Massive renal arteriovenous fistula presenting as a pulsatile abdominal mass.
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Abdominal Neoplasms↗
Biomedical subjects
R S Lord
Publications and source records attributed to R S Lord.
Management of gunshot wounds at a Sydney teaching hospital.
BACKGROUND: Injuries caused by firearms account for only a small percentage of trauma admissions and deaths in Australia but are frequently the subject of media and public attention. The present study examines the epidemiology and management of firearm injuries presenting to St Vincent's Hospital, which is located at the edge of the central business district of Sydney. METHODS: The medical records of all patients presenting to St Vincent's with a gunshot wound (GSW) from January 1988 to December 1998 were analysed. Additional details were acquired from New South Wales State Coroner's Court reports and media archives, especially major newspapers. RESULTS: Seventy-four patients presented to St Vincent's Hospital with 103 GSW. The age (mean +/- SD) was 31+/-11 years. Sixty-seven patients (91%) were male. Alcohol was identified as a factor in 24 cases (32%) while other drugs were indicated in four cases (5%). Ten patients (14%) had intentionally self-inflicted wounds, seven (9%) had accidental wounds and 57 (77%) had wounds that were caused by crime-related violence. Sixty patients (81%) underwent operation for their injury. Thirty complications were seen in 18 patients (24%). Eleven patients (15%) died. The length of hospital stay (mean +/- SEM) was 18+/-9 days. CONCLUSIONS: The incidence of trauma due to firearms has not increased at St Vincent's hospital in the period 1988-98. Most GSW were inflicted in the setting of criminal violence, with a high proportion due to handguns. Patients were mostly young men, and alcohol or other drugs were frequently involved. Outcomes are comparable to other centres managing large volumes of penetrating trauma.
Adolescent↗
Dendritic cells in aortocoronary saphenous vein bypass grafts.
Dendritic cells are specialised leucocytes responsible for capturing and presenting antigens to T lymphocytes, which in turn mediate immune responses in various pathological conditions. The observations in this study demonstrate that dendritic cells are present in stenotic aortocoronary saphenous vein bypass grafts, which suggest that these cells may be involved in inflammatory actions which may subsequently contribute to graft failure.
Journal Article↗
Immune hemolytic anemia caused by sensitivity to a metabolite of etodolac, a nonsteroidal anti-inflammatory drug.
BACKGROUND: Immune hemolytic anemia can be caused by sensitivity to many different drugs. In some instances, the sensitizing compound can be identified by in vitro testing, but results are often negative. One reason for this is that a drug metabolite formed in vivo can be the sensitizing agent, but the responsible metabolites have rarely been identified at a chemical level. This report describes a patient who developed severe, Coombs-positive hemolytic anemia on two occasions after taking the nonsteroidal anti-inflammatory drug etodolac. Studies were performed to characterize etodolac metabolites to which this patient was sensitive. CASE REPORT: Serum was tested for antibody in the presence and absence of drug using conventional methods and urine from individuals taking etodolac as a source of drug metabolites. Urinary metabolites of etodolac were identified by high-pressure liquid chromatography analysis. Glucuronide conjugates of etodolac and the 6-OH metabolite of etodolac were synthesized in a rat liver microsomal system to obtain reference standards. RESULTS: The patient's serum gave only trace (+/-) reactions with normal RBCs in the presence of etodolac but reacted strongly (4+) in the presence of urine from an individual taking this drug. The active urinary metabolites were identified as etodolac glucuronide and 6-OH etodolac glucuronide. CONCLUSION: This patient appears to have experienced acute, severe immune hemolytic anemia on two occasions because of sensitivity to the glucuronides of etodolac and 6-OH etodolac. In patients suspected of having drug-induced immune hemolytic anemia, RBC-reactive antibodies can sometimes be detected by using urine from an individual taking the implicated medication as the source of drug metabolites in in vitro reactions. For patients who present with acute immune hemolysis, a careful history of drug exposure should be taken, and, where indicated, confirmatory testing should be performed to identify the sensitizing drug and prevent inadvertent reinduction of hemolysis at a later time.
Acute Disease↗
Maintaining carotid flow by shunting during carotid endarterectomy diminishes the inflammatory response mediating ischaemic brain injury.
