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Hepatic adenoma is an uncommon benign hepatic tumor that is oft discovered as an incidental finding at imaging [i]. Conservative handling past means of periodic observation with imaging can exist practical in patients with a modest lesion [2]. Large or multiple hepatic adenomas are generally resected surgically to avert the risk of hemorrhage and cancerous transformation [3]. Although the long-term utilise of oral contraceptives (OCs) and the use of steroid medications are considered the almost of import risk factors [4], other conditions have been proposed such as metabolic diseases, including diabetes and type I glycogen storage affliction (GSD), and built hepatic vascular abnormalities [5–7]. Conditions that predispose patients to develop multiple hepatic adenomas are not yet well established, to our noesis.

In recent studies, investigators have described cases of multiple adenomas in patients with liver steatosis [8–xi]. The rapidly ascension prevalence of nonalcoholic fatty liver illness in Western societies [12], often detected at CT and MRI of the liver, as well as its potential function for the evolution of cirrhosis and even hepatic malignancy has been described [xiii]. However, to our knowledge, less is known about the relationship between intrahepatocyte fat deposition and the evolution of benign liver tumors. The possible being of this association may accept consequences for the direction of patients with multiple adenomas because segmental or lobar resection of a fatty liver tin exist technically hard and can atomic number 82 to increased postoperative morbidity, including perihepatic abscesses, infectious complications, and hepatic insufficiency [14, 15].

The purpose of our study was to investigate the association between liver steatosis and hepatic adenomas. To provide statistical back up for this hypothesis, the prevalence of steatosis in patients with hepatic adenoma was compared with the prevalence of steatosis in patients with hepatic hemangioma, the nigh common benign liver tumor [16], in a case-command setting.

Our retrospective written report was compliant with HIPAA and was canonical by our institutional review lath; the need for patient informed consent was waived. This study was conducted at a university-based tertiary liver heart in the U.s.a..

Written report Group

A certified research coordinator searched the medical, radiology, and pathology databases for information obtained betwixt January 1999 and March 2007 using the terms "hepatic adenoma," "liver adenoma," "hepatic adenomatosis," and "liver adenomatosis." The search yielded the records for 39 patients with a proven diagnosis of hepatic adenoma. Fifteen patients were excluded because of lack of multiphasic CT or MR scans available for review; these images were considered essential for optimal lesion detection and identification of liver steatosis. Therefore, our study group included 24 patients (22 women, two men; age range, 23–57 years; mean age, 40 years); the hateful size (± SD) of the largest hepatic adenoma was seven.2 ± iii.7 cm. All had a histologically confirmed diagnosis of hepatic adenoma. The histologic specimen for the diagnosis was obtained at core needle biopsy in five patients (21%), liver resection in xvi (67%), and liver explantation in three (13%).

Twelve patients (l%) underwent CT or MRI performed specifically to evaluate a known or suspected liver mass, whereas 12 patients (l%) had hepatic adenoma discovered on CT or MRI performed to evaluate abdominal pain or other indications. Ix patients (38%) presented with symptoms that could be related to hepatic adenoma: v with pain or discomfort of the upper right abdominal quadrant and four with signs and symptoms of acute or recent hemorrhage. In iii patients (13%), hepatic adenoma was detected on imaging performed equally routine follow-up for GSD blazon I. No patients had clin ical, radiologic, or histologic evidence of viral hepatitis or cirrhosis, and no patient was imaged for elevated liver office test results or for a clinical suspicion of fatty infiltration of the liver. The clinical management of patients included observation in 5 (21%) later cadre needle biopsy results had excluded malignancy. Three patients (thirteen%) underwent orthotopic liver transplantation, two considering of adenomatosis and 1 considering of terminate-stage alcoholic liver affliction, and hepatic adenoma was revealed in the liver explant.

Control Grouping

The CT and MRI reports in the same time menstruation (i.e., from Jan 1999 to March 2007) were reviewed by a certified inquiry coordinator to identify patients with a diagnosis of hepatic hemangioma on multiphasic CT or MRI series. Patients with hepatic hemangioma were chosen as control subjects considering this tumor is considered the almost mutual hepatic primary lesion, reported in up to 20% of the full general adult population [17], and the diagnostic criteria are well established both at CT and MRI [18, 19]. In add-on, there is, to our cognition, no known relation between the prevalence of hemangioma and steatosis.

