Diffuse hepatocellular calcification developing in a patient on chronic hemodialysis after ischemic hepatitis

Diffuse hepatic calcification is a rare condition. Previous reports have described patients with end-stage renal disease who developed diffuse hepatic calcification after ischemic hepatitis caused by shock. We herein present a similar case. A 41-year-old man on chronic hemodialysis developed ischemic hepatitis due to shock induced by ventricular tachycardia, followed by progressive hepatic failure. Necropsy of the liver revealed diffuse hepatocellular calcification. Given the similarity by which our case and previously reported cases developed this rare condition, we postulate that chronic renal failure is involved in the pathogenesis of diffuse hepatic calcification.     

LDH在缺血性肝炎诊断与鉴别诊断中的临床意义

目的探讨LDH在缺血性肝炎诊断与鉴别诊断中的临床意义。方法回顾性分析45例缺血性肝炎和34例急性病毒性肝炎患者的临床特点。结果缺血性肝炎患者,TBil、γ-GT、AKP多在正常范围内,LDH水平则明显升高。急性病毒性肝炎与之相反,TBil、γ-GT、AKP明显升高,LDH水平在正常范围内。心脏源性缺血性肝炎LDH水平明显升高,与失血性低血容量性缺血性肝炎患者相比,有显著差异。结论面对明显肝功能异常的患者,若LDH明显升高,而TBil、γ-GT、AKP水平不高,则应考虑缺血性肝炎可能,反之应考虑急性病毒性肝炎。面对LDH明显升高的缺血性肝炎患者,应首先考虑心脏功能不全引起缺血性肝炎的可能。     

Incidence and outcome of ischemic hepatitis complicating septic shock

Aim:  The specific incidence of ischemic hepatitis in septic shock patients remains unknown. The aim of this study was to evaluate the incidence of ischemic hepatitis in septic shock and its relationship with mortality.
Methods:  We retrospectively studied 181 patients with septic shock admitted to the intensive care unit (ICU). We defined ischemic hepatitis as having a value of serum aminotransferases equal to or higher than 1000 IU/L. We recorded the age, sex, comorbidity, site of infection, the Sequential Organ Failure Assessment (SOFA) score on admission to the ICU, maximum SOFA score and inadequate antibiotic therapy.
Results:  Twenty-five (13.8%) patients developed ischemic hepatitis. In-hospital mortality was 57% (103 patients). In the ischemic hepatitis group, mortality increased up to 84.0% (21 patients) compared with 52.6% (82 patients) in patients without ischemic hepatitis (control group) (odds ratio [OR]: 4.7; 95% confidence interval [CI]: 1.6–14.4; P  = 0.003). The development of ischemic hepatitis, age, maximum SOFA score and inadequate antibiotic therapy were independently associated with an increased risk of death. The odds of death increased by 247% in ischemic hepatitis (OR: 3.47; 95% CI: 1.02–11.8; P  = 0.047).
Conclusion:  Ischemic hepatitis is a common complication in septic shock patients, associated with a high mortality.     

Rapid improvement of distal vasculitis in PAN related to hepatitis B with alprostadil infusion: a case report

Polyarteritis nodosa (PAN) related to hepatitis B is an uncommon vasculitis that is sometimes associated with the rapid progression of distal ischemia. A few recent reports have proposed the use of antiviral therapy. However, there is not yet a consensus for the standard treatment of this disease entity and none of these treatments have been focused on fast symptomatic improvement. We describe here a 39-year-old female patient with PAN related to hepatitis B infection who completely recovered from the acutely progressing ischemic manifestations of her distal extremities with the use of alprostadil infusion (prostaglandin E1). The reactivation of her hepatitis B infection after glucocorticoid and cyclophosphamide therapy was successfully managed by the antiviral lamuvudine therapy. Most importantly, the vasodilator together with the conventional therapy may be desirable in the early stages of the disease before irreversible ischemic tissue damage can occur.     

