Lobular capillary hemangioma of the liver

BACKGROUND:Lobular capillary hemangioma(LCH) is a benign vascular tumor that is rare in adults and has never been reported in the liver.This vascular lesion usually presents on the skin or mucous membranes,and predominantly affects children. METHODS:LCH as a large asymptomatic hepatic mass was seen in a 35-year-old female.Imaging and pathologic characteristics of the mass are reviewed,and the relevant literature is also reviewed. RESULTS:A large vascular hepatic lesion was observed in an asymptomatic 35-yea...     

Cystic cavernous hemangioma of the liver

We report an unusual case of multilocular cystic cavernous hemangioma of the liver. The patient was a 61-year-old woman without liver disfunction but who had multicystic mass lesions in the liver. Although cavernous hemangiomas are usually accurately diagnosed by the various imaging modalities, our case showed atypical features.     

Curious manifestations in cavernous hemangioma of the liver

We report a cavernous hemangioma of the liver with some curious findings. Angiography showed a hypervascular lesion and the arterioportal shunt which commonly is regarded as a pathognomonic sign of malignancy. Laparoscopy showed a well-defined, reddish-purple elevated lesion with a central umbilication. As the patient was a painter and dealing with vinyl chloride monomer, we suspected the possibility of hemangiosarcoma. The lesion proved to be a cavernous hemangioma with central fibrous replacement probably in consequence of thrombosis of some cavernous spaces.     

Rapid growth of liver hemangioma following interferon treatment for hepatitis C in a young woman

Liver hemangioma is the most common benign liver tumor. Giant hemangiomas can grow and give various clinical symptoms. We describe a case of rapid growth of liver hemangioma in a seventeen-year-old girl. She was treated with interferon alpha 2b for hepatitis C. About 12 months later she was admitted to the hospital with symptoms of large epigastric mass, anemia and thrombocytopenia. Ultrasound scan and computed tomography confirmed the clinical picture, suggesting giant liver hemangioma. During surgery large cavernous hemangioma deeply penetrating into normal liver parenchyma was found. In view of recent hepatitis C infection the resection procedure (left extended hemihepatectomy) was assessed as being dangerous for the patient's life. Ligation of the left branches of hepatic artery and portal vein reducing tumor blood supply was performed. The postoperative period was uneventful; the hemangioma in the left lobe had shrunk. Ultrasound and CT scans performed one and two years after surgery showed that the size of the hemangioma remained stable and the patient was asymptomatic. In this described case three potential factors stimulating the growth of hemangioma (puberty, hepatitis C infection and interferon treatment) are discussed. The potential role of vascular endothelial growth factor and fibroblast growth factor is raised.     

Giant liver hemangioma in three sisters

We describe a patient, in whom giant liver hemangioma (GLH) was found by ultrasound study in screening for hypertension. Two of her sisters also had GLH. One of them had become symptomatic and the hemangioma was successfully removed. The other sisters were carefully watched. Our patient didn't need any intervention in 4 years of follow-up. The pathogenesis of GLH is still unknown. Recent investigations show a role of the TIE receptor/angiopoietin system in vascular malformations. In literature we only found two other reports about a familial occurrence of liver hemangiomas. A genetic defect in familial GLH has not yet been identified.     

Incidental hepatic schistosomiasis in a liver transplant recipient

E. Ariza‐Heredia & R.R. Razonable. Incidental hepatic schistosomiasis in a liver transplant recipient.
Transpl Infect Dis 2011. All rights reserved Abstract: Hepatic schistosomiasis is a well recognized cause of chronic liver disease and portal hypertension. Herein, we describe a case of a 62‐year‐old Kuwaiti man who underwent liver transplantation for non‐alcoholic steatohepatitis and, as an incidental finding in the histopathology of the explanted liver, eggs consistent with Schistosoma were found. In endemic regions, hepatic schistosomiasis is often observed as an incidental finding in explanted livers of patients who receive liver transplantation for other indications. In the context of this case, we provide a brief review of the management of schistosomiasis in transplant recipients.     

Radiotherapy of hemangioma cavernosum of the liver.

Four patients with massive cavernous hemangioma of the liver were treated with 6 Mev X-ray, and favorable results were obtained in 3. Patient 1 was treated with a total tumor dose of 940 rads without response. The 2nd patient was given a total tumor dose of 1900 rads over 54 days, with a daily dose of 50 to 100 rads. Although the hemangioma regressed after treatment, the response was transient. A total tumor dose of 2940 rads was given over 41 days with a daily dose of 100 to 200 rads as a second course, and the hemangioma regressed with no sign of reenlargement. Patients 3 and 4 were given 150 to 200 rads every other day to a total of about 3000 rads, with a satisfactory response. Follow-up studies showed the latter 3 patients to be well 8, 5, and 4 years after radiotherapy, respectively.     

