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        <title>Journal of Medical Case Reports - Most accessed articles</title>
        <link>http://www.jmedicalcasereports.com</link>
        <description>The most accessed research articles published by Journal of Medical Case Reports</description>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.jmedicalcasereports.com/content/6/1/106" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/106">
        <title>Vancomycin-induced Henoch-Schonlein purpura: a case report</title>
        <description>IntroductionHenoch-Sch&#246;nlein purpura is a small-vessel systemic vasculitis. Although its exact pathophysiology remains unknown, Henoch-Sch&#246;nlein purpura has been reported in association with various medical conditions including hypersensitivity. We report the case of a patient with vancomycin-induced Henoch-Sch&#246;nlein purpura.Case presentationA 42-year-old Caucasian man who had previously undergone a heart transplant was diagnosed as having an intra-abdominal abscess after he underwent a Hartmann procedure. At 15 days after initiation of antibiotic therapy including vancomycin, he developed a purpuric rash of the lower limbs, arthralgia, and macroscopic hematuria. At that time, our patient was already on hemodialysis for end-stage renal disease. Henoch-Sch&#246;nlein purpura was diagnosed. After a second 15-day course of vancomycin, a second flare of Henoch-Sch&#246;nlein purpura occurred. Skin biopsies showed leucocytoclastic vasculitis with IgA deposits and eosinophils in the peri-capillary inflammatory infiltrate, suggesting an allergic mechanism. After vancomycin was stopped, we did not observe any further flares. Only five cases of isolated cutaneous vasculitis, one case of lupus-like syndrome and one case of Henoch-Sch&#246;nlein purpura after vancomycin treatment have been described to date in the literature.
Conclusions:
Clinicians should be aware that systemic vasculitis can be induced by some treatments. Vancomycin is a widely prescribed antibiotic. Occurrence of rare but serious Henoch-Sch&#246;nlein purpura associated with vancomycin requires its prompt discontinuation.</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/106</link>
                <dc:creator>Stanislas Bataille</dc:creator>
                <dc:creator>Aurelie Daumas</dc:creator>
                <dc:creator>Anne Marie Tasei</dc:creator>
                <dc:creator>Noemie Jourde Chiche</dc:creator>
                <dc:creator>Bertrand Dussol</dc:creator>
                <dc:creator>Stephane Burtey</dc:creator>
                <dc:creator>Solene Taugourdeau</dc:creator>
                <dc:creator>Yvon Berland</dc:creator>
                <dc:creator>Laurent Chiche</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:106</dc:source>
        <dc:date>2012-04-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-106</dc:identifier>
                            <dc:title>Severe Henoch-Schonlein purpura associated with Vancomycin</dc:title>
                            <dc:description>Henoch-Schonlein purpura, a systemic vasculitis effecting the skin, joints and kidneys in a patient treated with common antibiotic Vancomycin; the second reported case of this potentially serious side effect.</dc:description>
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        <prism:issn>1752-1947</prism:issn>
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        <prism:startingPage>106</prism:startingPage>
        <prism:publicationDate>2012-04-10T00:00:00Z</prism:publicationDate>
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        <title>Responsiveness of a patient in a persistent vegetative state after a coma to weekly injections of autologous activated immune cells: a case report</title>
        <description>IntroductionAn 82-year-old Caucasian woman had remained in a persistent vegetative state after a coma of seven months duration, which occurred after a stroke with hemiplegia, nine years previously. The persistent vegetative state could be reversed in part by weekly injections with activated immune cells. After therapy, our patient responded to commands in addition to regaining spontaneous movements of both arms and the ability to swallow. This is the first report on the treatment with activated immune cells of a patient in a persistent vegetative state after a coma.Case presentationAn 82-year-old Caucasian woman presented with a persistent vegetative state subsequent to a coma. She retained respiratory and autonomic functions. As contact was not possible, physiotherapy was passive. Her skin was yellowish, and our patient did not move by herself. Vomiting repeatedly resulted from tube feeding. After a once-weekly treatment with activated immune cells sampled from our patient&apos;s blood and activated in vitro, several of her functions gradually returned. Our patient opened her eyes in the requested direction and turned her head toward people entering the room. She &apos;supported&apos; nursing efforts, as the nurse noted a loss of spastic motions. The strength in both her arms returned, and she spontaneously moved her arm on the side experiencing hemiplegia. After three months, our patient could stick out her tongue upon demand. Finally, the swallow reflexes of our patient started to return. However, tube feeding was continued, and our patient died after aspiration of vomit following a feeding.
