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      A Case of a Ruptured Sclerosing Liver Hemangioma

      case-report

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          Abstract

          Hemangiomas are the most common benign tumors found in the liver, typically asymptomatic, solitary, and incidentally discovered. Although vascular in nature, they rarely bleed. We report a case of a 52-year-old woman with a previously stable hemangioma who presented to our hospital with signs and symptoms indicative of spontaneous rupture. We review the literature, focusing on diagnosis and management of liver hemangiomas.

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          Most cited references34

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          Cellular markers that distinguish the phases of hemangioma during infancy and childhood.

          Hemangiomas, localized tumors of blood vessels, appear in approximately 10-12% of Caucasian infants. These lesions are characterized by a rapid proliferation of capillaries for the first year (proliferating phase), followed by slow, inevitable, regression of the tumor over the ensuing 1-5 yr (involuting phase), and continual improvement until 6-12 yr of age (involuted phase). To delineate the clinically observed growth phases of hemangiomas at a cellular level, we undertook an immunohistochemical analysis using nine independent markers. The proliferating phase was defined by high expression of proliferating cell nuclear antigen, type IV collagenase, and vascular endothelial growth factor. Elevated expression of the tissue inhibitor of metalloproteinase, TIMP 1, an inhibitor of new blood vessel formation, was observed exclusively in the involuting phase. High expression of basic fibroblast growth factor (bFGF) and urokinase was present in the proliferating and involuting phases. There was coexpression of bFGF and endothelial phenotypic markers CD31 and von Willebrand factor in the proliferating phase. These results provide an objective basis for staging hemangiomas and may be used to evaluate pharmacological agents, such as corticosteroids and interferon alfa-2a, which accelerate regression of hemangiomas. By contrast, vascular malformations do not express proliferating cell nuclear antigen, vascular endothelial growth factor, bFGF, type IV collagenase, and urokinase. These data demonstrate immunohistochemical differences between proliferating hemangiomas and vascular malformations which reflect the biological distinctions between these vascular lesions.
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            Contrast-enhanced ultrasound of histologically proven liver hemangiomas.

            Differentiation of small and atypical hemangiomas from other hepatic masses using imaging methods can be difficult, especially in patients with underlying malignant disease. Therefore, contrast-enhanced ultrasound was assessed in patients with histologically confirmed hemangiomas with respect to contrast-enhancing kinetics and tumor characteristics. In 58 patients with indeterminate hepatic lesions demonstrated with at least 2 imaging methods (ultrasound/computed tomography/magnetic resonance imaging), ultrasound-guided liver biopsy revealed hemangioma. In all patients a hepatic neoplasm had been suspected because of underlying malignant disease (n=41), liver cirrhosis (n=15), or growth of the lesion (n=2). All patients underwent nonlinear, low mechanical index real-time contrast-enhanced ultrasound scanning with bolus injections of SonoVue. Peripheral nodular arterial enhancement was detected in 43 patients (74%), whereas the typical metastatic peripheral rim-like enhancement was not observed at all. Strong homogenous arterial enhancement was found in 9 of 58 (16%) patients. In 6 patients (10%), the arterial contrast enhancement pattern could not be determined because of the very small size of the lesions or fibrotic nodules. Forty-five (78%) of the hemangiomas showed homogenous centripetal filling within 180 seconds. Contrast-enhanced ultrasound demonstrates typical hemangioma imaging characteristics, that is, peripheral nodular contrast enhancement and iris-diaphragm sign in a high percentage of patients with undetermined lesions. This technique may therefore improve noninvasive functional characterization and differentiation of hemangiomas.
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              Natural history of hepatic haemangiomas: clinical and ultrasound study.

              Hepatic haemangiomas are the most common benign tumours of the liver and commonly present as incidental findings on sonographic examination of the abdomen. Since little is known of the natural course of these tumours, we performed a clinical and sonographic follow up of 123 haemangioma patients. Our prospective study investigated clinical and sonographic findings in 158 haemangiomas for periods of 12 to 60 months. Ninety nine haemangiomas measured less than 2 cm and had an echogenic pattern; 40 were between 2 cm and 5 cm with a mainly echogenic structure; 19 measured greater than 5 cm and showed a mixed echo pattern. At the first examination only eight patients, all with giant haemangiomas, presented symptoms which could be attributed to the tumour. During follow up only one haemangioma changed in shape and size. One patient who was symptom free at the first examination experienced right upper abdominal quadrant pain during follow up. No deterioration occurred in any of the patients with symptoms at the first examination, and all had a satisfactory quality of life. No complications arose during the follow up period. This study shows that in adults haemangiomas remain stable in size and echo patterns rarely change. Only haemangiomas greater than 5 cm may cause symptoms. Prolonged clinical and sonographic follow up of small and medium sized haemangiomas is not warranted.
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                Author and article information

                Journal
                Int J Hepatol
                IJHEP
                International Journal of Hepatology
                SAGE-Hindawi Access to Research
                2090-3448
                2090-3456
                2011
                31 May 2011
                : 2011
                : 942360
                Affiliations
                1Division of Hepatology, University of Miami Miller School of Medicine, 1500 NW 12th Avenue, Suite 1101, Miami, FL 33136, USA
                2Department of Pathology, University of Miami Miller School of Medicine, 1611 NW 12th Avenue, Holtz Building, Room 2042, Miami, FL 33136, USA
                3Department of Radiology, University of Miami Miller School of Medicine, 1611 NW 12th Avenue, Miami, FL 33136, USA
                4Miami Transplant Institute, University of Miami Miller School of Medicine, Highland Professional Building, 1801 NW 9th Avenue, 3rd Floor, Miami, FL 33136, USA
                Author notes
                *Haris Papafragkakis: papafragakish@ 123456gmail.com

                Academic Editor: Yo-ichi Yamashita

                Article
                10.4061/2011/942360
                3170855
                21994877
                8107717e-037d-460f-858d-28ac99d941d7
                Copyright © 2011 Haris Papafragkakis et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 December 2010
                : 11 April 2011
                Categories
                Case Report

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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