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ID PMID Title PublicationDate abstract
27866180 Positive Effects of Uyakujunkisan Therapy (Kampo Medicine) for Postherpetic Neuralgia With 2016 Nov Context • The hallmark of herpes zoster (HZ) is a painful, blistering rash, but neuropathic pain can persist beyond the clearing of the rash and is diagnosed as postherpetic neuralgia (PHN), a chronic pain syndrome. However, the pain in PHN is often refractory to treatment. Objective • The study investigated the ability of Uyakujunkisan (UJS), or Kampo medicine, a traditional herbal medicine, to treat PHN successfully. Design • The study was observational, with discussion of 2 cases. Setting • The study took place in the Department of Japanese Oriental Medicine at Gunma Central and General Hospital (Maebashi, Gunma, Japan). Participants • The participants in cases 1 and 2 were a 70-y-old male and a 70-y-old female, respectively. The woman in case 2 also had rheumatoid arthritis. Both had been treated for HZ with antiviral drugs but continued to experience pain and were diagnosed with PHN. Intervention • Both participants were treated with a decoction of UJS that was administered 3 ×/d before meals. Outcome Measures • The patients completed a visual analogue scale. Results • In case 1, the patient's pain had almost disappeared after 8 wk of treatment. In case 2, the patient's pain had disappeared by 4 mo after starting the UJS treatment. Conclusions • Treatment with UJS may be a useful option as a therapeutic strategy for refractory PHN, especially in older adults.
27004724 Two new eunicellin diterpenoids from the East China Sea gorgonian Muricella sp. 2016 Sep A phytochemical investigation on gorgonian Muricella sp. from East China Sea resulted in the isolation of eight eunicellin diterpenoids including two new ones, muricellins A-B (1, 2). Chemical structures of these compounds were elucidated by spectroscopic techniques (1D and 2D NMR and MS) and by comparison with data reported in the literature. Anti-rheumatoid arthritis activities of 1, 3, 4, and 6 have been evaluated.
26845207 [Management of antirheumatic drugs in kidney failure]. 2015 Nov The nephrologist deals with the management of patients with rheumatic disease, both diagnostically and therapeutically. He must determine whether the renal pathology is related to the rheumatologic disease, mostly through the use of the renal biopsy. In the second case, he must know the nephrotoxic potential of the drugs prescribed and adjust their use to the degree of renal impairment. This task is made difficult by the absence of controlled clinical trials regarding their use on patients with renal insufficiency or on chronic dialysis. For this reason, the prescription will have to take into account the pharmacokinetics of the drugs. Kidney failure can affect the metabolism of antirheumatic drugs determining their accumulation, which can lead to increased toxicity, either renal or systemic. On the other hand, dialysis can cause excessive drug removal, leading to sub-therapeutic pharmacological effects and to the need for additional doses. In this brief review, we will consider the nephrotoxic effects of some important drugs used in rheumatology and examined individually, with specific reference to rheumatoid arthritis: methotrexate, leflunamide, hydroxychloroquine, cyclosporine, biological DMARDs. In the past, therapeutic success in rheumatic diseases associated with kidney impairment was severely limited by the well- known nephrotoxicity of drugs such as gold salts, D-penicillamine, NSAIDs, COX-2 inhibitors. Although generally effective, they are contraindicated in case of kidney failure. Biologic therapies have recently opened new therapeutic perspectives. Nevertheless, it is worth stressing how our knowledge of their action is still incomplete and this may result in exposure to immune-mediated renal disease.
26768963 The role of HIF in immunity and inflammation. 2016 Feb Uncontrolled or non-resolving inflammation underpins a range of disease states including rheumatoid arthritis, inflammatory bowel disease and atherosclerosis. Hypoxia is a prominent feature of chronically inflamed tissues. This is due to elevated oxygen consumption by highly metabolically active inflamed resident cells and activated infiltrating immunocytes, as well as diminished oxygen supply due to vascular dysfunction. Tissue hypoxia can have a significant impact upon inflammatory signaling pathways in immune and non-immune cells and this can impact upon disease progression. In this review, we will discuss the relationship between tissue hypoxia and inflammation and identify how hypoxia-sensitive signaling pathways are potential therapeutic targets in chronic inflammatory disease.
