A technique for vascular reconstruction of pancreaticoduodenal allograft. A literature review and case report

In most cases, whole pancreaticoduodenal allograft vessels can be reconstructed using a segment of donor common iliac artery bifurcation. An alternative way to bridge the splenic artery and the superior mesenteric artery (SMA) is to use a short segment of distal SMA as an interposition graft, as described herein.     

Secondary hyperparathyroidism and acute tubular necrosis following renal transplantation

In the present study we investigated the relationship betweensecondary hyperparathyroidism in renal graft recipients andpost-transplantation acute tubular necrosis (ATN). Patientswere divided into two groups according to graft function: groupA consisted of 28 patients who had an uneventful postoperativeperiod and did not require haemodialysis. Group B comprised26 patients with primary non-function of the graft due to biopsy-provenATN who required continued haemodialysis for the first postoperativeweek or longer (mean 14.2 ±8.7 days). Both groups hadcomparable donor characteristics, HLA-matching and ischaemiatimes. All patients were given cyclospo-rin and low-dose prednisolonefor immunosuppression. Pretransplant levels of intact PTH weresignificantly greater in group B than in group A (203.5 ±193.1pg/ml versus 81.7±45.2 pg/ml, P<0.01). Group B patientshad more transplant biopsies (50 versus 7) and a longer hospitalizationtime (33.4 ± 10.9 days versus 21.9 ± 11.9 days,P<0.01), although serum creatinine on the day of dischargewas higher in group B (1.77 ± 0.51 mg/dl versus 1.5±0.45mg/dl, P<0.05). We conclude that patients with secondaryhyperparathyroidism as assessed by measuring circulating levelsof intact PTH have an increased incidence of ATN.     

Heart rate and late mortality in cardiac transplant recipients

There are currently 104 patients at this centre who have survivedat least 3 months after orthotopic cardiac transplantation.Seven of these long-term survivors have subsequently died andin three cases death was sudden and unexpected. All three ofthese patients had been noted to have inappropriately high restingheart rates (>130 b.min^–1) The rhythm was sinus tachycardia,supraventricular tachycardia or both intermittently. The heart rates of all 104 long-term survivors were recordedfrom ECGs taken at routine follow-up visits every 3 months forone year and annually thereafter. The overall mean heart ratewas 100±13.2 b.min^–1. Four patients, including the three identified above, had meanheart rates greater than the 95th centile. The mortality ratein this group is 75%. Four deaths have occurred in the remaining100 patients (P <0.001). In our series, an inappropriately high resting heart rate dueto sinus tachycardia or supraventricular tachycardia in long-termsurvivors of cardiac transplantation, is an adverse prognosticsign.     

Effect of a protein binding change on unbound and total plasma concentrations for drugs of intermediate hepatic extraction

For substances eliminated from blood by the liver, the effect of a change in unbound fraction of drug (fu _b )on steady state total (C _b )and unbound (Cu _b )blood concentrations has hitherto only been considered for the two limiting cases, i.e., at the upper and lower extremes of hepatic intrinsic clearance (CL _int ).For a substance of very low CL _int ,if fu _b changes, C _t will change and Cu _b will remain constant, whereas if CL _int isvery high, Cu _b will change and C _b will remain constant.The present study defines the effects of a change in fu _b on C _b and Cu _b over the whole CL _int range. Computer simulations were undertaken which predicted that, for a given change in fu _b ,absolute and relative changes in C _b would decreasenonlinearly with increasing CL _{int, twhile the relative change in} Cu _{b would} increasewith CL _int .The absolute change in Cu_b would be independent of CL _int .Significant changes in C_b and Cu _{b would be observed at intermediate values of} CL _{int not just at the high and low extremes. These theoretical predictions were investigated experimentally in the isolated perfused rat liver by examining the effects of a change in} fu _{b of sodium taurocholate a substance with intermediate} CL _int (such that at fu _b =0.27,hepatic extraction ratio=0.71) induced by concurrent administration of sodium oleate. Sodium 24- ¹⁴ C-taurocholate (specific activity 52 Ci/mmol) was infused into the reservoir in a recycling system at 30 mol/hr for 105 min (n=6). At 45 min a bolus dose of sodium oleate (50 mmol) was administered to the reservoir, followed by a constant infusion of 143 mmol/hr for 1 hr. Following the administration of oleate, taurocholate fu _{b fell promptly by 55% (0.27–0.12). There was a relative increase of taurocholate} C _{b of 22.7% and a relative decrease in} Cu _{b of 45.4%, in accordance with the simulations (p<0.05). We conclude that important changes in unbound steady-state concentration, the pharmacologically active moiety, can occur upon changes in unbound fraction with compounds of intermediate hepatic intrinsic clearance}.This study was supported by the National Health and Medical Research Council of Australia.     

