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Vascular Abnormalities (vascular + abnormality)

Distribution by Scientific Domains

Medical Sciences	75%
Life Sciences	20%

Distribution within Medical Sciences

Dermatology	20%
Hepatology	13%

Selected Abstracts

Protein kinase C and the development of diabetic vascular complications

DIABETIC MEDICINE, Issue 12 2001
K. J. Way
Abstract Hyperglycemic control in diabetes is key to preventing the development and progression of vascular complications such as retinopathy, nephropathy and neuropathy. Increased activation of the diacylglycerol (DAG)-protein kinase C (PKC) signal transduction pathway has been identified in vascular tissues from diabetic animals, and in vascular cells exposed to elevated glucose. Vascular abnormalities associated with glucose-induced PKC activation leading to increased synthesis of DAG include altered vascular blood flow, extracellular matrix deposition, basement membrane thickening, increased permeability and neovascularization. Preferential activation of the PKC, isoform by elevated glucose is reported to occur in a variety of vascular tissues. This has lead to the development of LY333531, a PKC, isoform specific inhibitor, which has shown potential in animal models to be an orally effective and nontoxic therapy able to produce significant improvements in diabetic retinopathy, nephropathy, neuropathy and cardiac dysfunction. Additionally, the antioxidant vitamin E has been identified as an inhibitor of the DAG-PKC pathway, and shows promise in reducing vascular complications in animal models of diabetes. Given the overwhelming evidence indicating a role for PKC activation in contributing to the development of diabetic vascular complications, pharmacological therapies that can modulate this pathway, particularly with PKC isoform selectivity, show great promise for treatment of vascular complications, even in the presence of hyperglycemia. Diabet. Med. 18, 945,959 (2001) [source]

Impaired lymphangiogenesis due to excess vascular endothelial growth factor-D/Flt-4 signalling in the skin of patients with systemic sclerosis

BRITISH JOURNAL OF DERMATOLOGY, Issue 4 2010
N. Honda
Summary Background, Vascular abnormalities are one of the primary pathological components of systemic sclerosis (SSc). However, it has not been determined if there are also abnormalities in the formation of lymphatic vessels in SSc. Objective, To evaluate lymphangiogenic activity in SSc skin. Methods, The numbers of D2-40-positive lymphatic vessels in skin specimens from healthy control subjects and patients with SSc were counted and compared. Quantitative real-time polymerase chain reaction (PCR) was performed to determine mRNA levels of vascular endothelial growth factor (VEGF)-D and Flt-4 (fms-related tyrosine kinase 4, VEGFR-3, one of the receptors for VEGF-D) in the skin. Serum VEGF-D levels were measured with specific enzyme-linked immunosorbent assays. Results, The number of lymphatic vessels in patients with SSc was significantly decreased compared with healthy control subjects. Mean relative transcript levels of FIGF (VEGF-D) and FLT4 (Flt-4) in skin tissue from patients with SSc were significantly increased compared with healthy control subjects. By the analysis of the association between serum VEGF-D levels and the clinical or laboratory features, we found that patients with SSc with higher serum VEGF-D levels more frequently have skin ulcers than those with normal VEGF-D levels. Conclusions, A systemic increase of VEGF-D, as well as local overexpression of FIGF and FLT4, may be the cause of disturbed lymphangiogenesis in SSc skin and play a role in the pathogenesis of SSc. We showed the possibility that regulation of VEGF-D/Flt-4 signalling could lead to new treatment of skin ulcers in SSc by controlling the formation of lymphatic vessels. [source]

