Anastomosing hemangioma: report of two renal cases and analysis of the literature.

BACKGROUND: Anastomosing hemangioma (AH) is a very rare vascular tumor mimicking angiosarcoma, predominately observed in kidney and less frequently in other organs. We present two new renal cases of AH at opposite ends of the clinical presentation spectrum, provide review of the literature and compare the epidemiological, clinical and pathological profiles of renal and non-renal cases. CASE PRESENTATION: The first occurred in a 64-year-old woman presented with back pain and the second, a multifocal lesion, in a 47-year-old man with end stage renal disease (ESRD). Histology disclosed a vascular tumor with striking anastomosing pattern, minimal nuclear atypia and locally infiltrative pattern, mimicking superficially angiosarcoma. Extramedullary hematopoiesis, extensive perirenal fat entrapment and increased number of mast cells were additional features in the second lesion. Both patients are well, without disease, 25 and 14 months after diagnosis. CONCLUSION: Comprehensive review and analysis of the published literature show that the growing number of non-renal AHs exhibits similar epidemiologic, clinical, biologic and histologic characteristics with renal AHs and most mild differences vanish after exclusion of cases associated with ESRD. Better understanding of AH pathogenesis will contribute to optimal treatment choices.

Glucagonoma syndrome: survival 21 years with concurrent liver metastases.

A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described. Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor. No specific treatment was administered. The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.

A fatal case of postinfantile giant cell hepatitis in a patient with chronic lymphocytic leukaemia.

Postinfantile giant cell hepatitis has been associated with various aetiologies, including drug taking, autoimmune diseases and viral infections. We present a fatal case of giant cell hepatitis in a patient with chronic lymphocytic leukaemia. No liver biopsy was available ante-mortem. The patient was treated with corticosteroids and aciclovir for suspected autoimmune hepatitis and reactivation of Epstein-Barr virus in the context of his haematological malignancy. Post-mortem liver biopsy showed severe giant cell hepatitis while the study of liver tissue by electron microscopy revealed paramyxo-like viral particles in the cytoplasm of the affected hepatocytes similar to those observed in previous reports of giant cell hepatitis. This case illustrates that the diagnosis of the underlying cause of giant cell hepatitis may be complicated because a heterogeneous group of different aetiologies needs to be investigated. The identification of the causative agent is essential before commencing any kind of therapy. A few sporadic case reports of paramyxo-like virus related, postinfantile giant cell hepatitis have shown that ribavirin was quite effective treatment but further clinical evaluation is needed.

Fulminant hepatic failure in a pediatric patient with active GB virus C (GBV-C)/hepatitis G virus (HGV) infection.

We describe a rare case of a pediatric patient with active GB virus C (GBV-C)/hepatitis G virus (HGV) infection who died of fulminant hepatic failure within less than a month after the onset of jaundice. The child tested negative for all other known hepatitis viruses and had no history of blood transfusions. This observation suggests that although GBV-C/HGV is usually not pathogenic to the liver, it may be associated with certain idiopathic forms of fulminant hepatitis. Whether this association is etiological or circumstantial remains to be seen.

IFN-alpha2b monotherapy in patients with chronic hepatitis C and persistently normal or near normal aminotransferase activity: a randomized, controlled study.

To determine the effect of interferon-alpha2b (IFN-alpha2b) on the long-term suppression of hepatitis C virus (HCV) RNA in patients with persistently normal or near normal alanine aminotransferase (ALT) activity, 76 previously untreated patients with serum HCV RNA and ALT levels <1.5 times the upper limit of normal (ULN) were randomized to receive either interferon-alpha2b (IFN-alpha2b) 5 MU three times a week for 24 weeks (n = 37) or no treatment (n = 39). HCV RNA testing was performed at the end of treatment and after a 6-month follow-up period. Intention-to-treat analysis showed that HCV RNA was detected significantly less frequently in treated than in untreated patients, at the end of both treatment and follow-up (43.2% vs. 7.7%, p < 0.001, and 21.6% vs. 5.1%, p = 0.033, respectively). Among treated patients, sustained virologic response was significantly higher in non-1 than in genotype 1 patients (8 of 26 or 30.8% vs. 0 of 11, p = 0.038). According to multiple logistic regression, untreated patients had a 13.5 times greater risk to be HCV RNA-positive compared with treated patients (p = 0.040). ALT levels flared up in 3 treated and 9 untreated patients (p = 0.07), suggesting that these flare-ups are related to the natural course of chronic HCV infection rather than to IFN-alpha2b. Thus, such patients could benefit from an IFN-alpha2b in combination with ribavirin regimen.