Conclusion:
The success of treatment with autologous activated immune cells in this patient may have resulted from the production of neuroactive substances, such as neurotrophin-3 and brain-derived neurotrophic factor, by activated immune cells. The deterioration of our patient could be reversed, as demonstrated by the restoration of motor strength in her hemiplegic side. In addition, our patient was able to induce motor responses upon request. It seems reasonable to conclude that activated immune cells may improve the chronic vegetative state in some patients.</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/6</link>
                <dc:creator>Barbara Fellerhoff</dc:creator>
                <dc:creator>Barbara Laumbacher</dc:creator>
                <dc:creator>Rudolf Wank</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:6</dc:source>
        <dc:date>2012-01-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-6</dc:identifier>
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        <prism:issn>1752-1947</prism:issn>
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        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2012-01-10T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/112">
        <title>Fabry disease presenting with sudden hearing loss and otosclerosis: a case report</title>
        <description>IntroductionFabry disease is an X-linked lysosomal storage disorder resulting in a multiple-system disorder with a wide spectrum of physical signs and symptoms, predominantly affecting the central and peripheral nervous systems, skin, heart, kidneys, and eyes.Case presentationWe describe the case of a 26-year-old European Caucasian man who had Fabry disease and who presented with episodic sudden unilateral hearing loss and was treated with glucocorticoids, pentoxifylline, hyperbaric oxygen, and fluoride because of concomitant audiometric evidence of otosclerosis. This case demonstrates the partial and transient beneficial effect of standard treatment for sudden hearing loss not related to Fabry disease and analyzes the possible connection between typical Fabry disease inner-ear lesions and otosclerosis. Whereas hearing loss has been described in connection with Fabry disease, otosclerosis-associated hearing loss in Fabry disease has not yet been described.
Conclusions:
Although progressive hearing loss in patients with Fabry disease seems to be influenced by replacement therapy, few data concerning treatment of sudden hearing loss are available. The lack of literature concerning the pathogenesis of the otological involvement in Fabry disease makes it impossible to identify a connection between the latter and otosclerosis. Therefore, this report may help to reinforce the importance of a thorough evaluation of hearing in patients with Fabry disease and may be of help with therapeutic decision-making.</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/112</link>
                <dc:creator>Giovanni Felisati</dc:creator>
                <dc:creator>Elisabetta Salvatici</dc:creator>
                <dc:creator>Carlotta Pipolo</dc:creator>
                <dc:creator>Sara Portaleone</dc:creator>
                <dc:creator>Enrica Riva</dc:creator>
                <dc:creator>Marcello Giovannini</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:112</dc:source>
        <dc:date>2012-04-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-112</dc:identifier>
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        <prism:issn>1752-1947</prism:issn>
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        <prism:startingPage>112</prism:startingPage>
        <prism:publicationDate>2012-04-16T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/122">
        <title>A 43 year old woman on Triptorelin presenting with Pseudotumor Cerebri - A Case Report</title>
        <description>IntroductionTo our knowledge, this is the first time Triptorelin has been reported to cause BIH.Case presentationA 43 years old Caucasian woman who suffered from chronic menorrhagia was commenced on Triptorelin, a gonadotrophin releasing hormone (GnRH) analogue. Three days later, she developed gradually worsening headaches accompanied by bilateral visual disturbances. Examination revealed bilateral papilledema and enlarged blind spots on visual fields. A diagnosis of benign intracranial hypertension (BIH) was made confirmed on MRI scan.
Conclusion:
We recommend that the high risk patients (female overweight patients of reproductive age group) who are using any GnRH analogue (e.g. Triptorelin) should be periodically monitored for the possible development of BIH.Keywordsbenign intracranial hypertension, pseudotumor cerebri, GnRH analogue, Triptorelin</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/122</link>
                <dc:creator>Uday Kumar Bhatt</dc:creator>
                <dc:creator>Imran Haq</dc:creator>
                <dc:creator>Venkata Avadhanam</dc:creator>
                <dc:creator>Kim Bibby</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:122</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-122</dc:identifier>
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                <prism:publicationName>Journal of Medical Case Reports</prism:publicationName>
        <prism:issn>1752-1947</prism:issn>
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        <prism:startingPage>122</prism:startingPage>
        <prism:publicationDate>2012-05-03T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/121">
        <title>Capsule impaction presenting as acute small bowel perforation: a cases series.</title>
        <description>IntroductionPerforation  caused by CE impaction is extremely rare and, at present, only 5 cases of perforation from CE impaction are reported in the literature.Case presentationWe report here 2 cases of patients with undiagnosed small bowel stenosis presenting acute perforation after CE. Strictures in the small bowel were likely the inciting mechanism leading to acute SB obstruction and subsequent distension and perforation above the capsule in the area of maximal serosal  tension.Case 1 was a 55-years-old Italian woman who underwent CE because of recurrent  postprandial cramping pain and iron deficiency anemia, in the setting of negative abdominal US,  upper endoscopy, colonoscopy,  and small bowel follow-through radiograph. She developed a symptomatic bowel obstruction approximately 36 hours after ingestion of CE. Emergent surgery was performed to remove the capsule, which was impacted at a previously undiagnosed structuring ileal adenocarcinoma leading to perforation.Case 2 was a 60-year-old Italian male with recurrent episodes of abdominal pain and diarrhea who underwent CE after conventional modalities, including  comprehensive blood and stool studies, CT, abdominal ultrasound, upper endoscopy,  colonoscopy, barium enema, and small bowel follow-through, were not diagnostic. The patient developed abdominal distension,  acute periumbilical pain, fever and leukocytosis 20 hours after capsule ingestion. Emergent surgery was performed to remove the capsule, which was impacted at a previously undiagnosed ileal Crohn&apos;s stricture leading to perforation.
