Invited Review: Pharmacogenetics of estrogen replacement therapy

2001 ◽  
Vol 91 (6) ◽  
pp. 2776-2784 ◽  
Author(s):  
David M. Herrington ◽  
Karen Potvin Klein

There are a number of genetic factors that likely modulate both the beneficial and adverse effects of estrogen. An important domain of consideration is the relationship of estrogen and thrombosis risk. Gene polymorphisms among the key elements of the coagulation and fibrinolytic cascade appear to influence the effects of estrogen on risk for venous thromboembolic events and possibly arterial thrombosis as well. Emerging data also suggest that allelic variants in the estrogen receptor-α may modulate estrogen's effects, especially with respect to bone and lipid metabolism.

PEDIATRICS ◽  
1978 ◽  
Vol 62 (6) ◽  
pp. 1104-1113
Author(s):  
Thomas M. Mack

Recent studies concerning the relationship of exogenous estrogens and endometrial cancer have been reviewed and the objections to their conclusions discussed. Even considering the most serious of these reservations, it is difficult to avoid the tentative conclusion that estrogens are causally linked to endometrial cancer and that the attributable risk is numerically sizable. Whether the medical costs will be ultimately shown to outweigh the benefits of estrogen replacement therapy will depend largely on whether or not a relationship to breast cancer is shown and on the magnitude of the effect of estrogens in preventing serious complications of ovarian failure. For the time being, treatment of menopausal symptoms with estrogens should be as brief as possible, should use the lowest dose possible, and should probably be given in cyclic fashion, particularly to women with intact uteruses. Every attempt should be made to give patients a quantitative understanding of both potential risks and benefits before they decide in favor of or against estrogen therapy.


2015 ◽  
Author(s):  
Elena Peretokina ◽  
Natalia Mokrysheva ◽  
Lyudmila Rozhinskaya ◽  
Ekaterina Zakharova

2020 ◽  
Vol 10 (3) ◽  
pp. 1-2
Author(s):  
Joseph A Caprini

The appearance of the coronavirus pandemic has prompted a renewed interest in thrombosis risk assessment, particularly since this disease is associated with a high risk of thrombotic events. It is known that the number one preventable cause of death in hospitalized patients including those having surgical procedures is fatal pulmonary emboli. There is also high-quality data that the use of anticoagulant drugs in the proper dose, and for the period of time shown to be efficacious, will prevent most fatal events. It is true that even with the use of the best anticoagulant regimes venous thromboembolic events (VTE) can still occur but are rarely fatal. We also realize that providing adequate anticoagulant prophylaxis for the entire period of risk is the key to preventing these deaths.  Thrombosis risk scoring identifies who's at risk for these emboli and guides physician choices for appropriate preventive measures.


2020 ◽  
Vol 26 ◽  
pp. 107602962097790
Author(s):  
Xin Zhong ◽  
Zhongze Cao ◽  
Jiayi Song ◽  
Yuanmeng Liu ◽  
Qiang Guo

The biomarkers for predicting venous thromboembolic events (VTEs) after oncologic surgery are still lacking. The current study aimed to analyze the relationships of CD62P and GP IIb/IIIa with hypercoagulation after oncologic surgery. A total of 76 patients with primary abdominopelvic tumors in our hospital were enrolled. The patients were divided into groups A (malignancy with no VTE group), B (malignancy with VTE group), and C (benign with no VTE group). Twenty healthy volunteers were selected as control. The plasma CD62P (4.69 ± 2.55 vs. 1.76 ± 0.48) and the GP IIb/IIIa (9.28 ± 3.79 vs. 1.76 ± 0.48) levels in group A were significantly higher than those in the control group preoperatively. The CD62P (31.46 ± 17.13 vs. 13.51 ± 7.43, P < 0.05), GP IIb/IIIa (42.33 ± 21.82 vs. 13.51 ± 7.43, P < 0.05), and D-dimer (7.33 ± 2.34 vs. 2.03 ± 0.55, P < 0.05) levels in group B were markedly higher 7 days after operation compared with those in group A. The CD62P and the GP IIb/IIIa exhibited a positive correlation with the hypercoagulable state after oncologic surgery.


Maturitas ◽  
2004 ◽  
Vol 49 (2) ◽  
pp. 163-169 ◽  
Author(s):  
Juan Manuel Malacara ◽  
Elva Leticia Pérez-Luque ◽  
Sandra Martı́nez-Garza ◽  
Francisco Javier Sánchez-Marı́n

Twin Research ◽  
2000 ◽  
Vol 3 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Michael J Lyons ◽  
Jonathan Huppert ◽  
Rosemary Toomey ◽  
Rebecca Harley ◽  
Jack Goldberg ◽  
...  

