Contrast-enhanced ultrasonography in diagnosing liver metastases.

BACKGROUND: Dual-phase spiral computed tomography (CT) is still the primary imaging technique in the diagnosis of focal liver lesions. Contrast-enhanced ultrasonography (CEUS) is the most sensitive sonographic technique. The purpose of this study was to investigate the efficacy of CEUS in detecting liver metastases compared with CT as the standard of reference. MATERIAL/METHODS: The examined group consisted of 51 patients (24 men and 27 women, age range: 27-84 years, mean: 57.4 years) suspected of liver metastases. The routine diagnostic approach consisted of B-mode US, CEUS, and CT. Final diagnosis was made at cytologic (n=18) or histologic examination (n=14) and in 9 patients by combining information from CT scans, medical history, and clinical and biochemical investigations. RESULTS: Liver cysts and abscesses were detected in 10 patients. They were excluded from the further analyses. In the remaining 41 patients a total of 134 metastases were detected. In 15 patients with metastases, US images of the liver appeared normal. CEUS detected metastases in 36 patients. The sensitivities of the methods per patient were US 63.4% and CEUS 90.2%. Sensitivities of the methods per lesion were US 60.9%, CT 77.6%, and CEUS 90.2%. Application of contrast media (SonoVue) significantly increased diagnosing of liver metastases compared with standard sonography and CT. CONCLUSIONS: CEUS increased diagnostic confidence in the detection and characterization of hepatic metastases compared with standard sonography. Real-time contrast-enhanced sonography is particularly advantageous in detecting small metastases.

Effect of endothelin-1 receptor antagonists on histological and ultrastructural changes in the pancreas and trypsinogen activation in the early course of caerulein-induced acute pancreatitis in rats.

AIM: To assess the effect of non-selective ET(A/B) (LU 302872) and selective ET(A) (LU 302146) antagonist on pancreatic histology and ultrastructure of acinar cells in connection with trypsinogen activation in early caerulein-induced AP. METHODS: Male Wistar rats with caerulein-induced AP, lasting 4 h, were treated i.p. with 10 and 20 mg/kg b.w. of each antagonist. Edema, inflammatory infiltration, necrosis and vacuolization of acinar cells in the pancreas were scored at 0-3 scale. Free active trypsin (FAT), total potential trypsin (TPT) after activation with enterokinase, and index of trypsinogen activation (%FAT/TPT) were assayed in pancreatic homogenates. RESULTS: In untreated AP, the edema, inflammatory infiltration, necrosis and vacuolization increased as compared to control healthy rats (P<0.01). None of the treatment exerted any meaningful effect on the edema and inflammatory infiltration. The selective antagonist increased slightly the necrosis score to 0.82+/-0.06 at higher dose (P<0.05) vs 0.58+/-0.06 in untreated AP. The non-selective antagonist increased slightly the vacuolization score to 2.41+/-0.07 at higher dose (P<0.01) vs 1.88+/-0.08 in untreated AP. The decrease in the number of zymogen granules, disorganization of endoplasmic reticulum, autophagosomes and cytoplasmic vacuoles were more prominent in treated AP than in untreated AP groups. %FAT/TPT in untreated AP increased about four times (18.4+/-3.8 vs 4.8+/-1.3 in control group without AP, P<0.001). Treatment of AP with both antagonists did not affect significantly augmented trypsinogen activation. CONCLUSION: The treatment with endothelin-1 receptors (non-selective ET(A/B) and selective ET(A)) antagonists has essential effect neither on the edema and inflammatory infiltration nor on trypsinogen activation observed in the early course of caerulein-induced AP. Nevertheless a slight increase of the necrosis and vacuolization score and some of the ultrastructural data could suggest the possibility of their undesired effects in caerulein-induced AP at investigated doses.

Assessment of proliferative activity of thyroid Hürthle cell tumors using PCNA, Ki-67 and AgNOR methods.