Conclusions:
The present report shows that although the risk of acute complication is very low, the patient should be informed of the risks involved in capsule endoscopy, including the need for emergency surgical exploration</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/121</link>
                <dc:creator>Giovanni De Palma</dc:creator>
                <dc:creator>Stefania Masone</dc:creator>
                <dc:creator>Marcello Persico</dc:creator>
                <dc:creator>Saverio Siciliano</dc:creator>
                <dc:creator>Francesca Salvatori</dc:creator>
                <dc:creator>Francesco Maione</dc:creator>
                <dc:creator>Dario Esposito</dc:creator>
                <dc:creator>Giovanni Persico</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:121</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-121</dc:identifier>
                                <prism:require>/content/figures/1752-1947-6-121-toc.gif</prism:require>
                <prism:publicationName>Journal of Medical Case Reports</prism:publicationName>
        <prism:issn>1752-1947</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>121</prism:startingPage>
        <prism:publicationDate>2012-05-03T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/1/1/126">
        <title>Metformin induced lactic acidosis: two case reports </title>
        <description>IntroductionUnlike other agents used in the treatment of type 2 diabetes mellitus, metformin has been shown to reduce mortality in obese patients. It is therefore being increasingly used in higher doses. The major concern of many physicians is a possible risk of lactic acidosis. The reported frequency of metformin related lactic acidosis is 0.05 per 1000 patient-years; some authors advocate that this rate is equal in those patients not taking metformin.Case presentationWe present two case reports of metformin-associated lactic acidosis. The first case is a 77 year old female with a past medical history of hypertension and type 2 diabetes mellitus who had recently been prescribed metformin (3 g/day), perindopril and acetylsalicylic acid. She was admitted to the emergency department two weeks later with abdominal pain and psychomotor agitation. Physical examination revealed only signs of poor perfusion. Laboratory evaluation revealed hyperkalemia, elevated creatinine and blood urea nitrogen and mild leukocytosis. Arterial blood gases showed severe lactic acidemia. She was admitted to the intensive care unit. Vasopressor and ventilatory support was initiated and continuous venovenous hemodiafiltration was instituted. Twenty-four hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the sixth day. The second patient is a 69 year old male with a past medical history of hypertension, type 2 diabetes mellitus and ischemic heart disease who was on metformin (4 g/day), glycazide, acetylsalicylic acid and isosorbide dinitrate. He was admitted to the emergency department in shock with extreme bradycardia. Initial evaluation revealed severe lactic acidosis and elevated creatinine and urea. The patient was admitted to the Intensive Care Unit and commenced on continuous venovenous hemodiafiltration in addition to other supportive measures. A progressive recovery was observed and he was discharged from the intensive care unit on the seventh day.
