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BACKGROUND: Patients with severe aplastic anemia (SAA) frequently present with inflammatory episodes, and during flared inflammatory episodes, hematopoietic function is further exacerbated. The gastrointestinal tract is the most common site for infectious and inflammatory diseases, and its structural and functional features confer on it the most potent capacity to affect hematopoietic and immune functions. Computed tomography (CT) is a readily accessible approach to provide highly useful information in detecting morphological changes and guiding further work-ups. AIM: To explore CT imaging presentations of gut inflammatory damage in adult SAA patients during inflammatory episodes. METHODS: We retrospectively evaluated the abdominal CT imaging presentations of 17 hospitalized adult patients with SAA in search of the inflammatory niche when they presented with systemic inflammatory stress and exacerbated hematopoietic function. In this descriptive manuscript, the characteristic images that suggested the presence of gastrointestinal inflammatory damage and related imaging presentations of individual patients were enumerated, analyzed and described. RESULTS: All eligible patients with SAA had CT imaging abnormalities that suggested the presence of an impaired intestinal barrier and increased epithelial permeability. The inflammatory damages were concurrently present in the small intestine, the ileocecal region and the large intestines. Some readily identified imaging signs, such as bowel wall thickening with mural stratification ("water holo sign", "fat holo sign", intramural gas and subserosal pneumatosis) and mesenteric fat proliferation (fat stranding and "creeping fat sign"), fibrotic bowel wall thickening, "balloon sign", rugged colonic configuration, heterogeneity in the bowel wall texture, and adhered and clustered small bowel loop (including various patterns of "abdominal cocoon"), occurred at a high incidence, which suggested that the damaged gastrointestinal tract is a common inflammatory niche responsible for the systemic inflammatory stresses and the exacerbated hematopoietic failure in patients with SAA. Particularly, the "fat holo sign" was present in 7 patients, a rugged colonic configuration was present in 10 patients, the adhesive bowel loop was present in 15 patients, and extraintestinal manifestations suggestive of tuberculosis infections were present in 5 patients. According to the imaging features, a suggestive diagnosis of Crohn's disease was made in 5 patients, ulcerative colitis in 1 patient, chronic periappendiceal abscess in 1 patient, and tuberculosis infection in 5 patients. Other patients were diagnosed with chronic enteroclolitis with acutely aggravated inflammatory damage. CONCLUSION: Patients with SAA had CT imaging patterns that suggested the presence of active chronic inflammatory conditions and aggravated inflammatory damage during flared inflammatory episodes.
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PURPOSE: The role of NLRP3 inflammasome in the progression of many diseases has been increasingly recognized. However, the function of this molecular assembly in the development and progression of B-cell non-Hodgkin's lymphoma remains unclear. PATIENTS AND METHODS: In this study, we investigated the polymorphisms in the NLRP3 inflammasome associated genes in 281 patients with B-cell non-Hodgkin's lymphoma and 385 age- and gender-matched healthy controls. RESULTS: We found that IL-18 (rs1946518) and NFκB-94 ins/del (rs28362491) contributed to susceptibility to B-cell non-Hodgkin's lymphoma. Specifically, the allele "G" in IL-18 (rs1946518) and allele "ins" in NFκB-94 ins/del (rs28362491) were significantly associated with the risk of disease. The AA genotype of CARD8 (rs2043211) and the higher level of serum lactate dehydrogenase (LDH) led to statistically poorer B-cell non-Hodgkin's lymphoma survival. Less frequent genotype TT of CARD8 (rs2043211) was observed in patients with higher LDH level, clinical stages III-IV of disease, and IPI 3-5, although the relationship did not reach statistical significance. However, IPI is an independent prognostic factor for B-cell non-Hodgkin's lymphoma. CONCLUSION: IL-18 (rs1946518) and NFκB-94 ins/del (rs28362491) gene polymorphisms appear to be the factors influencing the risk of B-cell non-Hodgkin's lymphoma. CARD8 (rs2043211) polymorphisms are important factors for the survival of patients with this disease.
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BACKGROUND: Placenta growth factor (PLGF) is a member of the vascular endothelial growth factor (VEGF) family which is associated with the progression and metastasis of cancer. However, whether it can be used to predict prognosis in multiple cancer is still inconsistent. METHODS: A meta-analysis was performed by searching electronic databases updated to December 2014. Eligible studies which evaluated the relationship between PLGF expression level and survival of patients with multiple cancers were conducted. Overall survival (OS), progression-free survival (PFS), hazard ratio (HR), and 95% confidence intervals (CI) were calculated. RESULTS: Nineteen studies with a variety of cancers were included for the meta-analysis. Combined HR suggested that high expression of PLGF significantly associated with a poor OS (HR=1.69, 95% CI, 1.32-2.16), and PFS (HR=1.8, 95% CI, 1.33-2.44) in patients with different cancers. Moreover, a subgroup analysis based on cancer type demonstrated that high expression level of PLGF predict poor OS in both digestive system carcinoma (HR=1.63, 95% CI, 1.21-2.19; I(2)=80.7%, P<0.001) and respiratory system tumor (HR=1.75, 95% CI, 1.28-2.41; I(2)=0.0%, P=0.394). For PFS, the similar result was found in respiratory system tumor (HR=1.64, 95% CI, 1.23-2.19; I(2)=0.0%, P=0.807), but not in digestive system carcinoma (HR=1.81, 95% CI, 0.93-3.52; I(2)=80.2%, P<0.001). CONCLUSION: Our meta-analysis demonstrates that PLGF might be regarded as a poor prognostic fact for multiple cancers. More large-scale and well-designed studies are still needed to strengthen our findings.