Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HLA antigen studies indicate heterogeneity of allele of B locus and propedine factor based on racial differences, while confirming specificity of DR3-DR4 for IDDM. C-peptide reserve is indicative of some sparing of beta cell destruction due to pre-existing nutritional state with enzymatic modulations modifying ketosis in the atypical IDDM in North India. Specific diabetic vascular disease has lesser geographical predisposition though factors that promote its severity or restrain its progress are not well understood.
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PMID:Diabetes in tropics--perspectives of research. 668 May 43

Twenty-one children were diagnosed as having juvenile dermatomyositis on the basis of the strict criteria of Bohan and Peter. In addition to the typical skin and muscle changes, abnormalities of esophageal motility (eight of 19), pulmonary function (14 of 17), ECG (10 of 20), and gastrointestinal absorption of D-xylose (two of eight) with active disease were observed. Clinical signs of other collagen vascular disease appeared in five children. Serologic evaluation demonstrated that ANA and rheumatoid factor were transiently positive in six; one child developed a persistently positive rheumatoid factor after four years of disease inactivity. Antibody to ENA was negative in all, but antibody to PM-1 antigen was present in four of 18. Six had a low C3 or C4; evidence of immune complexes was demonstrated by Clq or Raji binding in eight with active disease. One child was IgA deficient. The HLA-B8 antigen was present in 72% of the Caucasian children as compared with the expected incidence of 21%. Therefore, classical dermatomyositis in children has more systemic involvement then previously appreciated, may be related to the presence of circulating immune complexes, and appears to be under immunogenetic control.
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PMID:Juvenile dermatomyositis: a clinical and immunologic study. 696 9

Between September 23, 1968 and March 22, 1980, primary renal allografts were performed in 373 uremic patients with insulin-dependent diabetes. After transplantation 65 of the diabetic patients (17%) underwent 151 amputations involving at least a digit or a limb. The lower extremity was involved in 72% of the amputations. Twenty-four patients had only one procedure, while 41 required multiple procedures. Mean interval from transplantation to first amputation was 25.2 +/- 2.4 (SE) months. Patient and graft loss (perioperative risk) in the first 3 months after amputation was 13%. Diabetic renal allograft recipients living long enough to require amputation have more severe manifestations of vascular disease. These amputees display both an 11% lower patient and graft survival after the first year following transplantation, as well as an accelerated rate of graft loss following amputation. Those diabetics requiring an amputation do significantly more poorly than nonamputees of the corresponding demographic category if diabetes onset occurred at age 10 to 20 years, diabetes duration prior to transplant was less than 20 years, age at transplant was less than 30 years, dialysis duration was less than 4 months, and donor type was HLA-nonidentical related. Nevertheless, more than 50% of the diabetics undergoing amputation will be alive with functioning allografts 4 years after amputation. On the other hand, diabetics not requiring amputation do particularly well if they survive 1 year, with more than 80% chance that they will be alive with a functioning graft 4 years after transplantation.
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PMID:Patient and graft survival in amputated versus nonamputated diabetic primary renal allograft recipients. 704 51

The antiphospholipid antibody syndrome (APS) is defined by widespread arterial and venous thromboses associated with elevated plasma levels of antiphospholipid antibodies (APLA). The primary antiphospholipid antibody syndrome (PAPS) appear to be a fairly homogeneous disease, and HLA, family and other studies provide new insights into this cause of thrombosis and vascular disease. We describe two patients with PAPS (lupus anticoagulant positive), whose family members were analyzed for clinical and laboratory abnormalities associated with APS. Familial screening seems to be important, in order to prevent the thrombotic events. Low dose aspirin is the first line treatment in asymptomatic subjects with APLA, previous or present thrombosis requiring long-term, possibly life-long anticoagulation.
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PMID:Familial lupus anticoagulant. 1184 63