Late hepatic allograft dysfunction

LIVER TRANSPLANTATION, Issue 11B 2001
Professor of Medicine Russell H. Wiesner MD
Key Points 1Lifelong monitoring of graft function, immunosuppressive levels, and screening for drug toxicity is required in all liver recipients. 2Late hepatic allograft dysfunction is common and is caused by a variety of etiologies including rejection, infection, biliary/vascular abnormalities, recurrence of disease, and drug hepatotoxicity. 3In all patients with late hepatic allograft dysfunction, liver biopsy should be performed to assess for the presence of rejection, and to thus avoid excessive use of bolus corticosteroid therapy and guide appropriate immunosuppressive management. 4Recurrence of disease is the most common cause of late hepatic allograft dysfunction. 5Hepatitis C universally reinfects the hepatic allograft, and is associated with decreased patient and graft survival and leads to the recurrence of cirrhosis in 28% of patients within 5 years of transplantation. 6Major advances have been made in preventing recurrence of hepatitis B by the use of hepatitis B immune globulin in combination with lamivudine therapy. 7Autoimmune liver diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis have a recurrence rate of approximately 20% to 30%. 8In patients developing recurrence of autoimmune hepatitis, steroid withdrawal is the most common cause. 9Recurrent hepatocellular cancer can be markedly reduced if strict guidelines are adhered to in selecting patients. 10Drug hepatotoxicity must always be considered in the differential diagnosis of late hepatic allograft dysfunction. [source]

Characterization of the cardiac phenotype in neonatal Ts65Dn mice

DEVELOPMENTAL DYNAMICS, Issue 2 2008
Austin D. Williams
Abstract The Ts65Dn mouse is the most-studied of murine models for Down syndrome. Homology between the triplicated murine genes and those on human chromosome 21 correlates with shared anomalies of Ts65Dn mice and Down syndrome patients, including congenital heart defects. Lethality is associated with inheritance of the T65Dn chromosome, and anomalies such as right aortic arch with Kommerell's diverticulum and interrupted aortic arch were found in trisomic neonates. The incidence of gross vascular abnormalities was 17% in the trisomic population. Histological analyses revealed interventricular septal defects and broad foramen ovale, while immunohistochemistry showed abnormal muscle composition in the cardiac valves of trisomic neonates. These findings confirm that the gene imbalance present in Ts65Dn disrupts crucial pathways during cardiac development. The candidate genes for congenital heart defects that are among the 104 triplicated genes in Ts65Dn mice are, therefore, implicated in the dysregulation of normal cardiogenic pathways in this model. Developmental Dynamics 237:426,435, 2008. © 2007 Wiley-Liss, Inc. [source]

Critical role for retinol in the generation/differentiation of angioblasts required for embryonic blood vessel formation,

DEVELOPMENTAL DYNAMICS, Issue 4 2004
Amanda C. LaRue
Abstract Numerous studies demonstrate that vitamin A (retinol) deficiency causes abnormal cardiovascular morphogenesis. We evaluated the impact of retinol deficiency on the regulation of the numbers of endothelial cells and angioblasts (endothelial progenitors) produced during embryonic quail development. At the one-somite stage, there were no discernible differences in the mean number of endothelial cells or angioblasts in normal and retinol-deficient embryos. However, retinol-deficient embryos at the three-somite stage had an increase in the mean number of endothelial cells but no difference in the mean number of angioblasts. By contrast, retinol-deficient embryos at the five-somite stage have 61% of the normal number of endothelial cells and 12% of the normal number of angioblasts. Similarly, retinol-deficient embryos at the 10-somite stage had 71% and 60% of normal numbers of endothelial cells in capillary-like networks and the sinuses venosus, respectively. Furthermore, we show that retinol deficiency did not elicit a global reduction in mesodermal cell numbers but was specific to cells of the endothelial lineage. Taken together, our findings suggest that vascular abnormalities observed under conditions of retinol deficiency are due to reduction in the number of angioblasts and consequently an insufficiency in the number of endothelial cells required to build complex vascular networks. Developmental Dynamics 230:666,674, 2004. © 2004 Wiley-Liss, Inc. [source]

