Venous filling defects on portal venous phase CT of the abdomen and pelvis: clinical implications and positive predictive value for diagnosing deep venous thrombosis

Purpose

To determine the prevalence, resulting clinical decisions, and the positive predictive value (PPV) of venous filling defects detected on portal venous phase (PVP) CT.

Methods

Over a 3-year period, 42412 consecutive patients underwent a PVP abdominopelvic CT; of these, 348 reports mentioned a filling defect concerning for deep venous thrombosis (DVT) in the IVC, iliac, or common femoral veins. Ninety-three patients underwent a reference standard venous imaging study.

Results

The prevalence of venous filling defects in CT reports was 0.82% (n = 348). Reports worded with higher degrees of certainty were statistically more likely to result in treatment, while lower certainty was correlated with additional confirmatory imaging. The PPV for detection of DVT was 77%. The presence of peri-vascular stranding or vessel expansion increased the PPV of PVP CT to 95% and 100%, respectively.

Conclusion

While the PPV for filling defects on PVP CT was modest, it was substantially improved if peri-venous stranding or vessel expansion was present.     

Cardiac perforation following transcatheter PFO closure.

From December 1998 to August 2001, transcatheter closure of patent foramen ovale (PFO) with an Amplatzer PFO occluder has been successfully performed in our center in 102 patients without severe complications. We are reporting the first known case of cardiac perforation by an Amplatzer PFO occluder.     

Prolactin-Producing Pituitary Adenoma and Carcinoma with Neuronal Components<197>A Metaplastic Lesion

Recent studies indicate that cells of various epithelial tumors are capable of transformation to neurons. Observing both neurons and neuropil in two prolactin-producing adenohypophyseal tumors, one benign and one malignant, we sought to assess their cellular differentiation, the presence of nerve growth factor receptor, and expression of the dopamine receptor gene using immunocytochemistry, electron microscopy, and in situ hybridization. Light and electron microscopy clearly revealed cells morphologically transitional between adenoma/carcinoma cells and neurons. Large neurons lacked proliferative activity. Neurons in varying number showed immunoreactivity for pituitary hormones including prolactin, growth hormone and alpha subunit in the adenoma and prolactin alone in the carcinoma. The distribution of nerve growth factor receptor staining was similar. In both tumors, in situ hybridization showed mRNAs for prolactin and dopamine receptor within adenohypophyseal cells and neurons. Our results indicate that the occurrence of neurons and neuropil in growth hormone and prolactin-producing pituitary tumors appears to be the result of metaplasia. The process is not limited to benign tumors and may be due to the production of tropic substances by the adenohypophysial cells, which by paracrine/autocrine mechanisms result in transformation of adenoma cells to nerve cells.     

Direct isolation of Candida spp. from blood cultures on the chromogenic medium CHROMagar Candida

CHROMagar Candida is a selective and differential chromogenic medium that has been shown to be useful for identification of Candida albicans, Candida krusei, Candida tropicalis, and perhaps Candida glabrata. Colony morphology and color have been well defined when CHROMagar Candida has been used to isolate yeast directly from clinical specimens, including stool, urine, respiratory, vaginal, oropharyngeal, and esophageal sources. Direct isolation of yeast on CHROMagar Candida from blood cultures has not been evaluated. We evaluated whether the color and colony characteristics produced by Candida spp. on CHROMagar Candida were altered when yeasts were isolated directly from blood cultures. Fifty clinical isolates of Candida were inoculated into aerobic and anaerobic blood culture bottles and incubated at 35 degrees C in an automated blood culture system. When growth was detected, an aliquot was removed and plated onto CHROMagar Candida. As a control, CHROMagar Candida plates were inoculated with the same isolate of yeast grown on Sabouraud dextrose agar simultaneously. No significant difference was detected in color or colony morphology between the blood and control isolates in any of the tested organisms. All C. albicans (n = 12), C. tropicalis (n = 12), C. glabrata (n = 9), and C. krusei (n = 5) isolates exhibited the expected species-specific colony characteristics and color, whether isolated directly from blood or from control cultures. CHROMagar Candida can be reliably used for direct isolation of yeast from blood cultures. Direct isolation could allow mycology laboratories to more rapidly identify Candida spp., enable clinicians to more quickly make antifungal agent selections, and potentially decrease patient morbidity and mortality.     

Analysis of selected oncogenes (AKT1, FOS, BCL2L2, TGFbeta) on chromosome 14 in granulosa cell tumors (GCTs): a comprehensive study on 30 GCTs combining comparative genomic hybridization (CGH) and fluorescence-in situ-hybridization (FISH)

In previous studies, we have demonstrated a number of cytogenetic alterations in granulosa cell tumors (GCTs), especially on chromosomes X, 12, 14, and 22. However, little is known about specific loci on 14q, which could play an important role in tumor pathology. Therefore, we assessed four important genes in 30 GCTs using fluorescence-in situ-hybridization (FISH). Comparative genomic hybridization (CGH) was performed on paraffin-embedded material. Then, we applied FISH with gene-specific DNA probes for AKT1 (14q32.32), FOS (14q24.3), BCL2L2 (14q11.2-q12), and TGFbeta3 (14q24), and tried to find a correlation between CGH, FISH, tumor stage, and survival. In CGH, 7 of 30 cases (23.3%) showed complete gains on chromosome 14. FISH of the four loci revealed gains of hybridization signals in 8 of 30 cases (26.6%), indicating trisomy of the whole chromosome arm. The same aberration was detected by FISH in 2 of 30 cases (6.6%), which were negative using CGH. One case (1 of 30; 3.3%) was found to have a gain on chromosome 14 by CGH, which could not be confirmed by FISH. A correlation with tumor stage or survival could not be established. Our results suggest that GCTs may be characterized by trisomy of chromosome 14. A specific oncogene that could play a particular role in the tumorigenesis of GCTs was not identified on chromosome 14.     

