scholarly journals OP0204 URATE CRYSTAL DEPOSITIONS ARE ASSOCIATED WITH INFLAMMATORY MARKERS AND CAROTID PLAQUES INDICATING SUBCLINICAL INFLAMMATION IN GOUT; BASELINE RESULTS FROM THE NOR-GOUT STUDY

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 123.1-123
Author(s):  
H. B. Hammer ◽  
S. Rollefstad ◽  
G. Jensen ◽  
L. Karoliussen ◽  
L. Terslev ◽  
...  

Background:In gout patients the extent of monosodium urate (MSU) crystal depositions can be quantitated by use of ultrasound. Gout may be associated with atherosclerotic disease which might be related to low-grade inflammation. Calprotectin is a major granulocyte protein reflecting the level of systemic inflammation.Objectives:To explore whether the extent of MSU crystal depositions is associated with low grade systemic inflammation as assessed by calprotectin/C-reactive protein (CRP) and with carotid pathologies in asymptomatic gout patients.Methods:The baseline data from NOR-GOUT, a prospective study of patients with crystal-proven gout with increased serum urate levels (>360 μmol/L), were used. All patients were assessed by ultrasound (GE Logiq E9 machine) to assess MSU depositions (OMERACT definitions; double contour (DC), tophi and aggregates) with bilateral assessment of wrist, MCP2, knee, ankle, MTP1 and insertions of triceps, quadriceps, proximal/distal patellar and Achilles tendons, all scored semi-quantitatively 0-3. Bilateral B-mode ultrasound assessments of the carotid arteries examined carotid intima-media thickness (cIMT; increased thickness >0.9mm). Atherosclerotic plaques were identified as protrusions of ≥1.5 mm or ≥ 2 times the adjacent IMT. Sum scores of each of the ultrasound elementary lesions for MSU depositions were calculated and the associations with calprotectin (plasma assessed by ELISA (Calpro), normal levels <910 µg/L), CRP (routine assessment, normal levels <4mg/L) as well as cIMT and presence of carotid plaque were explored. Correlations were performed by use of Spearman and differences between group was investigated by Mann-Whitney test.Results:A total of 202 gout patients without flare were included (95.5% men, mean (SD) age of 56.5 (13.8) years, 7.9 (7.7) years since first flare). The mean (SD) sum sore of DC was 4.4 (3.5), tophi 6.6 (6.6), aggregates 9.3 (5.6), calprotectin 801 (525) µg/L, CRP 7 (14) mg/L and serum urate (SUA) 499 (77) μmol/L. Carotid examinations were performed in 122 (60.4%) of the patients. Significant correlations were found between the MSU depositions and the inflammatory markers as well as cIMT. The 27% patients with increased calprotectin had the highest levels of each of the three elementary lesions (p=0.001) (Figure), and the 39% with elevated CRP levels had the highest levels of tophi and aggregates (p<0.05). The 18% with increased thickness of cIMT and the 53% of patients with carotid plaque had the highest levels of aggregates (p=0.003 and p=0.037, respectively).Conclusion:In asymptomatic gout patients, higher load of MSU crystal depositions was associated with increased levels of inflammatory markers, cIMT and presence of atherosclerotic plaques in the carotid arteries. This may indicate that crystal depositions cause subclinical inflammation with subsequent systemic implications, but future longitudinal studies are needed to confirm such causal relationships.Sum scoredouble contourSum scoretophiSum score aggregatesCalprotectin0.26**0.32**0.28**CRP0.20*0.25**0.18*Right IMTNSNS0.18*Left IMTNSNS0.21*Sum bilateral IMTNSNS0.22*Spearman’s correlations. NS; Not significant, *p<0.05, **p<0.001Disclosure of Interests:Hilde Berner Hammer Speakers bureau: AbbVie, Lilly and Novartis, Silvia Rollefstad: None declared, Gro Jensen: None declared, Lars Karoliussen: None declared, Lene Terslev Speakers bureau: Speakers fee from AbbVie, Janssen, Roche, Novartis, Pfizer, MSD, BMS and GE, Espen A Haavardsholm: None declared, Tore K. Kvien Speakers bureau: Tore K Kvien has received fees for speaking and/or consulting and/or research funding to Diakonhjemmet Hospital from AbbVie, Biogen, BMS, Celltrion, Egis, Evapharma, Ewopharma, Eli Lilly, Gilead, Hikma, MSD, Mylan, Novartis, Oktal, Pfizer, Sandoz, Sanofi and UCB., Anne Grete Semb: None declared, Till Uhlig: None declared