26684936 Antibodies against neo-epitope tTg complexed to gliadin are different and more reliable th 2016 Feb The neo-epitope tTg (tTg-neo) autoantibody, never challenged the anti-tissue transglutaminase (tTg) premiership, recommended by ESPGHAN, for celiac disease (CD) diagnosis. Pediatric CD (PCD), abdominal pains and normal children, normal adults, and rheumatoid arthritis patients, were tested using the following ELISAs detecting IgA, IgG or both IgA and IgG (check): AESKULISA® tTg (tTg; RUO) and AESKULISA® tTg-neo. Higher OD activity was detected for tTg-neo IgA, IgG and IgA+IgG than for tTg. tTg-neo IgA, IgG correlated better with intestinal damage than tTg. The tTg-neo combined IgA+IgG ELISA kit had higher sensitivity and a comparable specificity for the diagnosis of PCD. The drop in the % competition was much higher with the tTg-neo then the tTg antibodies. The false positivity of the tTg was significantly higher than the tTg-neo one. Serological diagnostic performances, reflection of intestinal damage, diverse epitopes and false positivity were better with the tTg-neo.
26308397 Identification of a new STAT3 dimerization inhibitor through a pharmacophore-based virtual 2016 Dec Signal transducer and activator of transcription 3 (STAT3) plays an essential role in cell growth regulation and survival. An aberrant STAT3 activation and/or expression is implied in various solid and blood tumors as well as in other pathologies like rheumatoid arthritis and pulmonary fibrosis, thus making the search for STAT3 inhibitors a growing field of study. With the aim of identifying new inhibitors of STAT3 dimerization, we screened a database including more than 1 320 000 commercially available compounds using a receptor-based pharmacophore model comprising the key protein-protein interactions identified in the STAT3 dimer and refining the search through docking and molecular dynamic simulations studies. STAT3 binding assays revealed a significant STAT3 inhibitory activity and selectivity versus Grb2 for one of the four top-scored compounds, thus verifying the reliability of the virtual screening workflow. Moreover, such compound could already be considered as a lead for the development of new and more potent STAT3 dimerization inhibitors.
25973436 The danger model approach to the pathogenesis of the rheumatic diseases. 2015 The danger model was proposed by Polly Matzinger as complement to the traditional self-non-self- (SNS-) model to explain the immunoreactivity. The danger model proposes a central role of the tissular cells' discomfort as an element to prime the immune response processes in opposition to the traditional SNS-model where foreignness is a prerequisite. However recent insights in the proteomics of diverse tissular cells have revealed that under stressful conditions they have a significant potential to initiate, coordinate, and perpetuate autoimmune processes, in many cases, ruling over the adaptive immune response cells; this ruling potential can also be confirmed by observations in several genetically manipulated animal models. Here, we review the pathogenesis of rheumatic diseases such as systemic lupus erythematous, rheumatoid arthritis, spondyloarthritis including ankylosing spondylitis, psoriasis, and Crohn's disease and provide realistic approaches based on the logic of the danger model. We assume that tissular dysfunction is a prerequisite for chronic autoimmunity and propose two genetically conferred hypothetical roles for the tissular cells causing the disease: (A) the Impaired cell and (B) the paranoid cell. Both roles are not mutually exclusive. Some examples in human disease and in animal models are provided based on current evidence.
25958049 Arthroscopic treatment of bony loose bodies in the subacromial space. 2015 INTRODUCTION: Multiple bony loose bodies in the subacromial space caused form cartilage or bone cells and continue to grow. PRESENTATION OF CASE: A 58-year-old man with two-year history of swelling and pain of the right shoulder. He had no history of tuberculosis and rheumatoid arthritis. Magnetic resonance (MR) images showed some bony loose bodies in the subacromial space. The removal of loose bodies and bursa debridement were performed arthroscopically. Histological diagnosis of them was synovitis with fibrous bodies. DISCUSSION: Extra-articular loose bodies is extremely rare, especially in the subacromial space, which maybe originated in the proliferative synovial bursa. Most authors recommend open removal to relive the pain, but there were choice to apply arthroscopy to remove them. CONCLUSION: The mechanism of formation of bony loose bodies is not clear, may be associated with synovial cartilage metaplasia. Arthroscopic removal of loose bodies and bursa debridement is a good option for treatment of the loose body in the subacromial space, which can receive good function.
