Database : MEDLINE
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[PMID]: 25284133
[Au] Autor:Basnet A; Cholankeril MR
[Ad] Address:Department of Internal Medicine, Trinitas Regional Medical Center, Seton Hall University of Graduate Medical Education, Elizabeth, USA.
[Ti] Title:Hemophagocytic Lymphohistiocytosis in a Patient with Goodpasture's Syndrome: A Rare Clinical Association.
[So] Source:Am J Case Rep;15:431-6, 2014.
[Is] ISSN:1941-5923
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening clinical syndrome. HLH can occur in the setting of an autoimmune disease, chronic immunosuppression, malignancy, and infection. We discuss a rare case of a young woman who was diagnosed with Goodpasture's syndrome that was most likely complicated by HLH. To the best of our knowledge, this is the first report of HLH in the setting of this rare autoimmune disease. Case Report A 31-year-old woman who was diagnosed with Goodpasture's syndrome 7 years prior presented with febrile neutropenia. She was initially receiving treatment with azathioprine and prednisone, which was subsequently switched to hydroxychloroquine. Over time, she had developed polyarthritis and was later diagnosed with MPO-ANCA-positive vasculitides. On this admission, her clinical status deteriorated from persistent pancytopenia. This was initially attributed to the immunosuppressive effect of hydroxychloroquine. A bone marrow biopsy was performed and revealed hypercellular bone marrow without any cytogenetic abnormalities. Due to a prolonged pancytopenia thought to be of autoimmune etiology, treatment with high-dose steroids was initiated. With the persistent febrile episodes, hepatosplenomegaly on examination, and laboratory workup that revealed hyperferritinemia and pancytopenia, HLH syndrome was suspected. A repeat bone marrow biopsy confirmed this diagnosis with the presence of hemophagocytosis, demonstrated by the presence of histiocytes engulfing erythroid cells. She also met 5 of 8 diagnostic criteria, which confirmed the diagnosis of HLH. The patient eventually died despite aggressive treatment with high-dose steroid therapy for her autoimmune disorder, as well intravenous antibiotics and supportive care for her underlying infections. Conclusions HLH is a syndrome marked by a hyper-inflammatory state aggravated by specific triggers. To make the diagnosis of HLH, at least 5 of the 8 criteria must be met. Treatment involves suppression of the overwhelming inflammatory response by the use of immunomodulators. The mortality rate can range from 50-90% due to delayed recognition and onset of treatment. Here, we present a rare case of Goodpasture's syndrome with overlap and pauci-immune vasculitis, which may have triggered the HLH. This correlation has not been described before in the literature.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.12659/AJCR.891067

  2 / 32350 MEDLINE  
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[PMID]: 25001084
[Au] Autor:Zikou AK; Kosmidou M; Astrakas LG; Tzarouchi LC; Tsianos E; Argyropoulou MI
[Ad] Address:Department of Radiology, Medical School, University of Ioannina, Ioannina, Greece.
[Ti] Title:Brain involvement in patients with inflammatory bowel disease: a voxel-based morphometry and diffusion tensor imaging study.
[So] Source:Eur Radiol;24(10):2499-506, 2014 Oct.
[Is] ISSN:1432-1084
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:OBJECTIVES: To investigate structural brain changes in inflammatory bowel disease (IBD). METHODS: Brain magnetic resonance imaging (MRI) was performed on 18 IBD patients (aged 45.16 ± 14.71 years) and 20 aged-matched control subjects. The imaging protocol consisted of a sagittal-FLAIR, a T1-weighted high-resolution three-dimensional spoiled gradient-echo sequence, and a multisession spin-echo echo-planar diffusion-weighted sequence. Differences between patients and controls in brain volume and diffusion indices were evaluated using the voxel-based morphometry (VBM) and tract-based spatial statistics (TBSS) methods, respectively. The presence of white-matter hyperintensities (WMHIs) was evaluated on FLAIR images. RESULTS: VBM revealed decreased grey matter (GM) volume in patients in the fusiform and the inferior temporal gyrus bilaterally, the right precentral gyrus, the right supplementary motor area, the right middle frontal gyrus and the left superior parietal gyrus (p < 0.05). TBSS showed decreased axial diffusivity (AD) in the right corticospinal tract and the right superior longitudinal fasciculus in patients compared with controls. A larger number of WMHIs was observed in patients (p < 0.05). CONCLUSIONS: Patients with IBD show an increase in WMHIs and GM atrophy, probably related to cerebral vasculitis and ischaemia. Decreased AD in major white matter tracts could be a secondary phenomenon, representing Wallerian degeneration. KEY POINTS: • There is evidence of central nervous system involvement in IBD. • Diffusion tensor imaging detects microstructural brain abnormalities in IBD. • Voxel based morphometry reveals brain atrophy in IBD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1007/s00330-014-3242-6

