BACKGROUND Fulminant type 1 diabetes mellitus(FT1DM)that occurs during pregnancy or the perinatal period is known as pregnancy-related FT1DM(PF),always without history of abnormal glucose metabolism.Here,we present fo...BACKGROUND Fulminant type 1 diabetes mellitus(FT1DM)that occurs during pregnancy or the perinatal period is known as pregnancy-related FT1DM(PF),always without history of abnormal glucose metabolism.Here,we present four patients who developed FT1DM during treatment but were first diagnosed with gestational diabetes mellitus(GDM).CASE SUMMARY The clinical data of four patients with GDM combined with FT1DM admitted to our hospital between July 2018 and April 2021 were collected,and the patients and their infants were followed up.All patients were diagnosed with GDM during the second trimester and were treated.The blood glucose level elevated suddenly during the third trimester and then were diagnosed with FT1DM.Two patients had an insulin allergy,and two had symptoms of upper respiratory tract infection before onset.One patient developed ketoacidosis,and three developed ketosis.Two patients had cesarean section deliveries,and two had vaginal deliveries.The growth and development of the infants were normal.C-peptide levels were lower than those at onset,suggesting progressive impairment of islet function.The frequencies of the DRB109:01,DQB103:03,DQA103:02,DPA101:03,DPA102:02,DPB105:01,DRB401:03,G 01:01,and G 01:04 human leukocyte antigen(HLA)-G alleles were high in the present study.CONCLUSION In comparison with pregnancy-associated FT1DM(PF),patients with GDM combined with FT1DM had an older age of onset,higher body mass index,slower onset,fewer prodromal symptoms,and less acidosis.The pathogenesis may be due to various factors affecting the already fragileβ-cells of GDM patients with genetically susceptible class II HLA genotypes.We speculate that GDM combined with FT1DM during pregnancy,referred to as“double diabetes,”is a subtype of PF with its own unique characteristics that should be investigated further.展开更多
Objective It is difficult to predict fulminant myocarditis at an early stage in the emergency department.The objective of this study was to construct and validate a simple prediction model for the early identification...Objective It is difficult to predict fulminant myocarditis at an early stage in the emergency department.The objective of this study was to construct and validate a simple prediction model for the early identification of fulminant myocarditis.Methods A total of 61 patients with fulminant myocarditis and 160 patients with acute myocarditis were enrolled in the training and internal validation cohorts.LASSO regression and multivariate logistic regression were selected to develop the prediction model.The selection of the model was based on overall performance and simplicity.A nomogram based on the optimal model was built,and its clinical usefulness was evaluated by decision curve analysis.The predictive model was further validated in an external validation group.Results The resulting prediction model was based on 4 factors:systolic blood pressure,troponin I,left ventricular ejection fraction,and ventricular wall motion abnormality.The Brier scores of the final model were 0.078 in the training data set and 0.061 in the internal testing data set,respectively.The C-indexes of the training data set and the testing data set were 0.952 and 0.968,respectively.Decision curve analysis showed that the nomogram model developed based on the 4 predictors above had a positive net benefit for predicting probability thresholds.In the external validation cohort,the model also showed good performance(Brier score=0.007,and C-index=0.989).Conclusion We developed and validated an early prediction model consisting of 4 clinical factors(systolic blood pressure,troponin I,left ventricular ejection fraction,and ventricular wall motion abnormality)to identify potential fulminant myocarditis patients in the emergency department.展开更多
AIM To evaluate the possibility of usingcultured human hepatocytes as a bridge betweenbioartificial liver and liver transplantation.METHODS In this experiment,the efficacy ofextracorporeal bioartificial liver support ...AIM To evaluate the possibility of usingcultured human hepatocytes as a bridge betweenbioartificial liver and liver transplantation.METHODS In this experiment,the efficacy ofextracorporeal bioartificial liver support system(EBLSS)consisting of spheriodal human livercells and cultured hepatocytes supernatant wasassessed in vivo using galactosamine inducedrabbit model of fulminant hepatic failure.RESULTS There was no difference of survivalbetween the two groups of rabbits,but in thesupported rabbits serum alanineaminotransferase,total bilirubin and creatininewere significantly lower and hepatocyte necrosiswas markedly milder than those in controlanimals.In addition,a good viability of humanliver cells was noted after the experiment.CONCLUSION EBLSS plays a biologic role inmaintaining and compensating the function ofthe liver.展开更多
BACKGROUND: Fulminant hepatic failure (FHF) is not uncommon in our clinical practice in Bangladesh. There was a rise in acute hepatitis E virus (HEV) in Bangladesh after the 2004 floods. At that time, most of the coun...BACKGROUND: Fulminant hepatic failure (FHF) is not uncommon in our clinical practice in Bangladesh. There was a rise in acute hepatitis E virus (HEV) in Bangladesh after the 2004 floods. At that time, most of the country was under water for more than a month, leading to sewage contamination of the water supply. The aim of this study was to investigate the etiology of FHF in Bangladesh. METHODS: In this retrospective study, 23 patients with FHF who presented with severe impairment of hepato- cellular function (i.e. encephalopathy, coagulopathy and jaundice) within 6 months of onset of symptoms were included. There were 17 men and 6 women, aged from 18 to 32 years. Four of the women were pregnant. Patients were tested for markers for common hepatotrophic viruses. A relevant history was taken and the Patient Record Book of the Unit was reviewed. RESULTS: 56.52% patients (13/23) had HEV infection, and all were anti-HEV IgM-positive tested by ELISA. HBV infection was detected in 34.78% patients (8/23), all of whom were tested positive for either HBsAg or anti-HBs IgM by ELISA. 8.7% patients (2/23) had a positive history for intake of alcohol and/or drugs. CONCLUSIONS: Acute HEV infection is the leading cause of FHF in Bangladesh. Sewage contamination of the water supply following floods contributes to a higher incidence of HEV infection. HBV infection is also important.展开更多
Wilson’s disease(WD)is an autosomal recessive inherited disorder of hepatic copper metabolism.WD can be present in different clinical conditions,with the most common ones being liver disease and neuropsychiatric dist...Wilson’s disease(WD)is an autosomal recessive inherited disorder of hepatic copper metabolism.WD can be present in different clinical conditions,with the most common ones being liver disease and neuropsychiatric disturbances.Most cases present symptoms at<40years of age.However,few reports exist in the literature on patients in whom the disease presented beyond this age.In this report,we present a case of late onset fulminant WD in a 58-year-old patient in whom the diagnosis was established clinically,by genetic analysis of the ATP7B gene disclosing rare mutations(G1099S and c.1707+3ins T)as well as by high hepatic copper content.We also reviewed the relevant literature.The diagnosis of WD with late onset presentation is easily overlooked.The diagnostic features and the geneticbackground in patients with late onset WD are not different from those in patients with early onset WD,except for the age.Effective treatments for this disorder that can be fatal are available and will prevent or reverse many manifestations if the disease is discovered early.展开更多