25861466 Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalanc 2015 Autoimmune diseases (ADs) are considered to be caused by the host immune system which attacks and destroys its own tissue by mistake. A widely accepted hypothesis to explain the pathogenic mechanism of ADs is "molecular mimicry," which states that antibodies against an infectious agent cross-react with a self-antigen sharing an identical or similar antigenic epitope. However, this hypothesis was most likely established based on misleading antibody assay data largely influenced by intense false positive reactions involved in immunoassay systems. Thus reinvestigation of this hypothesis using an appropriate blocking agent capable of eliminating all types of nonspecific reactions and proper assay design is strongly encouraged. In this review, we discuss the possibility that low immune function may be the fundamental, common defect in ADs, which increases the susceptibility to potential disease causative pathogens located in the gastrointestinal tract (GI), such as bacteria and their components or dietary components. In addition to these exogenous agents, aberrations in the host's physical condition may disrupt the host defense system, which is tightly orchestrated by "immune function," "mucosal barrier function," and "intestinal bacterial balance." These disturbances may initiate a downward spiral, which can lead to chronic health problems that will evolve to an autoimmune disorder.
25791770 The emerging role of rituximab in autoimmune blistering diseases. 2015 Jun Rituximab is a chimeric monoclonal antibody that selectively binds to the CD20 molecule on B cells, resulting in their lysis. In autoimmune blistering diseases, the auto-antibody-producing B cells are destroyed and auto-antibody levels are reduced or eliminated. In the majority of patients, rituximab produces rapid clinical response and early resolution. In part, this accounts for the increased use of rituximab. Rituximab does not distinguish normal from pathologic B cells. Hence, shortly after its use, B-cell levels are zero and remain so for several months. In most patients, the use of systemic corticosteroids and immunosuppressive agents are continued after rituximab therapy, while their dosages are significantly decreased. In the majority of patients rituximab is used according to the protocol used in treating lymphoma patients or patients with rheumatoid arthritis. Approximately 50% of patients experience a relapse, requiring additional therapy. Serious adverse events and fatal outcomes have been reported, although their incidence is less than that observed with conventional therapy. Nonetheless, the causes, i.e. infections and septicemia, are similar. Several gaps exist in our understanding of how to optimally benefit from the use of this valuable biological agent. Future studies need to be targeted in designing and implanting protocols that maximize the benefit of rituximab and result in producing sustained prolonged remissions with minimal adverse events and a high quality of life.
25648415 Three cases of previous smokers with rheumatoid arthritis who did not respond to tumor nec 2015 We report three cases of previous smokers who did not respond to TNF inhibitors but who responded successfully to an anti-interleukin-6 receptor antibody (tocilizumab (TCZ)). Case 1 is a 63-year-old woman whose smoking index was 200 and had been complaining of polyarthralgia since 1996. She started treatment with etanercept due to high disease activity, but her DAS28-CRP was 4.2. She was therefore switched to TCZ, which dramatically improved her symptoms; her DAS28-CRP had decreased to 2.1. Case 2 is a 64-year-old man whose smoking index was 1600 and had been complaining of polyarthralgia since 2006. Because his DAS28-CRP score increased over time to 5.9, etanercept and adalimumab were added sequentially, but he showed no response over the course of two years. The patient was therefore switched to TCZ, which dramatically improved his symptoms: his DAS28-CRP decreased to 2.7. Case 3 is a 48-year-old woman whose smoking index was 560 and had been complaining of pain in both knee joints since 2001. She was treated with adalimumab due to high disease activity but showed no response over the course of 1.5 years. The patient was therefore switched to TCZ, and her DAS28-CRP decreased to 1.8. An IL-6 blockade might be suitable for treating these 3 cases of previous smokers.
