Serological Inflammatory Markers Research Articles

Isolated abdominal aortic dissection in a young female patient

A 43-year-old woman presented with acute lower abdominal pain radiating to both sides of the groin. She had no history of smoking, drug abuse, surgeries, trauma, or any chronic diseases. There was no family history of vascular disease. On the admission physical examination, she was normotensive, had normal pulses on four limbs, and presented tenderness and pain on abdominal aortic palpation and in her lower abdomen. Contrastenhanced abdominal and thoracic computed tomography showed a distal infrarenal abdominal aortic dissection compromising both common iliac arteries (A) and a saccular dilation of the left common iliac dissected artery (B and C). The patient had partial remission of pain with opioids and elected to undergo an endovascular treatment. A coil embolization of the left internal iliac artery (the level at which the dissection ended) was performed, and then a unibody bifurcated endoluminal graft was deployed, covering most of the infrarenal aorta and both common iliac arteries. The patient recovered uneventfully, with total pain remission. The patient did not meet diagnostic criteria for Takayasu disease and had neither Marfan nor Ehlers-Danlos syndrome; her serologic inflammatory and infectious markers were negative, and she had no other radiologic signs of arterial disease of the aorta or its major branches. At 1-month follow-up, computed tomography angiography showed total thrombosis of the dissection’s false lumen as well as of the saccular dilation and patency of the infrarenal aorta and iliac arteries (D). Isolated abdominal aortic dissection, an extremely rare entity, is estimated to occur in 0.4% to 2% of all aortic dissections. It may be classified on the basis of etiology as iatrogenic, traumatic, or spontaneous. Most patients with spontaneous abdominal aortic dissections present with dissection of the infrarenal aortic segment, extending or not to the iliac arteries. Although there is no consensus in the literature on the treatment indications, most authors advocate treatment of all symptomatic patients and of those asymptomatic with radiologic evidence of aneurysmal dilation. There is no standardized technique, and although the endovascular approach used in this case was successfully undertaken, long-term follow-up is warranted to see how the device behaves in a young patient with small-caliber arteries.

Monocyte Subsets and Inflammatory Cytokines in Acute Decompensated Heart Failure

BackgroundDistinct monocyte subsets predict cardiovascular risk and contribute to heart failure progression in murine models, but they have not been examined in clinical acute decompensated heart failure (ADHF). Methods and ResultsBlood samples were obtained from 11 healthy control subjects (HCs) and at admission and discharge from 19 ADHF patients. Serologic markers of inflammation were assessed at admission and discharge. Monocyte populations were defined with the use of flow cytometry for cell-surface expression of CD14 and CD16: CD14++CD16− (classic), CD14++CD16+ (intermediate), and CD14+CD16++ (nonclassic). In ADHF patients, C-reactive protein (CRP) and interleukin-6 (IL-6) were higher compared with HCs (both P < .001) and decreased from admission to discharge (CRP: 12.1 ± 10.1 to 8.6 ± 8.4 mg/L [P = .005]; IL-6: 19.8 ± 34.5 to 7.1 ± 4.7 pg/mL [P = .08]). In ADHF patients, the admission proportion of CD14++CD16− monocytes was lower (68% vs 85%; P < .001) and that of CD14++CD16+ (15% vs 8%; P = .002) and CD14+CD16++ (17% vs 7%, P = .07) monocytes higher compared with HCs. Additionally, the proportion of CD14++CD16− monocytes increased (68% to 79%, P = .04) and the CD14+CD16++ monocytes decreased (17% to 7%, P = .049) between admission and discharge. ConclusionsFollowing standard treatment of ADHF, the monocyte profile and circulating inflammatory markers shifts to more closely resemble those of HC, suggesting a resolution of the acute inflammatory state. Functional studies are warranted to understand how specific monocyte subsets and systemic inflammation may contribute to ADHF pathophysiology.

Abstract 17623: A Case of Biopsy-proven Immunoglobulin G4-Related Disease Associated With Multiple Giant Coronary Artery Aneurysms, Peripheral Arterial Aneurysms, End Stage Renal Disease, and Heart Failure