AbstractThere have been long questions about the relationship of schizophrenia to other mental disorders. Lifetime DSM-III-R diagnoses of mood and anxiety disorders in twins with clinically diagnosed schizophrenia (n = 24) and their non-affected co-twins (n = 24) were compared with twins from pairs without schizophrenia (n = 3327) using a sample from the Vietnam Era Twin Registry. Schizophrenic probands had significantly elevated rates of all included disorders (bipolar disorder, major depression, dysthymia, generalized anxiety disorder, panic disorder, and PTSD) compared with controls (P < 0.01). The odd ratios comparing co-twins of schizophrenic probands with controls was greater than three for every disorder, but did not attain statistical significance. A similar pattern was observed when analyses were restricted to only monozygotic twins (n = 12). Consistent with other studies, schizophrenics appeared to have higher rates of a range of mental disorders. Our results suggest that schizophrenia per se represents a risk factor for other psychiatric disorders, but the absence of significantly elevated risk among non-schizophrenic co-twins suggested that family environmental and/or genetic factors that contribute to risk of schizophrenia do not increase the risk of mood and anxiety disorders to the same extent that the risk of these other disorders is increased by the presence of schizophrenia. Twin Research (2000) 3, 28–32.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Enkhmaa Byambaa ◽  
Kyoungmi Kim ◽  
Wei Zhang ◽  
Kevin Truax ◽  
Anuurad Erdembileg ◽  
...  

Abstract Introduction: An elevated level of lipoprotein(a) [Lp(a)] is an independent causal risk factor for cardiovascular disease. Non-genetic factors do not appreciably influence Lp(a) levels due to a strong genetic control. However, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has been shown to reduce Lp(a) levels. The association of PCSK9 with Lp(a) level and its major genetic determinant—apolipoprotein(a) [apo(a)] size—is not fully understood. In this study, we assessed the relationship between PCSK9, Lp(a) level, apo(a) size, age, and race/ethnicity. Methods: Healthy Caucasian and African-American families were recruited from the general population (age range: 6–74 years, N=267). PCSK9 and Lp(a) levels were assayed enzymatically; apo(a) isoform and LPA allele sizes and isoform-specific Lp(a) levels were determined. Results: In all participants, PCSK9 levels differed significantly by race/ethnicity, age, and sex. Thus, the mean PCSK9 levels were significantly higher in African-Americans vs. Caucasians (104 ± 29 vs. 95 ± 30 ng/mL, respectively, p=0.020), in adults vs. children (102 ± 29 vs. 92 ± 31 ng/mL, respectively, p=0.001) and in females vs. males (103 ± 30 vs. 94 ± 29 ng/mL, respectively, p=0.007). PCSK9 levels were not associated with total plasma Lp(a) levels neither in all participants nor in ethnicity-specific analyses. However, PCSK9 levels were significantly and positively associated with isoform-specific Lp(a) levels carried by the larger apo(a) size in all subjects (r=0.139, p=0.0361). In race/ethnicity analyses, a significant association was seen for African-Americans (r=0.268, p=0.0199), but not for Caucasians. In contrast, there were no significant associations of PCSK9 with isoform-specific Lp(a) levels for the smaller apo(a) sizes in all participants nor in ethnic-specific analyses. Of note, PCSK9 levels were significantly negatively associated with the larger apo(a) isoform sizes in all participants (r=-0.139, p=0.0366). Although significant in both groups, heritability of PCSK9 level was higher in Caucasians than in African-Americans (47% vs. 22%, respectively). Conclusions: Among African-Americans, but not Caucasians, PCSK9 levels were associated with isoform-specific Lp(a) levels carried on larger, but not smaller, apo(a) sizes. The findings illustrate a diverging relationship of PCSK9 with isoform-specific Lp(a) levels.


Author(s):  
O. P. Bobrova ◽  
N. A. Shnayder ◽  
M. M. Petrova ◽  
S. N. Zobova ◽  
Yu. A. Dykhno ◽  
...  

Aim. To develop a model for the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer based on an analysis of the relationship of clinical and genetic factors. Materials and methods. In 45 patients with pancreatic cancer, 54 clinical and genetic factors were studied for predicting the implementation of opioid-associated neurotoxicity, receiving a transdermal form of fentanyl. Results. A clinical genetic model of the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer was developed using the example of a transdermal form of fentanyl Conclusion. The clinical genetic model for predicting the risk of opioid-associated neurotoxicity in patients with pancreatic cancer is important from the perspective of personalized medicine.


2021 ◽  
Vol 03 (03) ◽  
pp. 93-103
Author(s):  
A.G. Ganiev ◽  

The importance of assessment in the educational process and international assessment systems were discussed. There is also information on the dependence of a child's educational opportunities on genetic factors and upbringing. In this regard, it is recommended to use Gardner's "theory of multiplicity of intelligence" to make the most of the child's potential. The article presents a map of the “multi-intelligence theory” of intellect and comments on the relationship of types of intellect to the cerebral hemispheres. A "Child Intelligence Diagram" is also recommended for practice.


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