Stella Douma

Stella Douma

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Stella Douma

3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University of Thessaloniki, 56403 Thessaloniki, Greece

Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 May 2020 in Nutrients
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ANASTASIOS VAMVAKISANASTASIOS VAMVAKIS
ANASTASIOS VAMVAKIS
EGEugenia Gkaliagkousi
Eugenia Gkaliagkousi
ALAntonios Lazaridis
Antonios Lazaridis
MGMaria G Grammatikopoulou
Maria G Grammatikopoulou
ATAreti Triantafyllou
Areti Triantafyllou
SDStella Douma
Stella Douma
Lifestyle modification is an important component of essential hypertension (EH) therapy. The aim of the Hypertension Intensive Nutrition Treatment (HINTreat) parallel, randomized controlled trial was to examine the effect of a 6-month intensive lifestyle treatment (ILT) (diet plus exercise with monthly visits) compared to the usual care. A total of 76 adults with stage 1 EH were randomized (38 in each group). Dietary analysis, anthropometry, physical activity, biochemical and urine profile, blood pressure (BP), asymmetric dimethylarginine (ADMA), central hemodynamics, β-stiffness index and carotid intima media-thickness were evaluated. The dietary inflammatory index (DII) was calculated for each participant from the intake of 29 nutrients/food components. At the end of the trial, participants in the ILT group reduced their 24h urinary Na excretion (p ≤ 0.001), daytime systolic BP (p ≤ 0.048) and mean carotid β-stiffness index (p ≤ 0.005) and ameliorated their lipidemic profile compared to the standard care. Univariate analysis for the total sample showed a strong association between DII and ADMA levels (β = 0.089, p ≤ 0.01). ILT is effective in improving the inflammatory components of the diet and selected cardiometabolic parameters, including arterial stiffness.

Verified
Journal Article
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ALAntonios Lazaridis
Antonios Lazaridis
Eleni GavriilakiEleni Gavriilaki
Eleni Gavriilaki
SDStella Douma
Stella Douma
EGEugenia Gkaliagkousi
Eugenia Gkaliagkousi
Essential hypertension (EH) is a highly heterogenous disease with a complex etiology. Recent evidence highlights the significant contribution of subclinical inflammation, triggered and sustained by excessive innate immune system activation in the pathogenesis of the disease. Toll-like receptors (TLRs) have been implied as novel effectors in this inflammatory environment since they can significantly stimulate the production of pro-inflammatory cytokines, the migration and proliferation of smooth muscle cells and the generation of reactive oxygen species (ROS), facilitating a low-intensity inflammatory background that is evident from the very early stages of hypertension. Furthermore, the net result of their activation is oxidative stress, endothelial dysfunction, vascular remodeling, and finally, vascular target organ damage, which forms the pathogenetic basis of EH. Importantly, evidence of augmented TLR expression and activation in hypertension has been documented not only in immune but also in several non-immune cells located in the central nervous system, the kidneys, and the vasculature which form the pathogenetic core systems operating in hypertensive disease. In this review, we will try to highlight the contribution of innate immunity in the pathogenesis of hypertension by clarifying the deleterious role of TLR signaling in promoting inflammation and facilitating hypertensive vascular damage.

8 November 2019 in Rheumatology International
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Journal Article
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OVOlga Vampertzi
Olga Vampertzi
KPKYRIAKI PAPADOPOULOU-LEGBELOU
KYRIAKI PAPADOPOULOU-LEGBELOU
ATAreti Triantafyllou
Areti Triantafyllou
SDStella Douma
Stella Douma
EPEfimia Papadopoulou-Alataki
Efimia Papadopoulou-Alataki

