Prolonged remission of recurrent cervical carcinoma following paclitaxel and carboplatin chemotherapy with paclitaxel maintenance chemotherapy.

Cervical cancer recurs in ~30% of cases, for which a favorable prognosis is often unattainable. We describe a cervical cancer patient who developed metastatic disease ~5 years after her initial diagnosis. She was subsequently treated with six cycles of paclitaxel (175 mg/m) and carboplatin area under the curve (AUC) 5 chemotherapy every 21 days, and paclitaxel (135 mg/m) maintenance therapy every 21 days; the patient has remained in clinical remission after more than 5 years of follow-up. Chemotherapy has not historically been effective in managing recurrent, persistent, or metastatic cervical cancer. However, our case study involving paclitaxel and carboplatin chemotherapy with maintenance chemotherapy represents one of the longest documented remission rates in association with the management of recurrent cervical cancer.

Large volume cervical varix bleeding in a gravid patient.

► Cervical varix during pregnancy is very rare and can coincide with massive bleeding. ► A gravid patient with a history of granulosa cell tumor presented with cervical varix. ► Cervical varix can potentially jeopardize the health of both the patient and fetus.

Spinal epidural metastasis in an endometrial carcinoma patient.

► The incidence of CNS metastases from endometrial cancer is quite uncommon. ► We report on an endometrial cancer patient who developed a metastatic epidural mass. ► Oncology physicians should remain vigilant in order to effectuate prompt treatment and potentially benefit the patient's outcome.

Transient Hepatic Attenuation Differences in Computed Tomography from Extrahepatic Portal Vein Compression.

OBJECTIVE: To describe the appearance of transient hepatic attenuation differences (THADs) of extrahepatic origin. MATERIALS AND METHODS: Five cases of THADs produced by compression of the extrahepatic portal vein at its confluence with the splenic vein were identified prospectively over a four-month period. Two additional cases of peripheral THADs resulting from main portal vein thrombosis were identified from retrospective review of a departmental database. RESULTS: Streamlining of portal venous flow resulted primarily in left lobar THADs when the portal vein is compressed at its confluence with the splenic vein. THADs were seen in the periphery of the liver in the two cases of main portal vein thrombosis. CONCLUSION: Lobar and/or peripheral THADs can be produced by compromise of splenic and extrahepatic portal venous flow. Radiologists should be familiar with the "central pseudotumor" created by the peripheral THAD that can result from portal vein thrombosis.

Stent-based controlled release of intravascular angiostatin to limit plaque progression and in-stent restenosis.

PURPOSE: To evaluate the importance of angiogenesis in plaque progression after stent placement, this study examines stent-based controlled delivery of the antiangiogenic agent, angiostatin, in a rabbit model. MATERIALS AND METHODS: Controlled release biodegradable microspheres delivering angiostatin or polymer-only microspheres (polylactic-co-glycolic-acid-polyethylene glycol; PLGA/PEG) were loaded in channeled stents, anchored, and deployed in the aorta of adult New Zealand white rabbits (n = 6 animals per group, three each per time point). The stented aortas were harvested at 7 days and 28 days and evaluated for neovascularization, local inflammation, vascular smooth muscle cell proliferation, and in-stent plaque progression. RESULTS: At 7 days, neovascularization was significantly decreased in the angiostatin groups (1.6 +/- 1.6 neovessels per mm(2) plaque) versus the control group (15.4 +/- 2.6 neovessels per mm(2) plaque; P =.00081), as were local inflammation where angiostatin-treated groups demonstrated significantly lower macrophage recruitment per cross section (34.9 +/- 4.9 cells per cross section) relative to the control group (55.2 +/- 3.84 cells per cross section; P =.0037). And a significant decrease in the overall vascular smooth muscle cell proliferation (143.8 +/- 26.3 Ki-67 positive cells per mm(2)) relative to the control group (263.2 +/- 16.6 Ki-67 positive cells per mm(2); P =.00074). At both 7 and 28 days, in-stent plaque progression in the angiostatin groups was successfully limited relative to the control group by 54% (0.255 +/- 0.019% of cross section; P =.00016) and 19% (1.981 +/- 0.080; P =.0033) respectively and resulted in reduction of in-stent restenosis relative to the control group. CONCLUSION: Angiostatin-eluting stents may limit neovascularity after arterial implantation, offer insight into in-stent restenosis, and allow future refinement of bioactive stent designs and clinical strategies, particularly in light of evidence that intimal smooth muscle cells may in part be marrow-derived.

Periaortic hematoma at diaphragmatic crura at helical CT: sign of blunt aortic injury in patients with mediastinal hematoma.