A 64-year-old woman was referred to our hospital with jaundice of the bulbar conjunctiva and general fatigue. After admission, she developed hepatic encephalopathy and was diagnosed with fulminant hepatitis based on t...A 64-year-old woman was referred to our hospital with jaundice of the bulbar conjunctiva and general fatigue. After admission, she developed hepatic encephalopathy and was diagnosed with fulminant hepatitis based on the American Association for the Study of Liver Disease(AASLD) position paper. Afterwards, additional laboratory findings revealed that serum ceruloplasmin levels were reduced, urinary copper levels were greatly elevated and Wilson's disease(WD)-specific routine tests were positive, but the Kayser-Fleischer ring was not clear. Based on the AASLD practice guidelines for the diagnosis and treatment of WD, the patient was ultimately diagnosed with fulminant WD. Then, administration of penicillamine and zinc acetate was initiated; however, the patient unfortunately died from acute pneumonia on the 28 th day of hospitalization. At autopsy, the liver did not show a bridging pattern of fibrosis suggestive of chronic liver injury. Here, we present the case of a patient with clinically diagnosed late-onset fulminant WD without cirrhosis, who had positive disease-specific routine tests.展开更多
BACKGROUND Heterogeneous macrophages play an important role in multiple liver diseases,including viral fulminant hepatitis(VFH).Fibrinogen-like protein 2(FGL2)is expressed on macrophages and regulates VFH pathogenesis...BACKGROUND Heterogeneous macrophages play an important role in multiple liver diseases,including viral fulminant hepatitis(VFH).Fibrinogen-like protein 2(FGL2)is expressed on macrophages and regulates VFH pathogenesis;however,the underlying mechanism remains unclear.AIM To explore how FGL2 regulates macrophage function and subsequent liver injury during VFH.METHODS Murine hepatitis virus strain 3(MHV-3)was used to induce VFH in FGL2-deficient(Fgl2-/-)and wild-type(WT)mice.The dynamic constitution of hepatic macrophages was examined.Adoptive transfer of Fgl2-/-or WT bone marrowderived macrophages(BMDMs)into WT recipients with macrophages depleted prior to infection was carried out and the consequent degree of liver damage was compared.The signaling cascades that may be regulated by FGL2 were detected in macrophages.RESULTS Following MHV-3 infection,hepatic macrophages were largely replenished by proinflammatory monocyte-derived macrophages(MoMFs),which expressed high levels of FGL2.In Fgl2-/-mice,the number of infiltrating inflammatory MoMFs was reduced compared with that in WT mice after viral infection.Macrophage depletion ameliorated liver damage in WT mice and further alleviated liver damage in Fgl2-/-mice.Adoptive transfer of Fgl2-/-BMDMs into macrophage-removed recipients significantly reduced the degree of liver damage.Inhibition of monocyte infiltration also significantly ameliorated liver damage.Functionally,Fgl2 deletion impaired macrophage phagocytosis and the antigen presentation potential and attenuated the proinflammatory phenotype.At the molecular level,FGL2 deficiency impaired IRF3,IRF7,and p38 phosphorylation,along with NF-κB activation in BMDMs in response to viral infection.CONCLUSION Infiltrated MoMFs represent a major source of hepatic inflammation during VFH progression,and FGL2 expression on MoMFs maintains the proinflammatory phenotype via p38-dependent positive feedback,contributing to VFH pathogenesis.展开更多
BACKGROUND Sinapic acid(SA)has been shown to have various pharmacological properties such as antioxidant,antifibrotic,anti-inflammatory,and anticancer activities.Its mechanism of action is dependent upon its ability t...BACKGROUND Sinapic acid(SA)has been shown to have various pharmacological properties such as antioxidant,antifibrotic,anti-inflammatory,and anticancer activities.Its mechanism of action is dependent upon its ability to curb free radical production and protect against oxidative stress-induced tissue injuries.AIM To study the hepatoprotective effects of SA against lipopolysaccharide(LPS)/Dgalactosamine(D-GalN)-induced acute liver failure(ALF)in rats.METHODS Experimental ALF was induced with an intraperitoneal(i.p.)administration of 8μg LPS and 800 mg/kg D-GalN in normal saline.SA was administered orally once daily starting 7 d before LPS/D-GalN treatment.RESULTS Data showed that SA ameliorates acute liver dysfunction,decreases serum levels of alanine transaminase(ALT),and aspartate aminotransferase(AST),as well as malondialdehyde(MDA)and NO levels in ALF model rats.However,pretreatment with SA(20 mg/kg and 40 mg/kg)reduced nuclear factor kappalight-chain-enhancer of activated B cells(NF-κB)activation and levels of inflammatory cytokines(tumor necrosis factor-αand interleukin 6).Also,SA increased the activity of the nuclear factor erythroid-related factor 2/heme oxygenase-1(Nrf2/HO-1)signaling pathway.CONCLUSION In conclusion,SA offers significant protection against LPS/D-GalN-induced ALF in rats by upregulating Nrf2/HO-1 and downregulating NF-κB.展开更多
BACKGROUND Fulminant myocarditis is the critical form of myocarditis that is often associated with heart failure, malignant arrhythmia, and circulatory failure. Patients with fulminant myocarditis who end up with seve...BACKGROUND Fulminant myocarditis is the critical form of myocarditis that is often associated with heart failure, malignant arrhythmia, and circulatory failure. Patients with fulminant myocarditis who end up with severe multiple organic failure and death are not rare.AIM To analyze the predictors of in-hospital major adverse cardiovascular events(MACE) in patients diagnosed with fulminant myocarditis.METHODS We included a cohort of adult patients diagnosed with fulminant myocarditis who were admitted to Beijing Anzhen Hospital from January 2007 to December2017. The primary endpoint was defined as in-hospital MACE, including death,cardiac arrest, cardiac shock, and ventricular fibrillation. Baseline demographics,clinical history, characteristics of electrocardiograph and ultrasonic cardiogram,laboratory examination, and treatment were recorded. Multivariable logistic regression was used to examine risk factors for in-hospital MACE, and the variables were subsequently assessed by the area under the receiver operating characteristic curve(AUC).RESULTS The rate of in-hospital MACE was 40%. Multivariable logistic regression analysis revealed that baseline QRS duration > 120 ms was the independent risk factor for in-hospital MACE(odds ratio = 4.57, 95%CI: 1.23-16.94, P = 0.023). The AUC of QRS duration > 120 ms for predicting in-hospital MACE was 0.683(95%CI: 0.532-0.833, P = 0.03).CONCLUSION Patients with fulminant myocarditis has a poor outcome. Baseline QRS duration is the independent risk factor for poor outcome in those patients.展开更多