OBJECTIVES: to assess whether shunting during carotid reconstruction affects the release of inflammatory mediators from the ipsilateral hemisphere. MATERIALS AND METHODS: a catheter was placed in the ipsilateral jugular bulb during carotid endarterectomy (CEA) in 20 patients. Eight patients with ICBP (internal carotid backpressure) <40 mmHg received a shunt during CEA and 12 patients with ICBP >40 mmHg were operated upon without a shunt. Four patients with a carotid body tumour were used as controls. Blood was taken from the catheter as well as from the radial artery; before clamping, 5, 15, 30 min after clamping and 5 min after declamping. The oxygen extraction (AVO(2)) was calculated. Plasma concentrations of interleukin-1beta (IL-1beta), phospholipase A(2)(PLA(2)), thromboxane B(2)(TXB(2)), 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha) and prostaglandin E(2)(PGE(2)) were measured by enzyme-linked immunosorbent assay (ELISA) technique. RESULTS: all patients had a normal postoperative course except for one patient in the no-shunt group, who suffered a stroke 1 h later due to occlusion of the endarterectomy site. The AVO(2)extraction increased during clamping in patients operated upon without a shunt (p <0.05). This increase was partly recovered to pre-clamp levels 5 min after reperfusion. The extraction remained stable in the non-shunted patients and the control group. The increased extraction in the non-shunted group correlated with increased levels of IL-1beta during clamping ( p <0.05) and reperfusion ( p <0.01). PLA(2)also increased during reperfusion in the non-shunted group ( p <0.05). An increased ratio between TXB(2)and 6-keto-PGF1alpha was noted during clamping ( p <0.05) and further increased during reperfusion. The levels of PGE(2)remained stable in both CEA groups. The PLA(2)levels, as well as TXB(2), 6-keto-PGF1alpha and PGE(2)levels, remained unchanged during the procedure in the control group. CONCLUSIONS: there is a metabolic response to carotid cross-clamping when no shunt is used. However, the clinical significance of this is unclear, since there were no intraoperative strokes.
Aged↗
Accumulation of lymphocytes, dendritic cells, and granulocytes in the aortic wall affected by Takayasu's disease.
The aim of this study was to analyze the cellular composition of the arterial wall in Takayasu's disease and to investigate the contribution of the various cell types to the immunoinflammatory processes and degenerative alterations of the vessel wall in this disease. Specimens of aorta were obtained at operation from 10 patients with Takayasu's arteritis. The duration of disease ranged from 2 months to 13 years. Immunohistochemical investigation was carried out using the antibodies CD3 (to identify T-cells), CD20 (B-cells), S-100 (dendritic cells), CD68 (macrophages), CD15 (granulocytes), von Willebrand factor (endothelial cells), and alpha-smooth muscle actin (smooth muscle cells). All specimens showed distinctive histologic features of Takayasu's arteritis and contained inflammatory infiltrates, but the degree of their accumulation within the aortic wall varied. Inflammatory infiltrates within the deep part of the intima, around areas of neovascularization and within the adventitia contained T-cells colocalizing with dendritic cells. Nodules formed by large numbers of intermingling T-cells and B-cells enriched with dendritic cells were observed in the adventitia. Massive accumulation of granulocytes and their destruction within the adventitia were prominent in all cases. This is the first study that establishes the presence of dendritic cells and granulocytes in Takayasu's disease. Dendritic cells are probably involved in the immunoinflammatory processes through their interaction with T-cells and B-cells. The present observations may help understanding of the pathogenesis of Takayasu's disease.
Adult↗
Pharmacokinetics, metabolism, and excretion of irinotecan (CPT-11) following I.V. infusion of [(14)C]CPT-11 in cancer patients.
This study determined the disposition of irinotecan hydrochloride trihydrate (CPT-11) after i.v. infusion of 125 mg/m(2) (100 microCi) [(14)C]CPT-11 in eight patients with solid tumors. Mean +/- S.D. recovery of radioactivity in urine and feces was 95.8 +/- 2.7% (range 92.2-100.3%, n = 7) of dose. Radioactivity in blood, plasma, urine, and feces was determined for at least 168 h after dosing. Fecal excretion accounted for 63.7 +/- 6.8 (range 54.2-74.9%, n = 7) of dose, whereas urinary excretion accounted for 32.1 +/- 6.9% (range 21.7-43.8%; n = 7) of dose. One patient with a biliary T-tube excreted 30.1% of dose in bile, 14.2% in feces, and 48.2% in urine. Quantitative radiometric HPLC revealed that CPT-11 was the major excretion product in urine, bile, and feces. Aminopentane carboxylic acid (APC) and SN-38 glucuronide (SN-38G) were the most significant metabolites in urine and bile, whereas SN-38 and NPC, a primary amine metabolite, were relatively minor excretion products. SN-38 and APC were the most significant metabolites in feces. The relatively higher amount of SN-38 in feces compared with bile is presumably due to hydrolysis of SN-38G to SN-38 by enteric bacterial beta-glucuronidases. There was close correspondence between quantitative fluorescence HPLC and mass balance findings. CPT-11 was the major circulating component in plasma (55% of the mean radiochemical area under the curve), and CPT-11, SN-38, SN-38G, and APC accounted for 93% of the mean radiochemical AUC. These results show that the parent drug and its three major metabolites account for virtually all CPT-11 disposition, with fecal excretion representing the major elimination pathway.
