Extramedullary plasmocytoma relapsing at differents sites: an unusual presentation

Extramedullary plasmacytoma (EMP) is an uncommon plasma cell neoplasm results from plasma cell proliferation and consists of monoclonal plasmacytic infiltration, without bone marrow involvement and any other systemic characteristics of multiple myeloma. EMP accounts for 3% of all plasma cell neoplasms and approximately 80% to 90% of EMP involve submucosa of the upper aerodigestive, while scrotal, dermis and retroperitoneal infiltration are very rare. There are no consensus guidelines for treatment, but EMP is highly radiosensitive, surgery may be considered for some sites, but 11 at 30% can progress in multiple myeloma. We report here an exceptional case of recurrent EMP in much localization. It's about a man 72 years old with initially testicular plasmocytoma who generalized the plasmacytic infiltration after 16 months in skin and progressively in mediastinal and retroperitoneal plasmacytoma, without any medullar and bone involvement.Pan African Medical Journal 2013; 14:3

Perflubron Distribution During Transition From Gas to Total Liquid Ventilation

Total liquid ventilation (TLV) using perfluorocarbons has shown promising results for the management of neonatal respiratory distress. However, one important safety consideration for TLV is a better understanding of the early events during the transition to TLV, especially regarding the fate of residual air in the non-dependent-lung regions. Our objective was to assess perflubron distribution during transition to TLV using electrical impedance tomography, complemented by fluoroscopy, in a neonatal lamb model of induced surfactant deficiency. Eight lambs were anesthetized and ventilated in supine position. Surfactant deficit was induced by saline lung lavage. After deflation, lungs were filled with 25 ml/kg perflubron over 18 s, and TLV was initiated. Electrical impedance tomography data was recorded from electrodes placed around the chest, during the first 10 and at 120 min of TLV. Lung perfusion was also assessed using hypertonic saline injection during apnea. In addition, fluoroscopic sequences were recorded during initial lung filling with perfluorocarbons, then at 10 and 60 min of TLV. Twelve lambs were used as controls for histological comparisons. Transition to TLV involved a short period of increased total lung volume (p = 0.01) secondary to recruitment of the dependent lung regions. Histological analysis shows that TLV was protective of these same regions when compared to gas-ventilated lambs (p = 0.03). The non-dependent lung regions filled with perflubron over at least 10 min, without showing signs of overdistention. Tidal volume distribution was more homogenous in TLV than during the preceding gas ventilation. Perflubron filling was associated with a non-significant increase in the anterior distribution of the blood perfusion signal, from 46 ± 17% to 53 ± 6% (p = 0.4). However, combined to the effects on ventilation, TLV had an instantaneous effect on ventilation-perfusion relationship (p = 0.03), suggesting better coupling. Conclusion: transition to TLV requires at least 10 min, and involves air evacuation or dissolution in perflubron, dependent lung recruitment and rapid ventilation-perfusion coupling modifications. During that time interval, the total lung volume transiently increases. Considering the potential deleterious effect of high lung volumes, one must manage this transition phase with care and, we suggest using a real-time monitoring system such as electrical impedance tomography

Pro-Resolving Effects of Resolvin D₂ in LTD₄ and TNF-α Pre-Treated Human Bronchi

<div><p>Inflammation is a major burden in respiratory diseases, resulting in airway hyperresponsiveness. Our hypothesis is that resolution of inflammation may represent a long-term solution in preventing human bronchial dysfunctions. The aim of the present study was to assess the anti-inflammatory effects of RvD₂, a member of the D-series resolving family, with concomitant effects on ASM mechanical reactivity. The role and mode of action of RvD₂ were assessed in an <i>in vitro</i> model of human bronchi under pro-inflammatory conditions, induced either by 1 μM LTD₄ or 10 ng/ml TNF-α pre-treatment for 48h. TNF-α and LTD₄ both induced hyperreactivity in response to pharmacological stimuli. Enhanced 5-Lipoxygenase (5-LOX) and cysteinyl leukotriene receptor 1 (<a href="http://www.ejog.org/action/doSearch?searchType=quick&occurrences=all&ltrlSrch=true&searchScope=series&searchText=CysLTR1&seriesISSN=0301-2115" target="_blank">CysLTR1</a>) detection was documented in LTD₄ or TNF-α pre-treated human bronchi when compared to control (untreated) human bronchi. In contrast, RvD₂ treatments reversed 5-LOX/β-actin and CysLTR1/β-actin ratios and decreased the phosphorylation levels of AP-1 subunits (c-Fos, c-Jun) and p38-MAP kinase, while increasing the detection of the ALX/FPR2 receptor. Moreover, various pharmacological agents revealed the blunting effects of RvD₂ on LTD₄ or TNF-α induced hyper-responsiveness. Combined treatment with 300 nM RvD₂ and 1 μM WRW4 (an ALX/FPR2 receptor inhibitor) blunted the pro-resolving and broncho-modulatory effects of RvD₂. The present data provide new evidence regarding the role of RvD₂ in a human model of airway inflammation and hyperrresponsiveness.</p></div

Effect of RvD₂ on LTD₄–pretreated human bronchi in response to pharmacologically-induced tone and 5-LOX/CysLTR1 expression.