Imaging criteria to certificate hemangioma included marked hyperintensity on T2-weighted MR images, hypointensity on T1-weighted MR images, and nodular peripheral and centripetal contrast textile enhancement on dynamic CT and MR images obtained afterward IV contrast assistants [eighteen, nineteen]. In our establishment, for detection and characterization of both hepatic adenoma and hemangioma, a multiphasic CT or MR examination is indicated. For each case, the closest matching control subject for age at diagnosis, sex, and imaging technique was selected (Table 1). Among the 24 patients in the command group, 21 (88%) were women and 3 (12%) were men (p = ane.00, compared with the report group), with the age at diagnosis ranging from 26 to 54 years (mean age, 43 years; p = 0.227).

TABLE 1: Characteristics of Study and Control Groups According to the Selection Variables

CT and MRI

For 23 report patients (96%) and 22 control subjects (92%), abdominal CT images were available for review (p = 1.00), whereas 8 patients (33%) in the study grouping and two patients (eight%) in the control grouping had MRI series avail able (p = 0.033). Among these, both CT and MRI were bachelor for review in seven patients (29%) in the study group and none (0%) in the control group. In those cases, data obtained from the CT images were included in the analyses to achieve maximum comparability with the control group. Comparison of CT and MR images showed concordant results for steatosis and number of lesions in vii of the 7 patients (data non shown).

CT series consisted of biphasic abdominal heli cal CT, which included contrast-enhanced im aging through the liver with both hepatic arter ial and portal venous phases with delays of 25–35 seconds and 60–70 seconds, respectively, afterwards initiation of IV injection of dissimilarity material. All CT scans were obtained on MDCT scanners. All patients received nonionic 4 dissimilarity material (ioversol [Optiray 350, Mallinckrodt Imaging]) that was administered at three or 4 mL/southward at a volume of 125–150 mL. In addition, for 16 patients and 15 control subjects, unenhanced scanning of the liver before contrast material administration was performed.

MRI was performed on a ane.5-T system (Signa Excite Hd, GE Healthcare) using a variety of software upgrades that continuously evolved during the report flow. Standard liver imaging sequences included T1-weighted in-stage and opposed-phase gradient-echo and T2-weighted fast spin-echo sequences. T1-weighted imaging was repeated in all patients after contrast cloth assistants during the hepatic arterial (delay = 20–25 seconds), portal venous (delay = 60–seventy seconds), and delayed (delay = iii–v minutes) phases. All patients received a gadolinium chelate at a dose of 0.i mmol/kg of torso weight followed past a 20-mL saline flush.

Qualitative Analysis

Images were reviewed on a PACS workstation (Stentor, Philips Healthcare) independently by two abdominal radiologists with 5 and 4 years of experience, respectively, and discordance was resolved by consensus. Because we were not attempting to determine the accurateness of CT and MRI for the diagnosis of focal hepatic lesions, the readers had knowledge of the diagnosis of hepatic adenoma or hemangioma but were blinded to all clinical information and to the purpose of the study. In each patient, the CT and MR images obtained before and afterwards contrast injection were reviewed to assess whether steatosis was present and, if so, the distribution of steatosis in the surrounding liver parenchyma, the total number of lesions, and the maximum bore of the index lesion. In addition, every lesion with imaging features different from the characteristic findings of hepatic adenoma or hemangioma was recorded.

For the assessment of liver steatosis on CT images, each reader obtained attenuation measurements in Hounsfield units (HU) from the average of two regions of involvement (ROIs) drawn in the most representative fatty infiltrated area of the liver and ane ROI in the spleen. Steatosis was considered nowadays when the difference in attenuation between the liver and spleen (measured equally liver – spleen) was less than –10 HU on unenhanced images or less than –30 HU on portal venous phase images [20, 21].

On MRI, the presence of steatosis was qualitatively evaluated; the readers assessed for substantial bespeak intensity loss on the T1-weighted opposed-phase gradient-echo images in comparing with the in-stage images [22]. The distribution of fat in the liver was described using the following terms: diffuse, lobar, or focal or multifocal [23].

Additional Information Collection

The clinical reports of each patient were reviewed past three investigators for the patient'due south weight and height to summate body mass index (BMI) and history of OC use, steroid intake, diabetes, and GSD.

