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ID PMID Title PublicationDate abstract
25498205 Dry mouth: a critical topic for older adult patients. 2015 Jan PURPOSE: Diminished salivary flow, or dry mouth impacts the oral health of many older adults, dentate and edentulous. As a result typical oral conditions can prove more challenging to both the patient's comfort and home care and the treatment selected by the clinician. This paper will review issues of dry mouth from a clinical and symptomatic perspective and will include the condition's causes, treatment and prevention. STUDY SELECTION: We performed a review of PubMed using the words: older adults, dry mouth, xerostomia, radiation-induced xerostomia, and salivary gland hypofunction. We selected 90 articles with a clinical application perspective. RESULTS: When it comes to treatment of dry mouth conditions, either objective or subjective, there are no easy answers as to the best course of action for a specific individual. While most of the cited studies have examined the most difficult cases of dry mouth (e.g., Sjögren's syndrome, and that seen during and post head and neck cancer treatments), there are many older adults who demonstrate dry mouth from the use of multiple medications. This paper presents a summary of the etiology, diagnosis, prevention, and pharmacological and non-pharmacological treatment of dry mouth (salivary hypofunction and xerostomia in older adults). CONCLUSIONS: It is important to understand the causes of dry mouth and to educate our patients. Starting a prevention program as early as possible considering the most practical, cost effective and efficient treatments with the best risk-benefit ratio will help to diminish dry mouth symptoms and sequelae.
24952023 The Differential Diagnosis of Dry Eyes, Dry Mouth, and Parotidomegaly: A Comprehensive Rev 2015 Dec Primary Sjögren's syndrome (pSS) is a frequent autoimmune systemic disease, clinically characterized by eyes and mouth dryness in all patients, salivary gland swelling or extraglandular systemic manifestations in half of the patients, and development of lymphoma in 5 to 10 % of the patients. However, patients presenting with sicca symptoms or salivary gland swelling may have a variety of conditions that may require very different investigations, treatments, or follow-up. Eye and/or mouth dryness is a frequent complaint in clinical setting, and its frequency increases with age. When evaluating a patient with suspected pSS, the first step is to rule out its differential diagnoses, before looking for positive arguments for the disease. Knowledge of normal and abnormal lachrymal and salivary gland physiology allows the clinician to prescribe the most adapted procedures for evaluating their function and structure. New tests have been developed in recent years for evaluating these patients, notably new ocular surface staining scores or salivary gland ultrasonography. We describe the different diagnoses performed in our monocentric cohort of 240 patients with suspected pSS. The most frequent diagnoses are pSS, other systemic autoimmune diseases, idiopathic sicca syndrome and drug-induced sicca syndrome. However, other diseases are important to rule out due to their specific management, such as sarcoidosis, granulomatosis with polyangeitis, IgG4-related disease, chronic hepatitis C virus or human immunodeficiency virus infections, graft-versus-host disease, and head and neck radiation therapy. At the light of these data, we propose a core of minimal investigations to be performed when evaluating a patient with suspected pSS.
28002901 Homologous platelet-rich plasma for the treatment of knee involvement in primary Sjögren 2016 Oct Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease characterized by dry eyes, dry mouth, and other clinical manifestations. The most common extraglandular manifestation of pSS is articular involvement and to date their management is unclear. The aims of the current pilot study were to assess the safety and the outcomes of homologous platelet-rich plasma (HPRP) injections in pSS cohort affected by knee arthralgia/arthritis at short-term follow up. This pilot study provides the first evidence that HPRP injections are a safe treatment and induce a short-term clinical improvement. Although the lack of a control group, randomization and long-term follow up prevents the assessment of the real effectiveness of this treatment, further studies are needed to confirm these findings and to determine the mechanism of action, biological changes and disease-modifying properties of PRP.