Mortality rates attributable to fulminant Clostridium difficile(C.difficile) colitis remain high and are reported to be 38%-80%.Historically,the threshold for surgical intervention has been judged empirically because ...Mortality rates attributable to fulminant Clostridium difficile(C.difficile) colitis remain high and are reported to be 38%-80%.Historically,the threshold for surgical intervention has been judged empirically because level I evidence to guide decision making is lacking.Studies of the surgical management of C.difficile infection have been limited by small sample size and the lack of a standard definition of fulminancy.Multiple small and medium-sized series have examined the surgical management of C.difficile.However,because of a lack of prospective,randomized studies,it has been difficult to identify the optimal point for surgical intervention in patients with severe fulminant C.difficile colitis.Our goal was to analyze the existing body of literature in an attempt to define host constellations,which would predict the development of the more aggressive form of this disease and hence justify an early or earlier surgical intervention.A Pubmed search was conducted using the keywords "fulminant","clostridium difficile","surgery",and "colitis".Reviews and Meta-analyses proposing indications for surgical consultation or operative management in patients with C.difficile colitis were included.After analyzing current literature,we identified a number of parameters that are associated with unfavorable outcomes.The parameters include age greater than 65 years old,peritoneal signs on physical examination,abdominal distension,signs of end-organ failure,hypotension less than 90 mmHg systolic blood pressure,tachycardia greater than 100 bpm,vasopressor requirement,elevated WBC count of greater than at least 16 × 10 9 /μL,serum lactate of greater than 2.2 mmol/L,and lastly,radiologic findings suggestive of pancolitis,ascites,megacolon,or colonic perforation.Even though fairly strong evidence exists in contemporary literature,we recommend use of these identified parameters with caution in clinical practice when it comes to the actual decision to treat certain patients more aggressively.The identified risk factors should be used to lower surgeons' threshold for operative treatment early in the course of the展开更多
Fulminant type 1 diabetes mellitus(FT1DM)is a subtype of type 1 diabetes mellitus characterized by an abrupt onset and a rapid and complete functional loss of isletβcells.It is a very rare disease generally associate...Fulminant type 1 diabetes mellitus(FT1DM)is a subtype of type 1 diabetes mellitus characterized by an abrupt onset and a rapid and complete functional loss of isletβcells.It is a very rare disease generally associated with ketoacidosis and the absence of circulating pancreatic islet-related autoantibodies.Diabetic ketoacidosis with normal blood glucose levels has been reported during sodiumglucose co-transporter 2(SGLT2)inhibitor therapy.CASE SUMMARY The patient was a 43-year-old woman that consulted a medical practitioner for malaise,thirst,and vomiting.Blood analysis showed high blood glucose levels(428 mg/dL),a mild increase of hemoglobin A1c(6.6%),and increased ketone bodies in urine.The patient was diagnosed with type 2 diabetes mellitus.The patient was initially treated with insulin,which was subsequently changed to an oral SGLT2 inhibitor.Antibodies to glutamic acid decarboxylase were negative.Four days after receiving oral SGLT2 inhibitor,she consulted at Mie University Hospital,complaining of fatigue and vomiting.Laboratory analysis revealed diabetic ketoacidosis with almost normal blood glucose levels.The endogenous insulin secretion was markedly low,and the serum levels of islet-related autoantibodies were undetectable.We made the diagnosis of FT1DM with concurrent SGLT2 inhibitor-associated euglycemic diabetic ketoacidosis.The patient's general condition improved after therapy with intravenous insulin and withdrawal of oral medication.She was discharged on day 14 with an indication of multiple daily insulin therapy.CONCLUSION This patient is a rare case of FT1DM that developed SGLT2 inhibitor-associated diabetic ketoacidosis with almost normal blood glucose levels.This case report underscores the importance of considering the diagnosis of FT1DM in patients with negative circulating autoantibodies and a history of hyperglycemia that subsequently develop euglycemic diabetic ketoacidosis following treatment with a SGLT2 inhibitor.展开更多
Fulminant hepatitis (FH) is a rare and devastating syndrome caused by a variety of hepatic insults. It characterized by severe metabolic derangements, neurologic complications and ultimately, multiorgan failure. Liver...Fulminant hepatitis (FH) is a rare and devastating syndrome caused by a variety of hepatic insults. It characterized by severe metabolic derangements, neurologic complications and ultimately, multiorgan failure. Liver transplantation is the gold standard therapy for patients with irreversible FH. The major areas of current research in this field include the development of: hepatic support devices, strategies to accelerate hepatic regeneration and criteria for accurate prognostic classification of patients. This review aims to focus on the definitions, aetiologies and management strategies for FH.展开更多
Fulminant hepatic failure(FHF) is a critical illness that can be comorbid to primary liver damage.FHF shows a high mortality rate,and patients with FHF require intensive therapy,including plasma apheresis.However,inte...Fulminant hepatic failure(FHF) is a critical illness that can be comorbid to primary liver damage.FHF shows a high mortality rate,and patients with FHF require intensive therapy,including plasma apheresis.However,intensive care at the present is not enough to restore the severe liver damage or promote hepatocellular reproduction,and a standard therapy for the treatment of FHF has not been established.An 86-year-old female with FHF was admitted to our hospital.Her manifestation demonstrated a clinical situation of systemic inflammatory response syndrome(SIRS) and disseminated intravascular coagulation.A diagnosis of fulminant hepatitis was made according to the definition given in the position paper of the American Association for the Study of Liver Diseases.Her serum hepatocyte growth factor(HGF) level had increased to 11.84 ng/m L.The HGF level indicated massive liver damage as seen in FHF.Recombinant thrombomodulin(r TM) was administered daily from the admission day for 1 wk at 380 U/kg.The patient's white blood cells and C-reactive protein responded to the r TM treatment within a few days.The HGF level and PT recovered to the normal range.The levels of proinflammatory cytokines(tumor necrosis factor-α and interleukin-1β) were suppressed by the administration of r TM.The patient's hepatic function(e.g.,PT and albumin) completely recovered without plasma exchange.r TM may modulate the over-response of SIRS with the improvement of proinflammatory cytokines.The underlying mechanism is thought to be the inhibitory effect of r TM on highmobility group box 1(HMBG1).The pathogenesis of HMBG1 protein in fulminant hepatic failure has beenalready known.A novel favorable effect of r TM for SIRS would be promising for FHF,and the wide application of r TM for SIRS should be considered.展开更多
BACKGROUND: Hepatocyte nuclear factor 4 alpha (HNF4α) plays an important role in regulating cytokine-induced inflammatory responses. This study aimed to investigate the role of HNF4α in the development of fulminant ...BACKGROUND: Hepatocyte nuclear factor 4 alpha (HNF4α) plays an important role in regulating cytokine-induced inflammatory responses. This study aimed to investigate the role of HNF4α in the development of fulminant hepatic failure (FHF) induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN). METHODS: The FHF model was induced by simultaneous intraperitoneal injection of LPS/D-GalN in mice. Three days prior to LPS/D-GalN administration, HNF4α short-hairpin interfering RNA expression plasmid or physiological saline was injected via the tail vein with a hydrodynamics-based procedure. The degree of hepatic damage and cumulative survival rate were subsequently assessed. RESULTS: The expression of HNF4α was increased in the early stage after LPS/D-GalN administration. Inhibiting the expression of HNF4α reduced serum levels of alanine aminotransferase and aspartate aminotransferase, alleviated histological injury, and improved the survival of mice with FHF. In addition, both serum and hepatic tumor necrosis factor alpha expression were suppressed when HNF4α expression was inhibited in mice with FHF. CONCLUSION: Inhibiting HNF4α expression protects mice from FHF induced by LPS/D-GalN, but the exact mechanism behind this needs further investigation.展开更多