Statistical Assay

Continuous variables were described as a mean ± SD or as a median and range and categoric variables, equally a number (percent). The chi-square test was performed to compare the prevalence of steatosis in the patients versus the control subjects. Later, the chi-square test was used to compare the prevalence of steatosis in the patients with a single adenoma versus those with multiple adenomas in a subgroup assay. No attempt was made to examination the interobserver differences or accuracy because, in most cases, no absolute standard was available to found the exact number, size, and nature of the hepatic lesions. A p value of less than 0.05 was indicative of a statistically meaning difference. Data analyses were performed with commercially avail able software (SPSS 2004 for Microsoft Windows, version 13.0, SPSS).

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Fig. 1A —31-year-onetime woman with multiple hepatic adenomas and liver steatosis. Transverse unenhanced CT scan shows two modest hepatic adenomas (arrows) in right and left lobes of liver. Nodules announced hyperattenuating compared with surrounding liver parenchyma because of diffuse hepatic steatosis.

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Fig. 1B —31-twelvemonth-old woman with multiple hepatic adenomas and liver steatosis. Transverse dissimilarity-enhanced CT scan corresponding to A shows persistent enhancement of hepatic adenomas (arrows). Five boosted lesions with identical characteristics were identified (non shown).

Study Group

Among the 24 patients in the study group, liver steatosis was identified in fourteen (58%) (Table ii). The diagnosis was established using unenhanced CT images in 13 patients (Fig. 1A , 1B ) and by MR in-stage and opposed-stage gradient-echo images in one patient (Fig. 2A , 2B , 2C , 2D ).

Tabular array 2: Imaging and Clinical Features of Patients with Hepatic Adenoma (Report Group) Versus Patients with Hemangioma (Control Grouping)

13 patients (54%) had a single adenoma and 11 (46%) had multiple adenomas (range, i–20 lesions; median, iv lesions) identified at imaging. The maximum bore of the alphabetize lesion ranged from 2 to 17 cm with a median of seven.5 cm. In one patient, one additional lesion with imaging characteristics of focal nodular hyperplasia (FNH), which has a known association with hepatic adenoma [24], was identified. In two other patients with hepatic adenoma, a pocket-sized hemangioma (< ii cm) was also observed in nonsteatotic liver parenchyma.

Control Group

Amid the 24 patients in the control group, liver steatosis was identified in seven subjects (29%) (Table ii). The diagnosis was achieved by ways of unenhanced CT images in six subjects and MR in-stage and opposed-phase slope-echo images in one subject.

Fifteen control subjects (62%) had a single hemangioma and nine (38%) had multiple hemangiomas (range, 1–v lesions; median, 1 lesion) identified at imaging. The maximum diameter of the index lesion ranged from 1 to 24 cm with a median of 3 cm. No lesions with imaging findings different from hemangioma could be identified in the studies available.

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Fig. 2A —35-year-quondam woman with multiple hepatic adenomas and liver steatosis presenting with abdominal pain. Transverse in-phase MR prototype (TR/TE, 145/4.ii) shows biopsy-proven hepatic adenoma (pointer) as slightly hypointense lesion in right liver lobe.

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Fig. 2B —35-year-old woman with multiple hepatic adenomas and liver steatosis presenting with intestinal pain. Transverse opposed-phase MR prototype (145/2.1) respective to A shows indicate drop of liver parenchyma due to fatty deposition and "sparing" of area (arrowheads) surrounding hyperintense adenoma (arrow).

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Fig. 2C —35-year-old woman with multiple hepatic adenomas and liver steatosis presenting with abdominal pain. Transverse gadolinium-enhanced arterial phase T1-weighted slope-echo MR images (4.0/one.8) at 2 dissimilar hepatic levels show enhancement of adenoma (arrow, C) associated with transient hepatic intensity defect (arrowheads, C) and two additional modest lesions (arrows, D) with identical imaging characteristics; these characteristics are compatible with those of other small hepatic adenomas.

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Fig. 2d —35-twelvemonth-old woman with multiple hepatic adenomas and liver steatosis presenting with abdominal pain. Transverse gadolinium-enhanced arterial phase T1-weighted gradient-echo MR images (4.0/i.eight) at two different hepatic levels show enhancement of adenoma (arrow, C) associated with transient hepatic intensity defect (arrowheads, C) and two additional minor lesions (arrows, D) with identical imaging characteristics; these characteristics are uniform with those of other small hepatic adenomas.

