Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether hypertrophic cardiomyopathy is associated with a human leukocyte antigen (HLA) phenotype, we tissue-typed 70 unrelated afflicted patients and 86 of their asymptomatic family members (from nine separate kindreds). Forty-five per cent of the white patients had B-12 antigen as compared to 23 per cent in matched control subjects; 69 per cent of black patients had a B-5-complex antigen as compared to 33 per cent in matched controls. Patients with a B-12 or B-5-complex antigen were nonhypertensive and had family members with the disease. Patients without these antigens were severely hypertensive and had no affected family members. Linkage analysis of six families revealed a lod score of 7.7 for asymmetric septal hypertrophy and the HLA region of chromosome 6. We conclude that there is a heritable, nonhypertensive form of hypertrophic cardiomyopathy linked to the HLA loci on chromosome 6 and that a sporadic form is associated with severe, systemic hypertension.
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PMID:Hypertrophic cardiomyopathy and human leukocyte antigen linkage: differentiation of two forms of hypertrophic cardiomyopathy. 634 49

Data from a previous study concerning the distribution of human leukocyte antigen (HLA) haplotypes in siblings with essential hypertension suggested that at least one of the genes responsible for the genetic susceptibility to this disease is located in or near the HLA complex. The objective of the present study was to investigate if a given HLA-A, B, or DR gene could represent a marker for susceptibility to essential hypertension at the population level. Thus, the frequencies of HLA antigens were determined in Caucasian patients with essential hypertension (HLA-A and B antigens were determined in 89 cases, 85 of which were also typed for HLA-DR antigens). The results showed an increased frequency (p = 0.00064) of HLA-DR4, which was present in 34% of the patients and in 16% of local ethnically matched control subjects. We conclude that HLA-DR4 may represent a marker for susceptibility to essential hypertension in the Brazilian Caucasian population.
Hypertension 1992 Apr
PMID:Essential hypertension and histocompatibility antigens. An association study. 142 19

It is well established that genetic and environmental factors are involved in the etiology of essential hypertension. The presence of genes predisposing to essential hypertension in the human leukocyte antigen (HLA) complex is controversial because studies of an association between HLA antigens and essential hypertension have failed to yield consistent results. Our aim in the present study was to further investigate this issue through the method of linkage analysis. Analysis of 96 hypertensive siblings distributed in 31 families indicated a significant distortion (p = 0.0009) of the normal segregation pattern of inheritance of HLA haplotypes. Thus, our data indicate that at least one of the genes responsible for genetic predisposition to essential hypertension is located very near or within the HLA complex.
Hypertension 1989 Dec
PMID:Essential hypertension and histocompatibility antigens. A linkage study. 268 55

Although triple-drug immunosuppression with cyclosporine, prednisone, and azathioprine has reduced the incidence of acute graft rejection after cardiac transplant, its effect on the development of coronary artery disease is unknown. We have followed up 74 cardiac transplant recipients with yearly coronary angiograms. The probability of acute rejection was 10.8% at 1 year. The incidence of coronary artery disease was 8% at 1 year (six of 74 patients) and 24% at 2 years (11 of 30 patients). In patients who developed posttransplant coronary artery disease, there was a slightly higher, but not statistically significant, incidence of acute graft rejection and pretransplant idiopathic cardiomyopathy. No correlation was found between the incidence of coronary artery disease and recipient age, human leukocyte antigen (HLA) type, hypertension, diabetes, cholesterol level, triglyceride levels, weight gain after transplant, and smoking. These data indicate that triple-drug immunosuppression, despite having produced a significant reduction in the episodes of acute graft rejection, has not decreased the incidence of posttransplant coronary artery disease. Common risk factors for coronary disease and HLA mismatch are probably not important in the pathogenesis of coronary atherosclerosis after cardiac transplantation, whereas the risk for coronary artery disease may be increased by acute graft rejection and pretransplant idiopathic cardiomyopathy.
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PMID:Coronary artery disease in cardiac transplant patients receiving triple-drug immunosuppressive therapy. 280 89

