scholarly journals Intestinal Amyloidosis in Common Variable Immunodeficiency and Rheumatoid Arthritis

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
T. Meira ◽  
R. Sousa ◽  
A. Cordeiro ◽  
R. Ilgenfritz ◽  
P. Borralho
Keyword(s):  
Rheumatoid Arthritis ◽  
Common Variable Immunodeficiency ◽  
Chronic Diarrhea ◽  
Inflammatory Diseases ◽  
Amyloid Deposition ◽  
Prior History ◽  
Chronic Inflammatory Diseases ◽  
Reactive Amyloidosis ◽  
History Of ◽  
Common Variable

We present a case of reactive amyloidosis that developed secondary to common variable immunodeficiency and rheumatoid arthritis. A 66-year-old woman, with prior history of common variable immunodeficiency and rheumatoid arthritis, was referred to our clinic for chronic diarrhea investigation. The patient was submitted to colonoscopy with ileoscopy, which did not show relevant endoscopic alterations. However, undertaken biopsies revealed amyloid deposition. Since amyloidosis with GI involvement is a rare cause of chronic diarrhea, this pathology should be considered in etiologic investigation, especially when associated with chronic inflammatory diseases.

scholarly journals Lipid, fatty acid, carnitine- and choline derivative profiles in rheumatoid arthritis outpatients with different degrees of periodontal inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kathrin Beyer ◽  
Stein Atle Lie ◽  
Bodil Bjørndal ◽  
Rolf K. Berge ◽  
Asbjørn Svardal ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Fatty Acid ◽  
Mitochondrial Dysfunction ◽  
Inflammatory Diseases ◽  
Whole Body ◽  
Cross Sectional ◽  
Chronic Inflammatory Diseases ◽  
Periodontal Inflammation ◽  
Inflammatory Status ◽  
Lipid Fatty Acid

AbstractRheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases with several pathogenic pathways in common. Evidence supports an association between the diseases, but the exact underlying mechanisms behind the connection are still under investigation. Lipid, fatty acid (FA) and metabolic profile alterations have been associated with several chronic inflammatory diseases, including RA and periodontitis. Mitochondria have a central role in regulating cellular bioenergetic and whole-body metabolic homeostasis, and mitochondrial dysfunction has been proposed as a possible link between the two disorders. The aim of this cross-sectional study was to explore whole-blood FA, serum lipid composition, and carnitine- and choline derivatives in 78 RA outpatients with different degrees of periodontal inflammation. The main findings were alterations in lipid, FA, and carnitine- and choline derivative profiles. More specifically, higher total FA and total cholesterol concentrations were found in active RA. Elevated phospholipid concentrations with concomitant lower choline, elevated medium-chain acylcarnitines (MC-AC), and decreased ratios of MC-AC and long-chain (LC)-AC were associated with prednisolone medication. This may indicate an altered mitochondrial function in relation to the increased inflammatory status in RA disease. Our findings may support the need for interdisciplinary collaboration within the field of medicine and dentistry in patient stratification to improve personalized treatment. Longitudinal studies should be conducted to further assess the potential impact of mitochondrial dysfunction on RA and periodontitis.

Ischaemic heart disease and pregnancy

Heart ◽  
2018 ◽  
Vol 105 (3) ◽  
pp. 189-195 ◽  
Author(s):  
Matthew Cauldwell ◽  
Lucia Baris ◽  
Jolien W Roos-Hesselink ◽  
Mark R Johnson
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Maternal Morbidity ◽  
Inflammatory Diseases ◽  
Later Life ◽  
Shock Delivery ◽  
Chronic Inflammatory Diseases ◽  
Prevalence Of Obesity ◽  
History Of ◽  
In Pregnancy

