Thrombus in the non-aneurysmal, non-atherosclerotic descending thoracic aorta--an unusual source of arterial embolism.

INTRODUCTION: Mural thrombus of the thoracic aorta is a rare clinical finding in the absence of aneurysm or atherosclerosis. METHODS: The medical records of all patients diagnosed with a thrombus of a non-aneurysmatic and non-atherosclerotic descending thoracic aorta (NAADTA) and treated by the senior author between 04/1997 and 04/2010 were reviewed. RESULTS: Eight patients with mural thrombus of the NAADTA were identified. Arterial embolism was the main clinical finding in all cases and involved the lower extremities (n = 6), mesenteric (n = 3) or renal arteries (n = 2). Hypercoagulable disorders were present in 3 cases and a concurrent malignancy in another 3. Two patients underwent open surgery while 4 patients were treated conservatively with anticoagulation. Of the remaining 2 patients, one was treated with a thoracic stent-graft and aorto-biiliac bypass and the other one with transfemoral thrombectomy. Technical success was achieved in all surgical cases and thrombus resolution or stable disease in the conservative management group. No thrombus recurrence was observed during a mean follow-up of 49 months. CONCLUSION: The management of mural thrombus in NAADTA represents a challenge, especially in case of malignant disease or hypercoagulable disorder as a potential underlying pathology and should be individualized. Although no consensus exists in the literature, therapeutic anticoagulation is proposed as first-line therapy. The indication for surgical intervention results from contraindication to anticoagulation, mobile thrombus or recurrent embolism. Whenever possible, endovascular therapy should be preferred.

Angioimmunoblastic lymphadenopathy type of T-cell lymphoma and angioimmunoblastic lymphadenopathy: a clinicopathological and molecular biological study of 13 Chinese patients using polymerase chain reaction and paraffin-embedded tissues.

The morphological classification of angioimmunoblastic lymphadenopathy (AILD) or T-cell lymphoma of AILD-type (AILD-TCL) is still a subject of considerable difficulty and controversy. The aim of the current study was to examine the value of clinical, morphological, immunohistochemical variables in paraffin-embedded tissues in predicting the clonality of the respective lesion. Fifteen lymph node biopsies derived from 13 patients from Chengdu, China, were diagnosed as AILD or AILD-TCL and included in this study. The specimens were examined using a panel of monoclonal antibodies and a scoring system of morphological features. Clonality of the paraffin-embedded material was investigated using a novel polymerase chain reaction-technique to amplify rearranged T-cell receptor (TCR)-gamma sequences. Additional experiments were carried out to investigate the presence of clonal rearrangements of the immunoglobulin heavy chain (IgH) locus. We found clonal rearrangements of the TCR-gamma locus in 9 out of 15 lymph node biopsies. In 3 patients, the predominant cell clones carried clonal IgH and TCR-gamma rearrangements whereas 1 patient with polyclonal TCR-gamma pattern displayed IgH-monoclonality. The statistical evaluation of morphological and immunohistochemical data indicated that no single variable was able significantly to predict the clonality of the lesion. Furthermore, demonstrable clonality for the TCR-gamma or the IgH loci of a lesion did not correlate with a bad clinical course. Our data correlate with findings of other studies investigating AILD-TCL in Caucasian populations.

Single-cell analysis of T-cell receptor-gamma rearrangements in large-cell anaplastic lymphoma.

Large-cell anaplastic lymphomas (LCAL) are characterized by their distinctive morphology together with expression of the CD30 antigen. In addition, a chromosomal translocation, t(2;5) (p23; q35), can be detected in most cases. A significant proportion of LCALs carry rearrangements of the T-cell receptor-gamma (TCR-gamma) locus and display a T-cell phenotype. In about a third of the cases, another type of non-Hodgkin-lymphoma precedes LCAL. Early transformations of non-Hodgkin's lymphoma into LCAL might escape clinical detection in a significant number of cases. The existence of clonally related lymphoid cells within the lymph node infiltrates must be claimed in these cases. Recently, a small-cell-predominant variant of LCAL was described in which only few large tumor cells expressing the CD30 antigen are found together with numerous small lymphocytes, which are frequently CD30-. This observation in particular prompted us to investigate the clonal relationship of the tumor cell compartment and admixed small lymphocytes in one case of common LCAL with T-cell genotype. For this purpose, we chose to amplify rearranged TCR-gamma sequences from single cells isolated from immunostained frozen sections by using a micromanipulator. A total of 119 cells were investigated. Amplification products were obtained in 17 of 79 CD3+ cells, 12 of 30 CD30+ cells, and three of 10 CD20+ cells. The nucleotide sequences were determined in 28 cells by nonradioactive sequencing. In 11 CD30+ cells, the predominant rearrangement of TCR-gamma was identified. No clonal diversity was observed. The small CD3+ lymphocytes were unrelated to the anaplastic CD30+ tumor cells. This report describes a method to analyze rearrangements of the TCR-gamma in single cells isolated from immunostained frozen sections. Application of this technique revealed an absence of clonal diversity in a case of LCAL and documented the polyclonal nature of admixed small CD3+ lymphocytes.

Fluid transfer as a mechanism leading to endotension.

Some abdominal aortic aneurysms bridged with a minimally invasively introduced stent graft prosthesis increase in size without any diagnosable evidence of endoleakage (endotension). There are three possible pathways proposed through which undetectable low rates of blood flow may cause an aneurysm sac to be refilled: through the thrombus at the prosthesis attachment sites, through the clotted collaterals and through the clotted stent graft wall. If the inflow is more rapid than any drainage through the wall of the aneurysm is re-pressurised. However, critical magnitudes for the permeability of the clotted graft and the geometry of the thrombus at the aneurysm, necessary to inhibit endotension, are not known. The aim of this study was to determine which boundary conditions prevent endotension. An analytical model based on Darcy's Law was used to estimate the pressure in the aneurysm sac due to fluid transfer. Experimentally determined time- and pressure-dependent permeability of red and intraluminal thrombus, and of clotted graft materials were input into the model. The computational analysis showed that endotension is unlikely to be caused by fluid transfer from the collaterals or via the prosthesis attachment sites, but rather due to flow through the stent graft wall. Based on this study it can be stated that grafts with a permeability below 2e-13 mm(2) should diminish the occurrence of endotension.