26208812 Extrahepatic manifestations of hepatitis C infection: navigating CHASM. 2015 Sep This article describes the importance of extrahepatic systemic manifestations of chronic hepatitis C virus (HCV) infection. While most HCV literature focuses on liver injury and fibrosis progression, a spectrum of systemic disease processes, collectively called C hepatitis-associated systemic manifestations (CHASMs), are present in a high proportion of infected persons. These include thyroid disease (Hashimoto's thyroiditis, Graves disease, and thyroid cancer), cardiovascular disease (atherosclerosis, carotid artery disease, and coronary artery disease), renal disease (MPGN and glomerulosclerosis), eye disease (Mooren's ulcers and sicca syndrome), skin disease (PCT, vasculitis, and lichen planus), lymphomas (NHL and splenic T-cell), and diabetes. Mechanistic understanding of how HCV leads to CHASM processes could lead to development of new interventions. The role of early HCV treatment and cure may result in preventive strategies for a variety of complex disease states. Key Points • Systemic extrahepatic complications of HCV comprise a spectrum of disease states in many organs and systems.• Effective treatment of HCV may reduce or eliminate some but not all of these systemic complications.• Further research into early treatment intervention as a prevention strategy for systemic disease is warranted.
24803230 Lack of association of vitamin D receptor gene polymorphisms/haplotypes in Sjögren's synd 2015 Feb The vitamin D is involved in a wide variety of biological processes including bone metabolism, modulation of the immune response, and regulation of cell proliferation and differentiation. Vitamin D has several immunomodulatory effects through vitamin D receptor (VDR). A series of common single-nucleotide polymorphisms (SNPs) in the vitamin D receptor gene have been linked to numerous of diseases, including osteoarthritis, diabetes, cancer, cardiovascular diseases, tuberculosis, virus infections, urinary stones, and periodontitis. Several studies have reported that genetic variations of VDR might be a risk factor for the development of autoimmune diseases such as systemic lupus erythematosus (SLE), multiple sclerosis (MS), psoriasis, and autoimmune thyroid diseases (AITD). However, no data is available on the possible relationship between primary Sjögren's syndrome and VDR gene polymorphisms. Our aim was to determine VDR gene BsmI, ApaI, TaqI, and FokI polymorphism genotypes in pSS patients and healthy controls to analyze whether a relationship exists between polymorphisms in the VDR gene and susceptibility to Sjögren's syndrome. In the current study, 105 patients with pSS and 93 healthy controls were tested for VDR gene polymorphisms (BsmI, ApaI, TaqI, and FokI) genotypes. There were no statistical differences in the distribution of BsmI, TaqI, ApaI, and FokI genotypes and the common haplotypes between pSS patients and healthy controls. We hypothesized that the TaqI, BsmI, ApaI, and FokI polymorphisms of the VDR gene are not associated with the development of primary Sjögren's syndrome in the Hungarian population studied.
27957329 Adipose-derived mesenchymal stromal cells modulate experimental autoimmune arthritis by in 2016 Jun Modulation of innate immune responses in rheumatoid arthritis and other immune-mediated disorders is of critical importance in the clinic since a growing body of information has shown the key contribution of dysregulated innate responses in the progression of the disease. Mesenchymal stromal cells (MSCs) are the focus of intensive efforts worldwide due to their key role in tissue regeneration and modulation of inflammation. In this study, we define innate immune responses occurring during the early course of treatment with a single dose of expanded adipose-derived MSCs (eASCs) in established collagen-induced arthritis. eASCs delay the progression of the disease during the early phase of the disease. This is accompanied by a transient induction of Ly6C(+) monocytes that differentiate into IL10(+)F4/80(+) cells in arthritic mice. Strikingly, the induced IL10(+)F4/80(+) myeloid cells preferentially accumulated in the draining lymph nodes. This effect was accompanied with a concomitant declining of their frequencies in the spleens. Our results show that eASCs attenuate the arthritic process by inducing an early innate cell signature that involves a transient induction of Ly6C(+) monocytes in periphery that differentiate into IL10(+)F4/80(+) macrophages. Our findings demonstrate that early regulatory innate cell responses, involving the monocyte compartment, are targeted by the eASCs during the onset of collagen-induced inflammation.
27840652 The Extract of Chrysanthemum zawadskii var. latilobum Ameliorates Collagen-Induced Arthrit 2016 Chrysanthemum zawadskii var. latilobum (CZ) has been used for beverage or tea and also as folk medicine for the remedy of diverse inflammatory diseases. Nevertheless, the therapeutic effect of CZ on arthritis remains to be unknown. In this paper we aim to investigate the CZ's antiarthritic effect and mechanism of action both in vitro and in vivo. To assess CZ's antiarthritic effect, mouse models of type II collagen-induced arthritis (CIA) were used. Mice were used to gauge clinical arthritis index and histopathological changes. Reverse transcriptase-polymerase chain reaction (RT-PCR), western blotting, electrophoretic mobility shift assay (EMSA), and other biological methods were adopted to measure CZ's effect on arthritis and to understand the veiled mechanism of action. CZ greatly suppressed CIA, histopathological score, bone erosion, and osteoclast differentiation. Mechanistically, CZ inhibited the production of various inflammatory and arthritic mediators like inflammatory cytokines, matrix metalloproteinases (MMPs), and chemokines. Of note, CZ significantly suppressed the activation of the NF-κB pathway in vivo. CZ exerted an antiarthritic effect in CIA mice by curbing the production of crucial inflammatory and arthritis mediators. This study warrants further investigation of CZ for the use in human rheumatoid arthritis (RA).