AIM:To investigate the change in intestinal dendritic cell(DC)number in fulminant hepatic failure(FHF).METHODS:An animal model of FHF was created.Intestinal CD11b/c was detected by immunohistochemistry and Western blo...AIM:To investigate the change in intestinal dendritic cell(DC)number in fulminant hepatic failure(FHF).METHODS:An animal model of FHF was created.Intestinal CD11b/c was detected by immunohistochemistry and Western blot.Quantitative real-time polymerase chain reaction(PCR)was used to detect intestinal integrin-αm RNA expression.Intestinal CD83,CD86,CD74,CD3 and AKT were detected by immunohistochemistry,Western blot and PCR.Phosphorylated-AKT(p-AKT)was detected by immunohistochemistry and Western blot.RESULTS:In the FHF group[D-galactosamine(D-Galn)+lipopolysaccharide(LPS)group],the mice began to die after 6 h;conversely,in the D-Galn and LPS groups,the activity of mice was poor,but there were no deaths.Immunohistochemistry results showed that in FHF,the expression of CD11b/c(7988400±385941vs 1102400±132273,P<0.05),CD83(13875000±467493 vs 9257600±400364,P<0.05),CD86(7988400±385941 vs 1102400±13227,P<0.05)and CD74(11056000±431427 vs 4633400±267903,P<0.05)was significantly increased compared with the normal saline(NS)group.Compared with the NS group,the protein expression of CD11b/c(5.4817±0.77 vs 1.4073±0.37,P<0.05)and CD86(4.2673±0.69 vs 1.1379±0.42,P<0.05)was significantly increased.Itg-α(1.1224±0.3 vs 0.4907±0.19,P<0.05),CD83(3.6986±0.40 vs 1.0762±0.22,P<0.05)and CD86(1.5801±0.32 vs 0.8846±0.10,P<0.05)m RNA expression was increased significantly in the FHF group.At the protein level,expression of CD74in the FHF group(2.3513±0.52)was significantly increased compared with the NS group(1.1298±0.33),whereas in the LPS group(2.3891±0.47),the level of CD74 was the highest(P<0.05).At the gene level,the relative expression of CD74 m RNA in the FHF group(1.5383±0.26)was also significantly increased in comparison to the NS group(0.7648±0.22;P<0.05).CD3 expression was the highest in the FHF group(P<0.05).In the FHF,LPS and D-Galn groups,the expression of AKT at the protein and m RNA levels was elevated compared with the NS group,but there wasno statistical significance(P>0.05).The p-AKT protein expression in the FHF(1.54±0.06),LPS(1.56±0.05)and D-Galn(1.29±0.03)groups was higher than that in the NS group(1.07±0.03)(P<0.05).CONCLUSION:In FHF,a large number of DCs mature,express CD86,and activate MHC classⅡmolecular pathways to induce a T cell response,and the AKT pathway is activated.展开更多
Acute liver failure, also known as fulminant hepatic failure(FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral ...Acute liver failure, also known as fulminant hepatic failure(FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral edema and intracranial hypertension are common causes of mortality in patients with FHF. The management of patients who present acute liver failure starts with determining the cause and an initial evaluation of prognosis. Regardless of whether or not patients are listed for liver transplantation, they should still be monitored for recovery, death, or transplantation. In the past, neuromonitoring was restricted to serial clinical neurologic examination and, in some cases, intracranial pressure monitoring. Over the years, this monitoring has proven insufficient, as brain abnormalities were detected at late and irreversible stages. The need for real-time monitoring of brain functions to favor prompt treatment and avert irreversible brain injuries led to the concepts of multimodal monitoring and neurophysiological decision support. New monitoring techniques, such as brain tissue oxygen tension, continuous electroencephalogram, transcranial Doppler, and cerebral microdialysis, have been developed. These techniques enable early diagnosis of brain hemodynamic, electrical, and biochemical changes, allow brain anatomical and physiological monitoring-guided therapy, and have improved patient survival rates. The purpose of this review is to discuss the multimodality methods available for monitoring patients with FHF in the neurocritical care setting.展开更多
Serological methods were used to determine the cause of fulminant hepatitisin 207 patients. They were admitted to the isolation wards of 4 hospitals inShenyang between 1986-1990. The final diagnoses were: hepatitis ty...Serological methods were used to determine the cause of fulminant hepatitisin 207 patients. They were admitted to the isolation wards of 4 hospitals inShenyang between 1986-1990. The final diagnoses were: hepatitis type A 4 cas-es (2.0%), type B 144 cases (69.4% ),superinfections with A and B 3 cases (1.5%), hepatitis non-A non-B (NANB) 51 cases (24.6%), type D 2 cases (1.0%), type E 2 cases (1.0%) and cytomegalovirus (CW) infection 1 case (0.5%). The risk factors were found to be concerned with type D and several typesuper infections (prognosis poor).展开更多
We present a case of a healthy 72-year-old man with herpes simplex hepatitis (HSVH) development soon after ordinary surgery for biliary stones. A sudden onset of hepatitis associated with high fever and leukopenia eme...We present a case of a healthy 72-year-old man with herpes simplex hepatitis (HSVH) development soon after ordinary surgery for biliary stones. A sudden onset of hepatitis associated with high fever and leukopenia emerged on postoperative day 5, followed by a rapid and lethal course (died on day 9), despite an acyclovir therapy on day 8. Postmortem liver biopsy revealed positive immunostaining for herpes simplex virus(HSV) type-1. The serum tests(available after the death) were negative for anti-HSV immunogloblulins, but positive for HSV DNA. A review of 15 cases of postsurgical HSVH along with 42 cases of non-surgical HSH showed that (1): A wide spectrum of surgical procedures was involved; and (2): High mortality (87%) associated with lower rates of ante-mortem diagnosis (20%) and acyclovir treatment (20%). Due to the difficulty in diagnosis and lethal nature, an early clinical suspension and prompt empirical anti-viral intervention are imperative for postsurgical hepatitis with undetermined etiology, characterized by fever and leucopenia.展开更多
The model of fulminant hepatic failure induced by acetaminophen was established in dogs to observe the changes of hepatic hemodynamics and plasma histamine levels in portal vein (PV), hepatic vein (HV), abdominal aort...The model of fulminant hepatic failure induced by acetaminophen was established in dogs to observe the changes of hepatic hemodynamics and plasma histamine levels in portal vein (PV), hepatic vein (HV), abdominal aorta (AA) and inferior vena cava (ICV). The results showed that the portal vein resistance (PVR) was elevated and portal venous blood flow (PVF) was decreasedl hepatic artery resistance (HAR) was decreased and the hepatic artery blood flow (HAF),portal venous pressure (PVP), wedged hepatic venous pressure (WHVP) and inferior vena cava pressure (ICVP) had no changes. The histamine of the PV, HV,ICV and AA were all elevated after formation of fulminant hepatie failure. And the increasing wave Of the HV was the highest. The increased histamine in HV may be mediated by H, receptor.causing the contraction of hepatic venulae, result ing liver sinusoid congestion, increasing PVR and decreasing PVF which exacerbate the liver cell damage. Moreover, the more selvere liver damage, the more histamine was released, and a vicious circle may ensue. Our results also suggest the possibility of using,H1 receptor antagonist to treat the disturbance of liver hemodynamfics in severe acute liver damage. The increased histamine in systematic circulation as a vasodilator may lower blood pressure and accelerate heart beats.The increase of plasma histamine may play an important role in the changes of hepatic and systemic hemodynamics in fulminant hepatic failure.展开更多
基金Supported by National Natural Science Foundation of China,No.82270864.
