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PubMed1996

[Budd-Chiari syndrome associated with chronic myeloproliferative syndromes: analysis of 6 cases].

The chronic myeloproliferative disorders (CMPD) are considered the main etiology of Budd-Chiari syndrome in Western countries. Moreover, an occult CMPD has been recently identified in most patients with idiopathic hepatic vein thrombosis. In order to determine the frequency of the association between the above entities and to analyze the clinical and hematologic features of such patients, fourteen cases of Budd-Chiari syndrome diagnosed at a single institution over a five year period were reviewed. In 6 patients a CMPD was identified, with this being the first cause of the syndrome. Median age of the later six patients was 32 years (range: 14-54), and 4 were females. In all cases the CMPD was suspected due to the presence of hematological abnormalities, including a high hematocrit (5 cases), leucocytosis (4 cases) and thrombocytosis (3 cases). Five patients had polycythemia vera (PV) and one idiopathic myelofibrosis. In an additional Budd-Chiari patient with polycythemia, PV was ruled out on the basis of high serum erythropoietin and the absence of endogenous growth of erythroid colonies in the hematopoietic progenitor culture. The CMPD treatment included phlebotomies and hydroxiurea, whereas the Budd-Chiari syndrome was treated in most patients with transjugular intrahepatic portosystemic stent-shunt. One patient died from a gastrointestinal hemorrhage at 48 months from Budd-Chiari diagnosis, and the remaining five are alive after a median follow-up of 28 months.

Adolescent↗
PubMedDate not supplied

Histopathology of the liver in pediatric patients following transplantation.

Recognition of rejection and other hepatic complications by needle biopsy plays a significant role in the management of liver allograft recipients. In this report, 22 pediatric patients (below 18 years old) were selected from the 37 liver transplants. Seven of the 22 cases have an uneventful posttransplant course. The most common cause of allograft injury in these patients appeared to be acute cellular rejection. It occurred in 7 (31.8%) of the 22 cases and was the primary process in 8 of the 25 episodes of liver dysfunction. Other etiologies, such as opportunistic viral infection (3 cases), biliary obstruction (2 cases), preservation injury (1 case), and vascular obstruction (1 case) were less common. Acute graft rejection causing liver dysfunction was associated with a mixed portal inflammation, destruction of the interlobular bile ducts, and varied degree of venous endotheliitis, followed by centrilobular hepatocyte necrosis. Chronic rejection was not seen in our pediatric cases. Cold ischemic injury causing transient graft dysfunction as seen in one of our patients demonstrated focal, limited areas of hepatocyte necrosis, mild centrilobular hepatocyte ballooning, and cholestasis without evidence of bile duct damage. More severe ischemic injury resulted from vascular complication causing diffuse hepatocyte necrosis was seen in one patient with hepatic vein thrombosis. The histologic patterns observed were not pathognomic; however, liver biopsies were helpful in suggesting the probable cause of liver dysfunction and in predicting subsequent allograft recovery when used in conjunction with clinical information, radiologic, and other laboratory tests.

Adolescent↗
PubMed2005

[Portal vein thrombosis associated with hepatic encephalopathy].

A 54-year-old man who had been administered chlormadinone acetate 3 months after prostatectomy for prostate cancer, acutely developed disorientation and memory disturbance. Six days later, he experienced high grade fever and epigastralgia. He was suspected to have hepatic encephalopathy, because the Fischer ratio was low although serum ammonia level remained normal. Further examinations including abdominal echography and CT scan disclosed a thrombus extending from the portal vein to the superior mesenteric vein together with abnormal collateral vessels originating from the portal vein. He was successfully treated with warfarin potassium, urokinase and heparin sodium. It was suggested that the patient developed hepatic encephalopathy due to portal-systemic circulation shunting secondary to portal vein thrombosis.

Drug Therapy, Combination↗
PubMed1993

Hepatic actinomycosis with portal vein thrombosis mimicking hepatocellular carcinoma: a case report.

