Littoral cell angioma of the spleen: sonographic-pathologic comparison.

OBJECTIVES: The purpose of this study was to evaluate the sonographic and pathologic features of littoral cell angioma of the spleen in 7 patients. METHODS: The sonographic appearance in 7 cases of littoral cell angioma confirmed by surgical pathologic examination was retrospectively reviewed. All underwent color Doppler imaging. Two underwent contrast-enhanced sonography. The sonographic appearance was compared with pathologic findings. RESULTS: Splenic lesions were solitary in 5 cases and multiple in 2 cases. The masses ranged from 10 to 64 mm in maximum diameter. Five hypoechoic and 2 hyperechoic lesions on grayscale sonography corresponded to few and multiple blood-filled spaces on pathologic examination, respectively. Four hypovascular lesions, 1 hypervascular lesion, and the other 2 hypervascular lesions full of color flow signals on color Doppler imaging corresponded to few, several, and multiple arteries on pathologic examination. On contrast-enhanced sonography, 1 hypervascular lesion full of color flow signals showed homogeneous hyperenhancement for 8 minutes during the arterial and parenchymal phases. One hypovascular lesion showed inhomogeneous isoenhancement transiently during the arterial phase and became hypoechoic later. CONCLUSIONS: Littoral cell angioma is a primary vascular splenic neoplasm with variable features on grayscale sonography and color Doppler imaging as well as contrast-enhanced sonography. The sonographic appearance of littoral cell angioma mainly depends on the type and number of tumor vessels.

Serous cystic neoplasms of the pancreas: a clinicopathologic and immunohistochemical analysis.

OBJECTIVE: To clarify whether the various subtypes of serous cystic neoplasms (SCNs) of the pancreas can be distinguished from each other by marker profiles. METHODS: The immunoprofiles of 13 SCNs were defined by using antibodies against cytoskeletal, neuroendocrine, hormone receptor, and mucin markers. In addition, we examined the expression of calrentinin and alpha-inhibin. RESULTS: SCN included 7 cases of serous microcystic adenomas (SMA), 3 cases of serous oligocystic ill-defined adenomas (SOIA), 1 case of solid serous adenoma (SSA), 1 case of von Hippel-Lindau-associated cystic neoplasm (VHL-CN), and 1 case of serous cystadenocarcinoma (SCC). These neoplasms are histologically similar, but differ in their localization, gross appearance, gender distribution, and biological behavior. The various types of SCNs showed a very similar immunoprofile, characterized by positivity for cytokeratins (100%) and negativity for vimentin and synaptophysin. Other markers that were commonly expressed in the SCNs were alpha-inhibin (85%), MUC1 (69%) and MUC6 (77%). CONCLUSION: The results suggest that, despite their biologic differences, the various types of SCNs have the same (or a very similar) cell type and may therefore have a common direction of differentiation. A centroacinar origin is supported by the finding that a number of SCNs share MUC1 and MUC6 expression with pancreatic centroacinar cells. Alpha-inhibin, and MUC6 may be regarded as new markers for this type of pancreatic tumor.

Detection of herpes simplex virus type 1 in rheumatic valvular tissue.

BACKGROUND: Rheumatic heart disease (RHD) is the most important sequela of rheumatic fever (RF): evidence that streptococcal infection is aetiological is prominent, but sometimes contradictory. Acute HSV-1 infection in mouse leads to carditis and valvulitis whereas recurrent infection results in inflammatory granulomatous lesions that resemble Aschoff bodies. Cells containing HSV-1 inclusions or virus infected giant cells appear similar to Anitschkow cells or Aschoff cells respectively. We hypothesized that HSV-1 infection also may be involved in RHD. METHODS: Formalin-fixed, paraffin-embedded valvular tissue samples from 32 patients with RHD were investigated for evidence of HSV-1 infection. HSV-1 antigen was detected by immunohistochemistry, using HSV-1-specific monoclonal and polyclonal antibodies. HSV-1 glycoprotein D gene sequences were amplified by nPCR, using beta-globin gene amplification in the same samples as internal control. Valvular tissue from 5 cases of sudden death and 3 cases died of neisseria meningitis without a history of valvular disease was used for comparison. HSV-1-infected lung tissue was used as positive control. RESULTS: HSV-1 antigens were detected in valvular tissues from 21 of 32 (65.6%) patients. Fifteen of these 21 (46.9% of cases), but no antigen-negative sample, were positive also for HSV DNA. Nucleotide sequence of PCR products was homologous to the targeted region of the HSV-1 glycoprotein D gene. HSV-1 antigen was present also in one case of sudden death but viral DNA was not found in any tissue sample from the comparison group. Results from reagent and positive controls were as anticipated. CONCLUSIONS: This is the first study to show the presence of HSV-1 antigen and genomic DNA in valvular tissues from patients with RHD and provides evidence for an association of HSV-1 infection with some cases of rheumatic valvular disease.