文摘BACKGROUND Fulminant type 1 diabetes mellitus(FT1DM)that occurs during pregnancy or the perinatal period is known as pregnancy-related FT1DM(PF),always without history of abnormal glucose metabolism.Here,we present four patients who developed FT1DM during treatment but were first diagnosed with gestational diabetes mellitus(GDM).CASE SUMMARY The clinical data of four patients with GDM combined with FT1DM admitted to our hospital between July 2018 and April 2021 were collected,and the patients and their infants were followed up.All patients were diagnosed with GDM during the second trimester and were treated.The blood glucose level elevated suddenly during the third trimester and then were diagnosed with FT1DM.Two patients had an insulin allergy,and two had symptoms of upper respiratory tract infection before onset.One patient developed ketoacidosis,and three developed ketosis.Two patients had cesarean section deliveries,and two had vaginal deliveries.The growth and development of the infants were normal.C-peptide levels were lower than those at onset,suggesting progressive impairment of islet function.The frequencies of the DRB109:01,DQB103:03,DQA103:02,DPA101:03,DPA102:02,DPB105:01,DRB401:03,G 01:01,and G 01:04 human leukocyte antigen(HLA)-G alleles were high in the present study.CONCLUSION In comparison with pregnancy-associated FT1DM(PF),patients with GDM combined with FT1DM had an older age of onset,higher body mass index,slower onset,fewer prodromal symptoms,and less acidosis.The pathogenesis may be due to various factors affecting the already fragileβ-cells of GDM patients with genetically susceptible class II HLA genotypes.We speculate that GDM combined with FT1DM during pregnancy,referred to as“double diabetes,”is a subtype of PF with its own unique characteristics that should be investigated further.
文摘Objective It is difficult to predict fulminant myocarditis at an early stage in the emergency department.The objective of this study was to construct and validate a simple prediction model for the early identification of fulminant myocarditis.Methods A total of 61 patients with fulminant myocarditis and 160 patients with acute myocarditis were enrolled in the training and internal validation cohorts.LASSO regression and multivariate logistic regression were selected to develop the prediction model.The selection of the model was based on overall performance and simplicity.A nomogram based on the optimal model was built,and its clinical usefulness was evaluated by decision curve analysis.The predictive model was further validated in an external validation group.Results The resulting prediction model was based on 4 factors:systolic blood pressure,troponin I,left ventricular ejection fraction,and ventricular wall motion abnormality.The Brier scores of the final model were 0.078 in the training data set and 0.061 in the internal testing data set,respectively.The C-indexes of the training data set and the testing data set were 0.952 and 0.968,respectively.Decision curve analysis showed that the nomogram model developed based on the 4 predictors above had a positive net benefit for predicting probability thresholds.In the external validation cohort,the model also showed good performance(Brier score=0.007,and C-index=0.989).Conclusion We developed and validated an early prediction model consisting of 4 clinical factors(systolic blood pressure,troponin I,left ventricular ejection fraction,and ventricular wall motion abnormality)to identify potential fulminant myocarditis patients in the emergency department.
基金the national key project fund of the"9th Five Year Plan",No.96-920-12-02
文摘AIM To evaluate the possibility of usingcultured human hepatocytes as a bridge betweenbioartificial liver and liver transplantation.METHODS In this experiment,the efficacy ofextracorporeal bioartificial liver support system(EBLSS)consisting of spheriodal human livercells and cultured hepatocytes supernatant wasassessed in vivo using galactosamine inducedrabbit model of fulminant hepatic failure.RESULTS There was no difference of survivalbetween the two groups of rabbits,but in thesupported rabbits serum alanineaminotransferase,total bilirubin and creatininewere significantly lower and hepatocyte necrosiswas markedly milder than those in controlanimals.In addition,a good viability of humanliver cells was noted after the experiment.CONCLUSION EBLSS plays a biologic role inmaintaining and compensating the function ofthe liver.
文摘BACKGROUND: Fulminant hepatic failure (FHF) is not uncommon in our clinical practice in Bangladesh. There was a rise in acute hepatitis E virus (HEV) in Bangladesh after the 2004 floods. At that time, most of the country was under water for more than a month, leading to sewage contamination of the water supply. The aim of this study was to investigate the etiology of FHF in Bangladesh. METHODS: In this retrospective study, 23 patients with FHF who presented with severe impairment of hepato- cellular function (i.e. encephalopathy, coagulopathy and jaundice) within 6 months of onset of symptoms were included. There were 17 men and 6 women, aged from 18 to 32 years. Four of the women were pregnant. Patients were tested for markers for common hepatotrophic viruses. A relevant history was taken and the Patient Record Book of the Unit was reviewed. RESULTS: 56.52% patients (13/23) had HEV infection, and all were anti-HEV IgM-positive tested by ELISA. HBV infection was detected in 34.78% patients (8/23), all of whom were tested positive for either HBsAg or anti-HBs IgM by ELISA. 8.7% patients (2/23) had a positive history for intake of alcohol and/or drugs. CONCLUSIONS: Acute HEV infection is the leading cause of FHF in Bangladesh. Sewage contamination of the water supply following floods contributes to a higher incidence of HEV infection. HBV infection is also important.