A fatal case of hepatic actinomycosis with portal vein thrombosis is reported. The diagnosis of actinomycosis was delayed because of its rarity in Taiwan. This 63-year-old man was admitted due to body weight loss and poor appetite. No fever was noted before admission. Liver biochemical test showed a decreased serum albumin level with elevated serum levels of globulin and alkaline phosphatase. He was not a hepatitis B carrier and his serum level of alfafetoprotein was within normal range. Image studies (abdominal sonography and computed tomography) showed a hepatic mass over the medial segment of the left lobe with involvement of right lobe of the liver. Main portal vein thrombosis was also seen. Because of profound cachexia, he died of aspiration pneumonia and disseminated intravascular coagulation on the 11th day after admission. An autopsy revealed hepatic actinomycosis. High index of suspicion for early diagnosis and treatment is emphasized.

Actinomycosis↗
PubMed1993

Human hepatic infarction: histopathological and postmortem angiological studies.

Twenty hepatic infarction cases selected from 5420 consecutive autopsy cases were investigated to clarify the pathogenetic aspects of this disease. Additional postmortem angiological studies of 24 normal human livers obtained at autopsy were also further performed to analyse the effects of blocking vascular structures on lesion development. Seventeen of the 20 cases (85%) were clinically associated with systemic circulatory insufficiency, especially hepato- and/or renal failure. Histopathologically, there was a significantly closer relationship between the location of infarcted regions and portal vein thrombosis than with either hepatic vein thrombosis or hepatic arterial damage. The borders between infarcted regions and surviving hepatic parenchyma were located around central veins, corresponding with the microcirculatory periphery of the portal venous system. Postmortem angiographic studies revealed that hepatic lobuli mainly consist of portal vein branches. Moreover, postmortem embolization studies of six normal livers using glass beads and barium-gelatin injection showed that physical occlusion of portal vein branches produced defects in broad areas of the hepatic parenchyma. Therefore, it is suggested that the development of hepatic infarction principally depends on disturbances of the portal venous system. In addition, systemic circulatory insufficiency, which reduces the intrahepatic blood flow, probably contributes greatly to the development of hepatic infarction.

Adult↗
PubMed1998

Routine Doppler ultrasound for the detection of clinically unsuspected vascular complications in the early postoperative phase after orthotopic liver transplantation.

To assess the role of routine Doppler ultrasound in the detection of clinically unsuspected vascular complications in the early postoperative phase after orthotopic liver transplantation (OLT), the findings of 858 routinely performed Doppler ultrasound examinations were analyzed in 268 transplants. At various time intervals after OLT, we encountered 46 abnormal Doppler findings: hepatic artery (thrombosis), portal vein [anastomotic stenosis, (non)occlusive thrombosis or reversed flow], inferior vena cava [anastomotic stenosis with reversed flow, no flow, or (non)occlusive thrombosis], and hepatic veins (to-and-fro flow or stenosis with reversed flow) in 14, 20, 9, and 2 transplants, respectively. Most of these abnormal Doppler findings were confirmed by angiography, cavography, or surgery. The positive predictive value for hepatic artery thrombosis (HAT) was 12 out of 14, or 86%. In the first 2 weeks after OLT, routine Doppler ultrasound revealed 20 of the 46 abnormal findings (43%). Clinically unsuspected complications of the hepatic artery, portal vein, inferior vena cava, and hepatic veins were found in 9 of the 14 (64%), 6 of the 20 (30%), 3 of the 9 (33%), and 2 of the 2 (100%) transplants, respectively. The highest incidence--nine vascular complications--was found on the 1st day. On each of the remaining days (except for the 2nd and 9th days), one or two vascular complications were detected. HAT was found mainly in the 1st week. Vascular complications developed independently or concomitantly. We conclude that routine Doppler ultrasound is very important for the detection of clinically unsuspected vascular complications, particularly HAT, in the first 2 weeks after OLT. We recommend routine Doppler ultrasound of all hepatic vessels every 3 days in the early postoperative phase after OLT. Special attention should be paid to the 1st day.

Adolescent↗
PubMed1995

Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension.

