Hereditary Risk for Cancer

2005 ◽  
pp. 61-83
Author(s):  
Katherine S. Hunt
Keyword(s):  
2000 ◽  
Vol 83 (03) ◽  
pp. 404-407 ◽  
Author(s):  
Michael Klein ◽  
Hans Dauben ◽  
Christiane Moser ◽  
Emmeran Gams ◽  
Rüdiger Scharf ◽  
...  

SummaryRecently, we have demonstrated that human platelet antigen 1b (HPA-1b or PlA2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-1b does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-1b on the outcome in patients after coronaryartery bypass surgery. We prospectively determined the HPA-1 genotype in 261 consecutive patients prior to saphenous-vein coronaryartery bypass grafting. The patients were followed for one year. Among patients with bypass occlusion, myocardial infarction, or death more than 30 days after surgery, the prevalence of HPA-1b was significantly higher than among patients without postoperative complications (60 percent, 6/10, vs. 24 percent, 58/241, p <0.05, odds ratio 4.7). Using a stepwise logistic regression analysis with the variables HPA1b, age, sex, body mass index, smoking (pack-years), hypertension, diabetes, cholesterol and triglyceride concentration, only HPA-1b had a significant association with bypass occlusion, myocardial infarction, or death after bypass surgery (p = 0.019, odds ratio 4.7). This study shows that HPA-1b is a hereditary risk factor for bypass occlusion, myocardial infarction, or death in patients after coronary-artery bypass surgery.


2021 ◽  
pp. 49-56
Author(s):  
O. D. Ostroumova ◽  
S. A. Bliznyuk ◽  
A. I. Kochetkov ◽  
A. G. Komarova

One of the reasons for the development of hemolytic anemia (HA) can be drugs, including some antibacterial, non-steroidal anti-inflammatory, antitumor and antihypertensive drugs. It was found that the most common drug-induced hemolytic anemia (DIHA) develops against the background of taking antibacterial drugs. The true prevalence of DIHA is not known and is approximately one case per 1.0–1.2 million patients. The mechanisms of the occurrence of DIHA are divided into immune and metabolic (non-immune). The first mechanism is associated with the formation of haptens, the second option – with the formation of immune complexes, the third option is mediated by the formation of true autoantibodies to red blood cells, the fourth option of the immune mechanism of the occurrence of DIHA is non-immunological protein absorption on the membranes of red blood cells. The risk factors for the development of DIHA are not fully established. The most common hereditary risk factor for DIHA is glucose-6-phosphate dehydrogenase deficiency. The main method of diagnosing DIHA is a direct antiglobulin test (direct Coombs’ test). The temporal relationship between the use of the inducer drug and the development of HA symptoms is important. The treatment strategy of DIHA is determined by the severity of the disease. In all cases, treatment should be initiated with the identification and withdrawal of the drug that initiated the occurrence of HA. With the development of severe HA, hemodialysis may be required. Prevention of DIHA involves avoiding the use of drugs associated with a high risk of its development.


2013 ◽  
pp. 123-150
Author(s):  
Katherine S. Hunt ◽  
Jessica A. Ray ◽  
Joanne M. Jeter
Keyword(s):  

2002 ◽  
Vol 9 (6) ◽  
pp. 457-465 ◽  
Author(s):  
Mark E. Robson

Background Hereditary predisposition to breast and ovarian cancer, most commonly due to germline mutations in BRCA1 and BRCA2, has been recognized for many years. The optimal clinical management of individuals with such a predisposition is not yet completely defined. Methods The current literature regarding the clinical management of individuals at risk for hereditary breast and ovarian cancer was reviewed. Results Women with germline BRCA1 or BRCA2 mutations are at substantially increased risk for breast and ovarian cancer, although the risks may not be as high as originally reported. Current surveillance options are restricted in their effectiveness by both host and tumor factors as well as limitations of the techniques. Surgical prevention options, while effective, may be complicated by physical or psychological morbidity. Nonsurgical prevention options are under development. Conclusions The ability to define women as being at hereditary risk for breast and ovarian cancer facilitates the use of specialized surveillance and prevention strategies. Genetic testing, which plays a role in defining risk, requires careful pre- and post-test counseling to discuss the limitations of testing itself and available management strategies.


1997 ◽  
Vol 15 (5) ◽  
pp. 2139-2148 ◽  
Author(s):  
M A Andrykowski ◽  
R Lightner ◽  
J L Studts ◽  
R K Munn

PURPOSE Great interest in predictive testing for hereditary cancer syndromes has been reported. Prior research has focused on testing for specific hereditary syndromes and/or among individuals at high risk for positive carrier status. Given anticipated expansion of both the range of hereditary syndromes for which testing will be available, as well as the clinical settings in which testing will occur, assessment of interest in hereditary cancer risk testing and notification in the general public is warranted. METHODS As part of an annual statewide telephone survey, adults' (N = 654) interest in hereditary cancer risk testing and notification was assessed. RESULTS Interest in both risk testing (82%) and risk notification (87%) was high. Logistic regression analyses indicated that disinterest in risk notification was associated with female sex, performance of fewer health protective behaviors, and better perceptions of personal health. Disinterest in risk testing was associated with these same variables as well as older age, less concern over developing cancer, and a more extensive history of cancer in first degree relatives. CONCLUSION In the absence of risk-reducing behaviors with demonstrable efficacy, hereditary risk testing programs may have difficulty attracting the interest of those at greatest risk for carrier status. In contrast, many individuals at low risk for positive carrier status might seek testing, perhaps as a means of seeking reassurance regarding their low hereditary risk.


2016 ◽  
Vol 106 (3) ◽  
pp. e64
Author(s):  
T. Miki ◽  
A. Tanaka ◽  
M. Nagayoshi ◽  
S. Watanabe

2006 ◽  
Vol 4 (2) ◽  
pp. 59 ◽  
Author(s):  
M. Kriege ◽  
Brekelmans ◽  
A.I.M. Obdeijn ◽  
C. Boetes ◽  
H.M. Zonderland ◽  
...  

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