Conclusion:
We present two case reports of severe lactic acidosis most probably associated with high doses of metformin in patients with no known contraindications for metformin prescription. In both patients no other condition was identified to cause such severe lactic acidosis. Although controversial, lactic acidosis should be considered in patients taking metformin.</description>
        <link>http://www.jmedicalcasereports.com/content/1/1/126</link>
                <dc:creator>J Silvestre</dc:creator>
                <dc:creator>S Carvalho</dc:creator>
                <dc:creator>V Mendes</dc:creator>
                <dc:creator>L Coelho</dc:creator>
                <dc:creator>C Tapadinhas</dc:creator>
                <dc:creator>P Ferreira</dc:creator>
                <dc:creator>P Povoa</dc:creator>
                <dc:creator>F Ceia</dc:creator>
                <dc:source>Journal of Medical Case Reports 2007, null:126</dc:source>
        <dc:date>2007-10-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-1-126</dc:identifier>
                                <prism:require>/content/figures/1752-1947-1-126-toc.gif</prism:require>
                <prism:publicationName>Journal of Medical Case Reports</prism:publicationName>
        <prism:issn>1752-1947</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>126</prism:startingPage>
        <prism:publicationDate>2007-10-31T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/118">
        <title>Small-bowel necrosis complicating a cytomegalovirus-induced superior mesenteric vein thrombosis in an immunocompetent patient: a case report</title>
        <description>IntroductionSuperior mesenteric venous thrombosis as a result of acute cytomegalovirus infection is rare, with only a few cases reported in the literature.Case presentationWe present the case of a 40-year-old Caucasian man who was admitted to our hospital with a 5-day history of fever. His serological test and pp65 antigen detection of cytomegalovirus were positive, suggesting acute infection. On the sixth day after his admission, the patient complained of acute, progressive abdominal pain. Abdominal computed tomography revealed acute superior mesenteric venous thrombosis. An emergency laparotomy showed diffuse edema and ischemic lesions of the small bowel and its associated mesentery with a 50-cm-long segmental infarction of the proximal jejunum. An extensive enterectomy of about 100cm of jejunum that included the necrotic segment was performed, followed by an end-to-end anastomosis. Anti-coagulation therapy was administered pre-operatively in the form of small-fractionated heparin and continued postoperatively. The patient had an uneventful recovery and was discharged on the 11th postoperative day.
Conclusion:
Acute cytomegalovirus infection can contribute to the occurrence of mesenteric venous thrombosis in immunocompetent patients. It is important for physicians and internists to be aware of the possible thrombotic complications of cytomegalovirus infection. A high level of clinical suspicion is essential to successfully treat a potentially lethal condition such as superior mesenteric venous thrombosis.</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/118</link>
                <dc:creator>John Kalaitzis</dc:creator>
                <dc:creator>Paris Basioukas</dc:creator>
                <dc:creator>Evagelia Karzi</dc:creator>
                <dc:creator>Charalampos Markakis</dc:creator>
                <dc:creator>Emmanouil Liarmakopoulos</dc:creator>
                <dc:creator>Andreas Hadjimarkou</dc:creator>
                <dc:creator>Spyros Rizos</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:118</dc:source>
        <dc:date>2012-04-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-118</dc:identifier>
                                <prism:require>/content/figures/1752-1947-6-118-toc.gif</prism:require>
                <prism:publicationName>Journal of Medical Case Reports</prism:publicationName>
        <prism:issn>1752-1947</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>118</prism:startingPage>
        <prism:publicationDate>2012-04-24T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/6/1/111">
        <title>Stent implantation for a totally occluded right coronary artery in a 6-year-old boy after Kawasaki disease: a case report</title>
        <description>IntroductionCoronary stenting has previously been considered to be less feasible in children under 12 years old due to the limitation of vascular access. We report the case of a six-year-old boy who successfully underwent stent implantation for his totally occluded right coronary artery.Case presentationA Taiwanese boy aged six years and nine months old was found to have giant aneurysms after an acute episode of Kawasaki disease. An angiography revealed that his middle right coronary artery was totally occluded. A 0.014-inch guidewire was advanced to cross the totally occluded site. After pre-dilating the middle portion of his right coronary artery with a 1.5 mm balloon, stenting of his right coronary artery was accomplished using a 2.5 &#215; 28 mm and a 2.5 &#215; 18 mm bare metal stent. A final angiography demonstrated no residual stenosis or dissection.