Although ischaemic heart disease is currently rarely encountered in pregnancy, occurring between 2.8 and 6.2 per 100 000 deliveries, it is becoming more common as women delay becoming pregnant until later life, when medical comorbidities are more common, and because of the higher prevalence of obesity in the pregnant population. In addition, chronic inflammatory diseases, which are more common in women, may contribute to greater rates of acute myocardial infarction (AMI). Pregnancy itself seems to be a risk factor for AMI, although the exact mechanisms are not clear. AMI in pregnancy should be investigated in the same manner as in the non-pregnant population, not allowing for delays, with investigations being conducted as they would outside of pregnancy. Maternal morbidity following AMI is high as a result of increased rates of heart failure, arrhythmia and cardiogenic shock. Delivery in women with history of AMI should be typically guided by obstetric indications not cardiac ones.

scholarly journals Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Pascale Zwicky ◽  
Susanne Unger ◽  
Burkhard Becher
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Disease ◽  
Interleukin 17 ◽  
Clinical Perspective ◽  
Preclinical Models ◽  
Chronic Inflammatory Diseases ◽  
Recent Developments ◽  
Disease Entities ◽  
Barrier Tissues

Chronic inflammatory diseases like psoriasis, Crohn’s disease (CD), multiple sclerosis (MS), rheumatoid arthritis (RA), and others are increasingly recognized as disease entities, where dysregulated cytokines contribute substantially to tissue-specific inflammation. A dysregulation in the IL-23/IL-17 axis can lead to inflammation of barrier tissues, whereas its role in internal organ inflammation remains less clear. Here we discuss the most recent developments in targeting IL-17 for the treatment of chronic inflammation in preclinical models and in patients afflicted with chronic inflammatory diseases.

scholarly journals Expedited Desensitization to Canakinumab

2020 ◽  
Vol 11 ◽  
pp. 215265672093769 ◽  
Author(s):  
Neha Sanan ◽  
Jason Schend ◽  
Marija Rowane ◽  
Robert Hostoffer
Keyword(s):  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Alternative Therapy ◽  
Prior History ◽  
Intradermal Testing ◽  
Immune Modulators ◽  
Fever Syndromes ◽  
Gastrointestinal Intolerance ◽  
History Of ◽  
Desensitization Protocol

Introduction Interleukin-1 (IL-1) antagonists have been successful in the management of monogenic auto-inflammatory diseases, notably classic hereditary fever syndromes, such as Familial Mediterranean Fever (FMF). Anakinra (Kineret®), a human recombinant IL-1 receptor antagonist (IL-1Ra), has been clinically effective in the management of persistent auto-inflammation, such as FMF. Few studies report anaphylaxis in response to anakinra, which were resolved with an anakinra desensitization or the anti-IL-1β monoclonal antibody canakinumab (ILARIS®). We describe the first reported desensitization protocol to canakinumab. Case Report A 51-year-old man with a prior history of FMF presented with history of failed colchicine, nonsteroidal anti-inflammatory drug, and anakinra trials. Anakinra desensitization and canakinumab intradermal testing (IDT) resulted in anaphylactic and allergic symptoms, respectively. Expedited desensitization to canakinumab was successfully performed with 15-minute intervals between 13 doses of incremental increase to 150 mg. Discussion Biological agents are immune modulators that may evoke unanticipated hypersensitivity reactions, including anaphylaxis. These anaphylactic reactions to biologics have been infrequently reported, but the expanding market may increase the risk of IgE-mediated hypersensitivities and subsequent need for desensitization protocols. The current, expedited desensitization evaluated several published protocols involving anakinra desensitization to determine appropriate dosing for canakinumab. Conclusion We report the gastrointestinal intolerance and continued FMF flares on colchicine, followed by anaphylactic responses to anakinra and allergic reaction to IDT of canakinumab, in the present case of FMF. Our novel, expedited canakinumab desensitization protocol serves as an effective and alternative therapy in cases when other appropriate biologic agents are not tolerated.

scholarly journals Comparative analysis of various metrics of arterial compliance in the study of chronic inflammatory diseases

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P.L Kerkhof ◽  
R.B Djorai ◽  
A Maslyanskiy ◽  
E Kolesova ◽  
A.O Konradi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Ankylosing Spondylitis ◽  
Arterial Stiffness ◽  
Arterial Pressure ◽  
Inflammatory Diseases ◽  
Arterial Compliance ◽  
Poor Correlation ◽  
Funding Source ◽  
Chronic Inflammatory Diseases ◽  
The Impact