Protection of chlordecone-potentiated carbon tetrachloride hepatotoxicity and lethality by partial hepatectomy

Chlordecone (CD) pretreatment is known to markedly potentiate CCl₄ hepatotoxicity. Previous studies have shown that prior exposure to CD obtunds the increased hepatocellular regeneration and repair observed in non-treated rats challenged with a single, low dose of CCl₄. These observations allowed us to hypothesize that suppression of hepatic regeneration and tissue repair by CD + CCl₄ combination treatment might be involved in this interaction. To test this hypothesis, CCl₄ hepatotoxicity was evaluated in actively regenerating livers using CD-treated (10 ppm in the diet for 15 days), surgically partially hepatectomized (PH) male Sprague-Dawley rats. Rats undergoing no surgical manipulation (CTRL) and sham operation (SH) were included as appropriate controls. Surgical manipulations were conducted on day 15 of the dietary protocol. Based on liver-to-body weight ratios (LW/BW), mitotic indices, hepatic cytochrome P-450 content, and hepatic glutathione (GSH and GSSG) levels, PH-induced hepatocellular regeneration was not affected by pretreatment with CD. Thus, the PH model was considered valid for assessing the effects of CD + CCl₄ combination treatment. CCl₄ (100 l/kg; i.p.) was administered 1, 2, 4 or 7 days after the surgical manipulations. Hepatotoxicity was assessed 24 h later by measuring LW/BW and serum enzymes (SGPT, SGOT and ICD) in all four groups. Hepatic histopathological, histomorphometric and lethal effects were assessed in animals receiving CCl₄ 1 or 7 days after the surgical manipulations. CCl₄-induced increases in LW/BW were observed in CD + PH rats receiving CCl₄ 4 or 7 days post-PH, but not in the 1 or 2 day post-PH groups in which the hepatocellular regeneration was maximal. CCl₄-induced serum enzyme elevations were significantly less in the CD + PH rats as compared to CD + SH. This decrease in the serum enzyme elevations was most prominent in the 1 day post-PH group, where the hepatocellular mitotic activity was most pronounced. CCl₄ lethality, assessed in the 1 day post-surgical manipulation group, was also decreased in the CD + PH rats in comparison to CD + SH rats. Such a protection was not observed in rats receiving CCl₄ 7 days post-PH. These data are consistent with and are supportive of the hypothesis that a suppression of otherwise normally stimulated hepatocellular regeneration following low-dose CCl₄ administration is involved in the marked amplification of CCl₄ toxicity by CD.Abbreviations CD chlordecone - GSH reduced glutathione - GSSG oxidized glutathione - PH partial hepatectomy - SH shamhepatectomy - CTRL control, not surgically manipulated - N normal diet - LW/BW liver weight-to-body weight ratio - SGPT serum glutamic; pyruvic transaminase - SGOT serum glutamic oxaloacetic transaminase - ICD isocitrate dehydrogenase These studies were made possible by a grant from the US Environmental Protection Agency R-811072A preliminary report of these findings was presented at the 70th Annual Meetings of the Federation of American Societies for Experimental Biology at St. Louis, MO (Fed Proc 45: 1051, 1986)A. N. Bell is a Predoctoral Toxicology Trainee and Robert A. Young is a Postdoctoral Trainee supported by Toxicology Training grant from National Institute of Environmental Health Science ES-07045     

