Appearance and distinguishing features of retroperitoneal calcifications at computed tomography

OBJECTIVES: To describe the appearance of retroperitoneal calcifications seen at computed tomography (CT) and to investigate which CT features distinguish benign from malignant retroperitoneal calcifications. METHODS: We identified 25 patients with retroperitoneal calcifications by retrospective review of 39,931 abdominopelvic CT scans. Etiology of retroperitoneal calcifications was determined by examination of medical and histopathological records. By consensus, 2 abdominal radiologists recorded calcification number (solitary or multiple), location (suprarenal or infrarenal), morphology (globular or nonglobular), and the presence of soft-tissue components. The association between CT findings and etiology was assessed using the Fisher exact test. RESULTS: Retroperitoneal calcifications were malignant in 15 patients and benign in 10. Solitary calcifications were seen more commonly in patients with benign disease (6 of 10 vs. 1 of 15, P < 0.01). Suprarenal calcifications were seen only in patients with malignancy (13 of 15 patients, P < 0.01). Nonglobular calcifications were seen only in patients with benign disease (6 of 10, P < 0.01). Soft-tissue components were seen more commonly in patients with malignancy (14 of 15 vs. 4 of 10; P < 0.01). CONCLUSIONS: Retroperitoneal calcifications are rarely seen at CT and may be benign or malignant in etiology. Solitary or nonglobular retroperitoneal calcifications are likely to be benign while calcifications that are multiple, globular, suprarenal, or associated with noncalcified soft-tissue components are likely to be malignant.     

Giant fetal hepatic hemangioma. Case report and literature review

The purpose of this case report is to demonstrate the importance of prenatal imaging for treatment management of fetal giant hepatic hemangiomas. Prenatal ultrasound revealed an abdominal mass with several cystic areas and punctate calcifications in a fetus at 29 weeks' gestation. Doppler scans confirmed the highly vascular nature of the mass. In this case, ultrasound diagnosed the mass was of hepatic origin, while magnetic resonance imaging at 32 weeks' gestation was more equivocal with respect to the anatomy source of the lesion. Imminent hydrops caused by a rapidly enlarged liver tumor was sonographically demonstrated at 34 weeks' gestation. An elective C-section and immediate tumor resection was performed. At the age of 20 months the infant is thriving. This case supports the notion that the survival rates for giant hepatic hemangiomas improve when fetal hydrops is averted and specific pre- and postnatal treatment is applied based on correct prenatal imaging diagnostics.     

Is nutrition an aetiological factor for inflammatory bowel disease?

Inflammatory bowel disease (IBD) is a chronic inflammatory process, the aetiology of which is complex and probably multi-factorial. Nutrition has been proposed to be an important aetiological factor for IBD. The present review critically examines the relationship between components of the diet (such as sugar, fat, fibre, fruit and vegetables, and protein) and IBD, including ulcerative colitis and Crohn's disease. In addition, it investigates the possible role of infant feeding practices in the development of IBD.     

The effect of treatment on radiological progression in rheumatoid arthritis: a systematic review of randomized placebo-controlled trials

OBJECTIVE: To undertake a systematic review of randomized placebo-controlled trials to assess and rank the efficacy of pharmacological interventions in preventing radiological progression of rheumatoid arthritis. METHODS: The two outcome measures were the weighted standardized mean difference and the odds of progression of X-ray scores pooled as close to 12 months as possible to minimize heterogeneity. RESULTS: A total of 38 trials were identified. Of these, 13 were excluded, leaving data on 3907 subjects. Infliximab, cyclosporin, sulphasalazine, leflunomide, methotrexate, parenteral gold, corticosteroids, auranofin and interleukin 1 receptor antagonist were statistically better than placebo in terms of change in erosion scores. All agents were equivalent statistically, with the exception of infliximab (which was superior to the last five agents). There were similar findings for the odds of progression, with the exception of auranofin (P=0.06) and the infliximab-methotrexate comparison (P=0.07). Other agents did not reach statistical significance in either outcome measure. With the exception of the antimalarials, the magnitude of the effect was consistent with the effect seen in short-term disease activity trials. CONCLUSION: There is published evidence which supports the efficacy of nine agents in decreasing radiological progression in rheumatoid arthritis.     

