C J Kelly

Beaumont Hospital, Dublin, Leinster, Ireland

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Publications (72)161.44 Total impact

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    ABSTRACT: Introduction Les patients cancéreux ont un risque augmenté d'évènements thromboemboliques veineux. Certaines substances utilisées lors de chimiothérapies ont également été associées au développement de thromboses. Les cas rapportés d'épisodes ischémiques artériels aigus chez des patients cancéreux sont rares. Méthodes Les patients opérés chirurgicalement pour une ischémie aigue associée à une tumeur maligne dans un centre hospitalo-universitaire étaient identifiés sur une période de 10 ans. Les caractéristiques démographiques des patients, les types de cancer, l'utilisation de chimiothérapies, le site de la thrombose, les traitements et les résultats étaient notés. Résultats Quatre cents dix-neuf patients étaient opérés pour une ischémie aigue artérielle. Parmi eux, 16 patients (3,8%) avaient un cancer associé. Les sites les plus fréquents de cancer étaient le tractus urogénital (n = 5) et les poumons (n = 5). Huit patients (50%) avaient été diagnostiqués de leur cancer récemment, et quatre (25%) de ces cancers étaient découverts fortuitement après l'épisode d'ischémie aigue. Quatre patients (25%) développaient une ischémie aigue lors d'une chimiothérapie. L'artère fémorale superficielle était le site le plus fréquent d'occlusion (50%), suivie par les artères brachiales (18%) et poplitées (12%). Tous les patients avaient une thrombo-embolectomie, mais deux (12%) patients nécessitaient un pontage secondaire. Six patients (37%) perdaient leur membre, et la mortalité intra-hospitalière était de 12%. L'histologie révélait que toutes les occlusions étaient dues à une maladie thromboembolique, sans cellule tumorale identifiée. Lors du suivi, 44% de patients étaient vivants à 1 an. Conclusion Le cancer et la chimiothérapie peuvent prédisposer les patients à l'ischémie aigue artérielle. Au contraire d'autres rapports qui retrouvaient que cet évènement était préterminal et mieux traité par des mesures palliatives, dans cette série, un diagnostic et une intervention précoces permettaient un sauvetage de membre et la survie du patient.
    Annales de Chirurgie Vasculaire. 10/2011; 25(7):1016–1022.
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    ABSTRACT: Cancer patients have an increased risk of venous thromboembolic events. Certain chemotherapeutic agents have also been associated with the development of thrombosis. Reported cases of acute arterial ischemic episodes in cancer patients are rare. Patients who underwent surgery for acute limb ischemia associated with malignancy in a university teaching hospital over a 10-year period were identified. Patient demographics, cancer type, chemotherapy use, site of thromboembolism, treatment and outcome were recorded. Four hundred nineteen patients underwent surgical intervention for acute arterial ischemia, 16 of these patients (3.8%) had associated cancer. Commonest cancer sites were the urogenital tract (n = 5) and the lungs (n = 5). Eight patients (50%) had been recently diagnosed with cancer, and four (25%) of these cancers were incidental findings after presentation with acute limb ischemia. Four patients (25%) developed acute ischemia during chemotherapy. The superficial femoral artery was the most frequent site of occlusion (50%), followed by the brachial (18%) and popliteal (12%) arteries. All patients underwent thromboembolectomy, but two (12%) patients subsequently required a bypass procedure. Six patients (37%) had limb loss, and in-patient mortality was 12%. Histology revealed that all occlusions were due to thromboembolism, with no tumor cells identified. At follow-up, 44% of patients were found to be alive after 1 year. Cancer and chemotherapy can predispose patients to acute arterial ischemia. Unlike other reports that view this finding as a preterminal event most appropriately treated by palliative measures, in this series, early diagnosis and surgical intervention enabled limb salvage and patient survival.
    Annals of Vascular Surgery 08/2011; 25(7):954-60. · 0.99 Impact Factor
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    ABSTRACT: Down syndrome, or trisomy 21, has a characteristic constellation of clinical findings, including various congenital heart defects. We report a case of an adult male with Down syndrome who presented with a 3-week history of lower limb pain and swelling, attributed to cellulitis. Clinical and angiographic evaluation identified a below-knee mycotic pseudoaneurysm secondary to infective endocarditis. Surgical aneurysmal repair and revascularization were performed. Various management options are outlined in this report.