A 54-year-old man with remote large cell non-Hodgkin’s lymphoma in remission following R-CHOP and severe atopic dermatitis was transferred from another hospital with a non-ST elevation myocardial infarction. Over the preceding year, the patient had suffered recurrent admissions for acutely decompensated heart failure with a newly depressed left ventricular ejection fraction (LVEF) of 20% by echocardiography and rapidly progressive end-stage renal disease of unclear etiology requiring the initiation of hemodialysis. Prior workup had demonstrated an infrarenal abdominal aortic aneurysm and bilateral common iliac artery aneurysms with subsequent computed tomography (CT) additionally demonstrating a superior mesenteric artery aneurysm. The patient was taken for immediate coronary arteriography, which demonstrated giant aneurysms in the left main and right coronary arteries, as well as multivessel severe stenoses. CT coronary angiogram demonstrated significant circumferential wall thickening throughout the coronary vasculature. Given concern for IgG4-related disease (IgG4-RD), a renal biopsy was pursued that confirmed the diagnosis. 18F-fluorodeoxyglucose positron emission tomography-CT identified only mild aortic inflammation. The patient was treated with high-dose steroids and rituximab. The serological inflammatory markers improved, and he underwent coronary artery bypass grafting. Pericardial, aortic adventitial, left internal mammary artery, and saphenous vein biopsies showed cardiovascular involvement of IgG4-RD. The patient has been maintained on rituximab with normalization of his LVEF and no recurrence of chest pain over the past eighteen months. IgG4-RD is a fibroinflammatory systemic disease newly described in 2003 and only recently found to involve the cardiovascular system with several reports of peripheral aneurysmal disease. To our knowledge, the current case represents the first report of a patient successfully treated for biopsy-proven IgG4-RD associated with coronary artery disease and left ventricular systolic dysfunction. IgG4-RD may represent a novel mechanism underlying some forms of peripheral and coronary arterial disease and may offer new insights into vascular biology.

BIOLOGICAL THERAPY IN INFLAMMATORY BOWEL DISEASES: SAFETY PROFILE

Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic, progressive and disabling disorders characterized by a heterogeneous clinical course. Some years ago the main goal of the therapy was to achieve and maintain clinical remission, whereas at present the main goal of therapy is represented by the deep remission, characterized by sustained clinical remission, complete mucosal healing and normalization of serological markers of inflammation. In the last years new therapeutic approaches have been introduced which have led to a reduction in the mortality rate and have modified the natural history of inflammatory bowel diseases (IBD). In addition, several prognostic factors have been identified which have allowed to better stratify the disease and to choose the most appropriate therapy for the single patient. Moreover, early treatment with immunosuppressive drugs and/or biologics has changed, at least in the short term, the course of the disease by reducing hospitalization rate and the need for surgery. Therefore, the development of biologic therapies has represented an important step in the treatment of IBD, since these drugs induce remission and response rates that are not achieved by other therapies. Since their use can result in significant adverse events that increase morbidity, patients must be aware of the risks associated with treatment and must be strictly monitorized. Although treatment with biologic drugs is not successful in all patients and many of them lose clinical response, new therapies are currently under evaluation.

Selective oestrogen receptor modulators lasofoxifene and bazedoxifene inhibit joint inflammation and osteoporosis in ovariectomised mice with collagen-induced arthritis.

Objective. RA predominantly affects post-menopausal women and is strongly associated with development of generalised osteoporosis. To find treatments that target both joint manifestations and osteoporosis in RA is desirable. The third generation of selective oestrogen receptor modulators (SERMs) [lasofoxifene (LAS) and bazedoxifene (BZA)] are new treatment options for post-menopausal osteoporosis. The aim of this study was to investigate the effects of LAS and BZA on arthritic disease and inflammation-associated bone loss using CIA in mice.Methods. Female DBA/1 mice were ovariectomised and subjected to CIA as a model of post-menopausal RA. Mice received treatment with LAS, BZA, 17β-estradiol (E2) as reference or vehicle. Arthritis development was assessed and BMD was determined by peripheral quantitative CT of the femurs. Serologic markers of inflammation and cartilage destruction were analysed. Immune cells in lymph nodes were studied by flow cytometry.Results. LAS and BZA reduced the clinical severity of arthritis as well as the grade of histologic synovitis and erosions on cartilage and bone. Moreover, SERMs protected against generalised bone loss in CIA by increasing trabecular BMD. Both SERMs decreased serum marker of cartilage destruction and LAS reduced serum IL-6 levels. SERMs did not alter Th17 cells in lymph nodes as E2 did.Conclusion. The anti-osteoporotic drugs LAS and BZA were found to be potent inhibitors of joint inflammation and bone destruction in experimental arthritis. This study provides new important knowledge regarding the treatment regimen of post-menopausal women with RA who suffer from increased risk for osteoporosis.

Clinic-based Point of Care Transabdominal Ultrasound for Monitoring Crohn's Disease: Impact on Clinical Decision Making.