26207027 TLR5, a novel mediator of innate immunity-induced osteoclastogenesis and bone loss. 2015 Nov Accumulating evidence points to the importance of the innate immune system in inflammation-induced bone loss in infectious and autoimmune diseases. TLRs are well known for being activated by ligands expressed by bacteria, viruses, and fungi. Recent findings indicate that also endogenous ligands in inflammatory processes are important, one being a TLR5 agonist present in synovial fluid from patients with rheumatoid arthritis (RA). We found that activation of TLR5 by its specific ligand, flagellin, caused robust osteoclast formation and bone loss in cultured mouse neonatal parietal bones dependent on increased receptor activator of NF-κB ligand (RANKL):osteoprotegerin ratio, with half-maximal stimulation at 0.01 μg/ml. Flagellin enhanced Rankl mRNA in isolated osteoblasts by a myeloid differentiation primary response gene 88 and NF-κB-dependent mechanism. Injection of flagellin locally over skull bones in 5-wk-old mice resulted in increased mRNA expression of Rankl and osteoclastic genes, robust osteoclast formation, and bone loss. The effects in vitro and in vivo were absent in Tlr5(-/-) mice. These data show that TLR5 is a novel activator of RANKL and osteoclast formation and, therefore, a potential key factor in inflammation-induced bone erosions in diseases like RA, reactive arthritis, and periodontitis. TLR5 might be a promising novel treatment target for prevention of inflammatory bone loss.
26232056 Epidemiology of juvenile idiopathic arthritis in Oman. 2015 Aug 1 BACKGROUND: There is a worldwide variation in the prevalence and subtype distribution of juvenile idiopathic arthritis (JIA) which may be affected by ethnicity and genetic factors. The purpose of this study is to determine the prevalence, subtype distribution and characteristic features of JIA among Omani children and to compare our results with other ethnic populations worldwide. METHODS: A population-based, multicenter study among pediatric rheumatology clinics in the Sultanate over a 10 year period between 2004-2013. The diagnosis of JIA and identification of JIA subtypes was based on the ILAR 2004 revised criteria. The hospital charts of these patients were retrospectively reviewed and information was collected. All patients were screened for uveitis by an ophthalmologist using slit lamp examination during regular follow up visits. RESULTS: The study included a total of 107 cases of JIA in Oman over the study period. Among the 107 patients, 71 % (n = 77) were girls with a female:male ratio of 2.5:1. The mean age of disease onset was 6.85 ± 3.86 years (range 1-13years) while the mean disease duration of 4.8 ± 2.9 years (range 1-11 years). The incidence of JIA was estimated at 2/100,000 with a prevalence of JIA of 20/100,000. The prevalence of JIA in girls was 28/100,000 while the prevalence in boys was 12/100,000. According to disease distribution, the most frequent subtype was polyarticular JIA rheumatoid factor negative (39.2 %) followed by oligoarthritis (31.8 %), systemic (17.8 %), polyarticular JIA rheumatoid factor positive (7.5 %). The unique feature of the Omani cohort is the lack of occurrence of uveitis. CONCLUSIONS: This is the first epidemiological JIA study conducted in Oman that highlights unique geographical disease phenotype. Compared to Western counties, there were higher frequency of polyarticular disease and lack of occurrence of uveitis. Further studies are needed to evaluate the implications of genetic, ethnic and environmental differences of disease expression.