Aged↗
Electron-microscopic detection of apoptotic and necrotic cell death in non-atherosclerotic areas of stenotic aortocoronary saphenous vein bypass grafts.
Aortocoronary saphenous vein bypass grafts undergo structural alterations within the arterialized vein, resulting in graft stenosis and failure. Areas of the acellular intima contribute to fissuring, cracking and ulceration, while areas of the media become highly vascular but thinned. This study aimed to examine the ultrastructural features of cell death, including apoptosis and necrosis, in non-atherosclerotic areas of the stenotic aortocoronary saphenous vein bypass grafts. Thirteen stenotic vein grafts were obtained at redo coronary artery bypass grafting. The ultrastructural features of cell death were analysed by electron microscopy. Typical features of necrosis, including focal areas of cytoplasmic oedema, plasmalemmal destruction and nuclear condensation with cytoplasmic organelle destruction, were observed throughout the intima and media. Features of apoptosis, including the presence of apoptotic bodies, were also identified in the hyperplastic intima and its adjacent media. Our observations suggest that both apoptosis and necrosis occur in non-atherosclerotic areas of stenotic aortocoronary saphenous vein bypass grafts.
Aged↗
Neovascular expression of VE-cadherin in human atherosclerotic arteries and its relation to intimal inflammation.
OBJECTIVE: The present work aimed to investigate how the Ca(2+)-dependent cell adhesion molecule vascular endothelial (VE)-cadherin might be involved in atherogenesis. METHODS: Specimens of human carotid artery and aorta were obtained at operation. An immunohistochemical approach using cell-type specific antibodies examined how VE-cadherin expression in areas of neovascularisation related to the accumulation of immunocompetent and inflammatory cells within atherosclerotic plaque. Electron microscopy was used to examine the structural characteristics of neovessels and the cell composition in the surrounding intimal matrix. RESULTS: In all the non-atherosclerotic aortic segments, VE-cadherin expression was observed only in the adventitia and the outer third of the media. Within the atherosclerotic arterial segments, VE-cadherin was expressed in all layers of the arterial wall including the intima where VE-cadherin was expressed by endothelial cells in areas of neovascularization. In some neovessels, loss of VE-cadherin expression was associated with increased focal accumulation of T-cells, macrophages and dendritic cells. Electron-microscopic examination demonstrated varying degrees of endothelial continuity in the intimal neovessels. Within those neovessels which were surrounded by a large number of immunocompetent and inflammatory cells, some inter-endothelial cell contacts were open allowing the penetration of blood cells through patent intercellular zones. CONCLUSIONS: VE-cadherin is expressed in atherosclerotic lesions by endothelial cells associated with neovascularisation. Downregulation of VE-cadherin expression within some intimal neovessels is accompanied by increased entry of immunocompetent cells into the intimal matrix surrounding areas of neovascularization which suggests that disorganizing endothelial cell-to-cell interactions within neovessels is significant in atherogenesis.
Adult↗
Accumulation of co-localised unesterified cholesterol and neutral lipids within vacuolised elastin fibres in athero-prone areas of the human aorta.
To investigate whether there are alterations of elastin fibres in the arterial intima at the pre-atherosclerotic stage, grossly normal areas of human thoracic aorta were taken soon after death from 13 healthy trauma victims whose ages ranged from 16 to 40 years. Two areas were compared: atherosclerosis-prone (AP) areas localised to the dorsal aspect of the aorta along the rows of intercostal branch origins, and atherosclerosis-resistant (AR) areas from the ventral aorta. Electron microscopic analysis combined with cytochemical staining was applied. Unesterified cholesterol was identified using the filipin-staining technique while neutral lipids were visualised by the OTO-technique. Intimal features were studied by combining the filipin-staining and the OTO-technique. Electron microscopical examination showed that in both AR and AP areas, some elastin fibres in the intima were vacuolised. Unesterified cholesterol was found to be predominantly localised in the musculoelastic layer, in particular, inside the vacuolised elastin fibres. This localisation was seen in all 13 AP areas studied in contrast to the AR areas where it was observed in only four of 13 aortas studied (P < 0.0005, chi2-test). Accumulation of neutral lipids inside vacuolised elastin fibres was found in five out of 13 AP areas but was not observed in any of the AR areas (P=0.01, chi2). A combination of the filipin-staining and OTO-techniques showed that some deposits of neutral lipids and unesterified cholesterol within vacuolised elastin fibres were independently located from each other, but more frequently, neutral lipids were co-located with unesterified cholesterol. The present observations indicate a difference between AP and AR intimal areas which, in particular, relates to the structure of elastin fibres in the musculoelastic layer. The observations suggest that alterations of the extracellular matrix are involved in the trapping and retention of cholesterol and neutral lipids within the intima at an early stage in the development of atherosclerotic lesions.