The use of cross-sectional imaging is important to characterise inflammatory bowel disease [IBD] activity, extent, and location and to exclude complications, regardless of symptoms. The aim of this study was to evaluate the impact of routine use of sonography in the management of inflammatory bowel disease. A total of 49 patients with Crohn's disease were prospectively evaluated. Clinical symptoms (Harvey-Bradshaw Index [HBI]), disease character, serological markers of inflammation [C-reactive protein], and endoscopic evaluation were collected and reviewed by two independent IBD-specialty physicians. Clinical decisions regarding management were recorded. A separate, blinded physician then performed bowel ultrasound [US] and graded disease activity:] as inactive, mild, or active. A second blinded physician read and graded a sub-set of the US images. Clinical decisions of both IBD-physicians after US were independently recorded. Changes in clinical management following US information and inter-rater agreement on US disease activity parameters were evaluated. The concordance between US, CRP and clinical symptoms [HBI] were analysed. Follow-up data after US evaluation were collected. Clinical decisions were changed after ultrasound assessment in 30/49 [60%] and 28/48 [58%] of cases, for each physician respectively [p < 0.0001 for each]. Many [59%] of the patients seen in clinic were asymptomatic with an HBI of 3 or less [n = 29]; however, 52% [n = 15] of these had active disease found on US, resulting in alterations in clinical management. The agreement in overall score between the US reviewers was good, ĸ = 0.749 [0.5814, 0.9180], p < 0.001. Clinic-based point of care US can play a significant role in guiding therapeutic management and is an important adjunct to routine clinical and laboratory assessment.

Septic Arthritis and Acute Rheumatic Fever in Children

Joint pain and raised inflammatory markers are features of both acute rheumatic fever (ARF) and septic arthritis, often posing a diagnostic challenge to clinicians. Important differences in the presenting serological inflammatory marker profile may assist patient diagnosis, however, as clinical experience suggests that ARF is associated with a higher erythrocyte sedimentation rate (ESR), whereas other serological markers may be similarly elevated in these 2 conditions. The goal of this study was to determine the diagnostic value of serological inflammatory markers and white cell count (WCC) in children presenting with acute joint pain secondary to ARF or septic arthritis. Data were obtained from the Auckland regional rheumatic fever database and hospital computer records between 2005 and 2012. Records of all patients under the age of 16 years who were admitted with a new diagnosis of ARF or septic arthritis were analyzed. The diagnosis of ARF was defined on the basis of the New Zealand modification of the Jones Criteria, and the diagnosis of septic arthritis was defined on the basis of joint fluid cytology and culture. Baseline characteristics, serological inflammatory markers, and serum WCC were compared between the ARF and septic arthritis patient groups. Children with ARF displayed significantly higher ESR, higher serum C-reactive protein, and lower serum WCC than children with septic arthritis on presentation to hospital. In children presenting with monoarthritis, an ESR>64.5, serum WCC<12.1×109/L, and age above 8.5 years were found to be significant independent predictors of ARF. Children with all 3 predictors had a 71% risk for ARF and a 29% risk for septic arthritis. A significant proportion (30%) of children with the final diagnosis of ARF initially presented with monoarthritis; 14% of these children (5/34) had received nonsteroidal anti-inflammatory medication before hospital presentation, and 74% of these children (25/34) had abnormal echocardiograms on admission. ARF and septic arthritis are important diagnoses to consider in children presenting with acute joint pain in New Zealand. A significant proportion of patients with ARF initially present with acute monoarthritis. Serological inflammatory markers and WCC on presentation differ significantly between children with ARF and septic arthritis.

Evaluation of carotid plaque inflammation in patients with active rheumatoid arthritis using 18F-fluorodeoxyglucose PET-CT and MRI: a pilot study