25789331 Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody for juven 2015 OBJECTIVE: To estimate the diagnostic accuracy of the anti-CCP test in JIA and to evaluate factors associated with higher accuracy. METHODS: Two investigators performed an extensive search of the literature published between January 2000 and January 2014. The included articles were assessed by the Quality Assessment of Diagnostic Accuracy Studies tool. The meta-analysis was performed using a summary ROC (SROC) curve and a bivariate random-effect model to estimate sensitivity and specificity across studies. RESULTS: The bivariate meta-analysis yielded a pooled sensitivity and specificity of 10% (95% confidence interval (CI): 6.0%-15.0%) and 99.0% (95% CI: 98.0%-100.0%). The area under the SROC curve was 0.96. Sensitivity estimates were highly heterogeneous, which was partially explained by the higher sensitivity in the rheumatoid factor-positive polyarthritis (RF+ PA) subtype (48.0%; 95% CI: 31.0%-65.0%) than in the other subtypes (17.0%; 95% CI: 14.0%-20.0%) and the higher sensitivity of the Inova assay (17.0%; 95% CI: 14.0%-20.%%) than the other assays (0.05%; 95% CI: 2.0%-11.0%). CONCLUSIONS: Anti-CCP antibody test has a high specificity for the diagnosis of JIA. The sensitivity of this test is low and varies across populations but is higher in RF+ PA than in other JIA subtypes.
26176300 A retrospective study on 158 Thai patients with juvenile idiopathic arthritis followed in 2016 Dec AIM: To determine the outcomes of juvenile idiopathic arthritis (JIA) in Thai children. METHODS: A retrospective cohort study. All JIA patients in a rheumatology clinic, Ramathibodi Hospital, between July 1997 and December 2012 were enrolled. The patient data were reviewed from medical records. At the most recent follow-up visit, patient outcomes were assessed in three aspects: disease status, functional outcomes and structural damage. RESULTS: Of 168 patients, 158 (94.0%) were assessed in disease status and functional outcomes, with 114 patients (67.9%) assessed in three aspects over 4 years of disease. The most common JIA category was systemic JIA (SJIA) (33.8%), followed by enthesitis-related arthritis (ERA) (24.8%), oligoarthritis (18.5%), rheumatoid factor (RF)-negative polyarthritis (15.3%), RF-positive polyarthritis (7.6%) and one undifferentiated arthritis. SJIA had the highest remission rate due to early diagnosis and prompt treatment compared to other categories, whereas RF-positive polyarthritis carried the worst prognosis in three aspects, followed by ERA. Moreover, ERA patients had the highest failure rate in conventional therapy, half of whom had combined treatment with biologic agents and presence of human leukocyte antigen (HLA)-B27 was a predictor for biologic treatment in ERA patients. In addition, disease duration > 2 years or failure of conventional therapy was a predictor of structural bone damage. CONCLUSIONS: SJIA had the highest remission rate, whereas RF-positive polyarthritis had the worst outcome in three aspects. Prolonged disease duration or failure of conventional therapy was a predictor of structural bone damage, while HLA-B27 was a predictor for biologic treatment in ERA patients.
27534559 Resolvin D3 Is Dysregulated in Arthritis and Reduces Arthritic Inflammation. 2016 Sep 15 Uncontrolled inflammation is a unifying component of many chronic inflammatory diseases, such as arthritis. Resolvins (Rvs) are a new family from the endogenous specialized proresolving mediators (SPMs) that actively stimulate resolution of inflammation. In this study, using lipid mediator metabololipidomics with murine joints we found a temporal regulation of endogenous SPMs during self-resolving inflammatory arthritis. The SPMs present in self-resolving arthritic joints include the D-series Rvs, for example, RvD1, RvD2, RvD3, and RvD4. Of note, RvD3 levels were reduced in inflamed joints from mice with delayed-resolving arthritis when compared with self-resolving inflammatory arthritis. RvD3 was also reduced in serum from rheumatoid arthritis patients compared with healthy controls. RvD3 administration reduced joint leukocytes as well as paw joint eicosanoids, clinical scores, and edema. Taken together, these findings provide evidence for dysregulated endogenous RvD3 levels in inflamed paw joints and its potent actions in reducing murine arthritis.