    Vascular 10/2010; 18(5):297-8. · 0.86 Impact Factor
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    ABSTRACT: Peripheral arterial disease (PAD) and type 2 diabetes mellitus (DM) are both associated with excessive vascular calcification and elevated levels of inflammatory markers IL-6 and hsCRP. The recently identified Osteoprotegerin(OPG)/RANKL/TRAIL pathway has been implicated in vascular calcification, but data on levels in PAD and effect of co-existent DM are lacking. 4 groups of patients were recruited - 26 with PAD and DM, 35 with DM alone, 22 with PAD alone, and 21 healthy individuals. Serum OPG, RANKL, TRAIL, hsCRP and IL-6 were measured using commercial ELISA assays. Presence and severity of PAD was defined using ankle brachial index (ABI). Serum OPG (7.4±0.3 vs.5.8±0.2 pmol/l, p<0.0001), TRAIL (95.5±5.2 ng/ml vs. 76.2±4.4 ng/ml, p=0.006), hsCRP (2.6±0.3 vs. 1.8±0.3 mg/l, p=0.048), and IL-6 (4.1±0.4 vs. 2.9±0.4 pg/ml, p=0.06) were higher in patients with PAD. There was no difference in RANKL. Only OPG was significantly higher in PAD and DM (7.2±0.3 pmol/l) and PAD alone (7.7±0.4 pmol/l) compared to DM only (5.8±0.3 pmol/l) and healthy controls (5.6±0.4 pmol/l), p<0.01, but OPG was no higher in those with DM plus PAD versus those with PAD alone (p<0.3). Only OPG was associated with PAD severity, correlating negatively with ABI (r=-0.26, p=0.03), independent of age, gender, glycaemic status, hsCRP and IL-6. PAD is associated with higher serum OPG, regardless of the co-existence of DM. This finding, in addition to its correlation with severity of PAD, suggests that OPG may be a novel marker for the presence and severity of PAD, possibly by reflecting the degree of underlying vascular calcification.
    Thrombosis Research 10/2010; 126(6):e423-7. · 3.13 Impact Factor
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    ABSTRACT: The purpose of this study is to evaluate the use of endovascular stent grafts in the treatment of para-anastomotic aneurysms (PAAs) as an alternative to high-risk open surgical repair. We identified all patients with previous open aortic aneurysm repair who underwent infrarenal endovascular aneurysm repair (EVAR) at our institution from June 1998 to April 2007. Patient demographics, previous surgery, and operative complications were recorded. One hundred forty-eight patients underwent EVAR during the study period and 11 patients had previous aortic surgery. Of these 11 redo patients, the mean age was 62 years at initial surgery and 71 years at EVAR. All patients were male. Initial open repair was for rupture in five (45%) patients. The average time between initial and subsequent reintervention was 9 years. All patients were ASA Grade III or IV. Fifty-five percent of the PAAs involved the iliac arteries, 36% the abdominal aorta, and 9% were aortoiliac. Ten patients had endovascular stent-grafts inserted electively, and one patient presented with a contained leak. Aorto-uni-iliac stent-grafts were deployed in seven patients, and bifurcated stent-grafts in four patients. A 100% successful deployment rate was achieved. Perioperative mortality was not seen and one patient needed surgical reintervention to correct an endoleak. Endovascular repair of PAAs is safe and feasible. It is a suitable alternative and has probably now become the treatment of choice in the management of PAAs.
    CardioVascular and Interventional Radiology 08/2009; 32(6):1165-70. · 2.09 Impact Factor
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    ABSTRACT: There is lack of consensus regarding concurrent vs. staged approaches, and the prioritisation of staged procedures in cases presenting with colorectal carcinoma (CRC) and abdominal aortic aneurysm (AAA) synchronously. We aim to present our experience, review the literature on this therapeutic dilemma and examine the role of endovascular aortic repair (EVAR). An observational study of the experience of two centres and a systematic review of the published literature. Twenty-four patients were identified from the prospective databases of two tertiary referral centres between 2001 and 2006. Intervention for both malignancy and aneurysm was performed in 13 patients. In 10 patients, cancer resection was performed initially and was followed by open aneurysm repair (n=3) or EVAR (n=7). Two patients (AAA diameters: 7.0 and 8.0cm) underwent EVAR prior to colonic resection. One patient was selected for synchronous surgery. There were no interval AAA ruptures, graft infection or postoperative mortalities. Literature review identified 269 such cases; of these 101 were treated by combined surgery. In staged surgery, there were nine interval aneurysmal ruptures and one aortic graft infection. In our experience, staged management can be undertaken, without interval aneurysmal rupture. EVAR has an evolving role in preventing delay in CRC management, in high-risk patients, and during combined intervention.