Study and Control Groups

The prevalence of liver steatosis was significantly college in the patients with hepatic adenoma (58%) than in the control subjects (29%) (p = 0.042) (Table 2).

Information almost the use of OCs was available in 17 patients and xi command subjects. A positive history for OC utilize was present in 14 (82%) of the 17 hepatic adenoma patients (median time of use, 15 years) and in iv (36%) of the 11 control subjects (median time of utilise, 15 years) (p = 0.02). The BMI was calculated in 16 patients with adenoma and in ten patients with hemangioma (mean ± SD, 30.i ± vii.24 vs 28.1 ± 5.28, respectively; p = 0.456). Three report patients (13%) and no control subjects were affected by GSD type I (p = 0.023). 8 patients (33%) with hepatic adenoma and two control subjects (8%) with hemangioma had diabetes (p = 0.033).

Study Group: Single Versus Multiple Adenomas

Liver steatosis was present in five patients with a single hepatic adenoma (38%) and in 9 (82%) with multiple hepatic adenomas (Figs. 1A , 1B and 2A , 2B , 2C , 2d ). This difference was statistically meaning (p = 0.047) (Tabular array 3).

Tabular array 3: Prevalence of Liver Steatosis in Patients with Single Versus Multiple Hepatic Adenomas

Nine (82%) of the 11 patients with a single adenoma and five (83%) of six patients with multiple adenomas and available clinical data had a positive history of OC use (p = ane.00). BMI was calculated in seven patients with a unmarried adenoma and in 9 patients with multiple adenomas (mean ± SD, 32.v ± 7.three vs 28.three ± 7.0, respectively; p = 0.265). All 3 patients in our population with a diagnosis of GSD type I had multiple adenomas at imaging. Amid the eight patients with a history of diabetes, five had a single adenoma and iii had multiple adenomas (p = 0.679) (Table 3).

The goal of our report was to investigate the association between hepatic adenoma and liver steatosis. Co-ordinate to our results, the presence of liver fat deposition at CT and MRI was more frequently detected among the study group of patients with hepatic adenoma than in the command group of patients with hepatic hemangioma. In addition, in the study group, patients with multiple adenomas more than oft had signs of a fatty liver than patients with a unmarried adenoma. These results suggest that liver steatosis may play a role in the evolution of multiple hepatic adenomas.

Long-term exposure to exogenous estrogens by means of OCs is recognized as the principal chance gene for the evolution of the archetype single hepatic adenoma, or "pill adenoma," as commencement described by Baum et al. [25] and supported past others [4, 26]. However, the weather condition that predispose patients to develop multiple adenomas are not fully understood to our knowledge. In 1985, liver adenomatosis was described equally a dissever entity that is characterized by the presence of multiple adenomas (> 10) and lack of correlation with steroid medication intake or GSD that affects both men and women [27]. However, recent studies accept non been able to confirm this classification and take reported neither histologic nor radiologic differences among the adenomas arising as a single lesion, those arising as multiple lesions (2–10 lesions), and liver adenomatosis (> ten lesions) [11, 28]. Therefore, in our study we considered every patient to take multiple adenomas if imaging showed multiple lesions with identical characteristics in a patient with at least one pathologically confirmed adenoma. We did not consider "adenomatosis" as a distinct entity.

Recently, several groups of investigators reported or suggested an increased incidence of multiple adenomas in the setting of liver steatosis [eight–11]. Hepatic steatosis is due to fat accumulation inside the hepatocytes mainly resulting from alcoholic liver disease and nonalcoholic fatty liver affliction. The incidence of nonalcoholic fatty liver disease is rapidly increasing in the Western countries along with obesity [12, 29]. Although histologic analysis is considered the reference standard, CT and MRI are well-established noninvasive tests that accurately discover steatosis [twenty–22].

We hypothesize two possible mechanisms to explain the pregnant association between multiple hepatic adenomas and liver steatosis: The starting time hypothesis is that an increment in the intracellular content of lipid may lead to a hyperplastic reaction of the hepatocytes and finally to the germination of hepatic adenoma. Oxidative and inflammatory effects as well every bit alteration in hepatocyte regeneration accept been described to occur in fatty liver cells [30] and could peradventure be involved in a hyperplastic reaction. The 2d hypothesis is that the fat tissue may account for a continuous local estrogen generation, similar to what has been shown for peripheral fat tissues [31] through an increase in aromatase [32]. If this is indeed the case, one could speculate that a continuous local stimulus may change the hepatocyte growth rates more substantially than systemically elevated levels in OC users, resulting in the development of multiple tumors.

