial Finance Department,No.JLSWSRCZX2023-60Beijing iGandan Foundation Fund for Artificial Liver,No.iGandanF-1082023-RGG025.
文摘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 lifethreatening 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.
文摘BACKGROUND With the withdrawal of paraquat from the market,diquat is widely used,so the treatment of diquat poisoning has become one of the focuses of emergency poisoning diagnosis and treatment.CASE SUMMARY We studied the case of a 17-year-old male patient who drank 200 mL(20 g/100 mL)of diquat solution two hours before arriving at the hospital.Despite the use of treatments such as gastric lavage,hemoperfusion,continuous hemodialysis,glucocorticoids,and organ support,the patient’s condition rapidly progressed to multiorgan failure,and he died 23.5 h after admission.CONCLUSION We summarized the clinical characteristics and treatment strategies of diquat poisoning through this case and performed a literature review to provide a basis and direction for clinical treatment.
文摘AIM: To provoke persistent/chronic multiorgan inflammatory response and to contribute to stones formation followed by fibrosis in hepatobiliary and pancreatic tissues. METHODS: Tumor necrosis factor receptors 1 and 2(TNFR1/R2) deficient mice reared in-house were given dibutyltin dichloride(DBTC) twice within 10 d by oral gavage delivery. Sham control animals received vehicle treatment and na?ve animals remained untreated throughout the study. Animals were monitored daily for symptoms of pain and discomfort. The abdominal and hindpaw hypersensitivity were assessed with von Frey microfilaments. Exploratory behaviors were recorded at the baseline, after initiation of treatment, and before study termination. Histopathological changes were examined postmortem in tissues. Collagen accumulation and fibrosis were confirmed with Sirius Red staining. RESULTS: Animals lost weight after oral administration of DBTC and developed persistent inflammatory abdominal and hindpaw hypersensitivity compared to sham-treated controls(P < 0.0001). These pain related secondary mechanical hypersensitivity responses increased more than 2-fold in DBTC-treated animals. The drastically diminished rearing and grooming rates persisted after DBTC administration throughout the study. Gross as well as micropathology at one month confirmed that animals treated with DBTC developed chronic hepatobiliary injuries evidenced with activation of stellate cells, multifocal necrosis, fatty degeneration of hepatocytes, periportal infiltration of inflammatory cells, and prominent biliary ductal dilation. The severity of hepatitis was scored 3.7 ± 0.2(severe) in DBTC-treated animals vs score 0(normal) in shamtreated animals. Fibrotic thickening was extensive around portal ducts, in hepatic parenchyma as well as in lobular pancreatic structures and confirmed with Sirius Red histopathology. In addition, pancreatic microarchitecture was presented with distortion of islets, and parenchyma, infiltration of inflammatory cells, degeneration, vacuolization, and necrosis of acinar cells and distention of pancreatic ducts. Extent of pancreatic damage and pancreatitis were scored 3.6 ± 0.4(severe) for DBTC-treated in contrast to score 0(normal) in sham-treated animals. The gall bladder became expanded with ductal distention, and occasional bile stones were detected along with microscopic hepatic lesions. DBTC-treated animals developed splenic hypertrophy with increased weight and length(P < 0.01) along with thymic atrophy(P < 0.001). Finally, colitic lesions and colitis were prominent in DBTC-treated animals and scored 3.4 ± 0.3(moderately severe) vs 0(normal) for the sham-treated animals. CONCLUSION: This is the first report of chronic inflammatory multiorgan hepatobiliary pancreatitis, along with fibrosis and calculi formation induced reliably utilizing oral DBTC administration in TNFR1/R2 deficient mice.
文摘This editorial describes the indications and technical aspects of the simultaneous retrieval of thoracic and abdominal organs in Maastricht III donors as well as the preservation of such organs until their implantation.
文摘Clinical severity of scrub typhus ranges from mild to fatal. Acute pancreatitis with abscess formation is a rare complication among patients with scrub typhus. This paper reports a case of scrub typhus in a 75 years old man with acute pancreatitis with abscess formation and multiorgan failure. Abdominal computed tomography showed multiple infected pancreatic pseudocysts with peri-pancreatic infiltration. Multiorgan failure was successfully treated with doxycycline, ceftriaxone, and supportive management. The pancreatic abscess was successfully drained percutaneously and the sizes of pseudocysts decreased remarkably.
文摘BACKGROUND: Chronic pancreatitis following acute fatty liver of pregnancy is rarely reported.METHODS: We treated a 34-year-old woman who developed acute fatty liver of pregnancy (AFLP) after delivery by caesarean section at 32 weeks of gestation. AFLP was complicated by acute pancreatitis and multiple organ failure. The management of the disease was primarily supportive. She recovered from acute fulminant liver failure and multi-organ failure, apart from the development of symptomatic chronic pancreatitis thereafter. RESULTS: Investigations failed to identify any other causes of chronic pancreatitis. The patient responded very well to pancreatic enzyme supplement for the treatment of steatorrhoea.CONCLUSION: To our knowledge, this is the first report of chronic pancreatitis as a consequence of multi-organ dysfunction caused by AFLP.
