Value of high resolution compression elastography and color doppler sonography in characterisation of breast lesions: comparison of different high-frequency transducers.

PURPOSE: To evaluate the additional effect of higher frequent linear probes than 12.5 MHz in color Doppler sonography and free hand sonoelastography of benign and malignant breast masses and to compare different color encodings in sonoelastography. MATERIALS AND METHODS: From December 2012 to March 2013, 37 patients with benign or malignant breast masses were prospectively included in this study. All solid masses have been histologically proven. Two readers assessed sonoelastographic findings at 12.5 MHz vs. 17 MHz according to the tsukuba elasticity score and additionally different color encodings were compared. Results of Doppler sonography using a score of 0, 1 or 2, depending on the degree of perfusion, also were assessed at 12.5 MHz vs. 17 MHz. RESULTS: Among the 37 examined breast masses there were 10 cysts, 16 fibroadenomas and 11 carcinomas. Median participant age was 49.0 years. Use of color Doppler sonography enabled to distinguish cysts from solid breast masses (p < 0.001), without an improvement at 17 MHz. Additional sonoelastography significantly improved the specificity in solid breast masses (p < 0.001). No changes could be seen using different colors in sonoelastography. CONCLUSION: Combination of color Doppler sonography and sonoelastography can increase the accuracy in distinguishing benign from malignant breast masses. The use of linear probes with a higher frequency than 12.5 MHz does not show any benefit, neither in color Doppler sonography nor in sonoelastography.

Improving the follow up after EVAR by using ultrasound image fusion of CEUS and MS-CT.

PURPOSE: To evaluate whether the image fusion with contrast enhanced ultrasound (CEUS) and CT affects the diagnosis of endoleaks in unclear cases. METHODS AND MATERIALS: 35 patients with follow-up examinations after endovascular aneurysm repair (EVAR) were included in this retrospective study. Mean patient age was 73 years (range 54-83 y). B-scan, colour doppler and CEUS (1.2 ml SonoVue®, Bracco Imaging Germany) were performed in all patients by an experienced examiner using two different high-end ultrasound system (Siemens ACUSON S2000™, Siemens Healthcare, Erlangen, Germany or Logic E9, GE Healthcare, Milwaukee,WI, USA) with a multifrequency curved array transducer. The examiner was initially blinded to the CT results. Additional image fusion with CT-angiography (CTA) was then performed. The ultrasound examinations were later read by two blinded unbiased investigators with more than five years of clinical ultrasound in consensus. RESULTS: All patients were examined using all diagnostic ultrasound tools of the study. The results show that image fusion is easy and convenient to perform. Conventional ultrasound examination with B-scan and colour Doppler examination detected one Type I and one Type II endoleak, contrast enhanced ultrasound detected one Type I and three Type II endoleaks after EVAR whereas CTA depicted one Type I and two Type II endoleaks. Ultrasound image fusion with CT-angiography confirmed one Type I and three Type II endoleaks. CONCLUSION: In comparison to conventional ultrasound and CTA the use of CEUS improved the visualization and classification of endoleaks. CEUS shows even small blood flow which can be depicted due to the real time imaging of endoleaks. In unclear cases additional ultrasound image fusion with CEUS and CT angiography improves the visualisation of small endoleaks and this may cause a change in the follow-up interval. CEUS is a good alternative to CT in the detection and follow-up of endoleaks, especially in patients with contraindications to CT contrast agents due to allergies or renal failure, enabling reduced additional costs and exposure to radiation.

Identification of Mycobacterium shimoidei by molecular techniques: case report and summary of the literature.

A 53-year-old woman from Melbourne, Australia, with squamous cell carcinoma of the oesophagus was shown by computed tomography (CT) scan to have a left apical cavity and inflammatory changes in the right lung consistent with aspiration. Acid-fast bacilli isolated from bronchial washings were identified biochemically first as Mycobacterium terrae, but later as M. shimoidei on the basis of 1) restriction fragment analysis and 2) sequencing of polymerase chain reaction (PCR) amplified 16S rDNA. Nine other descriptions of patients with M. shimoidei isolates were collated. The salient feature of isolates considered to be pathogenic was pulmonary cavitation. Most patients had underlying lung disease, including past tuberculosis or malignancy. Six of eight patients died of progressive respiratory illness, although the contribution of M. shimoidei was not always clear, and two patients improved. One patient with the acquired immune-deficiency syndrome (AIDS) died with Salmonella enteritidis and M. shimoidei isolated from blood cultures. One isolate was regarded as a coloniser. There are insufficient clinical or sensitivity data on which to base recommendations for therapy, but a combination of ethambutol, rifabutin and pyrazinamide could be considered.

Aetiology of severe iron overload in a family with hereditary haemolytic anaemia.

Severe iron overload is a reported complication of certain erythroid disorders which are characterized by increased erythropoietic activity. Proposed mechanisms include enhancement of iron absorption secondary to increased erythroid activity and coexistent heterozygosity or homozygosity for haemochromatosis. We performed PCR-based analysis for the haemochromatosis-related HFE C282Y mutation in an extended family with inherited haemolytic anaemia in which several members exhibited iron overload. The results demonstrated iron overload was associated with homozygosity but not heterozygosity for this mutation. Such an association may also exist in other erythroid disorders in which iron overload has been reported.