26065426 B7-H3 Promotes Pathogenesis of Autoimmune Disease and Inflammation by Regulating the Activ 2015 B7-H3 is a cell surface molecule in the immunoglobulin superfamily that is frequently upregulated in response to autoantigens and pathogens during host T cell immune responses. However, B7-H3's role in the differential regulation of T cell subsets remains largely unknown. Therefore, we constructed a new B7-H3 deficient mouse strain (B7-H3 KO) and evaluated the functions of B7-H3 in the regulation of Th1, Th2, and Th17 subsets in experimental autoimmune encephalomyelitis (EAE), experimental asthma, and collagen-induced arthritis (CIA); these mouse models were used to predict human immune responses in multiple sclerosis, asthma, and rheumatoid arthritis, respectively. Here, we demonstrate that B7-H3 KO mice have significantly less inflammation, decreased pathogenesis, and limited disease progression in both EAE and CIA mouse models when compared with littermates; these results were accompanied by a decrease in IFN-γ and IL-17 production. In sharp contrast, B7-H3 KO mice developed severe ovalbumin (OVA)-induced asthma with characteristic infiltrations of eosinophils in the lung, increased IL-5 and IL-13 in lavage fluid, and elevated IgE anti-OVA antibodies in the blood. Our results suggest B7-H3 has a costimulatory function on Th1/Th17 but a coinhibitory function on Th2 responses. Our studies reveal that B7-H3 could affect different T cell subsets which have important implications for regulating pathogenesis and disease progression in human autoimmune disease.
25888974 Estrogen regulates T helper 17 phenotype and localization in experimental autoimmune arthr 2015 Feb 13 INTRODUCTION: The incidence and progression of many autoimmune diseases are sex-biased, which might be explained by the immunomodulating properties of endocrine hormones. Treatment with estradiol potently inhibits experimental autoimmune arthritis. Interleukin-17-producing T helper cells (Th17) are key players in several autoimmune diseases, particularly in rheumatoid arthritis. The aim of this study was to investigate the effects of estrogen on Th17 cells in experimental arthritis. METHODS: Ovariectomized DBA/1 mice treated with 17β-estradiol (E2) or placebo were subjected to collagen-induced arthritis (CIA), and arthritis development was assessed. Th17 cells in joints and lymph nodes were studied by flow cytometry. Lymph node Th17 cells were also examined in ovariectomized estrogen receptor α-knockout mice (ERα-/-) and wild-type littermates, treated with E2 or placebo and subjected to antigen-induced arthritis. RESULTS: E2-treated mice with established CIA showed reduced severity of arthritis and fewer Th17 cells in joints compared with controls. Interestingly, E2-treated mice displayed increased Th17 cells in lymph nodes during the early phase of the disease, dependent on ERα. E2 increased the expression of C-C chemokine receptor 6 (CCR6) on lymph node Th17 cells as well as the expression of the corresponding C-C chemokine ligand 20 (CCL20) within lymph nodes. CONCLUSIONS: This is the first study in which the effects of E2 on Th17 cells have been characterized in experimental autoimmune arthritis. We report that E2 treatment results in an increase of Th17 cells in lymph nodes during the early phase of arthritis development, but leads to a decrease of Th17 in joints during established arthritis. Our data suggest that this may be caused by interference with the CCR6-CCL20 pathway, which is important for Th17 cell migration. This study contributes to the understanding of the role of estrogen in the development of autoimmune arthritis and opens up new fields for research concerning the sex bias in autoimmune disease.
26343084 The evolution of time-intensity curves of contrast enhanced ultrasonography in early arthr 2015 Sep AIMS: The aim of the study was to assess the evolution of time-intensity curves parameters of contrast-enhanced ultrasonography (CEUS) after 6 months of conventional treatment in early arthritis patients with wrist involvement. MATERIAL AND METHODS: Patients diagnosed with early rheumatoid arthritis or undifferentiated arthritis on the basis of 2010 ACR/EULAR classification criteria, with bilateral wrist arthritis and both radiocarpal (RC) and intercarpal (IC) synovial hypertrophy identified by grey-scale ultrasonography, were enrolled. Synovial hypertrophy was semi-quantitatively scored (grade 0-3) by grey-scale and by Power Doppler at wrist level. CEUS was performed using Sonovue. The region of interest was selected as the area corresponding to the synovial hypertrophy of the RC and IC joints. Time-intensity curves parameters were calculated with Contrast Dynamic Software. The minimum and the maximum values of Peak, area under the curve (AUC), and slope were selected for each patient at baseline and after 6 months of conventional treatment. The difference between the visits was noted as "Δ". RESULTS: Eleven patients fulfilled the inclusion criteria. Maximum time-intensity curves parameters' difference significantly decreased at 6 months: Peak (30.00+/-5.90% vs 23.22+/-5.22%, p=0.008), AUC (1206.08+/-216.91%s vs 949.13+/-280.12%s, p=0.04) and slope (1.6 (1.4;2.3) %/s vs 1(0.7;1.2) %/s, p=0.03). Moderate correlations were found between maximum ΔPeak, maximum ΔAUC and maximum ΔPower Doppler grade (r=0.44, p=0.17; r=0.46, p=0.16, respectively). CONCLUSIONS: Peak and AUC for joints that had high baseline values significantly decreased following treatment with conventional synthetic drugs in EA patients with wrist arthritis. This decrease in Peak and AUC was moderately correlated with a decrease in US parameters. The joint with the highest values of these parameters may be used for evaluation of EA patients at follow-up.