文摘Wilson’s disease(WD)is an autosomal recessive inherited disorder of hepatic copper metabolism.WD can be present in different clinical conditions,with the most common ones being liver disease and neuropsychiatric disturbances.Most cases present symptoms at<40years of age.However,few reports exist in the literature on patients in whom the disease presented beyond this age.In this report,we present a case of late onset fulminant WD in a 58-year-old patient in whom the diagnosis was established clinically,by genetic analysis of the ATP7B gene disclosing rare mutations(G1099S and c.1707+3ins T)as well as by high hepatic copper content.We also reviewed the relevant literature.The diagnosis of WD with late onset presentation is easily overlooked.The diagnostic features and the geneticbackground in patients with late onset WD are not different from those in patients with early onset WD,except for the age.Effective treatments for this disorder that can be fatal are available and will prevent or reverse many manifestations if the disease is discovered early.
文摘A 64-year-old woman was referred to our hospital with jaundice of the bulbar conjunctiva and general fatigue. After admission, she developed hepatic encephalopathy and was diagnosed with fulminant hepatitis based on the American Association for the Study of Liver Disease(AASLD) position paper. Afterwards, additional laboratory findings revealed that serum ceruloplasmin levels were reduced, urinary copper levels were greatly elevated and Wilson's disease(WD)-specific routine tests were positive, but the Kayser-Fleischer ring was not clear. Based on the AASLD practice guidelines for the diagnosis and treatment of WD, the patient was ultimately diagnosed with fulminant WD. Then, administration of penicillamine and zinc acetate was initiated; however, the patient unfortunately died from acute pneumonia on the 28 th day of hospitalization. At autopsy, the liver did not show a bridging pattern of fibrosis suggestive of chronic liver injury. Here, we present the case of a patient with clinically diagnosed late-onset fulminant WD without cirrhosis, who had positive disease-specific routine tests.
基金Supported by the National Science and Technology Major Project,No.2017ZX10202201and the National Natural Science Foundation of China,No.NSFC 81700529。
文摘BACKGROUND Heterogeneous macrophages play an important role in multiple liver diseases,including viral fulminant hepatitis(VFH).Fibrinogen-like protein 2(FGL2)is expressed on macrophages and regulates VFH pathogenesis;however,the underlying mechanism remains unclear.AIM To explore how FGL2 regulates macrophage function and subsequent liver injury during VFH.METHODS Murine hepatitis virus strain 3(MHV-3)was used to induce VFH in FGL2-deficient(Fgl2-/-)and wild-type(WT)mice.The dynamic constitution of hepatic macrophages was examined.Adoptive transfer of Fgl2-/-or WT bone marrowderived macrophages(BMDMs)into WT recipients with macrophages depleted prior to infection was carried out and the consequent degree of liver damage was compared.The signaling cascades that may be regulated by FGL2 were detected in macrophages.RESULTS Following MHV-3 infection,hepatic macrophages were largely replenished by proinflammatory monocyte-derived macrophages(MoMFs),which expressed high levels of FGL2.In Fgl2-/-mice,the number of infiltrating inflammatory MoMFs was reduced compared with that in WT mice after viral infection.Macrophage depletion ameliorated liver damage in WT mice and further alleviated liver damage in Fgl2-/-mice.Adoptive transfer of Fgl2-/-BMDMs into macrophage-removed recipients significantly reduced the degree of liver damage.Inhibition of monocyte infiltration also significantly ameliorated liver damage.Functionally,Fgl2 deletion impaired macrophage phagocytosis and the antigen presentation potential and attenuated the proinflammatory phenotype.At the molecular level,FGL2 deficiency impaired IRF3,IRF7,and p38 phosphorylation,along with NF-κB activation in BMDMs in response to viral infection.CONCLUSION Infiltrated MoMFs represent a major source of hepatic inflammation during VFH progression,and FGL2 expression on MoMFs maintains the proinflammatory phenotype via p38-dependent positive feedback,contributing to VFH pathogenesis.
基金Deanship of Scientific Research at King Saud University,No.RG-1439-083.
文摘BACKGROUND Sinapic acid(SA)has been shown to have various pharmacological properties such as antioxidant,antifibrotic,anti-inflammatory,and anticancer activities.Its mechanism of action is dependent upon its ability to curb free radical production and protect against oxidative stress-induced tissue injuries.AIM To study the hepatoprotective effects of SA against lipopolysaccharide(LPS)/Dgalactosamine(D-GalN)-induced acute liver failure(ALF)in rats.METHODS Experimental ALF was induced with an intraperitoneal(i.p.)administration of 8μg LPS and 800 mg/kg D-GalN in normal saline.SA was administered orally once daily starting 7 d before LPS/D-GalN treatment.RESULTS Data showed that SA ameliorates acute liver dysfunction,decreases serum levels of alanine transaminase(ALT),and aspartate aminotransferase(AST),as well as malondialdehyde(MDA)and NO levels in ALF model rats.However,pretreatment with SA(20 mg/kg and 40 mg/kg)reduced nuclear factor kappalight-chain-enhancer of activated B cells(NF-κB)activation and levels of inflammatory cytokines(tumor necrosis factor-αand interleukin 6).Also,SA increased the activity of the nuclear factor erythroid-related factor 2/heme oxygenase-1(Nrf2/HO-1)signaling pathway.CONCLUSION In conclusion,SA offers significant protection against LPS/D-GalN-induced ALF in rats by upregulating Nrf2/HO-1 and downregulating NF-κB.
基金Supported by Beijing Natural Science Foundation,No.7184205Beijing Talents Fund,No.2017000021469G224Foundation of Beijing Anzhen Hospital,Capital Medical University,No.2016Z07
文摘BACKGROUND Fulminant myocarditis is the critical form of myocarditis that is often associated with heart failure, malignant arrhythmia, and circulatory failure. Patients with fulminant myocarditis who end up with severe multiple organic failure and death are not rare.AIM To analyze the predictors of in-hospital major adverse cardiovascular events(MACE) in patients diagnosed with fulminant myocarditis.METHODS We included a cohort of adult patients diagnosed with fulminant myocarditis who were admitted to Beijing Anzhen Hospital from January 2007 to December2017. The primary endpoint was defined as in-hospital MACE, including death,cardiac arrest, cardiac shock, and ventricular fibrillation. Baseline demographics,clinical history, characteristics of electrocardiograph and ultrasonic cardiogram,laboratory examination, and treatment were recorded. Multivariable logistic regression was used to examine risk factors for in-hospital MACE, and the variables were subsequently assessed by the area under the receiver operating characteristic curve(AUC).RESULTS The rate of in-hospital MACE was 40%. Multivariable logistic regression analysis revealed that baseline QRS duration > 120 ms was the independent risk factor for in-hospital MACE(odds ratio = 4.57, 95%CI: 1.23-16.94, P = 0.023). The AUC of QRS duration > 120 ms for predicting in-hospital MACE was 0.683(95%CI: 0.532-0.833, P = 0.03).CONCLUSION Patients with fulminant myocarditis has a poor outcome. Baseline QRS duration is the independent risk factor for poor outcome in those patients.
