The characteristics of liver injury induced by Amanita and clinical value of α-amanitin detection

Background:Amanita poisoning as a foodborne disease has raised concerning mortality issues.Reducing the interval between mushroom ingestion and medical intervention could greatly influence the outcomes of Amanita poisoning patients,while treatment is highly dependent on a confirmed diagnosis.To this end,we developed an early detection-guided intervention strategy by optimizing diagnostic process with performingα-amanitin detection,and further explored whether this strategy influenced the progression of Amanita poisoning.Methods:This study was a retrospective analysis of 25 Amanita poisoning patients.Thirteen patients in the detection group were diagnosed mainly based onα-amanitin detection,and 12 patients were diagnosed essentially on the basis of mushroom consumption history,typical clinical patterns and mushroom identification(conventional group).Amanita poisoning patients received uniform therapy,in which plasmapheresis was executed once confirming the diagnosis of Amanita poisoning.We compared the demographic baseline,clinical and laboratory data,treatment and outcomes between the two groups,and further explored the predictive value ofα-amanitin concentration in serum.Results:Liver injury induced by Amanita appeared worst at the fourth day and alanine aminotransferase(ALT)rose higher than aspartate aminotransferase(AST).The mortality rate was 7.7%(1/13)in the detection group and 50.0%(6/12)in the conventional group(P=0.030),since patients in the detection group arrived hospital much earlier and received plasmapheresis at the early stage of disease.The early detection-guided intervention helped alleviate liver impairment caused by Amanita and decreased the peak AST as well as ALT.However,the predictive value ofα-amanitin concentration in serum was still considered limited.Conclusions:In the management of mushroom poisoning,consideration should be given to the rapid detection ofα-amanitin in suspected Amanita poisoning patients and the immediate initiation of medical treatment upon a positive toxin screening result.

Analysis of imaging characteristics of blunt traumatic aortic dissection: an 8-year experience

BACKGROUND:Traumatic aortic dissection(TAD)has a low incidence but extremely high mortality.It always presents atypical clinical manifestations that are easily missed or misdiagnosed.This study mainly aims to describe the imaging characteristics and management of TAD patients.METHODS:A retrospective analysis of 27 blunt TAD patients was performed between 2013 and 2020.Demographic features,imaging characteristics,and management were analyzed.RESULTS:Twenty-seven patients with type B aortic dissection(age 56.04±16.07 years,20 men)were included.Aortic intimal tears were mostly initiated from the aortic isthmus.The sizes of the proximal intimal tears in the greater curvature were larger than those in the lesser curvature(1.78±0.56 cm vs.1.24±0.52 cm,P=0.031).Compared with those in the control group,the maximum diameters of the aortic arch,thoracic aorta,and abdominal aorta in the TAD patients were all significantly widened(all P<0.050).Multivariate logistic regression analysis showed that the maximum diameter of the thoracic aorta was an independent risk factor for TAD,with a predictive value with an area under the receiver operating characteristic curve(AUC)of 0.673.Finally,26 patients successfully underwent delayed thoracic endovascular aortic repair(TEVAR),and the remaining one patient was treated conservatively.No progression of aortic dissection or death occurred during the six-month follow-up period.CONCLUSIONS:In blunt trauma,the aortic isthmus is the most common site of proximal intimal tears.An accurate diagnosis of TAD requires an overall consideration of medical history and imaging characteristics.Delayed TEVAR might be an eff ective therapeutic option for TAD.

Roles of AKR1C3 in malignancy

The superfamily of aldo-keto reductases(AKRs)is composed of over 190 members and can be classified into 16 different families(visit www.med.upenn.edu/akr).AKR1C3(C3 subtype of aldosterone reductase family 1)refers to the first AKR in family 1,subfamily C,and is encoded by the AKR1C3 gene.AKR1C3 was first cloned and expressed from a human prostate cDNA library.This protein is a soluble monomeric NADP(H)(nicotinamideadenine dinucleotide phosphate or reduced form of nicotinamide adenine dinucleotide phosphate)dependent oxidoreductase.