PURPOSE: To evaluate periaortic hematoma (PH) near the level of the diaphragm at abdominal computed tomography (CT) as an indirect sign of acute traumatic aortic injury after blunt trauma in patients with mediastinal hematoma. MATERIALS AND METHODS: From 1998 to 2001, 97 patients with CT evidence of mediastinal hematoma after blunt thoracic trauma were retrospectively identified at two level 1 trauma centers. The presence or absence of PH near the level of the diaphragmatic crura was retrospectively established by a blinded reviewer at each institution. Aortic injury status was determined by reviewing angiographic, surgical, and clinical records. Sensitivity, specificity, positive and negative productive values, and positive and negative likelihood ratios were calculated. RESULTS: Among the 97 patients with mediastinal hematoma, 14 had both PH near the level of the diaphragm and aortic injury; six had aortic injuries without PH, five had PH near the level of the diaphragm without aortic injury, and 72 had no evidence of PH near the diaphragm and no aortic injury. Sensitivity for PH near the level of the diaphragm as a sign of aortic injury was 70%; specificity, 94%; positive predictive value, 74%; and negative predictive value, 92%. The positive likelihood ratio for the presence of aortic injury was 10.8, and the negative likelihood ratio was 0.3. CONCLUSION: PH near the level of the diaphragmatic crura is an insensitive but relatively specific sign for aortic injury after blunt trauma. The presence of this sign at abdominal CT should prompt imaging of the thoracic aorta to evaluate potential thoracic aortic injury.

Initial clinical results of tenecteplase (TNK) in catheter-directed thrombolytic therapy.

PURPOSE: To investigate the safety and immediate efficacy of 2 different doses of tenecteplase (TNK) in peripheral catheter-directed thrombolytic therapy of arterial occlusions and deep vein thrombosis (DVT). METHODS: Over a 20-month period, 63 nonconsecutive patients underwent catheter-directed thrombolytic therapy with either 0.25 mg/h or 0.50 mg/h of TNK in a nonrandomized, open-label study. Of these, 55 patients (60 limbs) were treated for DVT (36 limbs in 16 men and 15 women; mean age 41 years, range 21-73) or peripheral arterial occlusions (24 limbs in 16 men and 8 women; mean age 63 years, range 32-91). The primary endpoints were major bleeding complications and angiographic reduction in clot burden. RESULTS: The mean duration of infusion was 18 +/- 4 hours in patients with arterial occlusions and 30 +/- 13 in those with DVT. Twenty-one (87.5%) patients with occlusive disease had marked or complete lysis of clot. Thirty (83.3%) limbs with DVT had either marked or complete resolution of thrombus. There were 4 (7.3%) episodes of minor bleeding with 1 (1.8%) major hemorrhagic event. Fibrinogen levels dropped by an average of 23%. CONCLUSIONS: Preliminary evidence suggests that TNK doses of 0.25 mg/h to 0.50 mg/h appear to be safe and effective. The potential benefits of TNK therapy warrant further investigation.

In vivo vascular engineering of vein grafts: directed migration of smooth muscle cells by perivascular release of elastase limits neointimal proliferation.

PURPOSE: Saphenous vein bypass grafting for coronary revascularization procedures remains limited by accelerated neointima formation. It was hypothesized that creation of a modified chemotactic gradient in vivo could guide migration of smooth muscle cells (SMCs) peripherally instead of in a luminal direction and reduce intimal hyperplasia during vein graft arterialization. MATERIALS AND METHODS: Surgical bypass vein grafting to femoral arteries was performed in adult male New Zealand White rabbits (n = 8 per treatment group; five for 7 d and three for 28 d). Controlled-release microspheres delivering elastase or buffered polymer only were administered perivascularly at the vein graft site. At 7 days, five vein grafts per group were harvested and cross-sections were immunostained with anti-proliferating cell nuclear antigen (PCNA) to determine the number and distribution of proliferating SMCs. At 28 days, three vein grafts per group were harvested and intima-to-media (I/M) ratios were calculated after staining with Verhoeff von Gieson-Masson trichrome stain. RESULTS: Significant early outward-directed elastin degradation resulted from elastase treatment. Concurrently, proliferating SMCs migrated peripherally. PCNA(+) cells in the outer half of the wall increased 2.37 fold compared to procedural controls (P <.0001). Directional shifts in SMC migration underlie these results because overall SMC proliferation was not significantly different. At 28 days after vein graft surgery, a 38% reduction (P =.0008) in neointima was observed relative to procedural controls. CONCLUSION: Directional guidance of SMC responses through perivascular elastase release achieves favorable vein graft remodeling characteristics, including limited neointima development. This represents practical evidence that SMC migration can be directionally guided in vivo in a vein graft model and that plaque progression can be prevented by redistributing elastin without decreasing functional vein graft wall stability.