Ischemic hepatitis: clinical presentation and pathogenesis

BACKGROUND: The pathophysiology of ischemic hepatitis, otherwise known as "shock liver," is poorly understood, although it is believed to be the result of a reduction in systemic blood flow as typically occurs in shock. The aim of this study was to investigate the importance of this phenomenon as well as other clinical features in patients with ischemic hepatitis.METHODS: We identified a cohort of 31 patients (case group) who met the most commonly accepted definition of ischemic hepatitis (an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper limit of normal, excluding known causes of acute hepatitis or hepatocellular injury, in an appropriate clinical setting). We also evaluated the clinical features and serum aminotransferase levels in a cohort (the control group) of 31 previously healthy patients who sustained major nonhepatic trauma at San Francisco General Hospital, a major trauma center. Both groups of patients had documented systolic blood pressures <75 mm Hg for at least 15 minutes. Clinical and hemodynamic (invasive and noninvasive) data were recorded.RESULTS: Despite the marked reduction in blood pressure, no patient in the control group developed ischemic hepatitis. The mean (+/- SD) peak serum aspartate aminotransferase level in the control group was only 78 +/- 72 IU, in contrast with a mean peak of 2,088 +/- 2,165 IU in the case group. All 31 patients with ischemic hepatitis had evidence of underlying organic heart disease, 29 (94%) of whom had right-sided heart failure.CONCLUSIONS: Systemic hypotension or shock alone did not lead to ischemic hepatitis in any patient. The vast majority of patients with ischemic hepatitis had severe underlying cardiac disease that had often led to passive congestion of the liver. These data lead us to propose that right-sided heart failure, with resultant hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event.     

Ischemic colitis during pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C.

Rare cases of ischemic colitis associated with interferon-alpha (IFN-alpha) treatment for chronic hepatitis C (HCV) infection and metastatic cancer have been reported. The present study describes the first case of ischemic colitis attributable to pegylated IFN-alpha and ribavirin combination therapy in an HCV-infected patient after 34 weeks of treatment. The clinical presentation, endoscopic appearance and histopathology of the colon were consistent with ischemic colitis, and the patient's symptoms rapidly resolved with cessation of therapy. The association between the therapy and the pathogenesis of ischemic colitis is unclear, but immunoregulatory, vasospastic and procoagulant mechanisms have been proposed. Physicians should be aware of this complication, and should consider it in any HCV-infected patient taking pegylated IFN-alpha and ribavirin who develops abdominal discomfort and gastrointestinal bleeding.     

Digital ischemic necrosis caused by pegylated interferon in a patient with hepatitis C

Pegylated interferon plus ribavirin remains the firstline treatment for patients with hepatitis C virus(HCV) . Interferonαhas the most extensive clinical application and is used for the treatment of chronic hepatitis B virus and hepatitis D virus as well as acute and chronic HCV infections.The attachment of polyethylene glycol to interferon increases its half-life by reducing the rate of absorption after injection,reducing renal and cellular clearance and also decreasing immunogenicity.In this case report,we have described a patient with chronic hepatitis C who developed ischemic necrosis of her fingertips after completing her third course of pegylated interferon and ribavirin.The patient underwent a very extensive workup in order to determine the underlying cause of her digital ischemia which was finally determined to be secondary to the use of pegylated interferon.     

Anabolic steroid-induced cardiomyopathy underlying acute liver failure in a young bodybuilder

Heart failure may lead to subclinical circulatory disturbances and remain an unrecognized cause of ischemic liver injury. We present the case of a previously healthy 40-year-old bodybuilder, referred to our Intensive-Care Unit of Hepatology for treatment of severe acute liver failure, with the suspicion of toxic hepatitis associated with anabolic steroid abuse. Despite the absence of symptoms and signs of congestive heart failure at admission, an anabolic steroid-induced dilated cardiomyopathy with a large thrombus in both ventricles was found to be the underlying cause of the liver injury. Treatment for the initially unrecognized heart failure rapidly restored liver function to normal. To our knowledge, this is the first reported case of severe acute liver failure due to an unrecognized anabolic steroid-induced cardiomyopathy. Awareness of this unique presentation will allow for prompt treatment of this potentially fatal cause of liver failure.     