We have undertaken an attempt to compare the application efficacy of the proliferative activity markers in differential diagnosis of thyroid Hürthle cell tumors (HCT) using the PCNA and Ki-67 labeling and AgNOR visualisation techniques. The present work is a retrospective analysis of 78 Hürthle cell tumors: 20 Hürthle cell carcinomas (HCC), 32 Hürthle cell adenomas (HCA) and 26 hyperplastic nodules with Hurthle cell metaplasia (HCM). Five microm sections were stained according to AgNOR technique and labeled with antibodies against PCNA and Ki-67. AgNOR dot count in the nucleus and proliferative index (PI - percentage of cells expressing PCNA and Ki-67) in randomly chosen nuclei (100 in case of AgNOR and over 1000 in case of PI) were evaluated in each slide. The mean values of AgNOR dot count, PI-PCNA and PI-Ki-67 in HCC, HCA and HCM were respectively: 5.1, 61.3 and 54.9; 3.4, 42.4 and 38.6 and 2.5, 39.3 and 34.3. Statistically significant difference was found in all the proliferative activity markers between malignant and benign tumors: HCC:HCA (p<0.01) and HCC:HCM (p<0.001). There was no statistically significant difference between HCA and HCM.

The influence of nitric oxide synthesis modulation on the pancreatic acinar cells in caerulein-induced acute pancreatitis. An ultrastructural and morphometric study.

The goal of our study was to evaluate the influence of NO synthesis modulation on the ultrastructural changes in the pancreatic acinar cells in connection with morphometric assessment of the volume and numerical densities of mitochondria (Vvm, Nvm) and zymogen granules (Vvz, Nvz) in caerulein-induced acute pancreatitis (AP). During AP induction rats were treated with L-arginine--substrate for NO synthesis, N(G)-nitro-L-arginine (L-NNA)--NO synthase inhibitor, gliceryl trinitrate (NTG)--NO donor, L-arginine+L-NNA or saline. This study demonstrated that administration of L-NNA leads to the formation of numerous, large autophagosomes and mitochondria oedema in pancreatic acinar cells. Treatment with L-arginine or NTG during AP induction resulted in a diminution of the ultrastructural changes with a concomitant increase of Vvz. Vvm and Nvm were significantly lower in the L-arginine treated group compared to the untreated AP. The results indicate that: L-NNA enhances damage to acinar cells which may be indicative of a protective role for endogenous NO in oedematous AP. The application of L-arginine or NTG decreases the damage to acinar cells evaluated ultrastructurally, suggesting the morphological changes accompanying the onset of AP in rats after the administration of either substrate for endogenous NO synthesis or exogenous NO donor follow a favourable course.

AgNOR, Ki-67 and PCNA expression in fibroepithelial tumours of the breast in correlation with morphological features.

The authors retrospectively reviewed the cytological slides of 44 histopathologically confirmed fibroepithelial lesions of the breast, of which 11 were fibroadenoma (FA), 19 benign phyllodes tumours (PTLGM), 8 borderline (PTBM) and 6 malignant (PTHGM). The 2 FA misdiagnosed as PTLGM in cytological smears were both of cellular type. NORS were quantified in a series of the above cases using the silver-colloid method. Expression of Ki-67 and PCNA were evaluated by immunohistochemistry on sections from the corresponding paraffin blocks. The results were compared with morphological parameters. In phyllodes tumours (PT), the AgNOR scores showed a tendency to increase with degrees of malignancy. There was significant correlation between Ag- NOR counts and proliferation rates as determined by Ki-67 and PCNA immunostaining. Ki-67 and PCNA expression correlated with mitotic count, stromal overgrowth, cellularity and atypia in PT. Determination of the AgNOR number per cell revealed an overlap between FA and PTLGM. The proliferating activity determined by immunohistochemistry with Ki-67 and PCNA antibodies did not reveal any significant difference between FA and PTLGM. In summary, Ki-67 and PCNA expression is suggested as a marker of stromal element proliferation. The results obtained confirm the diagnostic difficulties in distinguishing PTLGM from FA of the cellular type using fine needle aspiration cytology.