2018 ◽  
Vol 11 (2) ◽  
pp. 128-134
Author(s):  
Niya A. Krasteva ◽  
Boiko R. Shentov ◽  
Adelaida L. Ruseva ◽  
Chaika K. Petrova ◽  
Simeon P. Petkov

Summary The rising incidence of bronchial asthma and obesity in children raises the question of whether there is a link between them. Chronic low-grade systemic inflammation could be one of the linking mechanisms. We aimed to determine the serum concentrations of high-sensitive C-reactive protein (hs-CRP), interleukin 6 (IL-6) and tumour necrosis factor a (TNF-a) in children with asthma and obesity and to seek a relationship between these inflammatory markers and asthma control. We investigated 88 children aged 6 to 17 years - 25 asthmatic obese children (AsOb), 25 asthmatic non-obese children (AsNOb), 19 obese non-asthmatic children (ObNAs), and 19 non-obese non-asthmatic children as controls. Serum levels of IL-6 and hs-CRP were significantly increased in asthmatic obese and ObNAs compared to AsNOb and the control group. Serum TNF-a concentration was similar in the four studied groups. There were no statistically significant differences in serum levels of these inflammatory markers between controlled and partially controlled/uncontrolled asthmatics (obese and non-obese). Knowing the possible mechanisms of interaction between bronchial asthma and obesity would contribute to a more effective therapeutic approach in these patients.


2022 ◽  
Vol 12 ◽  
Author(s):  
Per Wågström ◽  
Åsa Nilsdotter-Augustinsson ◽  
Mats Nilsson ◽  
Janne Björkander ◽  
Charlotte Dahle ◽  
...  

PurposeIndividuals with immunoglobulin G deficiency (IgGsd) often complain of fatigue. The correlation between systemic inflammation and fatigue is unknown. In this study perceived quality of life (QoL) and fatigue in individuals with IgGsd, on and off immunoglobulin replacement therapy (IgRT) were correlated to inflammatory markers in plasma to identify the subgroup that benefits from IgRT.MethodThirty-five IgGsd-patients were sampled on three occasions: at baseline, after being on IgRT for at least 18 months, and 18 months after discontinuation of IgRT. Short form 36, EQ-5D-5L visual analogue scale and fatigue impact scale questionnaires were used for evaluation of QoL and fatigue. Furthermore, a panel of 92 inflammatory markers were analysed in plasma. Thirty-two gender- and age-matched healthy individuals were included as controls and sampled on one occasion.ResultsQoL was lower and perceived fatigue higher in IgGsd compared to the controls. Severe fatigue and low QoL were associated with the need to restart IgRT (which is considered in IgGsd-individuals with a high burden of infections in Sweden). Twenty-five inflammatory factors were dysregulated in IgGsd and the plasma protein patterns were similar regardless of whether IgRT was ongoing or not. Enrichment analysis indicated IL-10 signalling as the most affected pathway. Severe fatigue was associated with decreased levels of the neurotrophic factors VEGFA and CSF-1.ConclusionFatigue is a major contributory factor to impaired health-related QoL in IgGsd and is related to the need for IgRT. Low-grade systemic inflammation is a potential driver of fatigue. In addition to the burden of infections, we suggest the degree of fatigue should be considered when the decision to introduce IgRT is made.


