Focal nodular hyperplasia of the liver

The management of focal nodular hyperplasia (FNH) of the liver requires a systematic approach. After a histologic diagnosis of FNH is obtained, asymptomatic lesions can be observed safely with regular follow-up and treated if they become symptomatic or enlargement occurs. In the case presented here, we have elected follow-up with serial CT scans because our patient is asymptomatic and the lesion has not significantly enlarged. Patients who have symptomatic lesions while taking an oral contraceptive can have conservative follow-up when they stop taking the oral contraceptive, because regression of FNH has been reported to occur after cessation of oral contraceptive use. If the patient remains symptomatic or if the lesion enlarges after discontinuance of oral contraceptive use, surgical resection is warranted. Other symptomatic patients, including those with a previous history of taking oral contraceptives, should be treated by surgical resection or, when resection is not possible, by embolization or ligation of the hepatic artery, because symptomatic patients are at risk for having malignant lesions misdiagnosed as FNH.     

Focal nodular liver hyperplasia of atypical presentation

Focal nodular hyperplasia is a benign hepatic tumor that usually appears in young women. Diagnosis of focal nodular hyperplasia is often incidental when an ultrasonography or computed tomography is performed by other reasons, because its course is generally asymptomatic; the presence of a central fibrous scar is characteristic. Management in focal nodular hyperplasia must be conservative, with ultrasonographic follow-up, and it only must be treated when patients are symptomatics or in case of tumoral enlargement. We report a case of FNH in which symptomatic presentation and the absence of central stellate scar in ultrasonography, computed tomography and magnetic resonance leads to a misdiagnostic of hepatic adenoma, that conditioned a surgical resection. The later examination was diagnostic of focal nodular hyperplasia.     

Focal nodular hyperplasia of the liver: a rational approach to treatment

Focal nodular hyperplasia of the liver in a 3 year old child has been successfully treated by ligation of the hepatic artery branches supplying the lesion. The prominence of the abnormal vasculature in the lesion and its possible aetiological involvement is stressed. Because of the risks of partial hepatectomy, hepatic artery ligation is suggested as the treatment of choice for focal nodular hyperplasia.     

Focal nodular hyperplasia in a young female

OBJECTIVE: To analyze data from a large multicenter study to determine whether pregnancy and delivery rates decrease with repeated IVF-ET cycles. DESIGN: Multicenter retrospective study. SETTING: Participating centers from the Society of Assisted Reproductive Technology. PATIENT(S): Fifty-four centers contributed 4,043 cycles of oocyte retrieval for uterine transfer. INTERVENTION(S): Oocyte retrieval for uterine transfer. MAIN OUTCOME MEASURE(S): Pregnancy and delivery rates, analyzed according to age, program success rate, and whether the program was doing assisted hatching. RESULT(S): Pregnancy and delivery rates for cycles 1, 2, 3, 4, and >4 were 33.7% and 27.0%, 33.9% and 27.4%, 28.9% and 23.4%. 25.9% and 16.1%, and 21.0% and 15.4%, respectively. The pregnancy rate decreased significantly for >4 cycle; delivery rate decreased significantly for cycles 4 and >4. Assisted hatching was strongly related to better odds of pregnancy (OR, 1.50) and delivery (OR, 1.44) in women under age 40, and for pregnancy (1.64) in women age 40-42 years. CONCLUSION(S): Success rates do not decrease markedly with repeated IVF attempts, and the decrease did not change with program success rate, suggesting the IVF population is not markedly heterogeneous. Uncontrolled studies of new treatments for cycle repeaters cannot assume that success rate is poor without a treatment change.     

Focal nodular hyperplasia of the liver: a clinicopathologic study and review of the literature

We received the clinical records and pathologic material of 20 patients with biopsy proven hepatic focal nodular hyperplasia. The majority of the patients were females of child bearing age, five of whom had a history of oral use of contraceptives. In every instance focal nodular hyperplasia was an incidental finding; liver function tests were always normal. Focal nodular hyperplasia is a distinct histopathologic entity, distinguishable from liver cell adenoma. Specifically it consists of nodular aggregates of cytologically normal hepatocytes with foci of intranodular bile duct proliferation. Focal nodular hyperplasia appears to be a benign entity, even in patients in whom the lesion was not excised. The association between focal nodular hyperplasia and oral use of contraceptives may be coincidental, although hormonally related vascular changes may be responsible for rupture of the lesion.     

