Intracerebral hemorrhage outcome: Apolipoprotein E genotype, hematoma, and edema volumes

Abstract

We investigated whether early hematoma or edema volumes could explain the adverse association between APOE epsilon4 and survival in intracerebral hemorrhage. Among 102 patients, epsilon4 carriers had a higher mortality rate than non-epsilon4 carriers (38 versus 24%, p = 0.05). Nonsurvivors had larger hematoma (75.5 cm3 versus 27.1 cm3, p<0.001) and edema volumes (37.5 cm3 versus 17.1 cm3, p<0.01), but these were not associated with epsilon4 after adjusting for race, age, and type of hemorrhage.

A study on-effect of hematoma and perihematomal edema volume on GCS at the time of admission in patients with spontaneous lobar and basal ganglia hemorrhage

“…Mean GCS was 8 (range [3][4][5][6][7][8][9][10][11][12][13][14][15] In our series we found GCS range 3-15, our findings were compared with the findings of other studies demonstrated in tabulated form below:…”

Apolipoprotein E and the Risk of Breast Cancer in African-American and Non-Hispanic White Women

“…The ε4 allele is catabolized three times faster than the ε2 allele in heterozygous ε2/ε4 subjects, suggesting that these alleles may have distinct metabolic pathways [9, 10]. Given differential metabolisms, the assorted alleles also have diverse effects on neuronal plasticity and survival [10, 11, 17, 18, 19, 20, 21, 22, 23]. The ε3 allele has been shown to support the effective repair and remodelling after injury by noxious agents in a dose-dependent fashion.…”

“…The APO E genetic polymorphism has been shown to modify the risk for a variety of diseases, including breast cancer [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55]. We refer the reader to important reviews by Mahley and Rall [1]and Smith [23], who provide detailed discussions of APO E on the risk of common human diseases and on ageing.…”

“…We refer the reader to important reviews by Mahley and Rall [1]and Smith [23], who provide detailed discussions of APO E on the risk of common human diseases and on ageing. Given the relative dearth of information regarding APO E and breast cancer risk, we shall begin by briefly exploring the relevance of the ε4 allele, on disease risk and impaired immune function in general [1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40]. What such studies generally highlight is that APO E is essential for repair at the cellular level [1, 2, 3, 42, 50], given that lipoproteins, including APO-E-containing lipoproteins and LDL, have the ability to either inhibit or stimulate antigen- and mitogen-induced T lymphocyte activation and proliferation [1, 42].…”

Apolipoprotein E knockout mice have accentuated malnutrition with mucosal disruption and blunted insulin-like growth factor I responses to refeeding

“…Several studies have highlighted the critical role of apoE in brain plasticity after injury (in vivo and in vitro models) [6][7][8][9][10]. On the other hand, to date, few studies have addressed the importance of apoE during early postnatal development, although apoE mRNA has been shown to increase at birth, during suckling, and after fasting in the rat liver [11].…”