Author(s):  
G Rozikhodjaeva ◽  
K Yokubov ◽  
S Hikmatov ◽  
S Hudoynazarov ◽  
L Pak

2014 ◽  
pp. 48-56
Author(s):  
Van Thi Tran ◽  
Van Bang Le ◽  
Thị Thu Huong Hoang

Aim: Some studies have linked the present of chronic obstructive oulmonary disease (COPD) to coronary artery disease (CAD). Low grade systemic inflammation occurs in patients with COPD as well as patients with CAD. This study was designed to find out the concentration differences of hs-CRP and TNF-a in patients having both chronic obstructive pulmonary and coronary artery diseases with those having either. Methods: A cross - sectional descriptive study was conducted in 200 patients undergoing a coronary artery angiography in the Heart Institute, Thong Nhat Hospital and 115 People Hospital. COPD was diagnosed using GOLD classification. Result: Our study had shown that the levels of hs-CRP and TNF-a were statistically increased in patients with COPD, CAD as well as in patients who had COPD with CAD (p<0,05). The levels of hs-CRP were higher in CAD than in COPD nad the levels of TNF-a were higher in COPD than in CAD. In patients with COPD and CAD, there were increased the levels of both hs-CRP and TNF-a in serum. Conclusion: Systemic inflammation presents in both COPD and CAD. Key words: hs-CRP, TNF-a, coronary artery disease (CAD).


Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Jessica Ellis ◽  
Keziah Austin ◽  
Sarah Emerson

Abstract Background/Aims  A 49-year-old female of Nepalese heritage was referred with right-sided headache, scalp tenderness, and a painful swelling overlying the right temple. She denied any visual or claudicant symptoms but felt systemically unwell with a fever. There were no symptoms suggestive of an inflammatory arthritis, underlying connective tissue disease or vasculitis. She was normally fit and well with no past medical history. She did not take any regular medications and denied using over the counter or illicit drugs or recent travel. On review she had a low grade fever. There was a large tender, erythematous swelling overlying the right temple. Bilaterally the temporal arteries were palpable and pulsatile. Peripheral pulses were normal with no bruits. There was no evidence of shingles (HSV) or local infection. Full systemic examination revealed no other abnormalities. Laboratory tests showed: PV 2.56, CRP 101, total white cell count 14.38 (eosinophils 0.4), albumin 33, Hb 115. Urine dip was normal. Renal function, liver function and immunoglobulins were normal. ANCA was negative. Hypoechogenicity surrounding the right frontal branch of the right temporal artery was seen on ultrasound. There were no discrete masses suggestive of cysts, abscess or tumours. Temporal artery biopsy confirmed the presence of vasculitis; histology demonstrated transmural lymphohistiocytic inflammation, disruption of the elastic lamina and intimal proliferation. Prednisolone was started at 40mg daily. Four weeks after initially presenting she was asymptomatic and her inflammatory markers had normalised. Methods  The case is discussed below. Results  Temporal arteritis, or GCA, is primarily a disease of older adults; with age 50 often used as an inclusion criteria, and is more common in Caucasian populations. Limited reports exist of GCA in younger cohorts, but these are rare. An important differential in younger patients, such as ours, is juvenile temporal arteritis. This rare localised vasculitis affects almost exclusively the temporal artery. It is typically a disease of young males, who present with non-tender temporal swelling. Systemic symptoms are unusual and inflammatory markers are normal. Clinical or laboratory evidence of organ involvement, peripheral eosinophilia or fibrinoid necrosis on histology should prompt consideration of an AAV or PAN. Incidence of GCA increases in correlation with Northern latitude, with highest rates reported in Scandinavian and North American populations. GCA is rare in Asian populations. Higher diagnostic rates in countries where physicians have increased awareness of GCA proposed as an explanation for this difference; however differences in incidence are still observed between Asian and Caucasian populations presenting to the same healthcare providers. Conclusion  GCA is an uncommon diagnosis in younger and non-Caucasian patients. Thorough investigation through ultrasound and biopsy helped increase our diagnostic confidence in this unusual case. Rheumatologists must be alert to atypical presentations in order to deliver prompt and potentially sight-saving treatment. Disclosure  J. Ellis: None. K. Austin: None. S. Emerson: None.