    European journal of vascular and endovascular surgery: the official journal of the European Society for Vascular Surgery 03/2009; 37(5):544-56. · 2.92 Impact Factor
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    ABSTRACT: AAA screening programmes have proven to be beneficial and cost effective worldwide for males greater than 65 years of age, with 4.9% males of 65-75 years of age having an un-diagnosed AAA at screening, resulting in a 42% reduction in the risk of rupture in an English population. This study assessed the incidence of AAA and risk factors for atherosclerosis in Irish males of 55-75 years. From April 2006 to December 2007, males between the ages of 55 and 75 years, living within the catchment area of Blanchardstown Hospital were invited for AAA screening using duplex ultrasound and cardiovascular risk factor screening. 1.9% (17/904) of the study population had previously un-diagnosed aneurysms detected, with sizes ranging from 3.0 cm to 5.8 cm (0.6% in 55-65 years old (yo) and 4.2% in 65-75 yo, p<0.01). 33% (302/904) of patients had hyperlipidaemia, while 16% of those with a previous diagnosis of hyperlipidaemia, were inadequately controlled on the test date. 31% of patients had a single elevated blood pressure reading, meriting further investigation for possible hypertension. 3% (28/904) of all patients had a raised glucose levels which had not previously been identified and of those who had a previous history of DM, 46% had abnormal glucose levels. 16% of patients (93/573) were morbidly obese (BMI>30) and 64% (292/573) were overweight. The incidence of AAAs in 65-75-year-old men is similar to international figures. This study confirms that screening for hyperlipidaemia, hypercholesterolaemia, obesity and hypertension may be worthwhile in all males over 55 years, while AAA screening should be reserved for 65-75-year-old Irish males.
    European journal of vascular and endovascular surgery: the official journal of the European Society for Vascular Surgery 12/2008; 37(3):300-4. · 2.92 Impact Factor
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    ABSTRACT: Shortened trainingtimes duetothe European Working Time Directive (EWTD) and increased public scrutiny of surgical competency have led to a move away from the traditional apprenticeship model of training. Virtual reality (VR) simulation is a fascinating innovation allowing surgeons to develop without the need to practice on real patients and it may be a solution to achieve competency within a shortened training period. A Medline search was performed to identify studies and commentaries on the use of VR simulators in endovascular training. Three studies on carotid stenting and four on peripheral vascular angioplasty demonstrate that simulator training is a valid, feasible and acceptable training tool. One randomised study reports that these skills learned on simulators are transferable to the operating room. VR simulators have a role in competency based, structured training of vascular interventionalists and should improve patient safety.
    The surgeon: journal of the Royal Colleges of Surgeons of Edinburgh and Ireland 09/2008; 6(4):214-20. · 1.97 Impact Factor
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    ABSTRACT: We present the case of a 36-year-old female with a three-week history of a pulsatile, tender mass in the anterior triangle of the neck. Radiology demonstrated that this was a vascular tumour deep to the sternocleidomastoid muscle. Pre-operative embolisation and complete surgical resection was performed. Histology revealed Castleman's disease. Unicentric hyaline vascular Castleman's disease is an unusual cause of neck mass. Surgical resection remains the best chance for cure in unicentric disease. Long term follow-up is necessary as the risk of subsequent malignancy exists.
    Irish Journal of Medical Science 01/2006; 175(1):79-80. · 0.51 Impact Factor
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    ABSTRACT: The aim of this study was to investigate whether inhibition of hydroxymethylglutaryl co-enzyme A reductase attenuates leucocyte-endothelial cell interactions and alters expression of endothelial constitutive nitric oxide synthase (ecNOS) and inducible nitric oxide synthase (iNOS) following exposure to endotoxin. Male Sprague-Dawley rats were randomized into control, lipopolysaccharide (LPS) and pravastatin + LPS groups (seven per group). Pravastatin sodium was gavaged at 0.4 mg per kg per day for 5 days, after which LPS 15 mg/kg was administered via the jugular vein. Intravital microscopy was used to determine leucocyte-endothelial cell interactions. Following the administration of LPS there was a significant reduction in leucocyte rolling velocity at 10 min (mean(s.e.m.) 69(3) versus 102(6) per cent of baseline value; P = 0.041), an increase in the number of adherent leucocytes at 10 min (4.5(0.5) versus 2.8(0.3) per 100 microm; P = 0.044) and an increase in the number of leucocytes undergoing transendothelial migration at 30 min (4.2(0.4) versus 1.7(0.4) per field; P = 0.008) compared with controls. Pretreatment with pravastatin significantly attenuated LPS-induced leucocyte-endothelial cell interactions (rolling velocity 89(6) per cent at 10 min, P = 0.038; adherent leucocytes 3.0(0.5) per 100 microm at 10 min, P = 0.038; migrating leucocytes 1.9(0.5) per field at 30 min, P = 0.001). This endothelial protection was associated with maintenance of ecNOS and reduced iNOS expression within mesenteric tissues. These data show that pravastatin produces anti-inflammatory effects in response to injurious stimuli by attenuation of leucocyte-endothelial cell interactions.