Although survival after cardiac transplantation has improved since the introduction of cyclosporine to clinical practice in 1980, the long-term hemodynamic results of transplantation in cyclosporine-treated recipients has not been reported. Annual cardiac catheterization data for 109 cyclosporine-treated recipients were analyzed and compared to those of a nonconcurrent group of 65 recipients treated with azathioprine and corticosteroids. Recipient age, donor age, sex, and human leukocyte antigen mismatch were comparable for the two groups. Satisfactory left ventricular function of the cyclosporine-treated heart was characterized on the first annual study by a normal ejection fraction (60% +/- 10%), cardiac index (3.0 +/- 0.8 L/min/m2) and stroke work index (53 +/- 15 gm-m/m2) associated with moderately increased left ventricular end-diastolic pressures (12 +/- 6 mm Hg) and significantly increased mean aortic pressures (116 +/- 8 mm Hg). With the exception of aortic diastolic pressure, which tended to increase with time, the mean values of each variable analyzed did not change significantly over the period of study. In comparison to the azathioprine group, the cyclosporine cohort displayed higher aortic, left ventricular end-diastolic, and pulmonary artery pressures and produced more stroke work at each annual study. Analysis of the azathioprine group over extended (8 year) follow-up suggested excellent preservation of graft function. In summary, the long-term hemodynamic function of the transplanted heart treated with cyclosporine was satisfactory, demonstrated no deterioration over 5 year follow-up, but manifested substantially greater hypertension than hearts from the pre-cyclosporine era.
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PMID:Long-term hemodynamic results after cardiac transplantation. 331 22

Five multigenerational kindreds with familial hypertension were typed for human leukocyte antigen (HLA) and blood group antigens to investigate genetic factors that influence variability in blood pressure. Pedigree analysis revealed that children of matings in which both parents were hypertensive had a significantly greater risk of hypertension than children of matings in which one parent or neither parent was hypertensive. Blood types N and MN were abnormally distributed among hypertensive as compared with normotensive members of white but not black families. The distribution of ABO and Rh types was not significantly different between hypertensive and normotensive siblings. When all possible pairings of siblings were examined for HLA haplotype sharing, abnormal distributions were observed among hypertensive sib pairs whereas the expected mendelian segregation was observed among hypertensive-normotensive sib pairs and normotensive-normotensive sib pairs. These results suggest the genetic factors controlling variation in blood pressure may include loci in the region of the MN locus on chromosome 4 and, possibly, the major histocompatibility complex on chromosome 6.
Hypertension 1987 Jun
PMID:Possible association of MN locus haplotypes with essential hypertension. 358 3

A pair-matched, case-control design was used to study exposure to Histoplasma capsulatum and other environmental factors, and to determine various host characteristics including human leukocyte antigen (HLA) typings in 94 young patients with macular choroidal neovascularization (CNV) and in 94 controls with other eye diseases. Patients with two types of retinal patterns were studied: Type I, or those with CNV with one or no chorioretinal atrophic spots in the posterior pole or periphery (n = 51), and Type II, or those with CNV and 2 or more chorioretinal atrophic spots (n = 43). Our purpose was to explore whether these two variants of idiopathic CNV have different and distinguishable epidemiologies which may or may not be related to prior exposure to Histoplasma. We found that histoplasmin skin tests were negative in all but two Type I cases. The combination of the HLA-B7 and HLA-DR2 markers (but not either marker alone) was significantly increased in Type I cases. Among Type II cases, HLA-B7, HLA-DR2, HLA-DQ1, a positive histoplasmin skin test, myopic refractive error, prior residence in a histoplasmosis endemic area, occupations involving exposure to animals, and hypertension were all significantly increased. Histoplasmin skin test responses were positive in 18 Type II cases (45%). In the multivariate analysis, only DR2 and the combined presence of DQ1 and a positive histoplasmin skin test remained predictive of Type II disease. Our findings suggest that histoplasmin sensitivity is associated with some, but not all, cases of Type II disease. However, histoplasmin sensitivity appears to have no relationship to Type I disease. HLA factors may play a role in both disease types, possibly by producing a modified immune response to Histoplasma and/or other unidentified agents.
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PMID:Risk factors for choroidal neovascularization in young patients: a case-control study. 888 85