BackgroundRheumatoid arthritis is associated with a 50% increased risk in cardiovascular mortality. Inflammation is thought to accelerate atherosclerosis and might also lead to an inflammatory rupture-prone plaque phenotype. We tested the hypothesis that patients with active rheumatoid arthritis also have carotid plaque inflammation and that plaque inflammation correlates with clinical and serological markers of inflammation. MethodsPatients with active rheumatoid arthritis, defined as the Disease Activity Score in 28 joints (DAS28) score of more than 3·2, were recruited to a single centre study in the UK. Patients with carotid plaque on ultrasound underwent carotid MRI followed by 18F-fluorodeoxyglucose (18F-FDG) PET-CT. Scans were co-registered and analysed by a physicist, masked to clinical information. The maximum standardised uptake values (SUVmax) were measured in the plaque area. The association of SUV with DAS28, C-reactive protein, and CD4+CD28– T-cell frequency was tested with non-parametric statistics. Ethics approval and informed consent were obtained. FindingsScans were done in 13 patients, nine of whom were women. Median age was 60 years (IQR 57–65), disease duration was 11 years (6–25), and DAS28 score was 4·52 (4·32–5·13). None had a history or symptoms of clinical cardiovascular disease or took statins. All plaques caused less than 70% stenosis, and tracer uptake in plaque was seen on PET in all 13 patients. Median SUVmax was 2·18 (IQR 2·00–2·65), and all cases had an SUVmax greater than 1·6 (the threshold for defining carotid plaque inflammation). There was a significant association with SUVmax and C-reactive protein (r=0·58, p=0·04) and quartiles of CD4+CD28– T-cell frequency (p=0·045), but not with low-density lipoprotein concentrations (r=-0·49, p=0·09) or DAS28 score (r=0·38, p=0·20). No association was found with age (r=0·13, p=0·69) or sex (p=0·64). InterpretationIn this small pilot study, plaque inflammation was seen in all patients and correlated with C-reactive protein. Whether this finding represents simultaneous joint and plaque inflammation, which might improve on treatment of joint disease, remains to be determined. CD4+CD28– T-cells are known to predict cardiovascular events in patients with angina. Their association with plaque inflammation in this study suggests a possible role in cardiovascular risk prediction in rheumatoid arthritis. Larger studies are warranted to investigate these findings further. FundingNorth West England MRC Clinical Pharmacology and Therapeutics Clinical Research Fellowship, National Institute for Health Research, AstraZeneca-University of Manchester Strategic Alliance Fund.

The Prognostic Impact of Inflammatory Factors for Survival in Patients with Newly Diagnosed Multiple Myeloma Who Were Treated with Thalidomide Containing Induction Chemotherapy Underwent Autologous Stem Cell Transplantation

Background: Many prognostic factors have been studied with the development of treatments for multiple myeloma (MM). Serologic inflammatory markers, such as serum beta2-microglobulin (B2MG), albumin, absolute lymphocyte count (ALC), C-reactive protein (CRP), lactate dehydrogenase (LDH), and serum ferritin level, which are easily tested in patients to determine disease status, have been reported to be correlated with prognosis in many studies. Therefore, the purpose of this study is to estimate the correlation between the frequency of the combined inflammatory parameters of ALC, LDH, B2MG, albumin, CRP, and ferritin and the prognosis for survival in patients with MM treated with induction chemotherapy containing thalidomide and who underwent autologous stem cell transplantation (ASCT).Methods: Data from patients at 13 university hospitals in South Korea between December 2005 and May 2013 were collected retrospectively. The patients were those who had been treated with thalidomide-containing chemotherapy and then underwent ASCT. An inflammatory score was determined for each inflammatory parameter, where an ALC level less than 1000/L, a B2MG level greater than 3.5 mg/L, a serum albumin level less than 3.5 g/dL and an LDH level greater than 450 IU/L were each assigned a score of 1 point, and the sum of these points was used as the total inflammatory score ranging from 0 to 4 points.Results: The median age of the 232 patients was 57 years (range, 33-82 years) and the male to female ratio was 1.09:1. The achieved response rates before and after ASCT were as follows: complete response (CR) or stringent CR (sCR) in 81 (34.9%) and 142 (60.2%) patients, very good partial response (VGPR) in 61 (26.3%) and 47 (20.3%), partial response (PR) in 79 (34.1%) and 32 (13.8%), and < PR in 7 (3.1%) and 5 (2.3%). The reason for the higher overall response rate (ORR) in this study compared to other studies was that it included patients who were treated with thalidomide induction chemotherapy and who underwent ASCT. The median progression free survival (PFS) was 31.93 months (range, 25.116 – 38.750) and the median overall survival (OS) was not reached during the follow-up duration. In the univariate analysis, the following factors were associated with a greater than 3-year PFS: lower B2MG (< 3.5 mg/L vs. ≥ 3.5 mg/L; 49.7% vs. 40.4%, p=0.022), lower LDH (< 450 IU/L vs. ≥ 450 IU/L; 47.9% vs. 31.5%, p=0.009), lower cytogenetic risks (standard vs. intermediate vs. high; 51.4% vs 26.2% vs 52.7%, p=0.022) and a lower inflammatory score (< 2 vs. ≥ 2; 53.6% vs. 35.1%, p=0.004). The following factors were associated with a greater than 3-year OS (Table 2): higher hemoglobin level (< 10 g/dL vs. ≥ 10 g/dL; 81.0% vs. 92.8%, p=0.042), higher platelet count (<100×109/L vs. ≥ 100×109/L; 48.5% vs. 89.5%, p=0.003), lower B2MG (< 3.5 mg/L vs. ≥ 3.5 mg/L; 95.2% vs. 81.1%, p=0.003), lower LDH (<450 IU/L vs. ≥ 450 IU/L, 91.6 vs. 69.5, p=0.003), lower cytogenetic risk (standard vs. intermediate vs. high; 89.1% vs. 81.7% vs. 81.0%, p=0.014), lower ISS (I, II, and III; 95.2%, 90.3%, and 78.3%, respectively; p=0.024) and a lower inflammatory score (<2 vs. ≥ 2; 95.1% vs. 77.1%, p<0.001). In the multivariate analysis, inflammatory score (<2) was the only independent prognostic factor for superior PFS (RR 0.618, 95% C.I. 0.409-0.933, p=0.022), and platelet count greater than 100×109/L as well as an inflammatory score less than 2 were independent prognostic factors for superior OS (RR 7.856, 95% C.I. 2.502-24.670, p<0.001 and RR 0.216, 95% C.I. 0.067-0.696, p=0.010, respectively).Conclusion:patients with two or more than two combined inflammatory factors who were treated with thalidomide induction chemotherapy and who underwent ASCT showed a significantly shorter survival compared to patients with less than two combined inflammatory factors, and these results might be helpful to predict prognosis in patients with MM. In the future, further prospective studies will be needed to confirm the correlations between prognosis and inflammatory factors including CRP, ferritin, and other cytokines in patients with MM treated with novel agents. DisclosuresNo relevant conflicts of interest to declare.