Oral contraceptive intake in women with focal nodular hyperplasia of the liver

This study examines the risk associated with oral contraceptive (OC) use in women with focal nodular hyperplasia (FNH). A total of 216 women (mean age, 36.2 years) with FNH were studied during 1989-98. The studied women were separated into five groups: no OC use (n = 28); high-dose OC use (50 mcg ethinyl estradiol, n = 46); low-dose OC use (30 mcg or less ethinyl estradiol, n = 98); low-dose and high-dose OC use (n = 33); pure progestagen use (n = 11). In each group, the mean diameter and the number of lesions per patient were assessed via magnetic resonance imaging (MRI). Findings revealed no differences between the five groups as to the number and the size of the lesions. The data showed that neither the intake nor the type of OC influenced the size and number of FNHs. A total of 128 women were followed up with serial MRI done after a mean of 23 months: 89 discontinued OCs, 14 remained without OCs, and 25 had taken or remained on low-dose OCs. In those who discontinued OCs, the FNH had decreased in size in two lesions and increased in size in one lesion. Despite continuation of OCs, the largest FNH disappeared 2 years after the first diagnosis, whereas the other FNH remained unchanged. Moreover, during this follow-up study, 12 women became pregnant; no increase in lesion size was seen during pregnancy. These findings indicate that low-dose OCs can be maintained in young women with FNH.     

Clonal analysis of focal nodular hyperplasia of the liver

Ligation of CD95 (APO-1/Fas) cell surface receptors induces death in apoptosis-sensitive cells. Induction of apoptosis in adherent gamma interferon-stimulated HT-29 and COLO 205 colon carcinoma cells by cross-linking CD95 with anti-APO-1 monoclonal antibody resulted in detachment of the cells from hyaluronate starting about 1 h after antibody exposure. Loss of adhesion was paralleled by a substantial reduction of the multifunctional cell surface adhesion molecule CD44. As evidenced by cycloheximide treatment, this effect was not caused by impaired protein synthesis. Depletion of surface CD44 was also not due to membrane blebbing, since cytochalasin B failed to inhibit ascension from hyaluronate. Instead, ELISA and time kinetics showed increasing amounts of soluble CD44 in the supernatant of CD95-triggered cells. SDS-PAGE revealed that soluble CD44 had an apparent molecular mass of about 20 kD less than CD44 immunoprecipitated from intact cells. Thus, CD95-triggering induced shedding of CD44. Shedding is a novel mechanism operative in early steps of CD95-mediated apoptosis. Shedding surface molecules like CD44 might contribute to the active disintegration of dying epithelial cells in vivo.     

Intrahepatic bile duct injury and nodular regenerative hyperplasia of the liver in a patient with polyarteritis nodosa

Although involvement of the hepatic vasculature in patients with polyarteritis nodosa is not unusual, biliary manifestations are very rare. We describe a patient with polyarteritis nodosa presenting with a febrile cholestatic anicteric syndrome. Histological examination of the liver revealed necrotizing arteritis of small hepatic arteries associated with significant lesions of intrahepatic bile ducts of the sclerosing cholangitis type, i.e. fibrous collar around the ducts, periductal inflammation and ductal proliferation. Concomitant nodular regenerative hyperplasia was found, a condition which has rarely been described in association with polyarteritis nodosa. We think that hepatic arteritis compromising arterial blood flow to the liver was responsible for the most likely ischemic nature of the bile duct injury and the nodular regenerative hyperplasia seen in our patient.     

Radiological features of focal nodular hyperplasia of the liver in children

BACKGROUND: Focal nodular hyperplasia (FNH) is an unusual hepatic tumour in children and should be distinguished from other hepatic lesions. OBJECTIVE: To describe the imaging characteristics of FNH in children. MATERIALS AND METHODS: We examined five patients (three boys and two girls, mean age 9.4 years) with pathologically confirmed FNH. The diagnosis was obtained by tumour resection (n = 4) and percutaneous needle biopsy (n = 1). One patient with multiple FNHs showed recurrent lesions after tumour resection. All patients were studied with US (including colour and power Doppler US [n = 3]) and CT. Dynamic enhanced CT scans were available in three patients. MRI (n = 2) or coeliac angiography (n = 1) was performed in three patients. RESULTS: Seven of eight FNH lesions in five patients were demonstrated by imaging. The average size of the lesions was 6.5 cm. Six lesions detected on US showed variable echogenicity with a central hyperechoic scar (n = 2). On Doppler examination, central or peripheral hypervascular areas were seen (n = 3). Six lesions detected on contrast-enhanced CT showed high attenuation (n = 4) or iso-attenuation (n = 2). On early phase scans, all the lesions (n = 3) showed high attenuation. Irregular linear or ovoid central scars were detected in two patients on CT. MR demonstrated three lesions in two patients, one of which had not been detected by US or CT. A central low signal intensity scar (n = 1) was seen on T2-weighted MRI. Coeliac angiography performed in one patient showed a hypervascular mass with homogeneous staining. CONCLUSION: FNH in children shows a wide spectrum of imaging findings on various radiological examinations and the typical central scar was not always seen on imaging studies. Dynamic enhanced CT obtained in the early phase and colour Doppler studies may be helpful in the diagnosis of FNH by allowing characterisation of tumour vascularity. FNH should be included in the differential diagnosis of liver mass in children.     