25034081 Safety and efficacy of etanercept in children with the JIA categories extended oligoarthri 2015 Jan The approval of etanercept for the treatment of the juvenile idiopathic arthritis (JIA) categories extended oligoarthritis (ExtOA), enthesitis-related arthritis (ERA) and psoriasis arthritis (PsA) was recently added to the approval for the treatment of polyarticular-course JIA (PA). This study aims to evaluate the efficacy and safety of etanercept in a large number of patients with the additional JIA categories. The Biologika in der Kinderrheumatologie (BIKER) registry documents baseline demographics, clinical characteristics and disease activity parameters. Efficacy was determined using the PedACR 30/50/70 response criteria and the Juvenile Arthritis Disease Activity Score (JADAS)-10. Safety assessments were based on adverse events' reports. Until December 2012, a total of 1,678 JIA patients, incorporating 238 ERA, 315 ExtOA and 127 PsA patients were included. JADAS-10 demonstrated marked improvement compared to baseline after 3 to 24 months in ExtOA [16.1 ± 7.6 (baseline), 5.1 ± 5.2 (3 months), 3.0 ± 3.5 (24 months)]; ERA (15.3 ± 7.2, 4.4 ± 4.7, 4.0 ± 4.9) and PsA (14.7 ± 6.4, 5.0 ± 4.6, 5.3 ± 6.4). Compared to patients with PA, the rate of serious adverse events [relative risk (RR) 1.39 (0.95-2.03, p = 0.08)] and nonserious [1.18 (1.02-1.35; p = 0.03)] adverse events were elevated. The rate of uveitis flares was significantly higher in PsA (3.3/100 patient-years), ExtOA (2.8/100 patient-years) and ERA (2.7/100 patient-years) than in rheumatoid factor (RF)-negative polyarticular JIA (1.3/100 pat.yrs) or RF-positive polyarticular JIA (0.27/100 patient-years). Reports on chronic inflammatory bowel disease were numerically more frequent in ExtOA, ERA and PsA. Administration of etanercept in patients with the JIA categories ExtOA, ERA and PsA is safe and very efficacious in children. Attention should be paid to the occurrence of extraarticular autoimmunopathies.
27756248 The impact of unrecognized autoimmune rheumatic diseases on the incidence of preeclampsia 2016 Oct 18 BACKGROUND: The burden of pregnancy complications associated with well defined, already established systemic rheumatic diseases preexisting pregnancy such as rheumatoid arthritis, systemic lupus erythematosus or scleroderma is well known. Systemic rheumatic diseases are characterized by a long natural history with few symptoms, an undifferentiated picture or a remitting course making difficult a timely diagnosis. It has been suggested that screening measures for these diseases could be useful but the impact of unrecognized systemic rheumatic disorders on pregnancy outcome is unknown. The objective of the study was to evaluate the impact of previously unrecognized systemic autoimmune rheumatic on the incidence of preeclampsia and fetal growth restriction (FGR). METHODS: A longitudinal cohort-study with enrolment during the first trimester of pregnancy of women attending routine antenatal care using a two-step approach with a self-reported questionnaire, autoantibody detection and clinical evaluation of antibody-positive subjects. The incidence of FGR and preeclampsia in subjects with newly diagnosed rheumatic diseases was compared to that of selected negative controls adjusting for potential confounders by logistic regression analysis. RESULTS: The prevalence of previously unrecognized systemic rheumatic diseases was 0.4 % for rheumatoid arthritis (19/5232), 0.25 % (13/5232) for systemic lupus erythematosus, 0.31 % (16/5232) for Sjögren's syndrome, 0.3 % for primary antiphospholipid syndrome (14/5232) and 0.11 % (6/5232) for other miscellaneous diseases. Undifferentiated connective tissue disease was diagnosed in an additional 131 subjects (2.5 %). The incidence of either FGR or preeclampsia was 6.1 % (36/594) among controls and 25.3 % (50/198) in subjects with unrecognized rheumatic diseases (excess incidence = 3.9 % (95 % CI = 2.6-9.6) or 34 % (95 % CI = 22-44) of all cases of FGR/preeclampsia). The incidence of small for gestational age infant (SGA) was higher among subjects with unrecognized rheumatic diseases (41/198 as compared to 46/594; adjOdds Ratio = 3.1, 95 % CI =1.96-4.95) than in controls. The excess incidence associated with unrecognized rheumatic diseases was 2.7 % (95 % CI = 1.5-4) or 25 % (95 % CI = 12.8-34.8) of all SGA cases. CONCLUSIONS: Unrecognized autoimmune systemic rheumatic disorders are associated with a significant proportion of preeclampsia and fetal growth failure, suggesting that their role in the etiology of adverse pregnancy outcome is probably undervalued.