Long-Term Results of Arthroscopic Wrist Synovectomy in Rheumatoid Arthritis

To investigate the effects of arthroscopic wrist synovectomy on the clinical course of rheumatoid arthritis in a large series with long-term follow-up. We performed arthroscopic synovectomy on 56 wrists in 49 patients with rheumatoid arthritis. At a mean follow-up of 7.9 years (range, 5-12 y), we evaluated pain and patient satisfaction using a visual analog scale and assessed overall function using the Mayo wrist score. Radiographic stage was graded according to Larsen stage. We determined clinical outcomes on the recurrence of wrist synovitis, which we evaluated by symptoms of pain and swelling and physical examination. Preoperative variables were statistically analyzed to find factors that could influence the results. The mean visual analog scale score for wrist pain decreased from 6.3 to 1.7, and the mean Mayo wrist score (evaluated in 39 wrists) improved from 48 (range, 5-70) to 76 (range, 55-100). The mean visual analog scale score for patient satisfaction was 7.9. At final follow-up, synovitis was controlled in 42 wrists (75%) and recurred in the others. The mean Larsen stage progressed from 2.2 to 3.3. Analysis of preoperative variables revealed no factors that significantly affected clinical outcomes in terms of sex, age, duration of wrist symptom, preoperative serologic inflammatory markers, or Larsen stage. Arthroscopic synovectomy of the wrist can provide pain relief and functional improvement with control of synovitis in 75% of rheumatoid wrists that have not responded to medication. Therapeutic IV.

Analysis of Skeletal Muscle Gene Expression Patterns and the Impact of Functional Capacity in Patients With Systolic Heart Failure

BackgroundDeclining physical function is common among systolic heart failure (HF) patients and heralds poor clinical outcomes. We hypothesized that coordinated shifts in expression of ubiquitin-mediated atrophy-promoting genes are associated with muscle atrophy and contribute to decreased physical function. MethodsSystolic HF patients (left ventricular ejection fraction [LVEF] ≤40%) underwent skeletal muscle biopsies (nondominant vastus lateralis) and comprehensive physical assessments. Skeletal muscle gene expression was assessed with the use of real-time polymerase chain reaction. Aerobic function was assessed with the use of cardiopulmonary exercise and 6-minute walk tests. Strength capacity was assessed with the use of pneumatic leg press (maximum strength and power). Serologic inflammatory markers also were assessed. Results54 male patients (66.6 ± 10.0 years) were studied: 24 systolic HF patients (mean LVEF 28.9 ± 7.8%) and 30 age-matched control subjects. Aerobic and strength parameters were diminished in HF versus control. FoxO1 and FoxO3 were increased in HF versus control (7.9 ± 6.2 vs 5.0 ± 3.5, 6.5 ± 4.3 vs 4.3 ± 2.8 relative units, respectively; P ≤ .05 in both). However, atrogin-1 and MuRF-1 were similar in both groups. PGC-1α was also increased in HF (7.9 ± 5.4 vs. 5.3 ± 3.6 relative units; P < .05). Muscle levels of insulin-like growth factor (IGF) 1 as well as serum levels of tumor necrosis factor α, C-reactive protein, interleukin (IL) 1β, and IL-6 were similar in HF and control. ConclusionExpression of the atrophy-promoting genes FoxO1 and FoxO3 were increased in skeletal muscle in systolic HF compared with control, but other atrophy gene expression patterns (atrogin-1 and MuRF-1), as well as growth promoting patterns (IGF-1), were similar. PGC-1α, a gene critical in enhancing mitochondrial function and moderating FoxO activity, may play an important counterregulatory role to offset ubiquitin pathway–mediated functional decrements.