文摘Mortality rates attributable to fulminant Clostridium difficile(C.difficile) colitis remain high and are reported to be 38%-80%.Historically,the threshold for surgical intervention has been judged empirically because level I evidence to guide decision making is lacking.Studies of the surgical management of C.difficile infection have been limited by small sample size and the lack of a standard definition of fulminancy.Multiple small and medium-sized series have examined the surgical management of C.difficile.However,because of a lack of prospective,randomized studies,it has been difficult to identify the optimal point for surgical intervention in patients with severe fulminant C.difficile colitis.Our goal was to analyze the existing body of literature in an attempt to define host constellations,which would predict the development of the more aggressive form of this disease and hence justify an early or earlier surgical intervention.A Pubmed search was conducted using the keywords "fulminant","clostridium difficile","surgery",and "colitis".Reviews and Meta-analyses proposing indications for surgical consultation or operative management in patients with C.difficile colitis were included.After analyzing current literature,we identified a number of parameters that are associated with unfavorable outcomes.The parameters include age greater than 65 years old,peritoneal signs on physical examination,abdominal distension,signs of end-organ failure,hypotension less than 90 mmHg systolic blood pressure,tachycardia greater than 100 bpm,vasopressor requirement,elevated WBC count of greater than at least 16 × 10 9 /μL,serum lactate of greater than 2.2 mmol/L,and lastly,radiologic findings suggestive of pancolitis,ascites,megacolon,or colonic perforation.Even though fairly strong evidence exists in contemporary literature,we recommend use of these identified parameters with caution in clinical practice when it comes to the actual decision to treat certain patients more aggressively.The identified risk factors should be used to lower surgeons' threshold for operative treatment early in the course of the
文摘Fulminant type 1 diabetes mellitus(FT1DM)is a subtype of type 1 diabetes mellitus characterized by an abrupt onset and a rapid and complete functional loss of isletβcells.It is a very rare disease generally associated with ketoacidosis and the absence of circulating pancreatic islet-related autoantibodies.Diabetic ketoacidosis with normal blood glucose levels has been reported during sodiumglucose co-transporter 2(SGLT2)inhibitor therapy.CASE SUMMARY The patient was a 43-year-old woman that consulted a medical practitioner for malaise,thirst,and vomiting.Blood analysis showed high blood glucose levels(428 mg/dL),a mild increase of hemoglobin A1c(6.6%),and increased ketone bodies in urine.The patient was diagnosed with type 2 diabetes mellitus.The patient was initially treated with insulin,which was subsequently changed to an oral SGLT2 inhibitor.Antibodies to glutamic acid decarboxylase were negative.Four days after receiving oral SGLT2 inhibitor,she consulted at Mie University Hospital,complaining of fatigue and vomiting.Laboratory analysis revealed diabetic ketoacidosis with almost normal blood glucose levels.The endogenous insulin secretion was markedly low,and the serum levels of islet-related autoantibodies were undetectable.We made the diagnosis of FT1DM with concurrent SGLT2 inhibitor-associated euglycemic diabetic ketoacidosis.The patient's general condition improved after therapy with intravenous insulin and withdrawal of oral medication.She was discharged on day 14 with an indication of multiple daily insulin therapy.CONCLUSION This patient is a rare case of FT1DM that developed SGLT2 inhibitor-associated diabetic ketoacidosis with almost normal blood glucose levels.This case report underscores the importance of considering the diagnosis of FT1DM in patients with negative circulating autoantibodies and a history of hyperglycemia that subsequently develop euglycemic diabetic ketoacidosis following treatment with a SGLT2 inhibitor.
文摘Fulminant hepatitis (FH) is a rare and devastating syndrome caused by a variety of hepatic insults. It characterized by severe metabolic derangements, neurologic complications and ultimately, multiorgan failure. Liver transplantation is the gold standard therapy for patients with irreversible FH. The major areas of current research in this field include the development of: hepatic support devices, strategies to accelerate hepatic regeneration and criteria for accurate prognostic classification of patients. This review aims to focus on the definitions, aetiologies and management strategies for FH.
文摘Fulminant hepatic failure(FHF) is a critical illness that can be comorbid to primary liver damage.FHF shows a high mortality rate,and patients with FHF require intensive therapy,including plasma apheresis.However,intensive care at the present is not enough to restore the severe liver damage or promote hepatocellular reproduction,and a standard therapy for the treatment of FHF has not been established.An 86-year-old female with FHF was admitted to our hospital.Her manifestation demonstrated a clinical situation of systemic inflammatory response syndrome(SIRS) and disseminated intravascular coagulation.A diagnosis of fulminant hepatitis was made according to the definition given in the position paper of the American Association for the Study of Liver Diseases.Her serum hepatocyte growth factor(HGF) level had increased to 11.84 ng/m L.The HGF level indicated massive liver damage as seen in FHF.Recombinant thrombomodulin(r TM) was administered daily from the admission day for 1 wk at 380 U/kg.The patient's white blood cells and C-reactive protein responded to the r TM treatment within a few days.The HGF level and PT recovered to the normal range.The levels of proinflammatory cytokines(tumor necrosis factor-α and interleukin-1β) were suppressed by the administration of r TM.The patient's hepatic function(e.g.,PT and albumin) completely recovered without plasma exchange.r TM may modulate the over-response of SIRS with the improvement of proinflammatory cytokines.The underlying mechanism is thought to be the inhibitory effect of r TM on highmobility group box 1(HMBG1).The pathogenesis of HMBG1 protein in fulminant hepatic failure has beenalready known.A novel favorable effect of r TM for SIRS would be promising for FHF,and the wide application of r TM for SIRS should be considered.
基金supported by grants from the 973 Program of China (2007CB512902)the National Natural Science Foundation of China (30972622)the National Science and Technology Major Project of China (2008ZX10002-006)
文摘BACKGROUND: Hepatocyte nuclear factor 4 alpha (HNF4α) plays an important role in regulating cytokine-induced inflammatory responses. This study aimed to investigate the role of HNF4α in the development of fulminant hepatic failure (FHF) induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN). METHODS: The FHF model was induced by simultaneous intraperitoneal injection of LPS/D-GalN in mice. Three days prior to LPS/D-GalN administration, HNF4α short-hairpin interfering RNA expression plasmid or physiological saline was injected via the tail vein with a hydrodynamics-based procedure. The degree of hepatic damage and cumulative survival rate were subsequently assessed. RESULTS: The expression of HNF4α was increased in the early stage after LPS/D-GalN administration. Inhibiting the expression of HNF4α reduced serum levels of alanine aminotransferase and aspartate aminotransferase, alleviated histological injury, and improved the survival of mice with FHF. In addition, both serum and hepatic tumor necrosis factor alpha expression were suppressed when HNF4α expression was inhibited in mice with FHF. CONCLUSION: Inhibiting HNF4α expression protects mice from FHF induced by LPS/D-GalN, but the exact mechanism behind this needs further investigation.
