scholarly journals Role of GDF-15 as an inflammatory marker in patients with psoriasis vulgaris

TURKDERM ◽  
2021 ◽  
Vol 55 (4) ◽  
pp. 184-188
Author(s):  
Mustafa Kaan Taşolar ◽  
Gamze Erfan ◽  
Onur Raimoğlu ◽  
Hülya Albayrak ◽  
Mehmet Emin Yanık
Author(s):  
Santiago R. Unda ◽  
Aldana M. Antoniazzi ◽  
David J. Altschul ◽  
Roberta Marongiu

<b><i>Introduction:</i></b> Peripheral and central nervous system inflammation have been linked to the classic symptoms of Parkinson’s disease (PD) and Alzheimer’s disease (AD). However, it remains unclear whether the analysis of routine systemic inflammatory markers could represent a useful prediction tool to identify clinical subtypes in patients with Parkinson’s and Alzheimer’s at higher risk of dementia-associated symptoms, such as behavioral and psychological symptoms of dementia (BPSD). <b><i>Methods:</i></b> We performed a multivariate logistic regression using the 2016 and 2017 National Inpatient Sample with International Classification of Diseases 10th edition codes to assess if pro-inflammatory white blood cells (WBCs) anomalies correlate with dementia and BPSD in patients with these disorders. <b><i>Results:</i></b> We found that leukocytosis was the most common WBC inflammatory marker identified in 3.9% of Alzheimer’s and 3.3% Parkinson’s patients. Leukocytosis was also found to be an independent risk factor for Parkinson’s dementia. Multivariate analysis of both cohorts showed that leukocytosis is significantly decreased in patients with BPSD compared to patients without BPSD. <b><i>Conclusions:</i></b> These results suggest a link between leukocytosis and the pathophysiology of cognitive dysfunction in both PD and AD. A better understanding of the role of systemic neuroinflammation on these devastating neurodegenerative disorders may facilitate the development of cost-effective blood biomarkers for patient’s early diagnosis and more accurate prognosis.


2012 ◽  
Vol 35 (6) ◽  
pp. ---
Author(s):  
Katharina Biller ◽  
Peter Fae ◽  
Reinhard Germann ◽  
Autar K. Walli ◽  
Peter Fraunberger

Abstract The role of procalcitonin (PCT) plasma levels as a diagnostic tool for intensive care patients has been intensively investigated during the past years. In particular for recognition of bacterial infections, PCT levels have been shown to be superior to other clinical and biochemical markers. Furthermore, some very recent studies show that in patients with lower respiratory tract infections PCT guided antibiotic therapy reduces antibiotic use and thereby may also reduce duration of stay of patients in hospital and thus cut hospitalisation costs. However, various studies indicate that the value of PCT as a prognostic marker is limited because of false positive or negative values. Despite these limitations PCT plasma levels are currently measured in intensive care units. The present study summarises the possible clinical uses of this laboratory marker as a diagnostic tool for the assessment of critically ill patients.


2020 ◽  
pp. 1-14
Author(s):  
Yaser H.A. Elewa ◽  
Osamu Ichii ◽  
Teppei Nakamura ◽  
Yasuhiro Kon

Diabetes is a devastating global health problem and is considered a predisposing factor for lung injury progression. Furthermore, previous reports of the authors revealed the role of mediastinal fat-associated lymphoid clusters (MFALCs) in advancing respiratory diseases. However, no reports concerning the role of MFALCs on the development of lung injury in diabetes have been published. Therefore, this study aimed to examine the correlations between diabetes and the development of MFALCs and the progression of lung injury in a streptozotocin-induced diabetic mouse model. Furthermore, immunohistochemical analysis for immune cells (CD3+ T-lymphocytes, B220+ B-lymphocytes, Iba1+ macrophages, and Gr1+ granulocytes), vessels markers (CD31+ endothelial cells and LYVE-1+ lymphatic vessels “LVs”), and inflammatory markers (TNF-α and IL-5) was performed. In comparison to the control group, the diabetic group showed lung injury development with a significant increase in MFALC size, immune cells, LVs, and inflammatory marker, and a considerable decrease of CD31+ endothelial cells in both lung and MFALCs was observed. Furthermore, the blood glucose level showed significant positive correlations with MFALCs size, lung injury, immune cells, inflammatory markers, and LYVE-1+ LVs in lungs and MFALCs. Thus, we suggest that the development of MFALCs and LVs could contribute to lung injury progression in diabetic conditions.