Microvascular structural entropy: A novel approach to assess angiogenesis in pituitary tumors

Entropy, a measure of the degree of disorder in a system, has recently been used in different morphologic studies to quantify regularity. Our aims were (a) to study the structural organization of the microvascular bed in prolactin (PRL)-producing adenomas and carcinomas, the most vascularized of pituitary tumors, by assessing microvascular structural entropy (MSE), and (b) to determine whether the degree of disorder of the capillary bed correlates with tumor cell proliferation as estimated by MIB-1 labeling, microvessel density (MVD), the most widely used method of quantifying blood vessel formation, and various clinicopathologic parameters (gender, age, tumor size and invasiveness). The morphometric study demonstrated statistically significant differences in MIB-1 labeling, MVD, and MSE between PRL-producing adenomas and carcinomas. Unlike MIB-1 labeling index (PRL-producing adenomas 1.5±0.27; carcinomas 15.0±4.04) and MVD (PRL-producing adenomas 2.7±0.34; carcinomas 4.2±0.72), the MSE values were significantly higher in adenomas (171.5±25.37) than in carcinomas (67.9±17.45). These results indicate that PRL-producing carcinomas have a less chaotic distribution of vessels than benign adenomas. In contrast to a lack of correlation between, microvessel density and other morphometric parameters, a strong negative correlation was found between MSE and MIB-1 labeling index (r=0.511, p=0.003). It thus appears that regular, less chaotic microvascular geometry contributes to increased proliferative activity in PRL cell tumors. Analysis of MSE may provide an independent parameter of tumor behavior, and contributes to a better understanding of the role of microvasculature in pituitary tumor progression.     

Restoration of innate immune activation accelerates Th1‐cell priming and protection following pulmonary mycobacterial infection

The immune mechanisms underlying delayed induction of Th1‐type immunity in the lungs following pulmonary mycobacterial infection remain poorly understood. We have herein investigated the underlying immune mechanisms for such delayed responses and whether a selected innate immune‐modulating strategy can accelerate Th1‐type responses. We have found that, in the early stage of pulmonary infection with attenuated Mycobacterium tuberculosis (M.tb H37Ra), the levels of infection in the lung continue to increase logarithmically until days 14 and 21 postinfection in C57BL/6 mice. The activation of innate immune responses, particularly DCs, in the lung is delayed. This results in a delay in the subsequent downstream immune responses including the migration of antigen‐bearing DCs to the draining lymph node (dLN), the Th1‐cell priming in dLN, and the recruitment of Th1 cells to the lung. However, single lung mucosal exposure to the TLR agonist FimH postinfection is able to accelerate protective Th1‐type immunity via facilitating DC migration to the lung and draining lymph nodes, enhancing DC antigen presentation and Th1‐cell priming. These findings hold implications for the development of immunotherapeutic and vaccination strategies and suggest that enhancement of early innate immune activation is a viable option for improving Th1‐type immunity against pulmonary mycobacterial diseases.     

Cells with regulatory function of the innate and adaptive immune system in primary Sjögren's syndrome

The aim of the present study was to describe subsets of cells with regulatory properties in primary Sjögren's syndrome (pSS), and to correlate these cell populations with clinical symptoms. Among the 32 investigated patients, 23 had extraglandular manifestations (EGMs), while nine had only glandular symptoms. Twenty healthy individuals served as controls. The percentages of natural killer (NK), natural killer T cells (NK T), interleukin (IL)‐10 producing T regulatory type 1 (Tr1) cells and CD4⁺CD25⁺ regulatory T cells (T_reg) cells were determined by flow cytometry and serum cytokine levels of IL‐4, IL‐6, IL‐10, tumour necrosis factor (TNF)‐α and interferon (IFN)‐γ were evaluated by enzyme‐linked immunosorbent assay (ELISA). Functional tests were carried out to assess the suppressor properties of T_reg cells in patients and controls. Peripheral NK, NK T and Tr1 cell percentages were elevated in pSS, while CD4⁺CD25⁺ T_reg cells showed reduced frequencies in patients compared to controls. In pSS, elevated percentages of NK T, Tr1 and CD4⁺CD25⁺ T_reg cells were observed in patients with EGMs, when compared to patients with sicca symptoms only. CD4⁺CD25⁺ T_reg cell percentages showed a negative correlation with sialometry values. The in vitro functional assay demonstrated lower suppression activity of CD4⁺CD25⁺ T_reg cells in patients compared to controls. Serum IL‐6 and TNF‐α levels were elevated, while IL‐10 was decreased in patients compared to controls. Negative correlation was found between IL‐10 levels and the percentages of Tr1 cells. Changes in the investigated subsets of regulatory cells in pSS may contribute to the development and progression of the disease.