Post-endovascular aneurysm repair (EVAR) testicular ischemia: A rare complication.

Endovascular aneurysm repair (EVAR) is a common modality of treating abdominal aortic aneurysms (AAA). Common complications include endoleak, bleeding, infection, contrast related injuries, and ischemia. We present the case of a patient who experienced a testicular infarction following repair of an infrarenal AAA. We also discuss the implications for this complication and review the available literature for similar cases and treatment options.

A retroperitoneal abscess caused by Haemophilus parainfluenza after endoscopic retrograde cholangiopancreatography and open cholecystectomy with a common bile duct exploration: a case report.

INTRODUCTION: Abscesses after open cholecystectomies have been reported to occur in less than 1% of patients. The majority of these abscesses are colonized by gastrointestinal tract flora. It is clearly known that Haemophilus parainfluenza is a normal inhabitant of the human respiratory tract. However, its origin and route of transmission into the gastrointestinal tract is unknown. CASE PRESENTATION: We present the case of a 68-year-old Caucasian female who developed a retroperitoneal abscess caused by H. parainfluenza after open cholecystectomy and common bile duct exploration. This presented nearly five weeks post-operatively. She underwent a second operation to drain the abscess, and was subsequently placed on appropriate antibiotics. CONCLUSION: A retroperitoneal abscess due to H. parainfluenza is extremely rare. It is a normal inhabitant of the human respiratory tract. To the best of our knowledge, there have been only a few reported cases of these abscesses, and they mainly involve the psoas muscle. The retroperitoneal abscess originated from the oropharynx, most likely after the endoscopic retrograde cholangiopancreatography was performed. With the advent of Natural Orifice Translumenal Endoscopic Surgery, oral decontamination will need to be considered to decrease the potential for such infections.

Intraparenchymal metastases to the spleen from ovarian cancer: a case report.

INTRODUCTION: Splenic tumors are rare and present a diagnostic dilemma. Metastatic carcinoma to the spleen is unusual. Visceral metastases in patients with ovarian cancer represent hematogenous spread of the disease; capsular involvement resulting from serosal and peritoneal seeding is more common. We present a patient with intraparenchymal splenic metastasis from ovarian carcinoma. This case demonstrates a rare etiology of an intraparenchymal solid splenic mass. CASE PRESENTATION: An 85-year-old woman presented with left upper quadrant pain. During her evaluation, a computed tomography scan revealed intraparenchymal splenic masses. An elective splenectomy was performed, during which ovarian cancer, which had not been revealed by the pre-operative computed tomography, was detected. There was no involvement of the splenic capsule by direct extension of the tumor, as is usually the case for ovarian cancer, but only intraparenchymal metastases. This mode of metastasis to the spleen has been described but is quite rare, and ovarian cancer presenting as a splenic mass is even more so. CONCLUSION: Splenic metastasis is a relatively rare event. It is often asymptomatic and is usually detected as part of multiorgan metastases. Symptomatic cases, though rare, do occur, and as in our patient, a thorough clinical evaluation is important to help direct the treatment plan. This case is a reminder to be cognizant of one of the less likely differential diagnoses of an intraparenchymal solid splenic mass.

Congenital absence of the left internal carotid artery.

The absence of the internal carotid artery (ICA) is a rare congenital anomaly, occurring in <0.01% of the population. Aplasia of the ICA may be harmless; however, the significance of ICA aplasia may be associated with conditions of clinical importance, such as in the setting of surgery, thromboembolic disease, and detection of cerebral aneurysms, and therefore should prompt further evaluation to rule out abnormalities. We present a case of left ICA aplasia diagnosed after work-up of neurological events. The incidence of intracranial aneurysm in association with aplasia has been reported as 25-43% compared to 2-4% in the general population. Mechanisms to explain the association between aplasia and intracranial aneurysms include embryological development or hemodynamic derangement. Recognition of this anomaly becomes important in thromboembolic disease as emboli in one cerebral hemisphere may be explained by atherosclerotic disease in the contralateral common carotid artery or vertebrobasilar system. Of significance, planning endarterectomy denotes consideration as both cerebral hemispheres may be dependent upon the atheromatous carotid. Recognizing this anomaly is important and may help prevent false diagnosis of carotid dissections or high-grade carotid stenosis.

Soluble fibrin inhibits lymphocyte adherence and cytotoxicity against tumor cells: implications for cancer metastasis and immunotherapy.

Circulating soluble fibrin (sFn) is elevated in many cancer patients. It is a marker for ongoing disseminated intravascular coagulation and may have prognostic significance. We have demonstrated that sFn inhibited monocyte adherence and cytotoxicity by a mechanism involving blockade of monocyte alphaMbeta2 and tumor cell CD54. It was, therefore, hypothesized that sFn also inhibits lymphocyte and interleukin-2-activated lymphocyte (LAK) adherence and cytotoxicity against tumor cells. This study sought to identify the lymphocyte subset responsible for adherence and killing of A375 melanoma cells and whether sFn inhibited these parameters. Lymphocyte and LAK cell adherence and cytotoxicity, which was adherence dependent, were inhibited by preincubation with purified or plasma-derived sFn. The lymphocyte and LAK cell activities were primarily a result of CD8(+) MHC (major histocompatibility complex) unrestricted cytotoxic T cells. These results suggest that elevated levels of circulating sFn may be immunosuppressive and may reduce the efficacy of adoptive immunotherapies.

Soluble fibrin inhibits monocyte adherence and cytotoxicity against tumor cells: implications for cancer metastasis.

BACKGROUND: Soluble fibrin (sFn) is a marker for disseminated intravascular coagulation and may have prognostic significance, especially in metastasis. However, a role for sFn in the etiology of metastatic cancer growth has not been extensively studied. We have reported that sFn cross-linked platelet binding to tumor cells via the major platelet fibrin receptor alphaIIb beta3, and tumor cell CD54 (ICAM-1), which is the receptor for two of the leukocyte beta2 integrins (alphaL beta2 and aM beta2). We hypothesized that sFn may also affect leukocyte adherence, recognition, and killing of tumor cells. Furthermore, in a rat experimental metastasis model sFn pre-treatment of tumor cells enhanced metastasis by over 60% compared to untreated cells. Other studies have shown that fibrin(ogen) binds to the monocyte integrin alphaM beta2. This study therefore sought to investigate the effect of sFn on beta2 integrin mediated monocyte adherence and killing of tumor cells. METHODS: The role of sFn in monocyte adherence and cytotoxicity against tumor cells was initially studied using static microplate adherence and cytotoxicity assays, and under physiologically relevant flow conditions in a microscope perfusion incubator system. Blocking studies were performed using monoclonal antibodies specific for beta2 integrins and CD54, and specific peptides which inhibit sFn binding to these receptors. RESULTS: Enhancement of monocyte/tumor cell adherence was observed when only one cell type was bound to sFn, but profound inhibition was observed when sFn was bound to both monocytes and tumor cells. This effect was also reflected in the pattern of monocyte cytotoxicity. Studies using monoclonal blocking antibodies and specific blocking peptides (which did not affect normal coagulation) showed that the predominant mechanism of fibrin inhibition is via its binding to alphaM beta2 on monocytes, and to CD54 on both leukocytes and tumor cells. CONCLUSION: sFn inhibits monocyte adherence and cytotoxicity of tumor cells by blocking alphaL beta2 and alphaM beta2 binding to tumor cell CD54. These results demonstrate that sFn is immunosuppressive and may be directly involved in the etiology of metastasis. Use of specific peptides also inhibited this effect without affecting coagulation, suggesting their possible use as novel therapeutic agents in cancer metastasis.