    British Journal of Surgery 09/2005; 92(8):1034-40. · 4.84 Impact Factor
  • The surgeon: journal of the Royal Colleges of Surgeons of Edinburgh and Ireland 07/2005; 3(3):160-3. · 1.97 Impact Factor
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    ABSTRACT: We hypothesize that treatment with Pravastatin, a HMG CoA reductase inhibitor would improve flow-mediated dilation (FMD), a nitric oxide dependent phenomenon and the earliest detectable marker of endothelial dysfunction, in asymptomatic patients with type-1 diabetes. FMD of the brachial artery in response to reactive hyperaemia was measured using high-resolution ultrasonography. Young male patients with type-1 diabetes (n=9) were compared with age matched non-diabetic controls (n=8). The FMD response in the control group was a median increase in diameter of 7.9 (range 3.8-12.6)%. In the diabetic group the FMD response was impaired when compared with controls with a median increase only of 4.4 (range 3.7-5.8)% (p<0.01). Following Pravastatin, 40 mg per day for one month in the diabetic group, there was a significant diameter change in response to reactive hyperaemia with a median of 8.4 (range 6.9-12.6)% (p<0.01). These data confirm the presence of endothelial dysfunction in young patients with type-1 diabetes. We have shown that 1-month of Pravastatin treatment normalizes FMD. This suggests that HMG CoA reductase inhibitors may have a role in the management of diabetes mellitus, even in the presence of normal serum cholesterol levels.
    European Journal of Vascular and Endovascular Surgery 05/2004; 27(4):432-7. · 2.82 Impact Factor
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    ABSTRACT: We have previously demonstrated that clinically applicable thermal preconditioning induces heat shock protein 72 (HSP72) and protects against a subsequent ischemia-reperfusion (I/R) injury in an animal model. A core component of I/R injuries is the interaction between activated leukocytes and endothelial cells. We hypothesized that the effects of clinically applicable thermal preconditioning are mediated through attenuation of this leukocyte-endothelial (L-E) interaction. Twenty-one male Sprague Dawley rats were divided into control, I/R, and preconditioning plus I/R groups. Preconditioning was done under general anesthesia and the animals' temperature raised by 1 degrees C for 15 minutes in a water bath. This was repeated once a day for 5 successive days. I/R injury was caused by occlusion of the superior mesenteric artery for 10 minutes followed by 1 hour of reperfusion. L-E interactions were analyzed using intravital microscopy of a mesenteric vessel in vivo. L-E interactions were determined using leukocyte velocity (which decreases as cells interact), and number of adherent and migrated leukocytes. HSP72 was assessed by Western blot. Ischemia-reperfusion caused a decrease in leukocyte rolling velocity at all timepoints (p < 0.05 versus controls). Preconditioning attenuated the effects of I/R, and leukocyte rolling velocity was significantly improved versus I/R (p < 0.05) to levels similar to those in controls. Similarly, the number of adherent and migrating leukocytes increased significantly (p < 0.05) after I/R versus control at all time points, and preconditioning attenuated these to control levels, (p < 0.05 versus I/R) at both the 30- and 60-minute postischemia time points. Upregulation of HSP72 was demonstrated on Western blot. These results demonstrate that the benefit of clinically applicable thermal preconditioning is at least partially because of an immunomodulatory role in attenuating leukocyte-endothelial interactions associated with an increased expression of HSP 72.
