B-cell lymphoma related iliac vein occlusion treated by endovenous stent placement.

Unilateral leg swelling is most often caused by deep vein thrombosis but other conditions may mimic this disorder. We describe the case of a patient with symptoms of unilateral lower extremity swelling caused by external compression of the iliac vein by a mass originating from the iliopsoas muscle. Initially this mass was diagnosed as an iliopsoas hematoma in a patient using anticoagulants. However, it proved to be B-cell non-Hodgkin lymphoma. Compression was relieved by placement of an endovenous stent in the left common iliac vein. Endovenous stenting is a relatively new treatment modality that is used to treat post-thrombotic venous occlusions and chronic venous insufficiency. Only a few case series have been described of stenting of compressed pelvic veins by adjacent structures such as gynecological malignancies. Although stent patency lasted only four weeks in this patient, venous stent placement quickly reliefs symptoms and should therefore be considered as an option to bridge time to allow development of sufficient venous collaterals.

Imaging the vulnerable carotid artery plaque.

Imaging plays a key role in the selection of patients for carotid artery surgery. Indication for carotid endarterectomy or stenting is based on symptomatology and degree of stenosis as determined by angiography, duplex ultrasonography or computed tomographic angiography. Degree of stenosis has long time been assumed the most reliable predictor of stroke-risk in patients with carotid artery stenosis and accordingly, traditional imaging methods were focused on luminal stenosis. There is, however, growing evidence that other factors than degree of stenosis determine whether a carotid plaque will result in acute neurologic events or not. Various morphological characteristics and molecular processes have proven to be highly related to carotid plaque instability and symptomatology. As a result, the focus of imaging techniques in carotid artery disease is more and more shifting towards identification of the vulnerable plaque rather than the high-grade stenosis. In traditional imaging modalities, new insights of imaging beyond degree of stenosis have been explored and may be able to detect morphological characteristics of plaque vulnerability. In addition, advanced molecular imaging methods have been developed and are able to identify molecular and cellular processes in the vulnerable carotid artery plaque. It is clear that recent developments in carotid imaging are of great potential in the identification of the vulnerable carotid plaque.

Advanced carotid plaque imaging.

Treatment of carotid artery stenosis by endarterectomy or stenting can significantly reduce stroke risk. In clinical practice, indication for surgery or stenting is primarily based on the degree of stenosis, but there is growing awareness that pathophysiological features within a vulnerable plaque play a key role in predicting stroke risk. Important molecular processes associated with plaque vulnerability are inflammation, lipid accumulation, proteolysis, apoptosis, angiogenesis and thrombosis. The rapidly emerging field of molecular and functional imaging strategies allows identification of pathophysiological processes in carotid artery stenosis. We aimed to review the literature regarding the current most promising advanced imaging techniques in carotid artery disease. Various advanced imaging methods are available, such as high-resolution magnetic resonance imaging (HR-MRI), single photon emission computed tomography (SPECT), positron emission tomography (PET) and near-infrared fluorescence (NIRF). Radionuclide and fluorescent tracers that identify inflammation, apoptosis and proteolysis, such as FDG, MMP probes and Annexin A5, are promising. A combination of activity of molecular processes and detailed anatomic information can be obtained, providing a powerful tool in the identification of the vulnerable plaque. With these developments, we are entering a new era of imaging techniques in the selection of patients for carotid surgery.

The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects.

Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

The acute inflammatory response in trauma / hemorrhage and traumatic brain injury: current state and emerging prospects

Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular; cellular; tissue; organ; and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned; dynamic; highly-regulated process that is not inherently detrimental; but rather required for immune surveillance; optimal post-injury tissue repair; and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines; but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice; rats; pigs; dogs; and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches; including those from the field of systems biology; may yield therapeutic breakthroughs in T/HS and TBI in the near future. Key words: Trauma; Hemorrhagic Shock; Taumatic Brain Injury; Inflammation; Systems Biology