P233 Early measurement of fecal calprotectin after intestinal resection is useful to predict postoperative recurrence in patients with Crohn's disease

Background: Serological Inflammatory markers can be used for assisting in the diagnoses of inflammatory bowel disease but are neither particularly sensitive nor specific. Aim of this study is to investigate the role of fecal Calprotectin in the diagnosis of inflammatory bowel disease along with the serological markers ESR, CRP and endoscopic and radiological means. Methods: Retrospective data of Fecal Calprotectin was collected from the online portal of Kings College Pathology Laboratory London, along with blood and colonoscopy reports from the iLab and Unisoft software of the Mid Western Regional Hospital Limerick respectively over period of 18 months. Statistical analysis was performed using Chi square and Student’s T test on SPSS. A P-value of 0.05 was taken as significant. Results: In the 18 months 97 patients had their faecal Calprotectin checked. Fifty-two (53.6%) of them subsequently had the diagnosis of inflammatory bowel disease made on the basis of colonoscopy, CT scan abdomen or small bowel follow through. We divided patients into 2 groups on the basis of faecal Calprotectin values. Patients in group 1 faecal Calprotectin values less than 60 (n = 27) group 2 had values above 60 to 2009 (70). Of those with normal faecal Calprotectin 21 did not have a diagnosis of IBD, whilst 6 had, of those with elevated faecal Calprotectin 23 did not have a diagnosis of IBD, whilst 47 did (Chi square test, p = 0.001). Six (22%) of group 1 had colitis while nineteen (27%) of group 2 were normal. Mean ESR in group 1 was 11.38 VS 17.65 in group 2 (P= 0.159 Student T Test) while mean CRP in group 1 was 10.6 VS 6.4 in group 2 (P= 0.226 Student T test). Those patients with subsequent diagnosis of IBD (52) had a mean faecal Calprotectin of 335.89 VS non IBD patients (45) mean faecal Calprotectin value was 138 (P= 0.0059 Student T test). Conclusions: This study shows that the use of faecal Calprotectin is a reliable indicator of IBD in the Irish population studied. It also shows that ESR and CRP levels do not correlate with or assist in the diagnosis of IBD in this population.

P232 Evaluation of the use of fecal calprotectin as a diagnostic aid for IBD in an Irish population

Background: Serological Inflammatory markers can be used for assisting in the diagnoses of inflammatory bowel disease but are neither particularly sensitive nor specific. Aim of this study is to investigate the role of fecal Calprotectin in the diagnosis of inflammatory bowel disease along with the serological markers ESR, CRP and endoscopic and radiological means. Methods: Retrospective data of Fecal Calprotectin was collected from the online portal of Kings College Pathology Laboratory London, along with blood and colonoscopy reports from the iLab and Unisoft software of the Mid Western Regional Hospital Limerick respectively over period of 18 months. Statistical analysis was performed using Chi square and Student’s T test on SPSS. A P-value of 0.05 was taken as significant. Results: In the 18 months 97 patients had their faecal Calprotectin checked. Fifty-two (53.6%) of them subsequently had the diagnosis of inflammatory bowel disease made on the basis of colonoscopy, CT scan abdomen or small bowel follow through. We divided patients into 2 groups on the basis of faecal Calprotectin values. Patients in group 1 faecal Calprotectin values less than 60 (n = 27) group 2 had values above 60 to 2009 (70). Of those with normal faecal Calprotectin 21 did not have a diagnosis of IBD, whilst 6 had, of those with elevated faecal Calprotectin 23 did not have a diagnosis of IBD, whilst 47 did (Chi square test, p = 0.001). Six (22%) of group 1 had colitis while nineteen (27%) of group 2 were normal. Mean ESR in group 1 was 11.38 VS 17.65 in group 2 (P= 0.159 Student T Test) while mean CRP in group 1 was 10.6 VS 6.4 in group 2 (P= 0.226 Student T test). Those patients with subsequent diagnosis of IBD (52) had a mean faecal Calprotectin of 335.89 VS non IBD patients (45) mean faecal Calprotectin value was 138 (P= 0.0059 Student T test). Conclusions: This study shows that the use of faecal Calprotectin is a reliable indicator of IBD in the Irish population studied. It also shows that ESR and CRP levels do not correlate with or assist in the diagnosis of IBD in this population.