Obliterative lesions in portal veins (PVs) and hepatic veins (HVs) of all sizes are known to occur in cirrhotic livers. PV lesions have generally been attributed to thrombosis, but the pathogenesis of the HV (veno-occlusive) lesions is unknown. We have studied 61 cirrhotic livers removed at transplantation to clarify the prevalence, distribution, and pathogenesis of venous lesions, as well as the association of these lesions with other morphological features and clinical morbidity. Intimal fibrosis that is highly suggestive of healed HV or PV thrombosis was found in at least 70% and 36% of livers, respectively. The distribution of HV lesions was patchy and largely confined to veins between 0.1 and 3 mm in diameter, suggesting multifocal origin in small veins. PV lesions were more uniform throughout the liver, suggesting origin in large veins with propagation to the small veins. HV lesions were associated with regions of confluent fibrosis (focal parenchymal extinction), and PV lesions were associated with regional variation in the size of cirrhotic nodules and a history of bleeding varices. These observations suggest that thrombosis of medium and large PVs and HVs is a frequent occurrence in cirrhosis, and that these events are important in causing progression of cirrhosis.

Budd-Chiari Syndrome↗
PubMed1986

'Lupus' anticoagulant and thrombosis of the hepatic veins (Budd-Chiari syndrome). Report of three patients and review of the literature.

Three patients with Budd-Chiari syndrome in association with the 'lupus' anticoagulant are described. This anticoagulant was looked for in our patients with an otherwise idiopathic hepatic venous thrombosis because of the presence of a pronounced thrombocytopenia, a prolonged activated partial thromboplastin time or a history of repeated abortions and deep leg vein thrombosis, respectively. An active search for the 'lupus' anticoagulant should be performed to lower the percentage of apparently idiopathic cases of Budd-Chiari syndrome.

Adult↗
PubMedDate not supplied

[Acute pre-hepatic portal thrombosis: diagnosis and therapy].

Portal vein thrombosis is a rare pathology. The etiopathogenetic causes that most frequently lead to this pathology are myeloproliferative syndromes. The authors present a case of acute pre-hepatic portal vein thrombosis and discuss its etiopathogenesis, diagnosis and therapy.

Acute Disease↗
PubMed1997

Prevalence of the factor V Leiden mutation in hepatic and portal vein thrombosis.

BACKGROUND: The factor V Leiden (FVL) mutation has been shown to be the most frequent cause of hereditary thrombophilia. The prevalence of the mutation in patients with Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT) has not been fully elucidated. AIMS: To investigate the association between the FVL mutation and BCS and PVT. PATIENTS: Thirty patients with BCS, 32 patients with PVT, and a control group of 54 patients with liver disorders and no history of thrombosis. METHODS: The factor V gene was analysed for the presence of the FVL mutation by a polymerase chain reaction (PCR) technique. The presence of the mutation was confirmed by DNA sequencing. RESULTS: Seven (23%) patients with BCS, one (3%) patient with PVT, and three (6%) patients in the control group were identified as having the FVL mutation. There of the BCS patients had coexisting hypercoagulable states. The prevalence of the FVL mutation was significantly higher in patients with BCS compared with patients with PVT and controls (p < 0.04). The FVL mutation was the second most common aetiology associated with BCS. CONCLUSION: The FVL mutation is an important factor in the pathogenesis of BCS and screening for the disorder must be included in the investigation of patients presenting with this condition. In contrast, the FVL mutation is not a major predisposing factor in the pathogenesis of PVT.

Adolescent↗
PubMed2003

[Portal vein thrombosis associated with factor V Leiden mutation in a woman who underwent exchange transfusion at birth].

We report the case of a 18-year-old woman with portal vein thrombosis and chronic hepatitis C virus. Portal vein thrombosis was diagnosed by chance on ultrasound examination during initial hepatitis C virus-positive patient screening. The patient interview revealed a history including exchange transfusion at birth, followed by necrotising ulcerocolitis and septicemia. The investigation of general factors favoring thrombosis showed acquired protein S deficiency and heterozygous factor V Leiden mutation. This case demonstrates the value of systematic investigations for general thrombophilic factors in cases of portal vein thrombosis even when a local cause is found.

Adolescent↗