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Allen Burke

Publications and source records attributed to Allen Burke.

15 recordsLinked to original sources
PubMed2006

Extra-oral plasmablastic lymphoma: report of a case and review of literature.

Plasmablastic lymphoma (PBL) of the oral cavity is classified as one subtype of diffuse large B-cell lymphoma that is most commonly seen in patients with human immunodeficiency virus infection. We report a rare case of PBL in the anal canal of a 33-year-old man with human immunodeficiency virus infection. The lymphoma cells were positive for CD138 and weakly positive for CD79a. In addition, these cells were also positive for CD10. The neoplastic cells were positive for Epstein-Barr virus and negative for human herpes virus 8. Review of the English medical literature revealed many more cases of extra-oral PBL. We propose that the term plasmablastic lymphoma of the oral cavity in World Health Organization classification be revised to simply plasmablastic lymphoma, which would include both oral and extra-oral PBLs, and the term to define the primary site of the lymphoma (ie, oral cavity) be dropped from the terminology used in World Health Organization classification.

Adult↗
PubMed2006

Review of isolated ascending aortitis: differential diagnosis, including syphilitic, Takayasu's and giant cell aortitis.

The image of tree-barking and proximal aortic root dilatation is firmly entrenched in the minds of practising pathologists as representing syphilis until proven otherwise. We discuss the differential diagnosis of syphilitic aortitis, Takayasu's disease, and giant cell aortitis, with a review of the literature and brief overview of other types of aortitis. As a starting point, we report a case of non-specific, or idiopathic, aortitis with aneurysm that was initially misdiagnosed as syphilitic aortitis. We then review the literature and emphasise the lack of histological data and histopathological criteria for the diagnosis of non-infectious aortitis and the implications for treatment in cases of isolated aortitis. Tree-barking is a non-specific finding in aortitis of any aetiology, and syphilitic aortitis in developed countries is rare. It is still unclear if there are histological features that separate Takayasu's disease and giant cell arteritis. In the majority of patients presenting with aortic root aneurysms, aortitis is an isolated finding not associated with autoimmune disease. Despite a plethora of literature, a histological classification of aortitis has yet to be attempted.

Aged↗
PubMed2006

Sudden cardiac death not related to coronary atherosclerosis.

Sudden cardiac death (SCD) accounts for approximately 300,000 cardiac events in the United States each year, representing an overall incidence of 0.1-0.2% per year. Although the vast majority of these may be attributed to coronary atherosclerosis, a wide variety of nonatherosclerotic-related cardiac diseases have been associated with SCD. This review highlights three general categories of cardiac disease not related to atherosclerosis: the cardiomyopathies, inflammatory myocardial diseases, and ion channel disorders. The important role played by genetics in some of these cardiovascular diseases is presented as well as toxic and drug-related etiologies.

Anti-Arrhythmia Agents↗
PubMed2006

Identification of novel missense mutations of cardiac ryanodine receptor gene in exercise-induced sudden death at autopsy.

Mutations in the cardiac ryanodine type 2 receptor (RyR2) gene are associated with catecholaminergic polymorphic ventricular tachycardia. We hypothesized that these mutations could be detected at autopsy in cases of exercise-triggered sudden death. Fourteen sudden death patients, eight males and six females, were studied at autopsy based on apparent sudden cardiac death, without significant anatomical abnormalities. The coding regions of arrhythmia genes were amplified by polymerase chain reaction and directly sequenced. Three novel RyR2 mutations, R414C, F2331S, and R2401L, were identified in three unrelated patients (two males and one female; mean age at death, 12 +/- 2 years), all performing strenuous activity at the time of death or collapse. These mutations were located in highly conserved regions where arrhythmia-linked RyR2 mutations clustered. Although G269S in the KVLQT1 gene was detected in a female with known family history of syncope and sudden cardiac death, no other mutations were found in any of the 14 cases, and no other mutations was found in 200 controls. The absence of structural cardiac disease in physical activity-induced sudden death and the finding of three novel RyR2 mutations suggest that mutation screening in such cases should include RyR2.

Adolescent↗
PubMed2005

Role of SCN5A Y1102 polymorphism in sudden cardiac death in blacks.

