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Length Polymorphisms in the Angiotensin I-Converting Enzyme Gene and the Serotonin-Transporter-Linked Polymorphic Region Constitute a Risk Haplotype for Depression in Patients with Coronary Artery Disease.
Biochemical Genetics ( IF 2.4 ) Pub Date : 2020-05-05 , DOI: 10.1007/s10528-020-09967-w
Thomas Meyer 1, 2 , Isabel Rothe 1 , Julia Staab 1 , Hans-Christian Deter 3 , Stella V Fangauf 1 , Stefanie Hamacher 4 , Martin Hellmich 4 , Jana Jünger 5 , Karl-Heinz Ladwig 6, 7 , Matthias Michal 8 , Katja Petrowski 9, 10 , Joram Ronel 11 , Wolfgang Söllner 12 , Cora Weber 3 , Martina de Zwaan 13 , Redford B Williams 14 , Christian Albus 15 , Christoph Herrmann-Lingen 1 ,
Affiliation  

Genetic variations affecting the course of depressive symptoms in patients with coronary artery disease (CAD) have not yet been well studied. Therefore, we set out to investigate whether distinct haplotypes of the two insertion/deletion polymorphisms in the serotonin-transporter-linked polymorphic region (5-HTTLPR) and the angiotensin I-converting enzyme (ACE) gene located on chromosome 17 can be identified as risk factors for trajectories of depression. Clinical and genotyping data were derived from 507 depressed CAD patients participating in the randomized, controlled, multicenter Stepwise Psychotherapy Intervention for Reducing Risk in Coronary Artery Disease (SPIRR-CAD) trial, of whom the majority had an acute cardiac event before study inclusion. Depression scores on the Hospital Anxiety and Depression Scale (HADS) were assessed at baseline and at five follow-up time points up to 2 years after study entrance. At baseline, depression scores did not significantly differ between patients carrying the risk haplotype ACE D/D, 5-HTTLPR I/I (n = 46) and the non-risk haplotypes (n = 461, 10.9 ± 2.7 versus 10.4 ± 2.5, p = 0.254). HADS-depression scores declined from study inclusion during the first year irrespective of the genotype. At each follow-up time point, HADS-depression scores were significantly higher in ACE D/D, 5-HTTLPR I/I carriers than in their counterparts. Two years after study inclusion, the mean HADS depression score remained 1.8 points higher in patients with the risk haplotype as compared to subjects not carrying this haplotype (9.9 ± 4.2 versus 8.1 ± 4.0, p = 0.009). In summary, the presence of the ACE D/D, 5-HTTLPR I/I haplotype may be a vulnerability factor for comorbid depressive symptoms in CAD patients.

中文翻译:

血管紧张素I转换酶基因中的长度多态性和血清素转运蛋白相关的多态性区域构成了冠状动脉疾病患者抑郁的危险单倍型。

尚未充分研究影响冠心病(CAD)患者抑郁症状进程的遗传变异。因此,我们着手研究在5-羟色胺-转运蛋白连锁的多态性区域(5-HTTLPR)和血管紧张素I转换酶(ACE)中两个插入/缺失多态性的不同单倍型)位于17号染色​​体上的基因可以被识别为抑郁症轨迹的危险因素。临床和基因分型数据来自507名抑郁CAD患者,他们参加了随机,对照,多中心循序渐进心理治疗降低冠状动脉疾病风险(SPIRR-CAD)试验,其中大多数在纳入研究前均患有急性心脏事件。在入院后两年内,在基线和五个随访时间点评估医院焦虑和抑郁量表(HADS)的抑郁评分。在基线时,携带风险单倍型ACE D / D,5-HTTLPR I / I(n  = 46)和非风险单倍型(n = 461,10.9±2.7与10.4±2.5,p  = 0.254)。在第一年,无论基因型如何,HADS抑郁评分均因纳入研究而下降。在每个随访时间点,ACE D / D,5-HTTLPR I / I携带者的HADS抑郁评分均明显高于其对应者。纳入研究两年后,具有风险单倍型的患者的平均HADS抑郁评分仍比未携带该单倍型的患者高1.8点(9.9±4.2对8.1±4.0,p  = 0.009)。总之,ACE D / D,5-HTTLPR I / I单倍型的存在可能是CAD患者合并抑郁症状的易感性因素。
更新日期:2020-05-05
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