基金Supported by National Natural Science Foundation of China,No.30871158 and No.81170604Outstanding Scientific Fund of Shengjing Hospital
文摘AIM:To investigate the change in intestinal dendritic cell(DC)number in fulminant hepatic failure(FHF).METHODS:An animal model of FHF was created.Intestinal CD11b/c was detected by immunohistochemistry and Western blot.Quantitative real-time polymerase chain reaction(PCR)was used to detect intestinal integrin-αm RNA expression.Intestinal CD83,CD86,CD74,CD3 and AKT were detected by immunohistochemistry,Western blot and PCR.Phosphorylated-AKT(p-AKT)was detected by immunohistochemistry and Western blot.RESULTS:In the FHF group[D-galactosamine(D-Galn)+lipopolysaccharide(LPS)group],the mice began to die after 6 h;conversely,in the D-Galn and LPS groups,the activity of mice was poor,but there were no deaths.Immunohistochemistry results showed that in FHF,the expression of CD11b/c(7988400±385941vs 1102400±132273,P<0.05),CD83(13875000±467493 vs 9257600±400364,P<0.05),CD86(7988400±385941 vs 1102400±13227,P<0.05)and CD74(11056000±431427 vs 4633400±267903,P<0.05)was significantly increased compared with the normal saline(NS)group.Compared with the NS group,the protein expression of CD11b/c(5.4817±0.77 vs 1.4073±0.37,P<0.05)and CD86(4.2673±0.69 vs 1.1379±0.42,P<0.05)was significantly increased.Itg-α(1.1224±0.3 vs 0.4907±0.19,P<0.05),CD83(3.6986±0.40 vs 1.0762±0.22,P<0.05)and CD86(1.5801±0.32 vs 0.8846±0.10,P<0.05)m RNA expression was increased significantly in the FHF group.At the protein level,expression of CD74in the FHF group(2.3513±0.52)was significantly increased compared with the NS group(1.1298±0.33),whereas in the LPS group(2.3891±0.47),the level of CD74 was the highest(P<0.05).At the gene level,the relative expression of CD74 m RNA in the FHF group(1.5383±0.26)was also significantly increased in comparison to the NS group(0.7648±0.22;P<0.05).CD3 expression was the highest in the FHF group(P<0.05).In the FHF,LPS and D-Galn groups,the expression of AKT at the protein and m RNA levels was elevated compared with the NS group,but there wasno statistical significance(P>0.05).The p-AKT protein expression in the FHF(1.54±0.06),LPS(1.56±0.05)and D-Galn(1.29±0.03)groups was higher than that in the NS group(1.07±0.03)(P<0.05).CONCLUSION:In FHF,a large number of DCs mature,express CD86,and activate MHC classⅡmolecular pathways to induce a T cell response,and the AKT pathway is activated.
文摘Acute liver failure, also known as fulminant hepatic failure(FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral edema and intracranial hypertension are common causes of mortality in patients with FHF. The management of patients who present acute liver failure starts with determining the cause and an initial evaluation of prognosis. Regardless of whether or not patients are listed for liver transplantation, they should still be monitored for recovery, death, or transplantation. In the past, neuromonitoring was restricted to serial clinical neurologic examination and, in some cases, intracranial pressure monitoring. Over the years, this monitoring has proven insufficient, as brain abnormalities were detected at late and irreversible stages. The need for real-time monitoring of brain functions to favor prompt treatment and avert irreversible brain injuries led to the concepts of multimodal monitoring and neurophysiological decision support. New monitoring techniques, such as brain tissue oxygen tension, continuous electroencephalogram, transcranial Doppler, and cerebral microdialysis, have been developed. These techniques enable early diagnosis of brain hemodynamic, electrical, and biochemical changes, allow brain anatomical and physiological monitoring-guided therapy, and have improved patient survival rates. The purpose of this review is to discuss the multimodality methods available for monitoring patients with FHF in the neurocritical care setting.
文摘Serological methods were used to determine the cause of fulminant hepatitisin 207 patients. They were admitted to the isolation wards of 4 hospitals inShenyang between 1986-1990. The final diagnoses were: hepatitis type A 4 cas-es (2.0%), type B 144 cases (69.4% ),superinfections with A and B 3 cases (1.5%), hepatitis non-A non-B (NANB) 51 cases (24.6%), type D 2 cases (1.0%), type E 2 cases (1.0%) and cytomegalovirus (CW) infection 1 case (0.5%). The risk factors were found to be concerned with type D and several typesuper infections (prognosis poor).
文摘We present a case of a healthy 72-year-old man with herpes simplex hepatitis (HSVH) development soon after ordinary surgery for biliary stones. A sudden onset of hepatitis associated with high fever and leukopenia emerged on postoperative day 5, followed by a rapid and lethal course (died on day 9), despite an acyclovir therapy on day 8. Postmortem liver biopsy revealed positive immunostaining for herpes simplex virus(HSV) type-1. The serum tests(available after the death) were negative for anti-HSV immunogloblulins, but positive for HSV DNA. A review of 15 cases of postsurgical HSVH along with 42 cases of non-surgical HSH showed that (1): A wide spectrum of surgical procedures was involved; and (2): High mortality (87%) associated with lower rates of ante-mortem diagnosis (20%) and acyclovir treatment (20%). Due to the difficulty in diagnosis and lethal nature, an early clinical suspension and prompt empirical anti-viral intervention are imperative for postsurgical hepatitis with undetermined etiology, characterized by fever and leucopenia.
文摘The model of fulminant hepatic failure induced by acetaminophen was established in dogs to observe the changes of hepatic hemodynamics and plasma histamine levels in portal vein (PV), hepatic vein (HV), abdominal aorta (AA) and inferior vena cava (ICV). The results showed that the portal vein resistance (PVR) was elevated and portal venous blood flow (PVF) was decreasedl hepatic artery resistance (HAR) was decreased and the hepatic artery blood flow (HAF),portal venous pressure (PVP), wedged hepatic venous pressure (WHVP) and inferior vena cava pressure (ICVP) had no changes. The histamine of the PV, HV,ICV and AA were all elevated after formation of fulminant hepatie failure. And the increasing wave Of the HV was the highest. The increased histamine in HV may be mediated by H, receptor.causing the contraction of hepatic venulae, result ing liver sinusoid congestion, increasing PVR and decreasing PVF which exacerbate the liver cell damage. Moreover, the more selvere liver damage, the more histamine was released, and a vicious circle may ensue. Our results also suggest the possibility of using,H1 receptor antagonist to treat the disturbance of liver hemodynamfics in severe acute liver damage. The increased histamine in systematic circulation as a vasodilator may lower blood pressure and accelerate heart beats.The increase of plasma histamine may play an important role in the changes of hepatic and systemic hemodynamics in fulminant hepatic failure.