Conclusion:
Coronary stenting could be a therapeutic option for children as young as six years old. Close follow-up is mandatory because the long-term outcome is still unclear, especially in a small child.</description>
        <link>http://www.jmedicalcasereports.com/content/6/1/111</link>
                <dc:creator>Ya-Chi Hsu</dc:creator>
                <dc:creator>Kae-Woei Liang</dc:creator>
                <dc:creator>Ming-Chih Lin</dc:creator>
                <dc:creator>Yun-Ching Fu</dc:creator>
                <dc:creator>Sheng-Ling Jan</dc:creator>
                <dc:source>Journal of Medical Case Reports 2012, null:111</dc:source>
        <dc:date>2012-04-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-6-111</dc:identifier>
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        <prism:startingPage>111</prism:startingPage>
        <prism:publicationDate>2012-04-16T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.jmedicalcasereports.com/content/2/1/166">
        <title>Pancreas divisum and duodenal diverticula as two causes of acute or chronic pancreatitis that should not be overlooked: a case report
</title>
        <description>IntroductionPancreas divisum is a congenital anatomical anomaly characterized by the lack of fusion of the ventral and dorsal parts of the pancreas during the eighth week of fetal development. This condition is found in 5% to 14% of the general population. In pancreas divisum, the increased incidence of acute and chronic pancreatitis is caused by inadequate drainage of secretions from the body, tail and part of the pancreatic head through an orifice that is too small. The incidence of diverticula in the second part of the duodenum is found in approximately 20% of the population. Compression of the duodenal diverticula at the end of the common bile duct leads to the formation of biliary lithiasis (a principal cause of acute pancreatitis), pain associated with biliary lithiasis owing to compression of the common bile duct (at times with jaundice), and compression of the last part of Wirsung&apos;s duct or the hepatopancreatic ampulla (ampulla of Vater) that may lead to both acute and chronic pancreatitis.Case presentationWe describe the radiological findings of the case of a 75-year-old man with recurrent acute pancreatitis due to a combination of pancreas divisum and duodenal diverticula.
Conclusion:
Magnetic resonance cholangiopancreatography is advisable in patients with recurrent pancreatitis (both acute and chronic) since it is the most appropriate noninvasive treatment for the study of the pancreatic system (and the eventual presence of pancreas divisum) and the biliary systems (eventual presence of biliary microlithiasis). Moreover, it can lead to the diagnostic suspicion of duodenal diverticula, which can be confirmed through duodenography with X-ray or computed tomography scan with a radio-opaque contrast agent administered orally.</description>
        <link>http://www.jmedicalcasereports.com/content/2/1/166</link>
                <dc:creator>Massimo De Filippo</dc:creator>
                <dc:creator>Emiliano Giudici</dc:creator>
                <dc:creator>Nicola Sverzellati</dc:creator>
                <dc:creator>Maurizio Zompatori</dc:creator>
                <dc:source>Journal of Medical Case Reports 2008, null:166</dc:source>
        <dc:date>2008-05-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-2-166</dc:identifier>
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        <prism:startingPage>166</prism:startingPage>
        <prism:publicationDate>2008-05-19T00:00:00Z</prism:publicationDate>
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        <title>Enterobacter cloacae infection of an expanded polytetrafluoroethylene femoral-popliteal bypass graft: a case report</title>
        <description>IntroductionEnterobacter cloacae infections are common among burn victims, immunocompromised patients, and patients with malignancy. Most commonly these infections are manifested as nosocomial urinary tract or pulmonary infections. Nosocomial outbreaks have also been associated with colonization of certain surgical equipment and operative cleaning solutions. Infections of an aortobifemoral prosthesis, an aortic graft, and arteriovenous fistulae are noted in the literature. To our knowledge, this is the first isolated account of an E. cloacae infection of a femoral-popliteal expanded polytetrafluoroethylene bypass graft.Case presentationA 68-year-old Caucasian man presented with fever and rest pain in the right lower extremity five months after the placement of a vascular expanded polytetrafluoroethylene graft for femoral-popliteal bypass. Computed tomography angiography demonstrated peri-graft fluid that was aspirated percutaneously with image guidance and cultured to reveal E. cloacae. The graft was revised and then removed. The patient completed a six-week course of ceftazidime and is currently without signs of infection. There were no other reports of E. cloacae graft infections in any patients receiving treatment in the same surgical suite within a month of this report.
Conclusion:
Isolated cases of E. cloacae infection of surgical bypass grafts are rare (unique in this setting). Clinicians should have a high index of suspicion for device contamination in such cases and should consider testing for possible microbial reservoirs. Graft removal is required due to the formation of biofilm and the recent emergence of Enterobacteriaceae producing extended-spectrum beta-lactamase in community acquired infections.</description>
        <link>http://www.jmedicalcasereports.com/content/4/1/131</link>
                <dc:creator>Ian Musil</dc:creator>
                <dc:creator>Vanessa Jensen</dc:creator>
                <dc:creator>Jolyon Schilling</dc:creator>
                <dc:creator>Boyd Ashdown</dc:creator>
                <dc:creator>Tyler Kent</dc:creator>
                <dc:source>Journal of Medical Case Reports 2010, null:131</dc:source>
        <dc:date>2010-05-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1752-1947-4-131</dc:identifier>
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        <prism:issn>1752-1947</prism:issn>
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        <prism:startingPage>131</prism:startingPage>
        <prism:publicationDate>2010-05-09T00:00:00Z</prism:publicationDate>
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