27325124 Hypogonadism and the risk of rheumatic autoimmune disease. 2016 Dec Testosterone deficiency has been linked with autoimmune disease and an increase in inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor, and interleukin-6 (IL-6). However, no large-scale longitudinal studies have examined this association. We examined whether untreated hypogonadism was associated with an increased risk of rheumatic autoimmune disease in a large nationally representative cohort. Using one of the nation's largest commercial insurance databases, we conducted a retrospective cohort study in which we identified 123,460 men diagnosed with hypogonadism between January 1, 2002 and December 31, 2014 and with no prior history of rheumatic autoimmune disease. We matched this cohort to 370,380 men without hypogonadism, at a 1 to 3 ratio, on age and index/diagnosis date. All patients were followed until December 31, 2014 or until they lost insurance coverage or were diagnosed with a rheumatic autoimmune disease. Cox proportional hazards regression was used to calculate adjusted hazard ratios (aHRs). Untreated hypogonadism was associated with an increased risk of developing any rheumatic autoimmune disease (HR = 1.33, 95 % CI = 1.28, 1.38), rheumatoid arthritis (HR = 1.31, 95 % CI = 1.22, 1.44), and lupus (HR = 1.58, 95 % CI = 1.28, 1.94). These findings persisted using latency periods of 1 and 2 years. Hypogonadism was not associated with the control outcome, epilepsy (HR = 1.04, 95 % CI = 0.96, 1.15). Patients diagnosed with hypogonadism who were not treated with testosterone had an increased risk of developing any rheumatic autoimmune disease, rheumatoid arthritis, and lupus. Future research should further examine this association, with particular attention to underlying mechanisms.
26675441 Discovery of highly potent and selective Bruton's tyrosine kinase inhibitors: Pyridazinone 2016 Jan 15 BTK inhibitor GDC-0834 (1) was found to be rapidly metabolized in human studies, resulting in a suspension of clinical trials. The primary route of metabolism was through cleavage of the acyclic amide bond connecting the terminal tetrahydrobenzothiophene with the central linker aryl ring. SAR studies were focused on reducing metabolic cleavage of this amide, and resulted in the identification of several central aryl linker substituents that conferred improved stability. The most promising substituted aryl linkers were then incorporated into an optimized pyridazinone scaffold, resulting in the identification of lead analog 23, possessing improved potency, metabolic stability and preclinical properties.
26550952 Bromo-honaucin A inhibits osteoclastogenic differentiation in RAW 264.7 cells via Akt and 2015 Dec 15 Osteoclasts are unique bone remodeling cells derived from multinucleated myeloid progenitor cells. They play homeostatic vital roles in skeletal modeling and remodeling but also destroy bone masses in many pathological conditions such as osteoporosis and rheumatoid arthritis. Receptor activation of NF-κB ligand (RANKL) is essential to osteoclastogenesis. In this study, we investigated the effects of bromo-honaucin A (Br-H A) isolated from Leptolyngbya crossbyana (cyanobacterium). To investigate the mechanism of the inhibitory effect of Br-H A on osteoclastogenesis, we employed Br-H Ain RANKL-treated murine monocyte/macrophage RAW 264.7 cells for osteoclastic differentiation in-vitro. The inhibitory effects on in-vitro osteoclastogenesis was evaluated by counting the number of Tartarate resistant acid phospatase (TRAP) positive multinucleated cells and by measuring the expression level of osteoclast-specific genes like matrix metalloproteinase 9 (MMP9), cathepsin K (CATH K), GRB2-associated-binding protein 2 (GAB2), c-terminal myc kinase (C-MYC), C-terminal Src kinase (C-SRC) and Microphthalmia-associated transcription factor (MITF). Moreover, Br-H A blocked the resorbing capacity of RAW 264.7 cells on calcium phosphate-coated plates. Finally, Br-H A clearly decreased the expression of Akt and also decreased the activation of ERK. Thus, the study identifies Br-H A as potent inhibitor potentialin the treatment of diseases involving abnormal bone lysis such as osteoporosis, rheumatoid arthritis, and periodontal bone degradation.