26415324 JAK INHIBITOR CLINICAL RESPONSE IN POLYARTHRITIS: CASE REPORT. 2015 Jun The heterogeneity of rheumatoid arthritis (RA) presentation and molecular signature of RA subclasses in patients with early changes of small peripheral joints still remains a challenging problem. In clinical setting, classification of the disease subtypes is not possible and treatment adjustment is based on the continuous Disease Activity Score for disease severity recognition. A new approach in the treatment appears with the novel non biologic targeted synthetic disease-modifying antirheumatic drugs from the group of Janus kinase 1 and 3 (JAKI and JAK3), blocking interleukin (IL)-2, IL-4, IL-7, IL-9, IL-15 and IL-21. We report a case of a 48-year-old patient who had suffered from polyarthritis from his age 40. Initial laboratory tests showed low inflammatory parameters and magnetic resonance imaging of both hands indicated an early stage of RA. Methylprednisolone and methotrexate therapy was initiated. The patient underwent additional tests, but there was not sufficient evidence for a precise diagnosis. According to the European League Against Rheumatism/American College of Rheumatology score-based algorithm, the patient was classified as seronegative RA based on joint involvement, duration of the disease, and synovitis not better explained by another disease. A partial clinical effect of the administered therapy (steroids as monotherapy and in combination, methotrexate and leflunomide) was noticed with the use of systemic steroids, but dramatic improvement was only achieved with a JAK inhibitor targeted therapy. Although the use of anti TNF-α blocker is a proposed procedure and the drug has not yet been registered in Europe, we took the opportunity to apply this new medication option. The patient, a construction worker, was treated for 20 months, which led to complete remission of the disease, without the need of basic or corticosteroid therapy. Full functional capacity necessary in his demanding job was also achieved. This result raised a question of timely introduction of immunomodulators in the polyarthritis treatment steps.
27066320 The melanocortin receptor type 3 agonist d-Trp(8)-γMSH decreases inflammation and muscle 2016 Mar BACKGROUND: Chronic inflammatory diseases induce cachexia that increases mortality and morbidity of the illness. Adjuvant-induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. Alpha-melanocyte stimulating hormone has an anti-inflammatory effect in arthritic rats and decreases muscle wasting. The aim of this work was to elucidate whether the anti-cachectic action of alpha-melanocyte stimulating hormone is mediated by the melanocortin receptor type 3 pathway. METHODS: Arthritis was induced in male Wistar rats by intradermal injection of Freund's adjuvant, and 6 days afterwards, arthritic rats were injected with the selective melanocortin receptor type 3 agonist d-Trp(8)-gammaMSH ( d-Trp(8)-γMSH) 500 µg/kg subcutaneously. or saline twice a day, for 10 days. RESULTS: d-Trp(8)-γMSH decreased the external signs of inflammation and body weight loss, but it was not able to modify the anorexigenic effect of arthritis or the increase in hypothalamic cyclooxygenase-2 (COX-2) expression. In contrast, d-Trp(8)-γMSH prevented arthritis-induced increase in hypothalamic IL-1β and serum corticosterone levels and the decrease in serum IGF-I levels. d-Trp(8)-γMSH treatment also prevented arthritis-induced NF-kB(p65) phosphorylation and tumour necrosis factor-α mRNA increase in the gastrocnemius. d-Trp(8)-γMSH administration to arthritic rats increased gastrocnemius mass, its cross-sectional area, and mean fast fibre area. Those effects of d-Trp(8)-γMSH were associated with a decreased expression of atrogin-1 and muscle ring-finger protein-1 in the gastrocnemius. In rats treated with saline, arthritis increased the expression of autophagy marker genes LC3b, Bnip-3, and Gabarap1 as well as the conversion of LC3b I to LC3b II by lipidation in the gastrocnemius. d-Trp(8)-γMSH decreased gastrocnemius LC3b, Bnip-3, and Gabarap1 mRNA expression and prevented the increase in LC3b II in arthritic rats. CONCLUSION: These data suggest that d-Trp(8)-γMSH administration prevents the effect of arthritis on corticosterone and insulin-like growth factor-I serum levels and decreases muscle wasting, by down-regulating atrogenes and autophagy through modifying the NF-kB(p65)/tumour necrosis factor-α signalling transduction pathway.