Verified
Journal Article
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Eleni GavriilakiEleni Gavriilaki
Eleni Gavriilaki
ISIoanna Sakellari
Ioanna Sakellari
PAPanagiota Anyfanti
Panagiota Anyfanti
IBIoannis Batsis
Ioannis Batsis
AVAnna Vardi
Anna Vardi
EGEugenia Gkaliagkousi
Eugenia Gkaliagkousi
(1) Background: survivors of allogeneic hematopoietic cell transplantation (alloHCT) suffer from morbidity and mortality due to cardiovascular events. We hypothesized that vascular injury and pro-coagulant activity are evident in alloHCT survivors without existing alloHCT complications or relapse. (2) Methods: we enrolled consecutive adult alloHCT survivors without established cardiovascular disease and control individuals matched for traditional cardiovascular risk factors (January–December 2019). Circulating microvesicles (MVs) of different cellular origins (platelet, erythrocyte, and endothelial) were measured by a standardized flow cytometry protocol as novel markers of vascular injury and pro-coagulant activity. (3) Results: we recruited 45 survivors after a median of 2.3 (range 1.1–13.2) years from alloHCT, and 45 controls. The majority of patients suffered from acute (44%) and/or chronic (66%) graft-versus-host disease (GVHD). Although the two groups were matched for traditional cardiovascular risk factors, alloHCT survivors showed significantly increased platelet and erythrocyte MVs compared to controls. Within alloHCT survivors, erythrocyte MVs were significantly increased in patients with a previous history of thrombotic microangiopathy. Interestingly, endothelial MVs were significantly increased only in alloHCT recipients of a myeloablative conditioning. Furthermore, MVs of different origins showed a positive association with each other. (4) Conclusions: endothelial dysfunction and increased thrombotic risk are evident in alloHCT recipients long after alloHCT, independently of traditional cardiovascular risk factors. An apparent synergism of these pathophysiological processes may be strongly involved in the subsequent establishment of cardiovascular disease.

6 November 2022 in Life
Verified
Journal Article
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AMAnastasia Margouta
Anastasia Margouta
PAPanagiota Anyfanti
Panagiota Anyfanti
ALAntonios Lazaridis
Antonios Lazaridis
BARBARA NIKOLAIDOUBARBARA NIKOLAIDOU
BARBARA NIKOLAIDOU
KMKonstantinos Mastrogiannis
Konstantinos Mastrogiannis
EGEugenia Gkaliagkousi
Eugenia Gkaliagkousi
Psoriasis is associated with accelerated rates of cardiovascular disease (CVD). Laser Speckle Contrast Imaging (LSCI) is a novel, non-interventional technique for the dynamic assessment of microvascular endothelial dysfunction, which represents an early precursor of CVD. We investigated whether skin microvascular reactivity is impaired in psoriasis and whether an association exists with large artery stiffening. Skin microvascular reactivity was assessed with LSCI combined with post-occlusive reactive hyperaemia protocol in psoriasis patients and controls in the absence of established CVD. Arterial stiffness and central hemodynamics were assessed throughout a whole 24 h period with the Mobil-O-Graph device. Most LSCI indices of microvascular reactivity were impaired in psoriasis patients (n = 90) compared to controls (n = 45) [baseline flux; occlusion flux; peak-to-baseline magnitude; baseline cutaneous vascular conductance (CVC); percentage increase in CVC, p < 0.001 for all comparisons]. In multivariate analysis, psoriatic disease predicted the above markers independently of classical CVD risk factors. Augmentation index, peripheral pulse pressure, and central systolic/diastolic blood pressure correlated with LSCI microvascular responses in the study population (n = 135). Pulse wave velocity significantly correlated with nearly all LSCI parameters, while the association with baseline flux was independent of CVD risk factors and psoriatic disease in multivariate analysis (beta = 0.096, p = 0.039). This study provides evidence of altered skin microvascular responses in psoriasis by use of LSCI, and interaction with macrovascular dysfunction, before the establishment of overt CVD. A non-interventional approach of skin microcirculation with LSCI might be used as an early indicator of vascular health in psoriasis.

5 November 2021 in Rheumatology International
Verified
Journal Article
Closed access
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OVOlga Vampertzi
Olga Vampertzi
KPKYRIAKI PAPADOPOULOU-LEGBELOU
KYRIAKI PAPADOPOULOU-LEGBELOU
ATAreti Triantafyllou
Areti Triantafyllou
NKNikolaos Koletsos
Nikolaos Koletsos
SASofia Alataki
Sofia Alataki
EPEfimia Papadopoulou-Alataki
Efimia Papadopoulou-Alataki