生物标志物联合检测在脓毒症相关急性肝损伤患者中的应用价值

目的:探讨生物标志物联合检测对脓毒症相关急性肝损伤患者的早期诊断和预后评估的价值。方法:收集内蒙古科技大学包头医学院第一附属医院重症医学科(ICU)2019年11月-2022年1月收治的104例脓毒症患者临床资料,按照入ICU时是否发生急性肝损伤分为脓毒症相关急性肝损伤组(n=42)和非肝损伤组(n=62),将脓毒症相关急性肝损伤患者按28 d是否存活分为存活组(n=16)和死亡组(n=26),记录104例患者入ICU 6 h内血清正五聚蛋白3(PTX-3)、C-反应蛋白(CRP)、降钙素原(PCT)、总胆红素(TBIL)、谷草转氨酶(AST)、谷丙转氨酶(ALT)、凝血酶原时间国际标准化比值(INR值)、凝血酶原时间(PT)、凝血酶原活动度(PTA)、血小板(PLT)、入ICU 24 h内急性生理与慢性健康状况评估量表II(APACHEII)评分最差值及序贯器官衰竭评估(SOFA)评分;同时记录脓毒症相关急性肝损伤患者28 d预后。PTX-3的相关性采用Spearman相关分析;绘制受试者工作特征曲线(ROC曲线),计算ROC曲线下面积(AUC),分析各指标单独检测以及联合检测对脓毒...     

慢加急性肝衰竭诊断标准的研究进展

慢加急性肝衰竭(ACLF)是指在慢性肝病基础上遭受急性打击后,出现严重的急性肝功能失代偿,其因病情进展迅速、短期死亡率极高,引起了全球肝病学家的关注。但由于不同国家(地区)ACLF的病因及临床特征等存在明显的差异,目前国内外ACLF的诊断标准多达十余种。本文通过回顾几种较为常用的ACLF定义,以及ACLF诊断标准相关研究,比较各ACLF诊断标准之间的差异,以期帮助临床医生更好地识别ACLF、优化临床决策。目前全球尚无公认的ACLF诊断标准,国内外ACLF的诊断标准存在着较大差异,临床医生在实际工作中选用何种ACLF诊断标准应根据患者慢性肝病的病因、临床特征等因素综合考虑。     

肝脏子宫内膜异位症一例

肝脏子宫内膜异位症是以肝内存在异位子宫内膜为特征的一种罕见子宫内膜异位症类型,因其缺乏典型临床症状且影像学诊断困难,易被误诊,组织学检查目前仍是肝脏子宫内膜异位症诊断的金标准。现报告1例海军军医大学第三附属医院收治的患者,反复经期右上腹疼痛,经超声检查发现右肝占位性病变,术后病理证实为肝脏子宫内膜异位症。     

Changes in the inducibility of a hepatic aldehyde dehydrogenase by various effectors

A hepatic soluble aldehyde dehydrogenase (ALDH), inducible by polycyclic aromatic hydrocarbons, was studied in Wistar rats in connection with substances known to affect drug metabolism or aldehyde dehydrogenase activity, such as phenobarbital (PB), disulfiram (DS), -diethylaminoethyl diphenylpropylacetate (SKF 525A) and calcium cyanamide (CC). 3-Methylcholanthrene (MC) was given as a model inducer of ALDH (100 mg/kg, i.p., as a single dose) and the animals were killed after 3 days. Pretreatment with PB (1 g/l drinking water, for 2 weeks) enhanced the inducing effect of MC. On the contrary, pretreatment with DS (100 mg/kg, i.p., daily x4) reduced by 70% the expected increase in ALDH activity. Neither SKF 525A (25 mg/kg, i.p., daily x4), nor CC (5 mg/kg, i.p., daily x4) could affect the action of the inducer. At the above doses, basal ALDH activity was inhibited by DS (30%) and CC (70%), but was not affected at all by PB or SKF 525A. The results were somewhat different when the various effectors tested were administered to animals already treated with MC (20 mg/kg, i.p., daily x6). In this case, DS did not affect the already induced ALDH activity. On the contrary, CC was still an effective inhibitor. Unexpectedly, post-treatment with SKF 525A further enhanced the initial induction brought about by MC. Our findings show that substances affecting microsomal drug metabolism can interfere with the process of ALDH induction by MC. The additive result of PB pretreatment is probably due to the enhanced accumulation of an active metabolite of MC. The opposite effect of DS on drug metabolism could explain the decreased ability of MC to induce ALDH activity. The MC-inducible ALDH isozyme can be effectively inhibited with CC, but not with DS.