Adolescent↗
Atherosclerotic lesions of apolipoprotein E deficient mice contain cells expressing S100 protein.
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Animals↗
Clustering of dendritic cells in athero-prone areas of the aorta.
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Adolescent↗
Familial carotid body paragangliomas and sensorineural hearing-loss: a new syndrome.
BACKGROUND: Carotid body paragangliomas are rare tumors that are sometimes familial, the transmission of which is thought to be by genomic imprinting. We have treated a family who exhibited co-inheritance of carotid body paraganglioma and sensorineural hearing-loss, a relationship that has not been previously reported. METHODS: We studied a large Australian family who exhibited familial carotid body paragangliomas, many of whose members also suffered tinnitus or hearing-loss. This relationship was examined by reviewing the medical records of family members with confirmed tumors, carrying out neck ultrasonic scanning or computed tomography on their relatives to look for previously unrecognized tumors, and arranging audiometric testing. This information was used to characterize the type of hearing-loss present in this family and to construct a pedigree for the two traits. RESULTS: The hearing-loss observed in this family was sensorineural in character. Of 15 family members studied over four generations, eight were confirmed positive for both carotid body paraganglioma and sensorineural hearing-loss, two for the tumor only (one of whom did not have his hearing assessed) and one for hearing-loss alone. Four family members were negative for both traits. CONCLUSIONS: The pedigree provides evidence of a previously undescribed association between familial carotid body paraganglioma and sensorineural hearing-loss, a combination that appears to be co-inherited in this family.
Adult↗
The blood supply of the hypoglossal nerve and its relevance to carotid endarterectomy.
Since the hypoglossal nerve is liable to injury during carotid endarterectomy and similar procedures, its blood supply was examined in microinjection studies of human cadavers. The nerve is supplied by arteries that arise from the ascending pharyngeal artery as it exits from the hypoglossal canal, the occipital artery as the nerve passes under its branch to the sternomastoid muscle, direct branches from the external carotid artery, and branches from the ascending pharyngeal artery just near the bifurcation of the common carotid artery. Within and close to the tongue, the nerve is supplied by branches from the lingual artery. Damage to the vessels supplying the nerve may account for some cases of hypoglossal palsy after carotid endarterectomy. Possible mechanisms are ischaemia, thermal or electrical injury from diathermy current conducted to the nerve, or intraneural haematoma from rupturing one or more of these fine vessels.
Arteries↗
The effect of increasing clamping forces on endothelial and arterial wall damage: an experimental study in the sheep.
PURPOSE: This study aimed to relate the level of physical force applied to the arterial wall by atraumatic clamps to the degree of endothelial and wall damage. METHODS: Sixteen sheep carotid and femoral arteries were each demarcated into four segments 1 cm apart (total 64 segments). Each segment was clamped for 15 min with a standard angled DeBakey vascular clamp. Four levels of force were generated by closing the clamp at three, four, five and six notches of closure. The extent of endothelial injury was assessed by using a dedicated computer assisted image acquisition program to measure the area stained by Evan's blue dye. The extent of damage to the layers of the arterial wall was analyzed and compared by scanning electron microscopy and light microscopy. RESULTS: For femoral arteries, the area of endothelial injury was considerably less for three notch (3.76 +/- 0.28 newtons) and four notch (5.68 +/- 0.29 newtons) closure compared with that for five notch (6.19 +/- 0.31 newtons) and six notch (6.61 +/- 0.16 Newtons) closure (p = 0.01). For carotid arteries, three notch (5.68 +/- 0.28 newtons) closure caused less damage than did four notch (7.98 +/- 0.29 newtons), five notch (9.17 +/- 0.40 newtons) and six notch (9.57 +/- 0.64 newtons) closure (P = 0.02). Scanning electron microscopy confirmed the extent and depth of arterial injury corresponded directly to the forces generated by the vascular clamps. CONCLUSIONS: The closing forces generated by arterial clamps correlated positively with the extent of artery wall injury. Vascular clamps should be applied at the minimum level of force that will arrest blood flow.