THREE GROUPS OF PRIMARY INFLAMMATORY MUSCLE DISEASES: The primary inflammatory muscle diseases comprise three main subsets: polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM). PM and DM are characterized by a proximal weakness that develops along weeks to months and by elevated creatine phosphokinase levels. Cutaneous involvement including both erythema and edema and infantile or adult onset are DM specific. PM and IBM only concern adults. Several PM/DM manifestations must be searched for because of their severity: swallowing disorders, various mechanisms of respiratory dysfunction (swallowing pneumopathies, interstitial lung disease, respiratory muscle deficiency) and cardiac involvement. DIAGNOSTIC ELEMENTS FOR PM AND DM: Two investigations, beside biopsy, are particularly useful: muscle MRI imaging showing inflammatory pattern and specific detection of antisynthetase autoantibodies (PM/DM with interstitial lung disease) and anti-Mi-1 and 2 in DM. PHYSIOPATHOLOGICAL DATA: PM and DM differ in their histological and physiopathological characteristics: perivascular B and CD4 lymphocyte infiltrates and complement deposits at the origin of humoral induced vascular disease in DM and perimysial CD8 lymphocytes inducing a cellular mediated cytotoxic injury in PM. Class I HLA antigen expression on the muscle fibers and production of cytokines play a crucial role in the pathogenesis of these two diseases. PM and DM may be associated with cancers, connective-tissue disease (overlap syndrome). Some PM are secondary to HIV, HTLV1 virus and toxoplasmosis infection. CHARACTERISTICS OF INCLUSION BODY MYOSITIS: IBM, the most frequent acquired myopathy after 50 years of age, is characterized by particular features: not only clinical (late onset, selective weakness, early distal involvement, slow course, unresponsiveness to corticosteroid and immunosuppressant agents); but also histological (rimmed vacuoles, filamentous inclusions) and pathogenic (cytotoxic and degenerative inflammatory process, similar to Alzheimer's disease, with beta-amyloid protein accumulation).
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PMID:[Polymyositis, dermatomyositis and inclusion body myositis, nosological aspects]. 1463 Dec 70

GREAT PROGRESS: The understanding of the physiopathology of Horton's syndrome has been made in view of the prevalence of the disease, the access to affected tissue and new molecular biology techniques. And it is now possible to specify the intricacy between the genetic, immunological and vascular components. HORTON'S SYNDROME, A GENETIC DISEASE: The preferential association of the disease with some alleles pf the HLA DR4 group has helped to emphasize the fundamental role of a few amino acids of the second hypervariable area of the HLA-DR molecule. An immunogenetic predisposition appears favourable, or even necessary, for the development of the disease. HORTON'S SYNDROME, AN IMMUNOLOGICAL DISEASE: The temporal arteries of patients presenting with Horton's syndrome are infiltrated by polymorphous inflammatory cells, fundamentally including CD4 T-cell lymphocytes, macrophages, and a few giant cells. Some CD4 lymphocytes have undergone clonal proliferation and show signs of recent antigenic recognition. A fraction of them secrete interferon gamma, which plays a crucial role in the onset, maintenance and orientation of the immunological response. The macrophages play multiple roles notably in maintaining the inflammatory reaction, but also in the destruction of certain structures of the arterial wall. HORTON'S SYNDROME, A VASCULAR DISEASE: The destruction of the arterial wall at the acute stage of the disease appears responsible, sometimes later on, for aneurismal dilatations observed on the aorta of certain patients. Moreover, intimal hyperplasia (mediated by the PDGF (platelet derived growth factor) A and B) and thrombosis (related to the inflammation) join up in reducing the arterial flow and enhancing the risk of ischemic complications during the acute stage. PATHOGENESIS, HYPOTHESES: Various candidate-antigens have been incriminated in the onset of the inflammatory reaction during Horton's syndrome. Some epidemiological and molecular studies are in favour of an exogenous antigen, possibly infectious, but no evidence has been demonstrated in the studies published. A parietal, endogenous antigen might also be at the origin of the cascade of events described during this disease.
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PMID:[Physiopathological data of Horton's syndrome]. 1502 23

The use of allogeneic venous grafts from postmortal organ donors allows for the reconstruction of critically affected arteries in patients with peripheral occlusive vascular disease. We were interested to determine the prevalence and specificity of anti-HLA antibodies in patients after allogeneic vein transplantation. Anti-HLA class I and II alloantibodies were analyzed by flowcytometric analysis using color-coded microbeads coated with HLA antigens including recombinant single antigens. Nine out of 10 patients involving 12 venous allografts were positive for anti-HLA alloantibodies. All antibody-positive patients carried both anti-HLA class I and II alloantibodies. Anti-donor HLA specificity of the anti-HLA alloantibodies was seen in seven out of nine patients for anti-class I antibodies and in eight out of nine patients for anti-HLA class II antibodies. A high rate of donor-specific allosensitization was seen after allogeneic venous transplantation. In conclusion, allosensitization not only includes a humoral response against the constitutively expressed class I antigens but also extends to class II antigens.
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PMID:Donor-specific sensitization by cadaveric venous allografts used for arterial reconstruction in peripheral arterial occlusive vascular disease. 1519 18