Noncirrhotic portal hypertension and nodular regenerative hyperplasia of the liver in dogs with mucopolysaccharidosis type I

Seventy six consecutive patients with T2-4, N0-1, M0 primary breast cancer (BC) received a median of 3 cycles of CMF (cyclophosphamide, methotrexate, 5-fluorouracil) regimen. Tamoxifen was concomitantly administered in patients with estrogen receptor positive (ER+) BC. Ki67 antigen was evaluated immunohistochemically in tumor specimens obtained before chemotherapy and at mastectomy. At post chemotherapy evaluation, tumor shrinkage greater than 50% was obtained in 60 patients (78.9%), 21 of them being complete responders (27.6%). As a whole, primary chemotherapy significantly decreased the number of Ki67 positive cells. More than 50% decrease in Ki67 expression was observed in 78.9% of patients attaining a clinical complete response (CR), in 44.7% of patients with partial remission (PR) and in 50.0% of non-responders, while an increase (>25%) in Ki67 expression was found in 5.3%, 18.4% and 18.7% of patients with CR, PR and non-response, respectively. Both CR and PR rates were superimposable in patients with ER+ and ER- primary BC, while the reduction in Ki67 expression was mainly found in ER+ cases. Patients with increased Ki67 expression from baseline, at the end of primary chemotherapy, had a shorter disease-free interval (70 months) with respect to patients with no change (88+ months) or decrease (87+ months), p<0. 05. To conclude, the activity of CMF + tamoxifen in primary BC does not seem superior to that expected administering CMF alone. The reduction in Ki67 expression, as a whole, correlated with clinical CR, but some individual discrepancies between tumor shrinkage and Ki67 pattern have been observed. The Ki67 reduction mainly confined to the ER+ primary BC suggests that tumor response in this subset may be linked to the reduction in proliferation activity, whereas other mechanisms such as apoptosis might be responsible for the tumor shrinkage in ER- tumors. Since the increase in proliferation activity after primary chemotherapy was associated with a greater recurrence rate and lower disease free interval, irrespective of tumor response, changes in proliferation activity after primary chemotherapy may represent a potentially available parameter that, in addition to the tumor response, can discriminate patients who would benefit from the cytotoxic treatment from patients who would not.     

The sonographic "scar sign" in focal nodular hyperplasia of the liver

The sonographic features of focal nodular hyperplasia of the liver as reported in the literature and nonspecific. However, a linear cluster of bright echoes was detected in the nodules of two of our patients with surgically proven focal nodular hyperplasia. Pathologically this finding correlated closely with the gross appearance of the characteristic fibrotic scar of focal nodular hyperplasia. When present, this "scar sign" should suggest the diagnosis of focal nodular hyperplasia, particularly in the typical clinical setting.     

Dynamic inversion recovery snapshot FLASH MRT of focal nodular hyperplasia of the liver

We report the regional assignment on Chromosome (Chr) 11q of two cDNA clones selected as sequences expressed in mature kidney and not expressed in Wilms' tumor. Clone T70 was identified as an alpha B-crystallin sequence (CRYA2). CRYA2 has previously been mapped to 11q22.3-23.1 by in situ hybridization. Clone 6.2 represents a new gene expressed in adult and fetal kidney, pancreas, and liver. In order to map sequences corresponding to clone 6.2 and to physically define the boundaries of the localization of CRYA2, we used somatic cell hybrids carrying either different human chromosomes or Chr 11 segments and a cell line established from a patient with an interstitial deletion of region 11q14.3-q22.1. We showed that CRYA2 lies proximal to the 11q23.2 breakpoint defined by the constitutional t(11;22) and distal to the 11q22.1 breakpoint (between D11S388 and D11S35) of a constitutional interstitial deletion. This is in agreement with previous data obtained by in situ hybridization and provides proximal and distal physical benchmarks for this localization. Clone 6.2-related sequence (D11S877E) was assigned to region 11q23.2-q24.2 defined by the breakpoints of the constitutional t(11;22) and of the Ewing's sarcoma neuroepithelioma t(11;22).     

Primary and secondary carcinomata with focal nodular hyperplasia in a multinodular thyroid: case report

A patient is described whose multinodular thyroid gland was found to have a primary papillary adenocarcinoma, a metastatic renal-cell carcinoma, and focal nodular hyperplasia. To our knowledge, this is the first case report of such an unusual combination. In a patient with known malignancy elsewhere, the possibility that a recent thyroid mass may be a metastasis should be considered.     

Focal epithelial hyperplasia: human-papillomavirus-induced disease with a genetic predisposition in a Venezuelan family

A study on the presence of human papillomavirus (HPV) DNA sequences and focal epithelial hyperplasia (FEH) in a family of Venezuelan ancestry has revealed that FEH is an HPV-induced disease presenting familial aggregation. The genealogical evidence indicates a genetic predisposition to the disease.