BACKGROUND: The Y1102 polymorphism of the cardiac sodium channel (SCN5A) gene has been found in 13% of black Americans. It has been linked to lethal arrhythmias in black families with ventricular tachycardia. The prevalence of the Y1102 polymorphism in a series of sudden death in blacks is unknown. METHODS AND RESULTS: We investigated the incidence of the Y1102 polymorphism in a series of 289 sudden deaths in blacks by sequencing an amplified segment of DNA that contained the polymorphic site extracted from prospectively sampled frozen splenic tissue. The deaths were classified as noncardiac controls (n=107), cardiac arrhythmias with clear anatomic substrate (n=117), cardiac arrhythmias with no anatomic substrate except mild to moderate cardiac hypertrophy (n=40), and unexplained cardiac arrhythmias (n=25). Cause of death was determined after complete forensic autopsy and postmortem cardiac examination. The overall frequency of the Y1102 polymorphism was 9.0%. The frequency was 5.6% in noncardiac deaths, 4.3% in cardiac deaths with obvious anatomic substrate, 20.0% in arrhythmias with moderate hypertrophy, and 28% in unexplained arrhythmias. Adjusted for age and sex, the relative risk of an unexplained arrhythmic death was 8.4 (95% CI 2.1 to 28.6, P=0.001) with the Y1102 allele compared with noncardiac deaths. The relative risk for cardiac arrhythmias with mild cardiac hypertrophy was 4.9 (95% CI 1.3 to 13.4, P=0.01). CONCLUSIONS: The Y1102 allele is a risk factor in blacks for sudden cardiac death in the absence of obvious morphological findings or mild to moderate cardiomegaly.

Adolescent↗
PubMed2005

Left ventricular noncompaction: a pathological study of 14 cases.

Left ventricular noncompaction (LVNC) has been recently proposed as a specific form of cardiomyopathy. There have been few pathological series describing gross and microscopic findings of this entity, especially in children. We present findings of 14 hearts (13 autopsy and 1 explant) with LVNC (isolated and associated with congenital heart disease), defined by poorly developed left ventricular (LV) papillary muscles and a noncompact inner LV myocardial layer comprising more than 50% of the LV thickness. The mean age at death/explant was 3.6 years (median, 2.5 months); there were 6 boys and 8 girls. The symptoms were sudden unexpected death (10) and heart failure (4). The diagnosis was suspected before death in only 1 of 13 autopsy cases. Right ventricular involvement (> 75% ventricular thickness comprised of noncompacted area with recess adjacent to tricuspid valve) was seen in 6 of 14 hearts. One patient had a sibling with pulmonary stenosis, but there was no other known familial cardiomyopathy. Endocardial fibroelastosis was a characteristic histological feature, as well as anastomosing or polypoid endocardial trabeculations, which resulted in staghorn-shaped, endocardial-lined recesses. There was a high rate of other cardiac anomalies, which often coexisted and were not clearly related to the LVNC, present in 8 cases (nonisolated LVNC): ventricular septal defect (4/14), anomalous venous pulmonary veins (1/14), coronary ostial stenosis (1/14), histiocytoid cardiomyopathy (1/14), polyvalvar dysplasia (2/14), and pulmonary stenosis (2/14). In the 6 isolated LVNC, there were 2 malformed atrioventricular valves (1 mitral and 1 tricuspid), which appeared part of the ventricular maldevelopment. There were no differences in histological or gross patterns of the noncompacted regions between the isolated and nonisolated LVNC. LVNC is frequently associated with other cardiac defects, especially when causing sudden death in infants and children. A clear-cut morphological distinction between "isolated" and "secondary" LVNC was not apparent. The pathologist should be aware of the entity because the diagnosis is often first established at autopsy.

Autopsy↗
PubMed2005

Effect of recombinant FVIIa in hypothermic, coagulopathic pigs with liver injuries.