肝硬化上消化道出血并发缺血性肝炎的临床特征与预后

目的 研究乙型肝炎肝硬化上消化道出血患者中缺血性肝炎的发生率、临床特点及其对预后的影响.方法 回顾性分析了264例乙型肝炎肝硬化合并上消化道出血患者的资料,其中缺血性肝炎患者11例,分层随机抽样法选择同期无缺血性肝炎患者30例为对照,分析缺血性肝炎的临床特点.各种构成比及率的比较采用x2检验或直接概率法;出血前后各指标比较采用配对t检验,组间比较采用两独立样本t检验. 结果缺血性肝炎的发生率为4.17%,平均年龄为(43.1±5.7)岁,较对照组[(52.3±11.1)岁]年轻(P<0.05).ALT、AST快速升高超过正常值上限20倍,10 d内迅速恢复,伴有总胆红素、乳酸脱氢酶、碱性磷酸酶、γ-谷氨酰转肽酶的明显升高,胆碱酯酶下降,尿素氮、肌酐及白细胞数明显升高,与对照组比较差异有统计学意义(P<0.05).缺血性肝炎组病死率为54.5%(6/11),明显高于对照组的16.7%(5/30),P<0.05;感染、肝肾综合征,肝性脑病是其主要的死亡原因.缺血性肝炎组患者失血量200～3600 ml不等,休克患者占63.6%(7/11),出血量与缺血性肝炎无明显的相关性.结论 年龄小、失血性休克、肝脏储备功能差是乙型肝炎肝硬化患者发生缺血性肝炎的危险因素.肝硬化消化道出血并发缺血性肝炎患者,及时应用抗菌素防治感染,减少内毒素血症对于改善预后很重要.     

Ischemic Hepatitis: Widening Horizons

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.     

肝硬化食管胃底静脉曲张破裂出血伴缺血性肝炎的危险因素分析

目的探讨肝硬化食管胃底静脉曲张破裂出血(esophageal and gastric varices bleeding,EGVB)继发缺血性肝炎的相关危险因素。方法回顾性分析2020年1月至8月沈阳市第六人民医院102例EGVB患者的临床资料,根据是否出现缺血性肝炎分为观察组和对照组。对一般资料、实验室指标、辅助检查结果、临床情况进行单因素分析,二元Logistic多因素分析EGVB后继发缺血性肝炎的相关危险因素。结果102例EGVB患者中,14例伴有缺血性肝炎(转氨酶升高>10倍正常值上限)纳入观察组,余88例纳入对照组。观察组死亡5例,是对照组的4.46倍。观察组ALT、AST峰值多出现在入院第2日,依次为791.00(555.25,1657.5)U/L、2541.50(1480.50,4594.00)U/L。单因素分析结果显示,观察组和对照组ALT、AST、γ-GGT、LDH、TBil、白细胞、血小板计数、脾长、脾门静脉、门脉主干内径、门静脉血栓、死亡、合并肝性脑病、合并脓毒症、Child-Pugh评分、腹腔积液等指标,差异有统计学意义(均P<0.05);二元logistic多因素分析显示,伴有肝癌(P<0.01)、白细胞计数(P=0.014)、γ-GGT(P=0.025)、Child-Pugh分级(P=0.050)与EGVB后出现缺血性肝损伤具有显著相关性。结论伴有肝癌、白细胞计数、肝硬化Child-Pugh分级是EGVB合并缺血性肝炎的危险因素。     