<p><b>a.</b> Corresponding bar graph showing mean contractile amplitudes induced by 1 μM methacholine (MCh), 1 μM histamine or 30 nM U-46619, either under control (untreated) conditions or after 1 μM LTD₄ pre-treatment in the absence or presence of 300 nM RvD₂ (n = 7–22, *<i>P</i> < 0.05). <b>b.</b> Western blot analyses of the 5-LOX / β-actin ratio assessing the putative effects of 1 μM LTD₄ and 1 μM LTD₄ + 300 nM RvD₂ on human bronchial homogenates compared with control conditions (<i>n</i> = 6, *<i>P</i> < 0.05). <b>c.</b> Western blot analyses using <a href="http://www.ejog.org/action/doSearch?searchType=quick&occurrences=all&ltrlSrch=true&searchScope=series&searchText=CysLTR1&seriesISSN=0301-2115" target="_blank">CysLTR1</a> and β-actin antibodies. Densities of the immunoreactive bands are expressed as a function of the β-actin-immunoreactive band (<i>n</i> = 6, * <i>P</i> < 0.05).</p

Effect of RvD₂ and WRW4 treatments on 5-LOX and CysLTR1 expression in TNF-α-pre-treated human bronchi.

<p><b>a.</b> Western blot analyses of bronchial homogenates derived from control, TNF-α, TNF-α + 300 nM RvD₂, TNF-α + 300 nM RvD₂ + 300 nM WRW4 and TNF-α + RvD₂ + 1 μM WRW4-pretreated bronchial rings for 48h, using specific antibodies against 5-LOX, <a href="http://www.ejog.org/action/doSearch?searchType=quick&occurrences=all&ltrlSrch=true&searchScope=series&searchText=CysLTR1&seriesISSN=0301-2115" target="_blank">CysLTR1</a> and β-actin, respectively. <b>b.</b> Quantitative analysis of various 5-LOX / β-actin density ratios (n = 5, * <i>P</i> < 0.05). <b>c.</b> Bar graph of mean <a href="http://www.ejog.org/action/doSearch?searchType=quick&occurrences=all&ltrlSrch=true&searchScope=series&searchText=CysLTR1&seriesISSN=0301-2115" target="_blank">CysLTR1</a> / β-actin density ratios in human bronchial homogenates (n <i>=</i> 5, * <i>P</i> < 0.05).</p

Effect of RvD₂ on TNF-α-induced reactivity and inflammation in human bronchi.

<p><b>a.</b> Bar graph of the contractile activity induced by bronchoactive agents (MCh, His and U-46619) on 48-h cultured human bronchi in control (untreated, n = 7–12) conditions, 10 ng/ml TNF-α (n = 14–19), TNF-α + 300 nM RvD₂ (n = 15–26), TNF-α + RvD₂ + 300 nM WRW4 (n = 11–14) or TNF-α + RvD₂ + 1 μM WRW4 (n = 10–11), *<i>P</i> < 0.05. <b>b.</b> Western blot analyses using specific antibodies against P-p38-MAPK and total p38-MAPK. Staining densities of P-p38-MAPK are expressed as a function of p38-MAPK levels (n = 5, * <i>P</i> < 0.05). <b>c.</b> Western blot analyses were performed using antibodies against p-c-Fos and total c-Fos. The relative density ratio of p-c-Fos to total c-Fos was used to quantify the comparative effects of RvD₂ on TNF-α-pretreated human bronchi (n = 5, * <i>P</i> < 0.05). <b>d.</b> Western blot analyses were performed using antibodies against p-c-Jun and total c-Jun. Staining densities of p-c-Jun are expressed as a function of c-Jun levels (n = 5, * <i>P</i> < 0.05).</p

Pharmacological effects of RvD₂ on ALX / FRP2 protein expression in TNF-α-pretreated human bronchi.

<p><b>a.</b> Human bronchial homogenates derived from control (untreated) bronchi or pre-treated with 10 ng/ml TNF-α, TNF-α + 300 nM RvD₂ or TNF-α + RvD₂ + 1 μM WRW4 were stained using specific antibodies against ALX / FRP2 and β-actin. <b>b.</b> Quantitative analyses of ALX / FRP2 density ratio. Staining densities of ALX / FRP2 are expressed as a function of β-actin staining level (n = 5, * <i>P</i> < 0.05).</p