Non-viral gene therapy for diabetic retinopathy

DRUG DEVELOPMENT RESEARCH, Issue 11 2006
*Article first published online: 9 FEB 200, Toshiyuki Oshitari
Abstract Diabetic retinopathy results from vascular abnormalities, such as an increase in the permeability of retinal vessels, and retinal neurodegeneration, which are irreversible changes that occur early in the course of diabetic retinopathy. To block the vascular and neuronal complications associated with the development and progression of diabetic retinopathy, a reasonable strategy would be to prevent the increased vascular permeability and to block the neuronal cell death. The purpose of this review is to present the non-viral strategies being used to block the neurovascular abnormalities and neuronal cell death that are observed in the early stages of diabetic retinopathy in order to prevent the onset or the progression of the diabetic retinopathy. Some of the non-viral gene therapeutic techniques being used are electroporation of selected genes, injections of antisense oligonucleotides, and injections of small interference RNAs. The results obtained by these methods are discussed as is the potential of these therapeutic strategies to prevent the onset or the progression of the neurovascular abnormalities in diabetic retinopathy. Drug Dev. Res. 67:835,841, 2006. © 2007 Wiley-Liss, Inc. [source]

Sural nerve and epidermal vascular abnormalities in a case of POEMS syndrome

EUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2006
L. Santoro
First page of article [source]

Molecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: A role for angiopoietin-1,

HEPATOLOGY, Issue 2 2010
Annette S. H. Gouw
Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion. In addition to features that are predominantly found in either FNH or HCA (e.g., dystrophic vessels in FNH and single arteries in HCA), FNH and HCA share morphological vascular abnormalities such as dilated sinusoids. We hypothesized that these anomalous vascular features are associated with altered expression of growth factors involved in vascular remodeling. This was based on reports of morphologically abnormal hepatic vasculature and nodular lesions in transgenic models of hepatocytic overexpression of angiopoietin-1 (Ang-1), a member of the angiopoietin family, which is crucially involved in vascular morphogenesis and homeostasis. We investigated gene and protein expression of members of the angiopoietin system and vascular endothelial growth factor A (VEGF-A) and its receptors in 9 FNH samples, 13 HCA samples, and 9 histologically normal livers. In comparison with normal samples, a significant increase in Ang-1 was found in FNH (P < 0.01) and HCA (P < 0.05), whereas no significant changes in Ang-2, receptor tyrosine kinase with immunoglobulin-like and EGF-like domains 2, VEGF-A, or vascular endothelial growth factor receptor 2 (VEGFR-2) were observed. Conclusion: Because of the different etiological contexts of a preceding vascular injury in FNH and a neoplastic growth in HCA, Ang-1 might exert different effects on the vasculature in these lesions. In FNH, it could predominantly stimulate recruitment of myofibroblasts and result in dystrophic vessels, whereas in HCA, it may drive vascular remodeling that produces enlarged vessels and arterial sprouting that generates single arteries. Hepatology 2010 [source]

Iron chelation prevents lung injury after major hepatectomy

HEPATOLOGY RESEARCH, Issue 8 2010
Konstantinos Kalimeris
Aim:, Oxidative stress has been implicated in lung injury following ischemia/reperfusion and resection of the liver. We tested whether alleviating oxidative stress with iron chelation could improve lung injury after extended hepatectomy. Methods:, Twelve adult female pigs subjected to liver ischemia for 150 min, 65,70% hepatectomy and reperfusion of the remnant liver for 24 h were randomized to a desferrioxamine (DF) group (n = 6) which received i.v. desferrioxamine to a total dose of 100 mg/kg during both ischemia and reperfusion, and a control (C) group (n = 6). We recorded hemodynamic and respiratory parameters, plasma interleukin-6 and malondialdehyde levels, as well as liver malondialdehyde and protein carbonyls content. Total non-heme iron was measured in lung and liver. Pulmonary tissue was evaluated histologically for its nitrotyrosine and protein carbonyls content and for superoxide dismutase (SOD) and platelet-activating factor acetylhydrolase (PAF-AcH) activities. Results:, Reperfusion of the remnant liver resulted in gradual deterioration of gas-exchange and pulmonary vascular abnormalities. Iron chelation significantly decreased the oxidative markers in plasma, liver and the lung and lowered activities of pulmonary SOD and PAF-AcH. The improved liver function was followed by improved arterial oxygenation and pulmonary vascular resistance. DF also improved alveolar collapse and inflammatory cell infiltration, while serum interleukin-6 increased. Conclusion:, In an experimental pig model that combines liver resection with prolonged ischemia, iron chelation during reperfusion of the remnant liver is associated with improvement of several parameters of oxidative stress, lung injury and arterial oxygenation. [source]