Long-term survival statistics for organ allografts have not improved substantially over time, despite improved immunosuppression and organ preservation and better surgical and perioperative management. Chronic rejection is the most important long-term limitation in allografts and increasingly seems to be caused by a multifactorial series of antigen-dependent and antigen-independent factors. Early injury is critical to late events, whether antigen driven (early acute rejection episodes and human leukocyte antigen mismatching) or antigen independent (ischemia/reperfusion injury and brain death). Ongoing alloimmunologic injury to the host and inadequate organ mass functioning (donor age, gender, race, and organ size) also seem to be important to this persisting process. Associated recipient conditions, which includes hypertension and hyperlipidemia, and postoperative complications, which include drug nephrotoxicity and infections, may affect this late-phase graft loss. These deleterious risk factors for chronic rejection of long-functioning allografts are an important subject for future investigation.
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PMID:Chronic allograft failure: the clinical problem. 914 41

A 51-year-old woman, who had both aortitis syndrome (Takayasu arteritis) and IgA nephropathy, presented with hypertension, fever, a high erythrocyte sedimentation rate, high C-reactive protein and serum IgG levels, proteinuria, and renal dysfunction. Renal arteriography showed stenosis and poststenotic dilatation at the origin of the right renal artery, as well as tortuosity of the left renal artery branches and marked atrophy of the left kidney. Renal biopsy showed IgA nephropathy with deposits of IgA, C3, and fibrinogen in the glomeruli and arteriolosclerosis. The present patient had human leukocyte antigen (HLA)-B 52, which is reported to be related to the aortitis syndrome, as well as HLA-DR 4, which is possibly related to IgA nephropathy, suggesting that HLA status may be involved in the pathogenesis of both diseases.
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PMID:A case of aortitis syndrome and IgA nephropathy: possible role of human leukocyte antigens in both diseases. 1021 60

Long-term prognosis in kidney transplant recipients depends on multiple factors. The purpose of this study was to quantify the influence of hyperuricemia and hyperglycemia (elements of the so-called 'syndrome X', i.e., a combination of metabolic disorders like hyperuricemia, diabetes mellitus, hyperlipidemia, and hypertension) on organ function in 350 kidney transplant recipients who had received 375 kidney transplants up to 1990 and in whom sex, age of recipient and donor, nephrologic disease, duration of dialysis, human leukocyte antigen (HLA) classification, and duration of transplant ischemia had been well matched. We found the influence of hyperuricemia on graft survival to be statistically significant (p < or = 0.05), while a statistically significant correlation between hyperglycemia and graft survival could not be detected in the present study. The transplant survival rates 2, 4, and 5 yr post-kidney-transplantation were 96.7, 80.7, and 78.7 in normogylcemic patients vs. 96.9, 85, and 82.7% in hyperglycemic ( > 100 mg,dL) kidney transplant recipients (p > 0.05). Transplant survival in hyperuricemic patients (male, > 8 mg dL; female, > 6.2 mg/dL) 2, 4, and 5 yr post-transplantation was significantly reduced (92.2, 70.6, and 68.8% vs. 98.1, 85.6, and 83.3%), as compared to normouricemic recipients. A combined presence of both hyperuricemia and hyperglycemia probably influencing the prognosis post-kidney-transplantation failed to reach the level of statistical significance. We found a significant correlation between age of recipients and plasma glucose (p < or = 0.01) and between serum uric acid concentrations and diuretic therapy (p < or = 0.05) and gender (p < or = 0.(5). In conclusion, hyperuricemia after kidney transplantation seems to reduce graft survival, whereas an influence of the carbohydrate metabolism has to be denied.
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PMID:Influence of hyperglycemia and hyperuricemia on long-term transplant survival in kidney transplant recipients. 1051 17


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