Recurrent Fever of Unknown Origin (FUO) Due to Periodic Fever, Aphthous Stomatititis, Pharyngitis and Adenitis (FAPA) Syndrome in an Adult.

FAPA syndrome (periodic fever, aphthous stomatititis, pharyngitis and adenitis) is a relatively new entity described in pediatric patients. In adults, reports of FAPA are limited to rare case reports. The differential diagnosis of FAPA in adults includes Behcet’s syndrome, familial Mediterranean fever (FMF), Hyper IgD syndrome and juvenile rheumatoid arthritis (JRA), i.e., adult Still’s disease. With FAPA syndrome, between episodes patients are completely asymptomatic and serologic inflammatory markers such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and white blood cell (WBC) count are normal. The etiology of FAFA is unknown, but lack of secondary cases or clustering in close contacts, lack of seasonality, and the lack of progression for years argue against an infectious etiology. We describe an extremely rare case of an adult with a recurrent FUO with profuse night sweats and prominent chills due to FAPA syndrome.

Epidemiological, clinical and viral characteristics of fatal cases of human avian influenza A (H7N9) virus in Zhejiang Province, China

The high mortality of avian influenza H7N9 in humans is a cause of great concern in China. We compared epidemiological, clinical and viral features of H7N9 influenza of 10 fatal cases and 30 survivors. Increasing age (p=0.021), smoking (p=0.04), underlying medical background (p=0.05) and chronic drug use (p=0.042) had a strong relationship with death due to H7N9 infection. Serological inflammatory markers were higher in fatal cases compared to survivors. Acute respiratory distress syndrome (100%), respiratory failure (100%), co-infection with bacteria (60%), shock (50%) and congestive heart failure (50%) were the most common complications observed in fatal cases. The median time from onset of symptoms to antiviral therapy was 4.6 and 7.4 days in those who survived and those who died, respectively (p=0.04). Viral HA, NA and MP nucleotide sequences of isolates from both study groups exhibited high molecular genetic homology. Age along with a history of smoking, chronic lung disease, immuno-suppressive disorders, chronic drug use and delayed Oseltamivir treatment are risk factors which might contribute to fatal outcome in human H7N9 infection.

AB1181 Psychological problems in saudi children with juvenile idiopathic arthritis is related to physical disability and disease status

ObjectivesThis study aimed at investigating the psychological functioning of Saudi children with poly-articular joint disease and its association with disease activity and disability.MethodsOne hundred and twenty Saudi children aged 6-16...

SP0194 Adult primary central nervous system vasculitis

Adult primary central nervous system vasculitis (aPCNSV) is an uncommon disorder of unknown cause that is limited to the brain and spinal cord. The median age of onset is 50...

Mo1286 Restorative Proctocolectomy With Ileal Pouch-Anal Anastomosis Improves Nutritional Status and Serological Inflammatory Markers in Ulcerative Colitis Patients in Both Short and Long Term

Mo1286 Restorative Proctocolectomy With Ileal Pouch-Anal Anastomosis Improves Nutritional Status and Serological Inflammatory Markers in Ulcerative Colitis Patients in Both Short and Long Term