肝血管瘤中VEGF的表达及其与AgNOR定量的关系

本文用肝血管瘤石蜡切片作血管内皮生长因子（ＶＥＧＦ）链霉亲和素—生物素—过氧化物酶免疫组织化学染色（即ＳＡＢＣ法）和核仁组成区相关嗜银蛋白（ＡｇＮＯＲ）计数方法，研究ＶＥＧＦ在肝血管瘤成因中的地位。结果显示:４８例肝血管瘤标本中，ＶＥＧＦ阳性表达率为７５．０％，其中（＋）者９例，（）者１１例，（）者１６例，且ＶＥＧＦ表达强度在不同的组别间ＡｇＮＯＲ计数差异显著（Ｐ＜０．０１）。提示ＶＥＧＦ在肝血管瘤的成因中可能具有重要意义。     

血管瘤中血管内皮生长因子及其受体KDR的表达和血管生成的研究

目的 探讨血管内皮生长因子(VEGF)及其受体KDR在血管瘤中的表达以及其与微血管密度(MVD)的关系.方法 采用免疫组化SP法检测35例婴幼儿血管瘤VEGF及KDR的表达和MVD.结果 35例血管瘤中VEGF、KDR的蛋白表达阳性率分别是66.5%,73.4%.其中增生期和消退期VEGF阳性率分别为92.1%、31.4%(P<0.01),KDR阳性率分别为89.3%、42.5%(P<0.01);MVD分别为75.7±13.71、28.9±8.5(P<0.01).KDR的表达与VEGF成正相关(P<0.01),KDR和VEGF与MVD都成正相关(P<0.01).结论 血管瘤增生期血管内皮细胞存在着血管内皮细胞生长因子及其受体KDR的相互作用,促进了新生微血管生成.     

Acute liver failure following the use of ecstasy (MDMA)

The use of "ecstasy" (Methylenedioxymethamphetamine) as a recreational drug is increasing in europe since the 1980's. Aside intended psychological effects the use of ecstasy can be followed by symptoms of intoxication; complications include toxic hepatic damage up to acute hepatic failure. This case-report is about a 17-year old female patient who regularly used "ecstasy" over a six-month period. Two days after the last use of "ecstasy", she reported to her general practitioner with nausea, vomiting, abdominal pain and jaundice. Within 10 days the patient developed acute liver failure. With criteria for liver transplantation fulfilled she was listed for orthotopic liver transplantation of high urgency which was carried out only one day later. Histological examination of the explanted liver showed evidence for a toxic fulminant hepatitis. After transplantation the patient made a full recovery and was released from hospital on day 26 after transplantation. At the first control after six months the patient was in good physical and nutritional condition, serological parameters were normal and ultrasound examination of the transplanted liver was unremarkable. The ethiopathology of "ecstasy"-induced hepatotoxicity, which can occur dose-independently with a symptom-free period from days to weeks after ingestion is not yet fully understood. Possible mechanisms of hepatic damage include influence of MDMA on body temperature regulation, harmful effects of the substance or further components of the "ecstasy"-tablets on the liver cell or a genetic vulnerability of some individuals against amphetamines and amphetamine derivates. There are no parameters existing which could predict the course and severity of "ecstasy"-induced hepatopathy. Especially in young patients with symptoms of hepatic damage frequent controls of clinical status and relevant laboratory parameters are of great importance. Patient transfer to a specialised centre should follow as early as possible; at the latest, when coagulopathy occurs.     

Giant cavernous hemangioma of liver.

An abscess forming in a giant cavernous hemangioma of the left lobe of the liver is reported. It was treated by lateral segmentectomy.     

Hemorrhagic hemangioma in the liver: A case report

Hemangioma is the most common type of benign tumor that arises in the liver. Although rupture and hemorrhage of hepatic hemangioma are rare complications, they can be the cause of mortality. The authors report a case of hemorrhagic hepatic hemangioma: in a 54-year-old woman who was admitted with epigastric pain. She had taken oral contraceptives several weeks prior. The results of a blood examination were normal. An abdominal computed tomography scan revealed a tumor in hepatic segment 4, and a hemorrhage inside the cystic mass was suspected. The mass was removed laparoscopically to confirm the tumor properties and control the hemorrhage. The pathologic findings of the resected mass were consistent with hepatic hemangioma with intratumoral hemorrhage. The patient was discharged 8 d after the surgery, without further complications or complaints, and the patient’s condition was found to have improved during follow-up.     