The 17q23 amplicon and breast cancer

A novel region of amplification in breast tumors was recently identified on chromosome 17q23. Extensive mapping of the amplicon by Southern blotting and fluorescence in situ hybridization (FISH) in breast cancer cell lines determined that the amplicon can be up to 4 Mbp in size and may contain 50 genes. Copy number analysis at 50–75 kb resolution in breast cancer cell lines and breast tumors identified several independently amplified regions within the amplicon, suggesting that a number of genes are selected for amplification because they independently contribute to tumor formation and progression. Support for this hypothesis comes from studies demonstrating that many of the amplified genes are over-expressed in breast cancer cell lines and tumors, and that the RPS6KB1, TBX2, and PPM1D genes from the region, that are amplified and over-expressed in breast tumors and cell lines, contribute to tumor formation and/or tumor progression. In this review we summarize the structural studies of the amplicon that have been carried out, we outline the evidence implicating the RPS6KB1, TBX2, and PPM1D genes as oncogenes, and we describe some of the other candidate oncogenes from the region.     

Suggestive Linkage of 2p22-25 and 11q12-13 with Low Bone Mineral Density at the Lumbar Spine in the Irish Population

Osteoporosis is a disease characterized by low bone mineral density (BMD) and poor bone quality. Peak bone density is achieved by the third decade of life, after which bone is maintained by a balanced cycle of bone resorption and synthesis. Age-related bone loss occurs as the bone resorption phase outweighs the bone synthesis phase of bone metabolism. Heritability accounts for up to 90% of the variability in BMD. Chromosomal loci including 1p36, 2p22-25, 11q12-13, parathyroid hormone receptor type 1 (PTHR1), interleukin-6 (IL-6), interleukin 1 alpha (IL-1) and type II collagen A1/vitamin D receptor (COL11A1/VDR) have been linked or shown suggestive linkage with BMD in other populations. To determine whether these loci predispose to low BMD in the Irish population, we investigated 24 microsatellite markers at 7 chromosomal loci by linkage studies in 175 Irish families of probands with primary low BMD (T-score –1.5). Nonparametric analysis was performed using the maximum likelihood variance estimation and traditional Haseman-Elston tests on the Mapmaker/Sibs program. Suggestive evidence of linkage was observed with lumbar spine BMD at 2p22-25 (maximum LOD score 2.76) and 11q12-13 (MLS 2.55). One region, 1p36, approached suggestive linkage with femoral neck BMD (MLS 2.17). In addition, seven markers achieved LOD scores >1.0, D2S149, D11S1313, D11S987, D11S1314 including those encompassing the PTHR1 (D3S3559, D3S1289) for lumbar spine BMD and D2S149 for femoral neck BMD. Our data suggest that genes within a these chromosomal regions are contributing to a predisposition to low BMD in the Irish population.     

Natural fluctuations of hepatitis C viral load in a homogeneous patient population: a prospective study

The aim of this study was to determine the variation in hepatitis C viral load over an extended period of patient follow up. Serum samples were collected from 49 female individuals who were identified as having been infected from the same source of hepatitis C-contaminated anti-D immunoglobulin during the period from 1977 (May) to 1978 (November). All patients attended the hepatitis C clinic at Cork University Hospital, Cork, Ireland. The study group was homogeneous with respect to gender, hepatitis C virus (HCV) genotype (1b), and duration of infection. None of the patients had received antiviral therapy at the time of completion of study. Viral load quantifications were assessed using the Roche Monitor (F. Hoffmann-La Roche, Ltd., Basel, Switzerland) assay. The mean age of the study group at time of infection was 30.3 years (SD +/- 6.1) with a range from 18.5 to 43 years. The mean time of follow-up was 4. 1 years (SD +/- 1.0) with a range from 1.2 to 5 years. The mean rate of change of viral load per year was 0.23 log(10) viral copies per mL serum for the study group (SD +/- 0.19) with a range of -0.18 to 0.78 that was significantly different from zero, P < 10(-10). The rate of change of viral load per year was negatively correlated with viral load at first determination, r = -.35, P =.01. Age at infection did not correlate with the slope of change of viral load, P =.10. In conclusion, most women infected with HCV 1b will have an increase in viral load over time but a few patients who acquire infection early in adult life will show a decrease in viral load.