27488446 [Diagnostics and treatment of polymyalgia rheumatica]. 2016 Sep Polymyalgia rheumatica (PMR) is the most common autoimmune inflammatory disease in older persons with an average age of onset of 73 years. Typical symptoms include acute or subacute bilateral shoulder pain with severe stiffness and often neck and bilateral hip pain. Giant cell arteritis (GCA) occurs in approximately 20 % of cases and up to two thirds of patients with GCA have symptoms of PMR. There are many disease which mimic PMR, elderly onset rheumatoid arthritis is frequently misdiagnosed as PMR. Although there are no specific laboratory tests, C‑reactive protein and erythrocyte sedimentation rates are elevated in over 90 % of patients. The diagnosis may be aided by imaging, especially ultrasonography and magnetic resonance imaging (MRI). Treatment currently consists of glucocorticoids at an initial dose of 12.5-25 mg prednisone equivalent daily. Treatment duration is typically 2‑3 years but may be longer. Under certain conditions low-dose methotrexate can be used as adjuvant therapy.
25735308 Pyrocarbon proximal interphalangeal joint arthroplasty: a medium to long term follow-up of 2015 Nov We retrospectively reviewed a consecutive single surgeon series of 57 Ascension pyrocarbon proximal interphalangeal joint arthroplasties, with a mean follow-up of 7.1 years (range 2 years to 11 years 6 months). We assessed the ranges of motion, deformity, stability and pain of the operated joints, grip strength of the hand and patient satisfaction. Of the cases, 44 were for osteoarthritis, five for rheumatoid arthritis and eight for post-traumatic arthritis. The median post-operative active arc of motion was from 0° to 60°. The median post-operative visual analogue pain score was 0.3 out of ten. Thirty six of the joints had no complications; 14 had minor complications (squeak, slight swan neck); three required early reoperation (joint release, flexor tenodesis); and five required implant removal. A total of 69% of our patients would have the same operation if they had to make the decision again. The Kaplan-Meier survival method estimates the mean implant survival to be 10.7 years (95% confidence intervals 9.96-11.37 years). All five failures occurred during the first 2 years.Level of evidence 4 (Case-series).
25461470 Autoimmune thyroid disorders. 2015 Feb Autoimmune thyroid diseases (AITD) result from a dysregulation of the immune system leading to an immune attack on the thyroid. AITD are T cell-mediated organ-specific autoimmune disorders. The prevalence of AITD is estimated to be 5%; however, the prevalence of antithyroid antibodies may be even higher. The AITD comprise two main clinical presentations: Graves' disease (GD) and Hashimoto's thyroiditis (HT), both characterized by lymphocytic infiltration of the thyroid parenchyma. The clinical hallmarks of GD and HT are thyrotoxicosis and hypothyroidism, respectively. The mechanisms that trigger the autoimmune attack to the thyroid are still under investigation. Epidemiological data suggest an interaction among genetic susceptibility and environmental triggers as the key factor leading to the breakdown of tolerance and the development of disease. Recent studies have shown the importance of cytokines and chemokines in the pathogenesis of AT and GD. In thyroid tissue, recruited T helper 1 (Th1) lymphocytes may be responsible for enhanced IFN-γ and TNF-α production, which in turn stimulates CXCL10 (the prototype of the IFN-γ-inducible Th1 chemokines) secretion from the thyroid cells, therefore creating an amplification feedback loop, initiating and perpetuating the autoimmune process. Associations exist between AITD and other organ specific (polyglandular autoimmune syndromes), or systemic autoimmune disorders (Sjögren's syndrome, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, cryoglobulinemia, sarcoidosis, psoriatic arthritis). Moreover, several studies have shown an association of AITD and papillary thyroid cancer. These data suggest that AITD patients should be accurately monitored for thyroid dysfunctions, the appearance of thyroid nodules, and other autoimmune disorders.