BACKGROUND: Previous experiments with diverse pig models to evaluate the ability of rFVIIa to reduce hemorrhage have provided divergent results. The current study was conducted to address concerns related to previous work by using larger sample sizes, and an extended observational period of 4 hours post-injury. The objectives were to evaluate further the hemostatic efficacy and safety of rFVIIa administration after traumatic, uncontrolled hemorrhage. METHODS: Anesthetized, splenectomized pigs (36.6 +/- 0.3 kg; n = 18/group) underwent an approximately 50% isovolemic blood exchange with 33 degrees C 6% hetastarch, and body temperature was adjusted to 32.5 +/- 0.5 degrees C. Subsequently, a Grade V liver injury was inflicted. After 30 seconds, either vehicle or treatment (180 microg/kg or 720 microg/kg rFVIIa) was administered intravenously as a bolus. Concomitantly, laparotomy pads were packed around the liver. Resuscitation with 33 degrees C lactated Ringer's solution (260 mL/min) was initiated and pigs were monitored for 4 hour post-injury or until death. Tissues were collected and examined histologically to assess the presence of disseminated intravascular coagulation (DIC). RESULTS: Liver injuries were comparable among all groups (p = 0.89). Measures associated with in vitro coagulation (prothrombin time, activated partial thromboplastin time, thromboelastographic split-point and R times) were enhanced by rFVIIa administration (p < 0.05). However, neither percent survival (p = 0.82), survival time (p = 0.56), nor blood loss (p = 0.63) were affected by treatment. DIC was not evident in lung or kidney tissue. CONCLUSIONS: These data indicate an inability of rFVIIa at these doses to reduce blood loss, or to increase survival time or percent survival in this pig model. Absence of DIC provides evidence for safe use of rFVIIa under conditions specific to this study.

Analysis of Variance↗
PubMed2004

Decorin promotes aortic smooth muscle cell calcification and colocalizes to calcified regions in human atherosclerotic lesions.

OBJECTIVE: Ectopic calcification localized to the intima of atherosclerotic plaque is a risk marker for cardiovascular events and increases the risk of aortic dissection during angioplasty. A variety of extracellular matrix molecules such as collagen type 1, bone sialoprotein, and osteopontin are known to regulate the biomineralization of bone and ectopic vascular calcification. In the present study, it was investigated whether decorin, a small leucine-rich proteoglycan expressed in bone and atherosclerotic plaque, is involved in arterial calcification. METHODS AND RESULTS: Calcification was induced in cultured bovine aortic smooth muscle cell (BASMC) by the addition of beta-glycerophosphate or inorganic phosphate. Northern and Western analysis revealed that decorin expression was strongly upregulated in mineralizing BASMC. Furthermore, overexpression of decorin using a retroviral expression vector resulted in a 3- to 4-fold elevation of calcium deposited on the BASMC monolayer. Increased calcification in response to decorin could also be mimicked by adding exogenous decorin to the cultures. In addition, human coronary atherosclerotic lesions taken from sudden-death patients showed marked colocalization of calcium deposits with decorin. CONCLUSIONS: Decorin induces calcification of arterial smooth muscle cell cultures and colocalizes to mineral deposition in human atherosclerotic plaque, suggesting that decorin functions as promoter of intimal calcification.

Animals↗
PubMed2004

Biocompatibility of a xenogenic elastin-based biomaterial in a murine implantation model: the role of aluminum chloride pretreatment.

We have investigated the long-term effect of aluminum chloride (AlCl(3)) treatment on the calcification and inflammatory reaction of a porcine elastin-derived biomaterial (PEB) in a novel subdermal adult mouse model. Untreated PEB disks and PEB treated with AlCl(3) were implanted subdermally in BALB/c mice for 30, 60, and 180 days. The calcification of the elastin disks was examined with histological analysis and atomic absorption analysis of calcium content. The inflammatory reaction was evaluated both with histological analysis of explants and by an enzyme-linked immunosorbent assay of the serum in each mouse to determine the production of antielastin antibodies. Robust calcification was evident in all untreated PEBs with calcium levels of 107.1 +/- 11.8, 151.4 +/- 14.4, and 227.2 +/- 23.8 microg/mg for 30, 60, and 180 days, respectively. AlCl(3) treatment only temporarily prevented the calcification of the elastin disks for 30 days. By 60 and 180 days, the AlCl(3)-treated materials had significant calcification with 88.7 +/- 17.4 and 105.3 +/- 27.0 microg/mg calcium, respectively. The inflammatory reaction was moderate for both types of implants. The AlCl(3)-treated implants displayed significantly more macrophage and lymphocyte infiltration at 180 days after implantation, and a trend to higher humoral responses at 30 and 60 days when compared with untreated PEBs. We conclude that PEBs extensively calcify in the adult mice model. AlCl(3) treatment of elastin enhances the long-term immunological response to xenogenic elastin implants and merely delays the onset of calcification.

Aluminum Chloride↗
PubMed2004

Optimal dye concentration and irradiance for laser-assisted vascular anastomosis.