Esophageal Causes of Sudden and Unexpected Death

JOURNAL OF FORENSIC SCIENCES, Issue 2 2006
Roger W. Byard M.D.
ABSTRACT: Gastrointestinal conditions are uncommon causes of sudden and/or unexpected death as compared to cardiovascular diseases, motor vehicle trauma, or suicide, and may involve an array of fatal mechanisms. Lethal esophageal conditions are encountered even less often, the manifestations of which include acute upper airway occlusion from tumors or foreign material, intraluminal hemorrhage from vascular abnormalities, or perforation with fistula formation resulting in hemorrhage and sepsis. When encountered at autopsy, a particular condition may also be a manifestation of a disease that does not primarily involve the esophagus. For this reason, a detailed autopsy investigation is required for evidence of systemic or remote disease when lesions are found within the esophagus. In this report, possible life-threatening esophageal conditions are reviewed with a description of lethal mechanisms, mention of rare associated diseases, and comment on difficulties that may arise at autopsy in the evaluation of such cases. [source]

Hepatopulmonary syndrome and extrahepatic vascular abnormalities

LIVER TRANSPLANTATION, Issue 7 2001
Michael J. Krowka MD
[source]

Review article: Managing bone complications after kidney transplantation

NEPHROLOGY, Issue 4 2009
RAHUL MAINRA
SUMMARY Chronic kidney disease mineral and bone disorder (CKD-MBD) describes the laboratory, bone and vascular abnormalities that exist in patients with CKD stages 3,5D and that may persist after transplantation. Persisting abnormalities of bone turnover and abnormal mineralization, together with bone mineral density (BMD) loss from glucocorticoids, may all predispose to a loss of structural integrity and increased fracture risk in kidney and kidney pancreas recipients. Vitamin D, calcitriol, calcitonin and bisphosphonates have all been used to preserve BMD following transplantation, despite a lack of safety data and the potential for some of these drugs to cause harm. A limited number of post-transplant studies utilizing these drugs have not yet documented improved fracture prevention or fracture-related mortality and have not considered allocation based on risk factors for fracture or markers of bone turnover. Targeted allocation of the available therapies based on a stratification of risk appears warranted. This might be achieved using an algorithm incorporating BMD, X-ray evaluation, laboratory investigations including bone turnover markers and the assessment of standard fracture risk factors at the time of and soon after transplantation. This approach, which is similar to protocols used in the general population, may result in more effective management of patients and fewer adverse effects such as adynamic bone disease. Although BMD is a surrogate for fracture risk in the general population it is not validated in this transplant population. Consequently, such an approach should be confirmed by studies that include bone biopsy data and an evaluation of patient level outcomes. [source]

Early indirect laser photocoagulation to induce regression of retinal vascular abnormalities in incontinentia pigmenti

ACTA OPHTHALMOLOGICA, Issue 2 2010
Figen Batioglu
No abstract is available for this article. [source]

A case of central visual loss in a child due to macular cavernous haemangioma of the retina

ACTA OPHTHALMOLOGICA, Issue 5 2002
Soheila Naftchi
ABSTRACT. Purpose:, To report a case of retinal cavernous haemangioma localized to the fovea. Methods:, Clinical examination, fluorescein angiographic study and magnetic resonance imaging are reported. Results:, A 9-year-old girl presented with acute loss of vision in the right eye. Ophthalmoscopy showed intraretinal bleeding in the macula, while fluorescein angiography showed a lesion typical of a small cavernous retinal haemangioma, localized in the central macula. Family history was negative. Conclusion:, Central cavernous retinal haemangioma is a rare cause of central visual loss and should be distinguished from other retinal vascular abnormalities with more profound systemic implications for the patient. [source]