2015 ◽  
Vol 114 (09) ◽  
pp. 498-518 ◽  
Author(s):  
Karin Müller ◽  
Madhumita Chatterjee ◽  
Dominik Rath ◽  
Tobias Geisler

SummaryPlatelets play a pivotal role in chronic inflammation leading to progression of atherosclerosis and acute coronary events. Recent discoveries on novel mechanisms and platelet-dependent inflammatory targets underpin the role of platelets to maintain a chronic inflammatory condition in cardiovascular disease. There is strong and clinically relevant crosslink between chronic inflammation and platelet activation. Antiplatelet therapy is a cornerstone in the prevention and treatment of acute cardiovascular events. The benefit of antiplatelet agents has mainly been attributed to their direct anti-aggregatory impact. Some anti-inflammatory off-target effects have also been described. However, it is unclear whether these effects are secondary due to inhibition of platelet activation or are caused by direct distinct mechanisms interfering with inflammatory pathways. This article will highlight novel platelet associated targets that contribute to inflammation in cardiovascular disease and elucidate mechanisms by which currently available antiplatelet agents evolve anti-inflammatory capacities, in particular by carving out the differential mechanisms directly or indirectly affecting platelet mediated inflammation. It will further illustrate the prognostic impact of antiplatelet therapies by reducing inflammatory marker release in recent cardiovascular trials.


2017 ◽  
Vol 26 (6) ◽  
pp. 951-963
Author(s):  
Akihiko Umazume ◽  
Takeshi Kezuka ◽  
Ryusaku Matsuda ◽  
Yoshihiko Usui ◽  
Hiroki Takahashi ◽  
...  

2001 ◽  
Vol 81 (3) ◽  
pp. 335-347 ◽  
Author(s):  
James B Rottman ◽  
Tammy L Smith ◽  
Kenneth G Ganley ◽  
Toyoko Kikuchi ◽  
James G Krueger

2012 ◽  
Vol 108 (8) ◽  
pp. 1435-1442 ◽  
Author(s):  
Andréa Name Colado Simão ◽  
Marcell Alysson Batisti Lozovoy ◽  
Larissa Danielle Bahls ◽  
Helena Kaminami Morimoto ◽  
Tathiana Name Colado Simão ◽  
...  

The aim of the present study was to verify the effects of fish oil and a soya-based product on inflammatory markers and endothelial function measured by NO in women with the metabolic syndrome (MetS). A total of sixty-five women (mean age: 47·9 (sd9·98) years) were studied in a 90-d parallel, randomised design. A control group maintained their usual diet; the second group received 29 g/d of soyabean (kinako); the third group received 3 g/d of fish oiln-3 fatty acids; and the fourth group received fish oil (3 g/d) and kinako (29 g/d). Anthropometric, blood pressure (BP), inflammatory markers, anti-inflammatory marker (adiponectin) and NO concentrations were evaluated. In relation to the baseline values, the group that received fish oil and kinako concomitantly presented a statistically significant decrease in systolic BP (SBP;P < 0·05), whereas there was a significant decrease in diastolic BP (DBP) in the control group (P < 0·05), kinako group (P < 0·01) and fish oil group (P < 0·01) after 90 d. There was a significant increase in adiponectin (P < 0·01) and NO values (P < 0·05) after 90 d in the kinako and fish oil groups. Differences between treatment groups verified a significant decrease (P < 0·05) in DBP in the kinako group after 90 d when compared to the results obtained from the fish oil and kinako groups. In conclusion, the findings of increased serum adiponectin and NO metabolite levels after 90 d, both in the fish oil and soya groups, reinforce the importance of the influence of adiponectin and NO levels on BP decrease in patients with the MetS.


2011 ◽  
Vol 31 (6) ◽  
pp. 343-352 ◽  
Author(s):  
Sema Becerik ◽  
Beral Afacan ◽  
Veli Özgen Öztürk ◽  
Harika Atmaca ◽  
Gülnur Emingil

Aim:The aim of the present study was to investigate gingival crevicular fluid (GCF) calprotectin, osteocalcin and cross-linked N-terminal telopeptide (NTx) levels in health along with different periodontal diseases.Material and methods:Twenty chronic periodontitis (CP), 20 generalized aggressive periodontitis (G-AgP), 20 gingivitis and 20 healthy subjects were included. Probing depth, clinical attachment level, plaque index and papillary bleeding index was recorded. GCF calprotectin, osteocalcin and NTx levels were analyzed by enzyme-linked immunosorbent assay (ELISA).Results:CP, G-AgP and gingivitis groups had higher GCF calprotectin total amount compared to healthy subjects (p< 0.008). CP and G-AgP groups had similar, but higher levels compared to gingivitis groups (p< 0.008). CP and G-AgP groups had lower GCF osteocalcin total amount compared to gingivitis and healthy groups (p< 0.008). CP group had higher GCF NTx but lower osteocalcin total amount and osteocalcin/NTx ratio than the G-AgP group (p< 0.008)Conclusions:Our results suggest that elevated GCF calprotectin levels play a role as a reliable inflammatory marker in the pathogenesis of periodontal disease. Fluctuating GCF levels of osteocalcin and NTx might point out to the abnormal bone turnover in periodontitis. Our data document for the first time the role of NTx in the pathogenesis of different periodontal diseases.


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