OBJECTIVE: This investigation was done in order to find optimal indocyanine green (ICG) concentration and energy irradiance in laser vascular welding. BACKGROUND DATA: Many studies have shown that laser tissue welding with albumin solder/ICG may be an effective technique in surgical reconstruction. However, there are few reports regarding optimal laser settings and concentrations of ICG within the albumin solder in laser-assisted vascular anastomosis. MATERIALS AND METHODS: Porcine carotid artery strips (n = 120) were welded in end-to-end by diode laser with 50% albumin solder of 0.01, 0.1, and 1.0 mM ICG at irradiance of 27.7, 56.7, and 76.9 W/cm(2), respectively. Temperature was measured by inserting thermocouples outside and inside the vessel. Tensile strength and histology were studied. RESULTS: Temperature and strength of the anastomosis significantly decreased (all p < 0.05) with increasing ICG concentration at 56.7 W/cm(2). Histological study showed minimal thermal injury limited to adventitia and no appreciable difference between all groups. CONCLUSIONS: ICG concentration within solder is the most important factor affecting both vascular temperature and tensile strength. The optimal balance between strength and minimal thermal injury may be achieved primarily at 56.7 W/cm(2) and 0.01 mM ICG.

Anastomosis, Surgical↗
PubMed2003

From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II.

Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

Animals↗
PubMed2003

From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.

Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

Acute Disease↗
PubMed2003

Gastrointestinal stromal tumors, intramural leiomyomas, and leiomyosarcomas in the duodenum: a clinicopathologic, immunohistochemical, and molecular genetic study of 167 cases.

In this study we analyzed the clinicopathologic features of duodenal smooth muscle or stromal tumors, including 156 GISTs, 6 leiomyomas (LMs), and 5 leiomyosarcomas (LMSs) from the files of the Armed Forces Institute of Pathology and the Haartman Institute of the University of Helsinki. GISTs were documented as KIT positive (n = 109); 47 tumors were also included because of their histologic identity to KIT-positive cases. GIST-specific c-kit gene mutations were documented in exon 11 in 9 of 30 cases (30%) and exon 9 in 4 of 30 cases (13%). The GISTs occurred in patients with an age range of 10-88 years (median 56 years); 54% were male. Ten patients had neurofibromatosis type I; six of them had multiple GISTs. The GISTs ranged from small asymptomatic intramural or external nodules to large masses that extended into the retroperitoneum (median size 4.5 cm). They were mostly spindle cell tumors; three malignant GISTs had an epithelioid morphology, and 81 cases had skeinoid fibers. The tumors often coexpressed CD34 and KIT (54%) and were variably positive for smooth muscle actin (39%) and S-100 protein (20%) but never for desmin. A total of 86% of patients with tumors >5 cm with >5 mitoses/50 high power fields (HPF) (n = 21) died of disease, whereas no tumor <2 cm with <5 mitoses/50 HPF (n = 12) recurred or caused death. Long latency was common between primary operation and recurrences or metastases; either one occurred in 49 of 140 patients with follow-up (35%). No formula could accurately predict metastases, which occasionally developed even if mitotic activity was <5/50 HPF and size <5 cm. Metastases were in the abdominal cavity, liver, and rarely in bones and lungs but never in lymph nodes. Four actin- and desmin-positive and KIT-negative benign intramural LMs were similar to those more often seen in the esophagus. There were five LMSs, one of which formed a polypoid intraluminal mass; all were actin positive and KIT negative. The great majority of duodenal mesenchymal tumors are GISTs, which have a spectrum from small indolent tumors to overt sarcomas. LMs and LMSs are rare.

Adolescent↗
PubMedDate not supplied

Takayasu aortitis with acute dissection and hemopericardium.

We report a case of a 57-year-old woman with an unremarkable past medical history who presented to the emergency department with maxillary pain that later radiated to the chest. She died less than 12 h after admission. CT findings were consistent with ascending aorta dissection with hemopericardium. Autopsy revealed a tear immediately proximal to the ostium of the brachiocephalic artery and a dissecting flap with false lumen, rupture, and hemopericardium. Histologically, there was a zonal medial necrosis with surrounding chronic inflammation, focal destruction of the media, and fibrosis of the intima and adventitia. A diagnosis of granulomatous necrotizing aortitis of Takayasu type was made. This case demonstrates a rare example of aortitis underlying aortic dissection and emphasizes the need for careful histologic examination in cases of aortic root disease.

Aortic Dissection↗