Stroke in children: inherited and acquired factors and age-related variations in the presentation of 48 paediatric patients

ACTA PAEDIATRICA, Issue 7 2009
Francesca Del Balzo
Abstract Aim:, Stroke is relatively rare in children and the clinical presentation of paediatric stroke is often subtle. Numerous predisposing risk factors are known, and these can be both inherited and acquired. They include cardiac disease, vascular abnormalities, endothelial damage, infectious diseases, collagen tissue diseases, certain inborn errors of metabolism and anticardiolipin antibody, lupus anticoagulant and deficiencies of protein C, protein S, antithrombin or plasminogen. In addition, abnormal activated protein C resistance (or Factor V Leiden), Factor II G20219A variant, and the thermolabile variant of methylenetetrahydrofolate reductase (MTHFR C677T) need to be considered. Methods:, To explore the prevalence of different predisposing conditions in paediatric stroke patients, we evaluated 48 patients, including subjects with ischaemic and haemorrhagic stroke subtypes. Results:, Only 7 out of 48 (14.5%) had no recognizable risk factors: the majority of paediatric stroke patients had pre-existing risk factors that predisposed to the condition. The major genetic risk factor in our series of patients was homozygosity for the MTHFR C677T mutation (7 out of 48 patients); three more patients were found to be heterozygous for the Factor V Leiden mutation. Acquired predisposing conditions were present in 23 out of 48 patients and included pulmunar stenosis, head trauma, hyperlipidaemia and varicella infection. A total of 17 patients had both genetic and acquired predisposing factors. Conclusion:, Our results emphasize that multiple predisposing risk factors commonly predispose to paediatric stroke. In addition, the primary clinical presentation appeared to differ between the older and younger children: hemiparesis was the typical presentation in children <1 year of age while seizure predominated in older children. [source]

Vascular anomalies in Proteus syndrome

CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 3 2004
P. H. Hoeger
Summary Proteus syndrome (PS) is a complex hamartomatous disorder defined by local overgrowth (macrodactyly or hemihypertrophy), subcutaneous tumours and various bone, cutaneous and/or vascular anomalies (VA). VA are manifold in PS, but their prevalence is unknown so far. In order to further characterize PS, we studied the prevalence of VA in 22 PS patients presenting to our outpatient clinic and reviewed 100 PS patients previously reported between 1983 and 2001. The diagnosis of vascular abnormalities was made on clinical grounds and supported with imaging studies and/or histology in 12 and seven patients out of 22, respectively. Thirty-five VA were identified in 22/22 (100%) of our patients, and more than one type of VA were present in 10 of them. Vascular tumours, portwine stains (PWS), and venous anomalies (varicosities, prominent veins) were equally common. A total of 118 VA were previously reported in 70/100 (70%) PS patients; vascular hamartomas were more prevalent (56/118 = 47.5%), whilst PWS (21.2%) and venous anomalies (22.9%) were slightly less common than in our series, but there is the possibility of under-reporting. Unlike Klippel,Trenaunay syndrome, where VA are mostly confined to the hypertrophic limb, major arteriovenous anomalies are rare, and ,,similar to the other hamartomas and naevi observed in PS (pigmentary naevi, epidermal naevi, subcutaneous tumours, exostoses) , VA appear to be distributed at random sites on the body. We conclude that VA are among the most common findings in PS. Their varying type and distribution lend further support to the concept of somatic mosaicism. [source]

Anomalous origin and cervical course of the vertebral artery in the presence of a retroesophageal right subclavian artery