Vitamin D-induction of secretory responses in rat pituitary tumour (GH4C1) cells.

1,25-Dihydroxyvitamin D3(1,25-(OH)2D3) selectively enhances prolactin gene expression in GH4C1 clonal rat pituitary tumour cells. Because this effect requires extracellular Ca2+, we studied the effect of 1,25-(OH)2D3 on another Ca2+-dependent process, agonist-induced hormone secretion. Pretreatment with 1,25-(OH)2D3 (1 nmol/l) caused at least 25-fold sensitization of GH4C1 cells to the voltage-sensitive Ca2+ channel agonist BAY K 8644 (methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyr idine -5-carboxylate) as a prolactin secretagogue. This inductive effect of 1,25-(OH)2D3 followed a similar time-course to the enhancement of prolactin production. 1,25-(OH)2D3 had no effect on basal or BAY K 8644-induced 45Ca2+ uptake. The Ca2+-selective divalent cation ionophore 11,19,21-trihydroxy-4,6,8,12,14,18,20- heptamethyl-9-oxo-22-(tetrahydro-5 methyl-5-tetra hydro-5-(1-hydroxyethyl)-5-methyl-2-furanyl)-10,16-docosadienoic acid (ionomycin; 12 nmol/l-1.2 mumol/l) caused no significant increase in prolactin secretion in the absence of 1,25-(OH)2D3, but in cells treated with 1,25-(OH)2D3-(1 nmol/l), it increased prolactin secretion by 73% at 12 nmol/l and by a maximum of 98% at 0.12 mumol/l. These data demonstrate that vitamin D markedly enhances the responsiveness of GH4C1 functional pituitary tumour cells to two secretagogues which acts primarily through Ca2+-dependent mechanisms. They support the proposal that 1,25-(OH)2D3 acts in this cultured cell model either by effecting a redistribution of intracellular Ca2+ or by increasing the response of a Ca2+-sensitive effector system, but not by enhancing agonist-induced Ca2+ uptake.

Steroid inhibition of calcitriol-induced prolactin production in GH4C1 cells. Specificity and sensitivity.

The induction of prolactin (PRL)-gene expression by calcitriol (1,25-dihydroxyvitamin D3, 1,25-dihydroxycholecalciferol) in clonal rat pituitary tumour (GH4C1) cells was selectively inhibited by cortisol [IC50 (concentration causing 50% inhibition) = 3.2-4.1 nM]. The steroid specificity of this effect was investigated and various steroids were found to inhibit calcitriol-stimulated PRL production with the following relative potencies: cortisol, 1; dexamethasone, 8; 11-deoxycortisol, 0.5; corticosterone, 0.4; aldosterone, 0.07; testosterone and oestradiol, less than 0.003. The steroid antagonist RU 38486 did not affect basal or calcitriol-stimulated PRL production, but antagonized the effect of 10 nM-cortisol in a concentration-dependent manner. Neither progesterone nor 11-deoxycortisol antagonized the effect of 10 nM-cortisol. Calcitriol-induced PRL production was 14 times more sensitive to dexamethasone inhibition than was non-stimulated PRL production. Growth-hormone production was stimulated by dexamethasone, in the presence or absence of calcitriol, with a concentration-dependence similar to that of dexamethasone inhibition of basal PRL production. These data indicate that steroid inhibition of calcitriol-stimulated PRL production is a specific glucocorticoid effect. The sensitivity of calcitriol-stimulated PRL production to dexamethasone was 14-26-fold greater than that of other measured responses in the same cells. Two of the possible explanations for this selectively increased sensitivity to glucocorticoids are: amplification of the glucocorticoid effect via an induced mediator; and the presence of very-high-affinity glucocorticoid-receptor-binding sites on DNA.

Glucocorticoids antagonize induction of prolactin-gene expression by calcitriol in rat pituitary tumour cells.

Clonal strains of rat pituitary tumour (GH4C1) cells are known to possess specific intracellular binding sites for calcitriol (1,25-dihydroxycholecalciferol, 1,25-dihydroxyvitamin D3). GH4C1 cells respond to calcitriol by a selective increase in prolactin(PRL)-gene expression. The interaction between calcitriol and glucocorticoids was studied by using this cultured-cell model. It was found that cortisol potently antagonized the induction of PRL mRNA and PRL production by calcitriol. The effects were concentration-dependent and were evident at glucocorticoid concentrations that did not alter basal PRL production. Inhibition was half-maximal at 3.2 nM-cortisol and 0.4 nM-dexamethasone. Calcitriol-induced PRL mRNA fell by more than 50% at 25 h and reached the control level 50 h after treatment with cortisol. The inhibition by cortisol of calcitriol induction of PRL production was selective when compared with effects on other inducers of PRL-gene expression [thyroliberin, epidermal growth factor and phorbol myristate acetate ('12-omicron-tetradecanoylphorbol 13-acetate')]. Potent antagonism by glucocorticoids of vitamin D action on specific gene expression has been demonstrated. Further studies with this cultured-cell model may help to explain the mechanism of this hormonal interaction, which assumes particular importance at major sites of vitamin D action such as the intestine.