Abstract Introduction Arterial compliance (AC), known to depend on age and sex, may be severely compromised in chronic inflammatory diseases. Apart from the various definitions for arterial stiffness that are in vogue, their constituent components are often not unique. Purpose This study compares vascular stiffness measures in various inflammatory diseases and explores a more comprehensive description of vessel wall properties by also considering inherent associated companion metrics. Methods We retrospectively analyzed arterial pressure, ventricular volume by echocardiography (Vivid-7 ultrasound system), along with carotid–femoral pulse wave velocity (PWV, by SphygmoCor, Atcor). Pulse pressure (PP) equals systolic arterial pressure (SAP) minus diastolic arterial pressure (DAP). Effective arterial elastance (Ea) = 0.9 × SAP/SV where SV is stroke volume. AC=SV/PP (Figure 1A). The intrinsic companion (C) to any established difference-based metric is calculated on the basis of the squared mean, e.g., PPC2 = (SAP2 + DAP2). Clearly, AC depends on two differences, each having a companion. Results A total of 177 patients (age range 18 to 80 years, 49 males), characterized by inflammatory disease (51 scleroderma, 62 atherosclerosis, 35 ankylosing spondylitis, and 29 rheumatoid arthritis), yielded reduced levels of vacular compliance irrespective of the method selected. Regression analysis showed weak correlations between the various approaches (i.e., Ea, AC, PWV). Average values for AC are comparable for all 4 diagnostic groups. Ea (P<0.03) and PWV (P<0.014) are lower for ankylosing spondylitis compared to all other groups, likely due to younger age and the higher prevalence of men. Ea is highest in atherosclerosis (P<0.026) versus all other groups. SV is significantly higher in atherosclerosis (P<0.03) compared to scleroderma and rheumatoid arthritis. However, the companions may differ (Figure 1B): PPC is significantly (P=0.017) higher in atherosclerosis (156.3±16.1 mmHg) vs scleroderma (147.2±23.0 mmHg), while SVC in ankylosing spondylitis is higher (P<0.013) than in all other groups. Conclusions Arterial stiffness measures show poor correlation, suggesting limitations to their utility when studying the diagnostic groups described here. Consideration of the companion associated with each difference-based metric is warranted in order to perform a comprehensive analysis of clinical data when evaluating the impact on risk factors and prognosis. Figure 1. A: Compliance components. B: Companions Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Russian Science Foundation

scholarly journals Cross-tissue, single-cell stromal atlas identifies shared pathological fibroblast phenotypes in four chronic inflammatory diseases

2021 ◽  
Author(s):  
Ilya Korsunsky ◽  
Kevin Wei ◽  
Mathilde Pohin ◽  
Edy Y. Kim ◽  
Francesca Barone ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Bowel Disease ◽  
Single Cell ◽  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Disease ◽  
Chronic Inflammatory Diseases ◽  
Single Cell Rna Sequencing ◽  
Inflammatory Bowel ◽  
Novel Therapeutic

SummaryPro-inflammatory fibroblasts are critical to pathogenesis in rheumatoid arthritis, inflammatory bowel disease, interstitial lung disease, and Sjögren’s syndrome, and represent a novel therapeutic target for chronic inflammatory disease. However, the heterogeneity of fibroblast phenotypes, exacerbated by the lack of a common cross-tissue taxonomy, has limited the understanding of which pathways are shared by multiple diseases. To investigate, we profiled patient-derived fibroblasts from inflamed and non-inflamed synovium, intestine, lung, and salivary glands with single-cell RNA-sequencing. We integrated all fibroblasts into a multi-tissue atlas to characterize shared and tissue-specific phenotypes. Two shared clusters, CXCL10+CCL19+ immune-interacting and SPARC+COL3A1+ vascular-interacting fibroblasts were expanded in all inflamed tissues and additionally mapped to dermal analogues in a public atopic dermatitis atlas. We further confirmed these human pro-inflammatory fibroblasts in animal models of lung, joint, and intestinal inflammation. This work represents the first cross-tissue, single-cell fibroblast atlas revealing shared pathogenic activation states across four chronic inflammatory diseases.

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