Central venulitis in pediatric liver allografts

Central venulitis (CV), a distinct histologic lesion described in adult liver transplants, can occur with acute portal tract rejection or in isolation (ICV). Possible etiologies include immunosuppressive drug toxicity, acute cellular rejection, viral hepatitis, ischemic injury, and recurrent disease. This study was designed to characterize ICV and to assess its potential etiology in pediatric liver recipients because this population generally does not develop recurrent disease or viral hepatitis. All posttransplantation liver biopsy specimens that were obtained from children who received liver allografts over a 4-year period were reviewed. ICV was identified in 12 of 127 posttransplantation biopsies and in 7 of 45 allograft recipients. Only 4 liver transplantations were performed for potentially recurrent diseases (primary sclerosing cholangitis). ICV first appeared in posttransplantation biopsy specimens significantly later than did portal rejection alone. The finding of CV was not significantly correlated with elevation of Tacrolimus levels, reason for transplantation, donor/recipient cytomegalovirus (CMV) status or blood type, cold ischemic times, or the incidence of outflow obstruction. The responses of CV to therapy were variable and, although the majority of cases resolved, several episodes persisted or recurred. In conclusion, ICV occurs in 16% of pediatric liver allograft recipients and does not appear to be related to recurrent disease, viral hepatitis, drug toxicity, or graft ischemia. CV may be a variant of acute rejection, but longer follow-up is required to determine the most adequate therapy for this entity.     

缺血性肝炎的生化和病理特点分析

目的探讨缺血性肝炎的生化和病理特点以及二者之间的关系,提高对该病的诊断水平。方法回顾性分析45例缺血性肝炎,并对9例缺血性肝炎患者行肝穿刺组织病理检查。结果缺血性肝炎患者ALT、AST、LDH明显升高,TBil、γ-GT、AKP多在正常范围内。随着肝脏缺血时间延长各项指标呈升高趋势,肝缺血时间6~12 h及〉12 h患者明显高于〈6 h患者,差异具有统计学意义。随着住院时间延长各项指标与入院当时相比明显下降,差异具有统计学意义。心脏源性缺血性肝炎与失血性低血容量性缺血性肝炎患者相比,LDH水平明显升高。不同病理分级患者生化变化差异无统计学意义。缺血性肝炎患者肝组织变化轻微,多为肝小叶中央轻-中度间质炎症。患者多死于原发病而非缺血性肝炎。结论缺血性肝炎患者生化变化明显,而组织变化轻微,显示出二者的不一致性。组织学的变化特点以及缺血性肝炎病因恰能更好的解释生化变化及其预后特点。从病理上,缺血性肝炎患者预后取决于原发病而非休克肝;积极治疗原发病,改善肝脏微循环是抢救成功的关键。     

Ischemic colitis during interferon-ribavirin therapy for chronic hepatitis C: a case report

Ischemic colitis is a rare complication of interferon administration. Only 9 cases in 6 reports have been described to-date. This report describes a case of ischemic colitis during pegylated interferon and ribavirin treatment for chronic hepatitis C, and includes a review of the relevant literature. A 48-year-old woman was treated with pegylated interferon α-2a and ribavirin for chronic hepatitis C, genotype Ib. After 19 wk of treatment, the patient complained of severe afebrile abdominal pain with hematochezia. Vital signs were stable and serum white blood cell count was within the normal range. Abdominal computed tomography showed diffuse colonic wall thickening from the splenic flexure to the proximal sigmoid colon, which is the most vulnerable area for the development of ischemic colitis. Colonoscopy revealed an acute mucosal hyperemic change, with edema and ulcerations extending from the proximal descending colon to the sigmoid colon. Colonic mucosal biopsy revealed acute exudative colitis. Polymerase chain reaction and culture for Mycobacterium tuberculosis were negative and the cultures for cytomegalovirus, Salmonella and Shigella species were negative. After discontinuation of interferon and ribavirin therapy, abdominal pain and hematochezia subsided and, following colonoscopy showed improvement of the mucosal ulcerations. Ischemic colitis cases during interferon therapy in patients with chronic hepatitis C reported so far have all involved the descending colon. Ischemic colitis is a rarely encountered complication of interferon administration in patients with chronic hepatitis C and should be considered when a patient complains of abdominal pain and hematochezia.     