    Journal of the American College of Surgeons 07/2003; 197(1):71-8. · 4.50 Impact Factor
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    ABSTRACT: Endothelial dysfunction initiated by monocyte-endothelial interactions has previously been observed in many vasculopathies, including chronic cigarette smoking. Taurine, a semiessential amino acid, and vitamin C, a naturally occurring antioxidant, have previously been shown to have endothelial protective effects when exposed to proinflammatory insults. Therefore, we hypothesized that taurine and vitamin C would restore endothelial function in young smokers by modifying monocyte-endothelial interactions. Endothelial-dependent vasodilatation was assessed in vivo using duplex ultrasonography, and monocyte-endothelial interactions were assessed in vitro using endothelial cell culture (human umbilical vein endothelial cells [HUVECs]) with monocyte-conditioned medium (MCM). Endothelial-dependent vasodilatation was significantly impaired in young smokers compared with nonsmokers. Pretreatment of young smokers for 5 days with 2 g/d vitamin C and, more significantly, with 1.5 g/d taurine attenuated this response. MCM taken from smokers impaired the release of nitric oxide and increased the levels of endothelin-1 release from HUVECs. When HUVECs were cultured with MCM from smokers who had been treated with taurine, the levels of nitric oxide and endothelin-1 returned toward control levels. This was attributed to an upregulation in endothelial nitric oxide synthase expression. These observations suggest that taurine supplementation has a beneficial impact on macrovascular endothelial function, and an investigation of its effect on altered endothelial function in dyslipidemic states is warranted.
    Circulation 02/2003; 107(3):410-5. · 15.20 Impact Factor
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    ABSTRACT: Thermal preconditioning has previously been shown to attenuate ischemia-reperfusion induced injuries, possible due to increased expression of heat shock proteins (HSP). The model of thermal preconditioning used, however, was not clinically relevant as preconditioning was to 41 degrees C, leading to cellular damage. Our aim was thus to establish a novel and clinically applicable method of preconditioning. Twenty-six male Sprague-Dawley rats were split into three groups (nine control, nine ischemia-reperfusion, and eight preconditioned followed by ischemia-reperfusion). To precondition the animals, they were anesthetized and, using a water bath, their core temperature was raised by 1 degrees C for 15 min once a day for five successive days. I/R injury consisted of 30 min of aortic cross-clamping followed by 120 min of reperfusion; control animals had a laparotomy only. Indicators of lung injury were tissue myeloperoxidase, broncho-alveolar lavage protein concentration, and tissue edema. Tissue heat shock protein expression was detected by Western blot analysis. Lower torso ischemia-reperfusion causes significant lung injury versus control, with raised levels of myeloperoxidase 4.53 iu/g to 7.88 iu/g (P < 0.05), raised B.A.L. protein concentration 419 microg/ml to 684 microg/ml (P < 0.05) and altered wet dry ratio 4.63 to 5.50. Clinically relevant thermal preconditioning attenuates all of these parameters back to control levels: myeloperoxidase 3.87 iu/g (P < 0.05 vs I/R), B.A.L. to 284 microg/ml (P < 0.01 vs I/R) and wet dry ratio to 4.44 (P < 0.05 vs I/R). Western blot demonstrated increased expression of H.S.P. 72 in the preconditioned group versus control and I/R alone. Western blot demonstrated increased expression of HSP72 in the preconditioned group vs control and I/R alone. We conclude that clinically applicable thermal preconditioning can attenuate ischemia-reperfusion induced lung injury, possibly through increased expression of HSP72.
    Journal of Surgical Research 02/2003; 109(1):24-30. · 2.02 Impact Factor
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    ABSTRACT: intimal hyperplasia (IH) is a major cause of re-stenosis post-vascular intervention. Induction of heat shock proteins (HSPs), by thermal pre-conditioning, reduces IH. Our aim was to investigate the effect of the pharmacological HSP inducer herbimycin A on IH in the rat carotid balloon injury model. Materials and Methods: thirty male Sprague-Dawley rats were randomized into three groups. All groups underwent balloon injury to the left carotid artery. Stress proteins were induced 18 h pre-operatively by heat shock or herbimycin A. Two weeks post-operatively, animals were sacrificed and carotid intima/media area ratio (I/M ratio) calculated using computerized planimetry. Neo-intimal proliferation was assessed immunohistochemically with PCNA (proliferating cell nuclear antigen). Western blot and immunohistochemistry for arterial HSP70 and HSP27 were performed. heat stress and herbimycin significantly reduced the I/M ratio (p < 0.05 vs balloon injury alone). Neo-intimal proliferation was significantly reduced in the heat stress and herbimycin groups (p < 0.05 vs balloon injury alone). Heat stress induced arterial HSP70 and HSP27. Herbimycin A increased arterial HSP27. herbimycin A significantly attenuates IH after balloon injury. HSP27 may be the HSP involved in mediating this response. Pharmacological inducers of HSPs may have a therapeutic role to play in preventing re-stenosis post-vascular intervention.