CLINICAL ANATOMY, Issue 4 2004
Valéria Paula Sassoli Fazan
Abstract The vertebral artery is usually described as the first branch of the subclavian artery, originating medial to the scalenus anterior muscle. During its cervical course, the vertebral artery presents a prevertebral segment and then enters the foramen transversarium of the sixth cervical vertebra. We describe a case of an unusual origin and course of the right vertebral artery in a cadaver specimen wherein the right vertebral artery originates from the right common carotid artery at the inferior border of the thyroid gland. In its cervical course the vertebral artery ascends outside and anteriorly to the foramen transversarium of vertebrae C VI to C III, and enters the foramen transversarium of the axis. In the same specimen, a retroesophageal right subclavian artery is also present. These vascular abnormalities are presented for physicians to keep in mind such variations during diagnostic investigation and surgical procedures of the neck. Clin. Anat. 17:354,357, 2004. © 2004 Wiley-Liss, Inc. [source]

Suspected involvement of the X chromosome in placental mesenchymal dysplasia

CONGENITAL ANOMALIES, Issue 4 2002
Masayoshi Arizawa
ABSTRACT, So far, 46 cases of placental mesenchymal dysplasia have been reported worldwide. We encountered 15 cases of placental mesenchymal dysplasia (PMD) including 7 cases delivered in our hospital. The incidence of PMD in our hospital was therefore, 7/30, 758 (0.02%). The PMD had a peculiar appearance. In the gross findings, large placenta with intestine-like dilatation of the vessels on the fetal side was reported. Microscopically, cistern-like dilatation of the stem villi, fetal artery thrombosis, and villous hemorrhage were reported. However, we believe most of these findings are secondary rather than the primary of mesenchymal dysplasia. Therefore, we investigated 15 other cases of mesenchymal dysplasia, and found including vascular abnormality of the stem, intermediate and terminal villi in all case of PMD. The abnormality was observed in the vessels of the periphery of the stem villi and their vessel walls were thin and appeared weak. The intermediate villous vessels were unusual, tangled. The terminal villous abnormalities showed chorangiosis and stromal hyperplasia. These findings are mesenchymal dysplasia origin. Moreover, PMD showed female-predominant. 14/15 was female among our cases, We discuss the relationship between mesenchymal dysplasia and the X chromosome in this paper. [source]

Reactive proliferation of endothelial cells and pericytes associated with arteriovenous malformation

THE JOURNAL OF DERMATOLOGY, Issue 4 2010
Masahito YASUDA
Abstract Arteriovenous malformation (AVM) is a structural vascular abnormality with no proliferation of cellular components. We report on a 53-year-old man who presented with a 15-year history of a progressively enlarging nodule on his lower lip. A dark-reddish, easy-bleeding nodule diagnosed as AVM was resected to reduce the volume and troublesome bleeding. Histologically, the nodule revealed that the proliferating cellular area was composed of endothelial cells and pericytes in addition to the area of dilated vessels. We speculated that the cell proliferation developed secondary to AVM. We also discuss the histological differential diagnosis of spindle cell hemangioma and pseudo-Kaposi's sarcoma. [source]

Bilateral Coats' disease: long-term follow up

ACTA OPHTHALMOLOGICA, Issue 1 2002
Anastassia Alexandridou
ABSTRACT. Purpose: To report on the long-term follow-up of a female patient with bilateral Coats' disease, who showed marked asymmetry between the two eyes. Methods: A five year old girl presented in 1978 with leukocoria in a blind right eye. A total exudative retinal detachment and extensive retinal telangiectasiae were noted. In the other eye, there was a localized area of retinal exudation and vascular abnormality in the supero-temporal periphery. Ultrasonography showed no evidence of intraocular tumour in the right eye and a clinical diagnosis of bilateral Coats' disease was made. Results: In 1995, the area or retinal exudation in the left eye increased and laser photocoagulation was applied successfully. To date, no disease recurrences have occurred. Conclusion: Although Coats' disease is usually unilateral, bilateral, asymmetrical involvement may occur on rare occasions. Long-term follow-up of the least affected eye is necessary so that late complications can be identified early and treated adequately to prevent visual loss. [source]