A case of liver hemangioma with markedly reduced tumor size after metformin treatment: a case report

A 52-year-old man with a 9-year history of hepatic hemangioma was treated with the anti-diabetic drug metformin, resulting in complete remission of the tumor. In 2006, a hemangioma with diameter of 20 × 25 mm was detected incidentally in the liver. The results of imaging studies including ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) were all compatible with that of hepatic hemangioma. The patient consequently underwent imaging annually from 2006 to 2015. The tumor size increased slightly, to 30 × 35 mm in 2012; however, the general tumor characteristics in imaging were not changed. Beginning May 2012, metformin (750 mg/day) was administered because of an increase in blood sugar and hemoglobin A1c levels. After the start of metformin treatment, the tumor size on US gradually decreased. Finally, in October 2015, the tumor was no longer detected. Dynamic CT study also demonstrated markedly reduced tumor size, with a decrease of 2–3 mm in diameter. These results indicate that metformin treatment strongly suppressed cell proliferation in liver hemangioma. The anti-angiogenic effect of metformin was indicated as a possible cause of the reduction in tumor size.     

Proton pump inhibitor use increases mortality and hepatic decompensation in liver cirrhosis

BACKGROUND Proton pump inhibitors(PPIs) are widely prescribed, often without clear indications. There are conflicting data on its association with mortality risk and hepatic decompensation in cirrhotic patients. Furthermore, PPI users and PPI exposure in some studies have been poorly defined with many confounding factors.AIM To examine if PPI use increases mortality and hepatic decompensation and the impact of cumulative PPI dose exposure.METHODS Data from patients with decompensated liver cirrhosis were extracted from a hospital database between 2013 to 2017. PPI users were defined as cumulative defined daily dose(c DDD) ≥ 28 within a landmark period, after hospitalisation for hepatic decompensation. Cox regression analysis for comparison was done after propensity score adjustment. Further risk of hepatic decompensation was analysed by Poisson regression.RESULTS Among 295 decompensated cirrhosis patients, 238 were PPI users and 57 were non-users. PPI users had higher mortality compared to non-users [adjusted HR =2.10,(1.20-3.67); P = 0.009]. Longer PPI use with cDDD 90 was associated withhigher mortality, compared to non-users [aHR = 2.27,(1.10-5.14); P = 0.038]. PPI users had a higher incidence of hospitalization for hepatic decompensation [aRR= 1.61,(1.30-2.11); P 0.001].CONCLUSION PPI use in decompensated cirrhosis is associated with increased risk of mortality and hepatic decompensation. Longer PPI exposure with cDDD 90 increases the risk of mortality.     

Case report: cavernous hemangioma of the liver.

Although cavernous hemangioma is the most common benign tumor of the liver, controversy persists regarding diagnosis and management of these lesions. With the development of multiple noninvasive modalities to visualize the liver, hepatic cavernous hemangiomas are recognized with increased frequency. The authors report the unusual case of a post-menopausal woman on no exogenous estrogen therapy who had a cavernous hemangioma that remained stable for approximately 10 years before dramatically increasing in size. This patient illustrates the vague symptoms associated with cavernous hemangiomas and the unpredictability of growth. Although estrogens have been reported trophic, this patient had no exogenous or endogenous estrogen supply, yet her lesion reached massive proportions. Modalities necessary to assure accurate diagnosis and factors influential in management are discussed.     

Reduction in myocardial neutrophil accumulation and infarct size following administration of thromboxane inhibitor U-63,557A

We examined the effects of a new selective thromboxane A2 (TXA2) synthetase inhibitor, U-63,557A, on myocardial infarct size 48 hours following left coronary ligation in rats. With a single 8 mg/kg dose of U-63,557A (furegrelate) administered prior to coronary ligation, platelet aggregation and serum TXA2 formation declined significantly (p less than 0.02) for up to 48 hours. Myocardial infarct size, as measured by planimetry of serial left ventricular sections, was decreased from 44 +/- 3% (saline-treated control rats) to 34 +/- 4% (p less than 0.05). Left ventricular creatine kinase (CK) following coronary ligation was also preserved in U-63,557A vs saline-treated control animals (p less than 0.05). These beneficial effects of U-63,557A were not accompanied by reduction in the indices of myocardial oxygen demand (heart rate and arterial pressure). Furthermore, neutrophil accumulation in the infarcted myocardium was significantly decreased by U-63,557A (26 +/- 6 vs 96 +/- 3/high-power field [p less than 0.01]). These data suggest that administration of a single dose of selective TXA2 synthetase inhibitor prior to coronary ligation modulates platelet function for up to 48 hours and reduces the extent of myocardial injury, which may, in part, relate to decrease in neutrophil accumulation.