Impact of Diabetes Mellitus

Kanter, Jenny E.; Bornfeldt, Karin E.

doi:10.1161/atvbaha.116.307302

Cited by 41 publications

(27 citation statements)

References 44 publications

(37 reference statements)

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“…But compared to nondiabetic patients with bacterial keratitis, DM1 patients with bacterial keratitis showed higher degree of in ammatory reaction in the anterior chamber of the eye at visit 1, p<0.05. Our data agree with the fact that DM patients have abnormal in ammatory reaction [18][19][20]. It was suggested that the janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway to be activated in the setting of diabetes.…”

Section: Discussionsupporting

confidence: 91%

Clinical Peculiarities of Bacterial Keratitis in Type 1 Diabetic Patients 

Zavoloka

2021

Preprint

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The purpose was to define the clinical peculiarities of bacterial keratitis in patients with type 1 diabetes mellitus (DM1) at visit 1. Methods. We retrospectively reviewed the results of 62 DM1 patients (62 eyes) with bacterial keratitis and 43 nondiabetic patients (43 eyes) with bacterial keratitis of the control group who were referred for visit 1 (before administering the treatment). Research methods were as follows: visual acuity, tonometry, slit-lamp biomicroscopy of anterior and posterior eye segments, bacteriological studies, fluorescein dye test, anterior eye OCT and non-contact corneal esthesiometry. Results. Compared to nondiabetic, DM1 patients with bacterial keratitis showed higher degree of inflammatory reaction in the anterior chamber of the eye at visit 1 (p<0.05) as well as 28.8% lower mean corneal sensitivity threshold (p<0.05). At visit 1, the degree of decreasing of corneal sensitivity in DM1 patients with bacterial keratitis was higher than in control group (p<0.05). Localization of bacterial keratitis, the degree of pericorneal injection, corneal ulcer defect size and depth, corneal infiltration as well as edema of the corneal tissue surrounding the ulcer did not depend on the presence of diabetes mellitus (р>0,05) at visit 1.Conclusions. There are clinical peculiarities of bacterial keratitis in patients with type 1 diabetes mellitus at visit 1.

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Section: Discussionsupporting

confidence: 91%

Clinical Peculiarities of Bacterial Keratitis in Type 1 Diabetic Patients 

Zavoloka

2021

Preprint

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“…Obesity is epidemic in westernized societies, driving a crushing wave of metabolic syndrome (MetS) and type II diabetes (T2D) 4 . Preclinical model of diet-induced obesity, insulin resistant diabetes, and arteriosclerotic disease 67–71 predicted the relationships between MetS, T2D, and valve and vascular calcification as subsequently established in MESA (Multiethnic Study of Atherosclerosis) 12, 13 .…”

Section: Preclinical Models Of Arterial Calcification In the Setmentioning

confidence: 99%

“…Not every approach will be successful. Therefore, given finite research resources and the disease burden and its consequences 4–6 , we must insist upon experimental design that embraces specific and relevant patient-oriented clinical settings to prioritize our pre-clinical research – with the goal of improving cardiovascular health and independence in our diabetic patients afflicted with arteriosclerotic disease.…”

Section: Translational Implications and Future Directionsmentioning

confidence: 99%

Arterial Calcification in Diabetes Mellitus

Stabley

Towler

2017

ATVB

108

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Diabetes increasingly afflicts our aging and dysmetabolic population. Type 2 diabetes (T2D) and the antecedent metabolic syndrome (MetS) represent the vast majority of the disease burden –increasingly prevalent in children as well as older adults. However, type 1 diabetes (T1D) is also advancing in preadolescent children. As such, a crushing wave of cardiometabolic disease burden now faces our society. Arteriosclerotic calcification is increased in MetS, T2D, and T1D – impairing conduit vessel compliance and function, thereby increasing the risk for dementia, stroke, heart attack, limb ischemia, renal insufficiency and lower extremity amputation. Preclinical models of these dysmetabolic settings have provided insights into the pathobiology of arterial calcification. Osteochondrogenic morphogens in the BMP-Wnt signaling relay and transcriptional regulatory programs driven by Msx and Runx gene families are entrained to innate immune responses – responses activated by the dysmetabolic state – to direct arterial matrix deposition and mineralization. Recent studies implicate the endothelial-mesenchymal transition (EndMT) in contributing to the phenotypic drift of mineralizing vascular progenitors. In this brief overview, we discuss preclinical disease models that provide mechanistic insights – and point to the emerging potential for translating these insights into new therapeutic strategies for our patients challenged with diabetes and its arteriosclerotic complications.

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“…Diyabet sadece yaşam kalitesini ve beklenen yaşam süresini düşürmekle kalmaz, aynı zamanda körlüğe, böbrek yetmezliğine, miyokard enfarktüsüne, felce ve uzuvların kesilmesi gerekliliğine yol açan bir dizi mikrovasküler ve makrovasküler komplikasyonların ana nedenidir. Bu nedenle dünya çapında diyabetle ilişkili komplikasyonların yükü önemli bir sağlık sorunudur (5).…”

Section: Tartişma Ve Sonuçunclassified