28163705 Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential. 2016 Over the last three decades, it has become clear that the role of vitamin D goes beyond the regulation of calcium homeostasis and bone health. An important extraskeletal effect of vitamin D is the modulation of the immune system. In the context of autoimmune diseases, this is illustrated by correlations of vitamin D status and genetic polymorphisms in the vitamin D receptor with the incidence and severity of the disease. These correlations warrant investigation into the potential use of vitamin D in the treatment of patients with autoimmune diseases. In recent years, several clinical trials have been performed to investigate the therapeutic value of vitamin D in multiple sclerosis, rheumatoid arthritis, Crohn's disease, type I diabetes, and systemic lupus erythematosus. Additionally, a second angle of investigation has focused on unraveling the molecular pathways used by vitamin D in order to find new potential therapeutic targets. This review will not only provide an overview of the clinical trials that have been performed but also discuss the current knowledge about the molecular mechanisms underlying the immunomodulatory effects of vitamin D and how these advances can be used in the treatment of autoimmune diseases.
28133600 MSC Therapeutics in Chronic Inflammation. 2016 Jun The utilization of mesenchymal stem cells (also known as mesenchymal stromal cells, or MSCs) as a cell-based therapy for diseases that have ongoing inflammatory damage has become increasingly available. Our understanding of the cell biology of MSCs is still incomplete. However, as a result of increasing numbers of pre-clinical and clinical studies, general themes are emerging. The capacity of MSCs to reduce disease burden is largely associated with their ability to modulate the activity of the host immune responses rather than to contribute directly to tissue regeneration. As a result, they have significant potential in the treatment of chronic inflammatory disease regardless of the affected tissue. For example, MSC based therapies have been developed in the context of diseases as diverse as rheumatoid arthritis and multiple sclerosis. Here we discuss some of the principles that link these conditions, and the aspects of MSC biology that contribute to their use as a therapy for chronic inflammatory conditions.
27682966 Human papillomavirus infection and cervical lesions in rheumatic diseases: a systematic re 2016 Jul An association between immune-mediated diseases and cervical pre-malignant and malignant lesions is described, having the human papillomavirus (HPV) infection a causal role. Related studies have been generally focused on systemic lupus erythematosus (SLE) patients, but relatively to other diseases, such as rheumatoid arthritis (RA), Sjögren's syndrome (SS) and systemic sclerosis (SSc), data has not been systematically evaluated. We conducted a systematic review analysis of the literature in PubMed, including articles published until March of 2015, in patients with RA, SS, SLE and SSc, to evaluate the frequency of HPV infection, cervical dysplasia and cervical cancer, and associated factors, with particular interest on the role of glucocorticoids and immunosuppressive treatment. Moreover, safety and efficacy of HPV vaccines in these patients was investigated. Of 476 articles identified, 27 were finally included. The studies showed an increased prevalence of cervical dysplasia and cancer, with the HPV infection being an important associated factor, in particular in SLE patients. The data relatively to other rheumatic diseases was very scarse, but an increased prevalence of smear abnormalities was also found in RA. Patients exposed to glucocorticoids and to long-term immunosuppression, particularly cyclophosphamide, have increased risk of presenting more pre-malignant lesions than the general population. The available vaccines seem to be generally safe and immunogenic in the short- period evaluation, but long-term follow-up is required to evaluate the impact of the vaccine in the protection against HPV infection and occurrence of high-grade cervical lesions.
27495134 Effect of inflammation on HDL structure and function. 2016 Oct PURPOSE OF REVIEW: Studies have shown that chronic inflammatory disorders, such as rheumatoid arthritis, systemic lupus erythematosus, and psoriasis are associated with an increased risk of atherosclerotic cardiovascular disease. The mechanism by which inflammation increases cardiovascular disease is likely multifactorial but changes in HDL structure and function that occur during inflammation could play a role. RECENT FINDINGS: HDL levels decrease with inflammation and there are marked changes in HDL-associated proteins. Serum amyloid A markedly increases whereas apolipoprotein A-I, lecithin:cholesterol acyltransferase, cholesterol ester transfer protein, paraoxonase 1, and apolipoprotein M decrease. The exact mechanism by which inflammation decreases HDL levels is not defined but decreases in apolipoprotein A-I production, increases in serum amyloid A, increases in endothelial lipase and secretory phospholipase A2 activity, and decreases in lecithin:cholesterol acyltransferase activity could all contribute. The changes in HDL induced by inflammation reduce the ability of HDL to participate in reverse cholesterol transport and protect LDL from oxidation. SUMMARY: During inflammation multiple changes in HDL structure occur leading to alterations in HDL function. In the short term, these changes may be beneficial resulting in an increase in cholesterol in peripheral cells to improve host defense and repair but over the long term these changes may increase the risk of atherosclerosis.