The purpose of this study was to evaluate the incidence of delayed graft function and its impact on the antigraft response after cadaver kidney transplantation. The analysis is based on 183 consecutive cadaver kidney transplantations performed in Vilnius University Hospital Santariskiu klinikos from January 2000 to December 2004. Delayed graft function occurred in 21.3% (39/183) of kidney transplantations. The frequency and severity of acute rejection episodes in recipients during first three months after transplantation and graft survival rate at one and two years were evaluated. Group 1 consisted of 39 patients with delayed graft function and group 2 (control group) of 144 patients with graft function immediately after transplantation. The maintenance immunosuppressive therapy consisted of cyclosporine, mycophenolate mofetil/azathioprine and prednisolone. The proportion of patients treated with monoclonal antibodies was similar in both groups (35.9% vs. 33.3%). Actuarial graft survival was estimated by the modified Kaplan-Meier method, graft loss was censored for death of recipient with functioning transplant and other causes of loss not related to rejection. There were no significant differences in the age of recipients (42.3+/-11.3 vs. 39.4+/-14.1), as well as in HLA matching (2.2/6 M vs. 2.2/6 M), in the number retransplanted patients (10.3% vs. 10.4%) and in highly sensitized patients (plasma renin activity >50.0%) (5.1% vs. 4.8%) between those groups. Significant differences were observed in donors over 50 year (33.3% vs. 18.7%; p<0.05), in cold ischemic time over 20 h (53.8 vs. 32.6%, respectively). The occurrence of acute rejection episodes was higher in group 1 than in group 2 (69.2% (27/39) vs. 34.7% (50/144); chi2=14.9945, p<0.05). Graft survival was 88.5%, 84.3% at one year and two years in group 1 and 94.7%, 93.8% at one year and two years in group 2 (ns). Donor age >50, cerebral vascular disease as cause of donor death, and cold ischemic time >20 h are the main risk factors for delayed graft function. Delayed graft function is a risk factor for acute rejection episodes, but it has no impact on graft loss due to immunological reason at one and two years. These data may serve for tailoring immunosuppressive protocols.
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PMID:[Delayed graft function and its impact on the antigraft response after cadaver kidney transplantation]. 1590 85

The limited availability of donated hearts is not sufficient to meet the needs of increasing numbers of heart transplant candidates. Thus, it is important to find the best recipient for each donated heart in order to achieve the best graft and patient survival. We investigated heart transplant outcomes in the US and the factors that influence them. We present information regarding 36,277 heart transplants reported to the OPTN/ UNOS Registry from January 1988-October 2004. The annual number of transplants ranged between 2,057-2,363 during the past 14 years and has not increased since 1990. One- and 5-year graft survival rates have gradually increased and have reached 87% and 72%, respectively, for adult recipients. Non-immunological factors, such as the circumstance of the donor's death, cause of death and ischemic time, the recipient's race, age, original disease, infection, systemic cerebro-vascular disease, whether or not they were on life support, renal function etc, significantly impacted on graft survival. Immunological factors, such as previous transfusion, previous transplantation, HLA mismatches, sensitization status, rejection episodes before discharge or within one year after transplant, were associated with lower graft survival rates. In conclusion, in order to achieve the best possible outcome for heart transplant patients, we must first find the most suitable candidate for an available donated heart; secondly, we must optimize immunosuppressive regimens and other medical and surgical therapies to prevent graft rejection and transplant-related complications.
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PMID:Heart transplantation in the United States 2004. 1670 61

The treatment of cardiovascular disease has benefited from advances in pharmacologic and intravascular intervention reducing the morbidity and mortality associated with this disease. To address the need in managing clinically complex vascular disease with limited therapeutic options studies have focused on cellular therapy as a means to augment compensatory mechanisms and to potentially prevent escalation and advancement of disease. Umbilical cord blood (UCB) is a rich source of hematopoietic stem cells (HSC) and thus may be a potential source of cells for this type of therapy. UCB can be collected at no risk to the donor, is immediately available, has a wider availability of HLA phenotypes with a possible lower immune reactivity and does not provoke ethically charged debates. Moreover, stem cells isolated from patients with chronic disease have impairment of their reparative abilities thus limiting their therapeutic impact. The potential of UCB HSC in augmenting this process has been studied extensively both in vitro and in vivo and has shown a benefit in acute and chronic vascular ischemia. Although studies suggest efficacy with no obvious safety concerns the mechanism for this therapeutic effect is unknown.
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PMID:Umbilical cord blood stem cells: implications for cardiovascular regenerative medicine. 1736 66


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