Other factors take been postulated in the development of multiple hepatic adenomas. Portal vein abnormalities (i.due east., portal vein agenesis or portal hepatic shunts) have been reported to facilitate the evolution of benign lesions, especially hepatic adenoma [29] and FNH [33], through a focal disturbance of the hepatic blood supply [34]. Even hepatocellular carcinoma in a child has been reported equally possibly related to hepatic vascular abnormalities [35]. Although in our serial hepatic adenoma was present in association with FNH and hemangioma (one and two cases, respectively), no patient had any identifiable vascular abnormality.

Investigators take reported that, in patients with diabetes, the accumulation of glycogen inside the cells, related to the defect in hepatic catabolism, can play a role in the hyperplastic reaction leading to the genesis of hepatic adenomas [5]. The obesity epidemic has paralleled the rapid increment in the prevalence of type 2 diabetes. In our report, there was a significant increased incidence of diabetes in the adenoma group versus the control group; nonetheless, no departure could be institute between patients with a single adenoma and those with multiple adenomas. Of interest, one man in the patient group had a history of diabetes mellitus as a unique potential caption for the presence of adenoma and a negative history of steroid intake or GSD.

In that location are limitations of our study that need to be best-selling. Because of its retrospective nature, complete information on all variables could not be retrieved. The lack of pinnacle and weight data limited the possibility of correlating BMI to the presence of steatosis in patients and command subjects. This correlation has been described as rather strong [36]; withal, our data did not suggest a college BMI in report patients versus command subjects or in patients with multiple versus single adenomas. With respect to the history of OC use, the unavailability of complete information prevented us from performing a multivariate analysis adjusting for OC employ. Investigators have reported that steroid hormones can be an independent run a risk gene in the development of liver steatosis [37], and OC use should, therefore, exist treated as a confounder in the relation betwixt steatosis and hepatic adenoma. However, the difference in availability of these data (i.e., data available for 71% of patients vs 46% of control subjects) could bias a multivariate analysis considering it is likely that physicians asked more specifically about OC use in patients with adenoma than in patients with hemangioma. All the same, the observation that multiple hepatic adenomas occur more frequently in fat livers is evident. The fact that this possibly includes a proportion of patients in whom steatosis is an intermediate in the pathway between OC and hepatic adenoma is perhaps non of direct cli nical relevance.

Other limitations of our study design could include underrepresentation of small hepatic adenomas in our serial considering those tumors are less likely to be biopsied or resected. State-of-the-fine art imaging, especially dynamic MR series, can be used to accurately diagnose hepatic adenoma and distinguish this tumor from FNH or malignancies on the basis of the described criteria in many cases [38]. However, histology results remain the reference standard and therefore only patients with a histologic diagnosis were included in this analysis. Another business concern that may arise is whether hemangiomas in steatotic livers could exist underrepresented considering fat infiltration may complicate the authentic detection of lesions. By including simply patients with dynamic imaging serial, on which hypervascular lesions are clearly visible, we tried to avoid the disproportional exclusion of control subjects with liver steatosis.

The handling for hepatic adenoma is not uniform. Some clinicians prefer a conservative approach; nonetheless, because of the hazard of hemorrhage and malignant degeneration, surgery is often advocated [39, 40]. The co-prevalence of multiple adenomas and steatosis may complicate the determination making for surgery versus observation in those patients because tumors are spread through the liver and steatosis increases the risk of surgical morbidity. Electric current MRI techniques can be of peachy value in providing the information needed to residual the risks versus the benefits of surgical intervention. In addition, the apply of standardized MRI protocols for patients with beneficial liver lesions could resolve many of the limitations of our study in future prospectively conducted enquiry. These studies are needed to confirm the association between hepatic adenoma and liver steatosis as suggested by our data.

In decision, the results of our study show the association of liver steatosis and hepatic adenoma in a case-command setting, which is a suitable study blueprint for uncommon conditions such as hepatic adenoma. Multiple adenomas were specially correlated with steatosis. In view of the increasing incidence of hepatic steatosis and obesity, this group of hepatic adenoma patients might be of growing importance and needs special attention.

A. Furlan and D. J. van der Windt contributed equally to this study.

Address correspondence to A. Furlan ([email protected]).

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