    European Journal of Vascular and Endovascular Surgery 01/2003; 25(1):40-7. · 2.82 Impact Factor
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    ABSTRACT: Systemic ischaemia-reperfusion (IR) injury is in part an oxidant injury mediated by neutrophils. Diethylmaleate (DEM), an intracellular pro-oxidant agent, has been shown to alleviate neutrophil-mediated tissue injury. The aim of this study was to evaluate whether DEM could have a protective effect on neutrophil-mediated lung injury in an animal model of lower-torso IR. Sprague-Dawley rats (seven per group) were randomized into three groups. The control group underwent midline laparotomy only; the IR group underwent laparotomy and clamping of the infrarenal abdominal aorta for 30 min followed by 2 h of reperfusion; and the third group was pretreated with DEM 6 mmol/kg intraperitoneally 1 h before the IR insult. IR resulted in a significant increase in both microvascular leakage and pulmonary neutrophil infiltration as measured by bronchoalveolar lavage protein concentration and pulmonary myeloperoxidase activity respectively. Pretreatment with DEM significantly attenuated both microvascular leakage and neutrophil infiltration. Preconditioning with DEM protected against IR-induced lung injury. This protective effect raises the possibility of using pro-oxidants to prevent inflammatory injury.
    British Journal of Surgery 05/2002; 89(4):482-5. · 4.84 Impact Factor
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    ABSTRACT: The purpose of this study was to determine if prereatment with taurolidine, a known anti-endotoxin agent, would attenuate the hemodynamic and respiratory responses associated with endotoxin induced lung injury in a large animal model in a randomized controlled study under license from the Department of Health. All animals underwent a general anesthetic. Vascular catheters were placed in the femoral artery and in the femoral vein. A Swan-Ganz Catheter was inserted for measurement of pulmonary artery pressure. Animals were randomized into three groups: Control, with measurements taken at baseline and half hourly up to 90 min; Endotoxin, receiving 5microg/Kg E. coli endotoxin intravenously after baseline measurements; and Endotoxin + Taurolidine, receiving 5g of taurolidine via intraperitoneal infusion 1 h before endotoxin administration. Main outcome measures were mean systemic arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), arterial oxygen tension (pO2), serum endotoxin concentration, and pulmonary myeloperoxidase. Endotoxin induced a significant lung injury characterized by an increase in pulmonary artery pressure, hypoxia, and systemic hypotension. Pretreatment with intraperitoneal taurolidine significantly attenuated these hemodynamic and respiratory changes. Serum endotoxin concentration was also significantly reduced as was lung myeloperoxidase. The data suggest that taurolidine may have a therapeutic role in preventing the lung injury seen in endotoxemia.
    Shock 05/2002; 17(4):308-11. · 2.61 Impact Factor
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    ABSTRACT: Conclusion The above data demonstrate that the endothelial dysfunction (FMD) previously demonstrated correlates with endothelial injury (vWF) and platelet abnormalities. These are early and possibly synergistic alterations in young smokers that contribute to the development of atherogenesis.
    Irish Journal of Medical Science 01/2002; 171:19-19. · 0.51 Impact Factor
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    ABSTRACT: Conclusion Using the above parameters, these data demonstrate that this population of type 1 diabetics have no evidence of platelet abnormalities. Further, they indicate that anti-platelet therapy is not required in the early stages of type 1 diabetes and that endothelial dysfunction precedes and is a potential mediator of diabetic platelet dysfunction.
    Irish Journal of Medical Science 01/2002; 171:45-45. · 0.51 Impact Factor

Publication Stats

645 Citations
161.44 Total Impact Points

Institutions

  • 1994–2011
    • Beaumont Hospital
      Dublin, Leinster, Ireland
    • Philadelphia University
      Philadelphia, Pennsylvania, United States
    • The Adelaide and Meath Hospital Ireland
      Dublin, Leinster, Ireland
  • 2008
    • Connolly Hospital Blanchardstown
      Dublin, Leinster, Ireland
  • 1991–2008
    • Royal College of Surgeons in Ireland
      • • Department of Surgery
      • • Department of Anatomy
      Dublin, Leinster, Ireland
    • University of Pennsylvania
      • Department of Surgery
      Philadelphia, PA, United States
  • 1997
    • Waterford Regional Hospital
      Waterford, Munster, Ireland
  • 1991–1993
    • Hospital of the University of Pennsylvania
      • Department of Surgery
      Philadelphia, PA, United States