We describe the case of a 77-year-old woman with chronic hepatitis C and well compensated cirrhosis in whom a single encapsulated 5.5 cm hepatocellular carcinoma was found in the right liver lobe. The patient was symptomatic with left upper quadrant pain and had elevated alfa-fetoprotein levels (3133 ng/ml). While she was waiting for liver resection and 2 months after the initial diagnosis the pain improved and alfa-fetoprotein levels normalized. A computerized tomography scan showed reduction in size of the lesion to 2.5 cm, with no central arterial enhancement, but with the demonstration of a peripheral rim enhancing in all dynamic phases. Follow up computerized tomography and magnetic resonance imaging examinations showed further reduction in size of the lesion to 1.3 cm with persistence of the enhancing rim 20 months after the initial diagnosis. The spontaneous and durable regression of the HCC and the persistent peripheral enhancing rim could be explained by a strong and persistent activation of the immune system directed against the neoplastic cells.

In their recent paper Van Bommel et al. demonstrated a greater antiviral activity of tenofovir at a dose of 300 mg/day compared to adefovir against lamivudine-resistant hepatitis B virus.1 This is the standard approved dose for HIV and HBV coinfected patients,2 but it may not be the optimal dose for HIV negative patients. Hepatitis B virus has a greater susceptibility to nucleotide analogues compared to HIV3 and is certainly less likely to develop resistant mutants. In the initial studies adefovir was used at doses up to 120 mg/day in order to achieve significant HIV inhibition, a dosage well above the approved dose for chronic hepatitis B. It is therefore feasible that tenofovir, like its parent drug adefovir could be used at a lower dosage in patients with HBV infection alone. To test this hypothesis we treated 10 chronic hepatitis B patients (8 of them had cirrhosis) with 75 mg/day of tenofovir for a median period of 82 weeks (range 44-144). The patients had a median age of 64 years (range 40-76), were all HBeAg negative, and had no other comorbidities. All had received lamivudine for a median duration of 24 months (range 10-39) and were shifted to tenofovir immediately after stopping lamivudine. Five of them had developed YMDD resistance, the others had wild-type virus and were changed to tenofovir to prevent the emergence of lamivudine resistance. Before starting tenofovir, 4 of the 5 patients with YMDD resistance had normal levels of alanine aminotransferase, negative serum branched HBV DNA (Versant HBV DNA 3.0 Bayer, sensitivity <2000 copies/mL), but viral HBV DNA could be detected by polymerase chain reaction (PCR; Innolipa HBV DR Amplification, Innogenetics, Ghent, Belgium, sensitivity <1000 copies/mL) with the presence of YMDD-resistant mutants (Innolipa Line Probe Assay, Innogenetics). The other patient with YMDD mutants had elevated levels of alanine aminotransferase and a serum HBV DNA of 4.8 × 106 copies/mL (b-DNA). Four of the 5 patients with lamivudine resistance, including the patient with high viremia, became HBV DNA negative by PCR assay after 2-6 months of tenofovir and remained negative throughout the entire period of treatment (median 64 weeks, range 44-144) The 5 patients without YMDD mutants were shifted from lamivudine to tenofovir when their serum HBV-DNA was undetectable by PCR and remained PCR negative while receiving tenofovir (median 84 weeks, range 64-100). The drug was well tolerated and no side effects were reported. In addition, no viral breakthrough was observed, confirming the low potential of this drug to induce phenotypic resistance, even using a dose as low as 75 mg. These excellent results have been observed in only 10 patients, all except one with very low HBV DNA levels, so they may not be generalized to all chronic hepatitis B patients, especially those with high viremia. We think, however, that a dose escalation study with a dose ranging from 75 to 300 mg/day may be warranted. The issue is clearly not safety, but cost and the fact that giving the lowest effective dose could significantly reduce the economic burden of this therapy. P. Del Poggio*, C. Jamoletti*, M. Zaccanelli*, * Hepatology Unit, Ospedale di Treviglio (Bg), Italy

A 58-year-old woman presented with a 2 cm hypoechoic lesion located in segment IV of the liver and incidentally discovered during an ultrasound examination. There was no posterior echo enhancement and the rim of the lesion was irregularly hyperechoic with some highly echogenic spots (panel A). A computed tomography (CT) scan showed an avascular unilocular cyst with density content in the soft tissue range (59 HU) and a magnetic resonance an increased signal on T2 weighted images (panel B). A fine needle aspiration yielded scattered mucous and ciliated columnar cells in a mucinous background (panel C: arrows). The presence of ciliated columnar cells is pathognomonic of the ciliated hepatic foregut cyst. These cysts originate from remnants of the primitive foregut and are typically located in the medial segments of the left hepatic lobe, underneath the anterior liver capsule [[1]Vick D.J. Goodman Z.D. Deavers M.T. Cain J. Ishak K.G. Ciliated hepatic foregut cyst: a study of six cases and review of the literature.Am J Surg Pathol. 1999; 23: 671-677Crossref PubMed Scopus (81) Google Scholar]. They are not associated with any other congenital hepatic lesions and are generally incidentally diagnosed. Their density at CT scan varies according to the mucinous content and at times differentiation from parasitic cyst, cystadenoma and metastatic lesions may be difficult [[2]Shoenut J.P. Semelka R.C. Levi C. Greenberg H. Ciliated hepatic foregut cysts: US, CT and contrast-enhanced MR imaging.Abdom Imaging. 1994; 14: 150-152Crossref Scopus (33) Google Scholar]. They are the only ciliated cystic lesions occurring in the liver and the diagnosis can be made by cytology alone, thus avoiding surgical resection. The irregularly hyperecogenic spots of the outer rim may be related to the constant presence of smooth muscle fibers within its wall. (panel D: arrow, operative specimen of another ciliated cyst). A regular follow up is advisable because of anecdotal reports of squamous cell carcinoma arising in these cysts.

We studied the stool samples of 151 school children in a district of the city of Portoviejo (Ecuador) in order to determine the prevalence and intensity of soil-transmitted helminthiasis (STH) and their relationships with anthropometric indices. The samples were analyzed with the semiquantitative Kato-Katz technique and the intensity of infections was categorized as light, moderate or high according to the thresholds set by the World Health Organization. Prevalence of soil transmitted helmintiasis was 65% (92 out of 141 collected samples), Ascaris lumbricoides was the most common STH (63%) followed by Trichuris trichiura (10%) and hookworm (1.4%). Heavy intensity infections were found in 8.5% of the stool samples, with T. trichiura showing higher worm burdens than A. lumbricoides. Sixteen percent of the children were below the third percentile for weight (wasted), while 27% were below the third percentile for height (stunted). A significant relationship was found between the worm burden and the degree of stunting. This study suggests that the periodic administration of an antihelminthic drug should be targeted to preschool and school children to allow a normal growth spurt and prevent stunting.

The case is described of a 63-year-old female with a multilocular liver cyst diagnosed as cystadenoma after imaging and fine needle aspiration. The lesion, however, proved to be an invasive cystadenocarcinoma at surgery. Cystadenoma cannot be differentiated, preoperatively, from cystadenocarcinoma and should always be considered for surgical resection.