Animals↗
Involvement of dendritic cells in long-term aortocoronary saphenous vein bypass graft failure.
Antigen-presenting dendritic cells are present in atherosclerotic lesions in human arterial intima, but have not been investigated in atherosclerotic and hyperplastic stenotic lesions that affect vein grafts used as arterial conduits. This study was undertaken to examine whether dendritic cells are present in aortocoronary artery saphenous vein bypass grafts affected by high-grade atheromatous stenosis. Stenotic saphenous vein coronary artery bypass grafts (angiographic luminal stenosis > 75%) were harvested from 10 patients (nine male, one female), aged 4271 years (mean 56.5) at re-do operation. The mean time interval from bypass surgery to the excision of stenotic grafts was 11.5 years (range 2-21). The specimens were fixed in 10% buffered formalin, embedded in paraffin blocks and the sections stained with antibodies to S-100 (to identify dendritic cells), CD3 (T cells), CD68 (macrophages), von Willebrand factor (endothelial cells) and alpha-smooth muscle actin (smooth muscle cells) using avidin-biotin complex immunoperoxidase technique. Normal veins were obtained during saphenous vein femoro-popliteal grafting. The stenotic venous grafts showed histological features typical of extensive arterialization, intimal hyperplasia, atherosclerotic plaque-like lesions, calcification and thrombosis. In areas of intimal hyperplasia, S-10O-positive cells were distributed irregularly among smooth muscle cells. S-100-positive dendritic cells were seen most frequently within atherosclerotic plaque-like lesions where they co-localized with CD3+ cells and CD68+ cells. S-100-positive dendritic cells were also seen accumulating within calcific foci. No S-100-positve cells were found in normal, ungrafted saphenous veins. We conclude that dendritic cells are present in aortocoronary saphenous vein bypass grafts affected by high grade stenosis. Dendritic cells are probably involved in immune mechanisms of atherogenesis through their interactions with T cells and macrophages. The accumulation of dendritic cells within calcific foci suggests their contribution to the calcification of stenotic venous grafts.
Adult↗
Dendritic cells in venous pathologies.
Dendritic cells are potent antigen-presenting cells responsible for the activation of T-lymphocytes in various immune responses. Their role in the initiation of immune reactions in allergies, autoimmune diseases, tumors, transplantation, and, more recently, in atherosclerosis has been well established, but their involvement in venous pathologies has not been previously investigated. The aim of this study was to determine whether dendritic cells are present in veins affected by varicosity and thrombophlebitis. Three groups of veins obtained at operation were studied: (1) varicose veins of the great saphenous vein from patients who were undergoing vein stripping for primary varicosity; (2) segments of the great saphenous vein from patients with varicosity complicated by thrombophlebitis; and (3) great saphenous veins without varicosity or thrombophlebitis from patients who were undergoing femoropopliteal bypass grafting. The specimens were fixed in 10% neutral buffered formalin and embedded in paraffin, and the sections were stained with antibodies to S-100 (to identify dendritic cells), CD3 (T-lymphocytes), CD68 (macrophages), von Willebrand factor (endothelial cells), alpha-smooth muscle actin (smooth muscle cells), and CD15 (mast cells) by use of avidin-biotin complex (ABC) immunoperoxidase technique. Immunohistochemical examination showed that no S-100-positive dendritic cells were present in normal saphenous veins. In contrast, S-100-positive cells with dendritic cell morphology were detected in the intima and media of veins with varicosity and thrombophlebitis, where they represented a minor cell population. S-100-positive dendritic cells were located between smooth muscle cells as well as around areas of neovascularization where they colocalized with T-lymphocytes. The present work suggests that dendritic cells might be involved in pathological processes in veins affected by varicosity and thrombophlebitis. The authors speculate that dendritic cells may be involved in the inflammatory mechanisms in these veins through their interaction with T-lymphocytes.
Adult↗
55-kD actin-bundling protein (p55) is a specific marker for identifying vascular dendritic cells.
Compared with other members of the dendritic cell family, the antigen profile of the recently recognized vascular dendritic cells has received limited attention. This study demonstrates that vascular dendritic cells in the human aorta and carotid arteries express 55-kD actin-bundling protein (p55), a specific marker for blood dendritic cells and Langerhans cells. This finding will facilitate screening of dendritic cells during their isolation from the arterial wall, as well as other investigations.(J Histochem Cytochem 47:1481-1486, 1999)
Actins↗