Prolonged cholestasis and disappearance of interlobular bile ducts following chlorpropamide and erythromycin ethylsuccinate. Case of drug interaction?

A 52-year-old man, having been treated for 4 months with chlorpropamide for diabetes mellitus type II, developed severe cholestatic hepatitis following a short course of erythromycin ethylsuccinate. Despite prompt withdrawal of both drugs, the cholestatic picture worsened and was associated with morphological evidence of disappearing interlobular bile ducts. After a 2-year course of profound cholestasis complicated by steatorrhea and striking hyperlipidemia, the patient died of ischemic cardiomyopathy. It is believed that this is the first published case of irreversible cholestasis with disappearance of ducts potentially related to a metabolic interaction between erythromycin ethylsuccinate and chlorpropamide.     

Ischemic hepatitis induced by mesenteric volvulus in a patient with chronic obstructive lung disease

A 66-year-old man with chronic obstructive lung disease was admitted to our hospital, presenting with mesenteric volvulus and mild liver injury. A superior mesenteric angiogram revealed that the arteries supplying the small intestine were twisted in the arterial phase, while the portal vein was not visualized in the late phase. A celiac angiogram demonstrated that portal blood flow from the splenic venous return was maintained. The patient's symptoms had almost resolved the day after admission, and his serum transaminases level had gradually decreased to normal with conservative therapy. A superior mesenteric angiogram on the 13th hospital day showed a normal arteriogram and the portal vein demonstrated blood flow from the superior mesenteric vein. Liver biopsy revealed hemorrhagic necrosis around the central veins, which was compatible with ischemic hepatitis. Since the patient's O₂ saturation level on admission was not low enough to have caused ischemic hepatitis by itself, we suspect that a sudden decrease in portal blood flow was the additional factor that allowed the threshold for the initiation of ischemic liver damage to be reached. Received: January 13, 1999 / Accepted: June 25, 1999     

Hepatitis C virus-associated pericardial effusion and tamponade in a liver transplant recipient

A liver transplant recipient with hepatitis C presented with unexplained dyspnea, fatigue and edema. Diagnostic evaluation revealed a pericardial effusion with echocardiographic features of tamponade. The patient underwent therapeutic pericardial drainage, resulting in symptomatic relief. The pericardial fluid tested positive for hepatitis C virus (viral quantitation of 200,000 copies/mL, genotype 1b) and negative for other plausible etiologies. Pericardial biopsy revealed normal tissue. This is the fifth case of hepatitis C virus-associated pericardial disease worldwide and the first case in North America. It is the first in a liver transplant recipient. In contrast to previous reports, this patient demonstrated tamponade in the absence of cryoglobulinemia or systemic extrahepatic manifestations of hepatitis C.     

Immune-mediated pathology following hepatitis B vaccination. Two cases of polyarteritis nodosa and one case of pityriasis rosea-like drug eruption

The association of hepatitis B virus infection and vasculitis or other immune-mediated manifestations is well documented. Reports on such manifestations in relation to hepatitis B vaccination are scarce, however. We report 2 patients who developed polyarteritis nodosa following vaccination against hepatitis B. In one patient this resulted in an ischemic and necrotic digital ulcus, necessitating surgical amputation. The other patient presented with typical cutaneous polyarteritis nodosa which responded well to corticosteroid treatment. A third patient developed a severe pityrias rosea-like eruption. He was treated with topical steroids with healing of the lesions, leaving only post-inflammatory hyperpigmentation. The literature on these associations is reviewed.     

Ischemic hepatitis

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (>5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.This study was supported, in part, by a grant from the James R. Dougherty, Jr. Foundation, Beeville, Texas.