2021 ◽  
Vol 22 (14) ◽  
pp. 7582
Author(s):  
Evgenii Gusev ◽  
Alexey Sarapultsev ◽  
Desheng Hu ◽  
Valeriy Chereshnev

The COVID-19 pandemic examines not only the state of actual health care but also the state of fundamental medicine in various countries. Pro-inflammatory processes extend far beyond the classical concepts of inflammation. They manifest themselves in a variety of ways, beginning with extreme physiology, then allostasis at low-grade inflammation, and finally the shockogenic phenomenon of “inflammatory systemic microcirculation”. The pathogenetic core of critical situations, including COVID-19, is this phenomenon. Microcirculatory abnormalities, on the other hand, lie at the heart of a specific type of general pathological process known as systemic inflammation (SI). Systemic inflammatory response, cytokine release, cytokine storm, and thrombo-inflammatory syndrome are all terms that refer to different aspects of SI. As a result, the metabolic syndrome model does not adequately reflect the pathophysiology of persistent low-grade systemic inflammation (ChSLGI). Diseases associated with ChSLGI, on the other hand, are risk factors for a severe COVID-19 course. The review examines the role of hypoxia, metabolic dysfunction, scavenger receptors, and pattern-recognition receptors, as well as the processes of the hemophagocytic syndrome, in the systemic alteration and development of SI in COVID-19.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohammad Z. Darabseh ◽  
Thomas M. Maden-Wilkinson ◽  
George Welbourne ◽  
Rob C. I. Wüst ◽  
Nessar Ahmed ◽  
...  

AbstractCigarette smoking has a negative effect on respiratory and skeletal muscle function and is a risk factor for various chronic diseases. To assess the effects of 14 days of smoking cessation on respiratory and skeletal muscle function, markers of inflammation and oxidative stress in humans. Spirometry, skeletal muscle function, circulating carboxyhaemoglobin levels, advanced glycation end products (AGEs), markers of oxidative stress and serum cytokines were measured in 38 non-smokers, and in 48 cigarette smokers at baseline and after 14 days of smoking cessation. Peak expiratory flow (p = 0.004) and forced expiratory volume in 1 s/forced vital capacity (p = 0.037) were lower in smokers compared to non-smokers but did not change significantly after smoking cessation. Smoking cessation increased skeletal muscle fatigue resistance (p < 0.001). Haemoglobin content, haematocrit, carboxyhaemoglobin, total AGEs, malondialdehyde, TNF-α, IL-2, IL-4, IL-6 and IL-10 (p < 0.05) levels were higher, and total antioxidant status (TAS), IL-12p70 and eosinophil numbers were lower (p < 0.05) in smokers. IL-4, IL-6, IL-10 and IL-12p70 had returned towards levels seen in non-smokers after 14 days smoking cessation (p < 0.05), and IL-2 and TNF-α showed a similar pattern but had not yet fully returned to levels seen in non-smokers. Haemoglobin, haematocrit, eosinophil count, AGEs, MDA and TAS did not significantly change with smoking cessation. Two weeks of smoking cessation was accompanied with an improved muscle fatigue resistance and a reduction in low-grade systemic inflammation in smokers.


Author(s):  
Chris L. de Korte ◽  
Stein Fekkes ◽  
Aart J. Nederveen ◽  
Rashindra Manniesing ◽  
Hendrik Rik H. G. Hansen

Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Muhammad F Kazmi

Abstract Background/Aims  Rheumatological conditions can present with a number of non-specific features like arthralgia, fever, fatigue, weight loss along with raised inflammatory markers and positive antibodies. Due to this, when similar symptoms are referred for input it is very important to consider other ‘mimics’. We report a case of Pigeon fancier’s lung presenting with these symptoms which was referred as likely connective tissue disease. Methods  A 52-year-old lady of South Asian origin was referred by her GP with six month history of 3kg weight loss, arthralgia, fatigue, low grade fever and persistently raised inflammatory markers (ESR ranging from 50-64 mm/hr, CRP 10-14 mg/L, normal BMI). On further questioning there was history of mouth ulcers, non-specific rash, occasional cough but no Raynaud’s or joint swelling. Blood investigations showed weakly positive ANA and RF but negative ENA, DNA, antiCCP , CK, C3,C4. C-ANCA was positive but PR3 negative. CXR was clear and tests for chronic infections including TB were negative. Due to lack of objective CTD signs, plan was to take a careful monitoring approach to see if clinical features evolved. A month later due to worsening cough, a CT chest/abdomen arranged by GP showed ground-glass changes consistent with pneumonitis and hence her rheumatology appointment was expedited to see if there was an autoimmune unifying diagnosis. She was also referred by her GP to the chest clinic in view of CT report and mild shortness of breath. Results  On further review, again there were no objective CTD signs. On direct questioning there was history of travelling before worsening chest symptoms to South Asia. Also around a year before her symptoms started she was given an African grey parrot. Based on this, serology for Avian precipitin was checked which showed strongly positive IgG antibodies to avian antigens (Budgerigar droppings and feathers, Pigeon feathers IgG Abs) confirming the diagnosis of pigeon fanciers lung. She fulfilled the diagnostic criteria and was asked to avoid the trigger. Urgent respiratory input was arranged where diagnosis was agreed with and disease was deemed sub-acute in presentation. Due to PFTs showing low transfer factor of 38%, Prednisolone was started with significant improvement within few days. Review of CT chest only showed inflammatory changes and no established fibrosis predicting excellent prognosis as delay in treatment can cause irreversible pulmonary fibrosis. Conclusion  A number of conditions can mimic rheumatological conditions which usually turn out to be either infectious or malignant in origin. This case highlights the importance of considering other differentials and along with taking a travel history also asking for other possible triggers like pets. In similar scenarios the diagnosis may be ‘cagey’ but as rheumatologists we are expected to answers questions which others can’t. Disclosure  M.F. Kazmi: None.


Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Xihai Zhao ◽  
Huilin Zhao ◽  
Feiyu Li ◽  
Jie Sun ◽  
Ye Cao ◽  
...  

Introduction Rupture of vulnerable atherosclerotic plaques in the intracranial and extracranial carotid arteries could trigger ischemic stroke. However, the incidence of high risk atherosclerotic lesions in these vascular beds is not well known. This study sought to investigate the incidence of high risk atherosclerotic lesions in intracranial and extracranial carotid arteries in stroke patients using magnetic resonance (MR) imaging. Methods Seventy-five patients (mean age 62.7 years, 56 males) with acute ischemic stroke underwent MR imaging for index carotid arteries, assigned as the same side as the brain lesions, with a Philips 3.0T MR scanner. Intracranial carotid MR angiography was performed using 3D TOF sequence with FOV of 23 × 23 cm 2 , matrix of 256 × 256, and a slice thickness of 1mm. The multi-contrast vessel wall images (3D TOF, T1W, T2W, and MP-RAGE) were acquired for extracranial carotid arteries with FOV of 14 × 14 cm 2 , matrix of 256 × 256, and slice thickness of 2 mm. The intracranial artery includes middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA). The extracranial carotid artery was divided into internal carotid artery (ICA), bulb, and common carotid artery (CCA). Luminal stenosis for each intracranial and extracranial carotid segment was measured and graded (normal or mild = 0-29%, moderate =30-69%, severe=70-99%). Normalized wall index (NWI = wall area/total vessel area × 100%), and presence/absence of calcification, lipid-rich necrotic core (LRNC), and intraplaque hemorrhage (IPH) and/or fibrous cap rupture in each extracranial carotid segment were determined. Results MCAs developed more severe stenotic lesions (24.6%), followed by extracranial carotids (16.5%), PCAs (5.4%), and ACAs (4.1%) in stroke patients ( Figure 1 A). For extracranial carotid arteries, ICAs showed the largest plaque burden as measured by NWI (44.3%±13.1%), followed by bulbs (39.4%±13%), and CCAs (37%±6.8%). Compared to CCAs, ICAs and bulb regions had more LRNCs (38.4% and 49.3% for ICA and bulb respectively) and IPH and/or rupture (11% and 9.6% for ICA and bulb respectively) ( Figure 1 B). Conclusions In patients with acute ischemic stroke, high risk atherosclerotic plaques can be found in both intracranial and extracranial carotid arteries, particularly in the MCA, ICA and bulb regions. Compared to extracranial carotid arteries, intracranial arteries develop more high risk lesions. The findings of this study suggest the necessity for early screening to detect high risk atherosclerotic lesions in these carotid vascular beds prior to cerebravascular events.


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