English

Introduction Periprosthetic joint infection is a frequent and dreadful complication after total joint arthroplasty. Serological inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are widely available and easy to use. As such, they are often used as preliminary diagnostic as well as follow-up tools during the course of treatment. The information they carry is not the same in every clinical scenario, and they should be interpreted accordingly. This review confronts the reader with different doubtful clinical situations and then provides the necessary tools to interpret ESR and CRP in each of them: the immediate postoperative period, the chronic painful arthroplasty and between two-staged revision of infected cases. Conclusion Serological inflammatory markers have different diagnostic thresholds in acute and chronic situations. Follow-up measurements during treatment are informative, but complete normalization is not a mandatory requirement for successful outcome. Introduction Total joint replacement, especially hip and knee, is one of the most successful surgeries in orthopaedics. The demand for total hip and knee joint arthroplasty is increasing and is expected to grow even further over the coming decades1. Infection is arguably the most challenging and certainly one of the most frequent complications after joint replacement2,3. Despite modern surgical prophylaxis, the incidence of this complication is rising worldwide4,5. It is therefore likely that an increasing number of orthopaedic surgeons and other clinicians will encounter this problem. Periprosthetic joint infection (PJI) is typically classified according to the timing of symptom development and the mechanism of bacterial contamination as acute postoperative, acute delayed (haematogeneous) or chronic. This simple classification scheme greatly influences treatment options. Timely recognition of this grievous complication is crucial as it may make the difference between successful and failed outcome. Definitive diagnosis is often challenging as a real ‘gold standard’ has yet to be determined6.Currently, it can only be determined after culture results of samples taken during surgery. As such, preoperative diagnosis is forced to rely on clinical suspicion as well as on careful scrutiny of laboratory and imaging modalities7. In this setting, serological inflammatory markers, specifically erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are often used as initial tests even when there is a low suspicion of PJI6. They are also commonly used in monitoring response to therapy since they are inexpensive, non-invasive and widely available tests. This review confronts the reader with real daily practice doubtful clinical situations and then provides the necessary tools to interpret ESR and CRP values in three different key periods: the immediate postoperative period, diagnosis of a suspected chronic infection and between stages of treatment of an infected total joint arthroplasty. The different thresholds and diagnostic accuracy in each instance will be presented. Discussion Immediate postoperative period Clinical case An otherwise healthy 73-year-old man underwent right total knee arthroplasty (TKA) for primary knee osteoarthritis. The first few days after the procedure were uneventful and the patient was discharged on the fifth postoperative day. On discharge, ESR and CRP values were 100 mm/h and 49.2 mg/L respectively. On the 18th postoperative day, the patient presented to the outpatient clinic with scarce serous wound drainage through a small area of maceratedlooking skin wound. Blood tests revealed normal leukocytes and elevated ESR and CRP: 84 mm/h and 6.2 mg/L respectively. The patient was sent home with no antibiotics and was seen again a week later. Small and seemingly superficial area of skin necrosis was present, and there was no drainage or obvious inflammatory signs (Figure 1). ESR was 102 mm/h and CRP was 7.9 mg/L. Is it normal? ESR is the rate at which red blood cells sediment in 1 h. It is a nonspecific haematological test routinely used as an indirect measure of inflammation. CRP is a major acute-phase protein produced by the liver and increases as a response to * Corresponding author Email: ricardojgsousa@gmail.com Department of Orthopaedics, Centro Hospitalar do Porto – Hospital de Santo Antonio, Porto, Portugal

Usefulness of (18)F-FDG PET/CT in Evaluating Disease Activity at Different Times in a Patient With Chronic Periaortitis.

We report the case of a 53-year-old man with a chronic periaortitis (CP) in whom Fluorine-18-Fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) has been useful in assessing the disease extent at diagnosis, in evaluating the treatment response, in diagnosing the relapse, and in monitoring the disease activity during follow-up (Fig. 1). This case highlights the usefulness of FDG-PET/CT at different times in patients with CP. Fig. 1 A 53-year-old man was admitted to our hospital for a suspected chronic periaortitis (CP) based on clinical (abdominal pain), laboratory data (increased serological inflammatory markers, such as erythrocyte sedimentation rate [ESR] and C reactive protein ... CP is a rare inflammatory disorder that affects the abdominal aorta and the retroperitoneum [1–3]. Imaging procedures are essential to diagnose and monitor the disease course [1–3]. Ultrasonography may be used as first-line screening test, and is particularly useful to monitor patients with hydronephrosis and aortic aneurysms. However, CT or magnetic resonance imaging (MRI) of the abdomen are currently considered the investigations of choice to diagnose CP [1–3]. In active CP, the periaortic mass usually enhances on CT and MRI. Both these methods can be used to monitor the disease course of CP and to evaluate response to treatment. A note of caution: signs of vasculitis seen on MRI and CT may persist for some time, despite achievement of clinical remission. A further limitation of abdominal CT and MRI is that neither technique can detect vasculitis in vessels other than the abdominal aorta, which has been described in 43 % of patients with CP [1]. FDG-PET/CT has been proposed as useful tool in inflammatory diseases, such as aortitis, because metabolic changes assessed by FDG-PET usually precede morphological changes assessed by conventional imaging methods [4–8]. Our case highlights the usefulness of FDG-PET/CT at different times in patients with CP. This method may be useful in assessing disease activity and extent at diagnosis, in evaluating the treatment response, in diagnosing the relapse, and in monitoring the disease during follow-up.