  3 / 32350 MEDLINE  
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[PMID]: 25107938
[Au] Autor:Medina G; González-Pérez D; Vázquez-Juárez C; Sánchez-Uribe M; Saavedra MA; Jara LJ
[Ad] Address:Clinical Research Unit, Hospital de Especialidades Centro Médico La Raza IMSS, Mexico City, Mexico Universidad Nacional Autónoma de México, Mexico City, Mexico....
[Ti] Title:Fulminant systemic vasculitis in systemic lupus erythematosus. Case report and review of the literature.
[So] Source:Lupus;23(13):1426-9, 2014 Nov.
[Is] ISSN:1477-0962
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Vasculitis in systemic lupus erythematosus (SLE) has a broad spectrum of clinical manifestations from cutaneous to visceral involvement and its prognosis ranges from mild to life-threatening. We report the case of a previously healthy 17-year-old woman with eight months' history of arthralgias and myalgias. Subsequently, she developed facial and lower limbs edema, and hair loss. Two weeks before admission to a secondary level hospital, she developed fever up to 40 ℃ followed by abdominal pain, rectal bleeding, hematemesis and blisters on both legs, reason for which she was hospitalized. With active bullous SLE with rapidly progressive glomerulonephritis suspected, she was treated with methylprednisolone pulses without response. After one week of treatment, she was transferred to a tertiary level hospital. On admission she presented acute arterial insufficiency of the lower extremities, respiratory failure with apnea, metabolic acidosis and shock; six hours later she died. Autopsy findings showed active diffuse lupus nephritis and diffuse systemic vasculitis that involved vessels from the skin, brain, myocardium, spleen, iliac and renal arteries. In addition, serositis of the small intestine and colon, acute and chronic pericarditis, pericardial effusion and myocarditis were found. Immunologic tests confirmed SLE diagnosis. In this case the fulminant course was the result of SLE high disease activity, visceral vasculitis of several organs and late diagnosis, referral and treatment. Early diagnosis, and opportune referral to the rheumatologist for intensive treatment can improve the outlook in these patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1177/0961203314546018

  4 / 32350 MEDLINE  
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[PMID]: 24969082
[Au] Autor:Böckle BC; Jara D; Aichhorn K; Junker D; Berger T; Ratzinger G; Sepp NT
[Ad] Address:Department of Dermatology, Innsbruck Medical University, Austria norbert.sepp@i-med.ac.at barbara.boeckle@i-med.ac.at....
[Ti] Title:Cerebral large vessel vasculitis in systemic lupus erythematosus.
[So] Source:Lupus;23(13):1417-21, 2014 Nov.
[Is] ISSN:1477-0962
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neuropsychiatric systemic lupus erythematosus (NPSLE) is defined by involvement of the central nervous system in systemic lupus erythematosus (SLE), with a wide range of both neurological and psychiatric manifestations. Although its aetiopathogenesis is not fully elucidated, NPSLE seems to be a consequence of cerebral vascular pathology including thromboembolism, small-vessel vasculopathy and, in rare cases, true vasculitis. Cerebral vasculitis is rare, and cerebral large-vessel vasculitis in SLE is even more unusual. We report the case of a female patient with the diagnosis of SLE. She presented with stroke-like symptoms, headache and vertigo, and palpable purpura on her legs. Further investigations revealed that she suffered from both vasculitis of the cerebral large vessels and coexisting cutaneous small-vessel vasculitis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1177/0961203314541689

  5 / 32350 MEDLINE  
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[PMID]: 23873874
[Au] Autor:Kambas K; Chrysanthopoulou A; Vassilopoulos D; Apostolidou E; Skendros P; Girod A; Arelaki S; Froudarakis M; Nakopoulou L; Giatromanolaki A; Sidiropoulos P; Koffa M; Boumpas DT; Ritis K; Mitroulis I
[Ad] Address:Laboratory of Molecular Haematology, Democritus University of Thrace, Alexandroupolis, Greece....
[Ti] Title:Tissue factor expression in neutrophil extracellular traps and neutrophil derived microparticles in antineutrophil cytoplasmic antibody associated vasculitis may promote thromboinflammation and the thrombophilic state associated with the disease.
[So] Source:Ann Rheum Dis;73(10):1854-63, 2014 Oct.
[Is] ISSN:1468-2060
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Antineutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) is characterised by neutrophil activation. An elevated prevalence of venous thromboembolic events has been reported in AAV. Because of the critical role of neutrophils in inflammation associated thrombosis, we asked whether neutrophil tissue factor (TF) may be implicated in the thrombotic diathesis in AAV. METHODS: Neutrophils from four patients and sera from 17 patients with ANCA associated vasculitis with active disease and remission were studied. TF expression was assessed by immunoblotting and confocal microscopy. Circulating DNA levels were evaluated. TF expressing microparticles (MPs) were measured by flow cytometry and thrombin-antithrombin complex levels by ELISA. RESULTS: Peripheral blood neutrophils from four patients with active disease expressed elevated TF levels and released TF expressing neutrophil extracellular traps (NETs) and MPs. TF positive NETs were released by neutrophils isolated from the bronchoalveolar lavage and were detected in nasal and renal biopsy specimens. Elevated levels of circulating DNA and TF expressing neutrophil derived MPs were further observed in sera from patients with active disease. Induction of remission attenuated the aforementioned effects. Control neutrophils treated with sera from patients with active disease released TF bearing NETs and MPs which were abolished after IgG depletion. Treatment of control neutrophils with isolated IgG from sera from patients with active disease also resulted in the release of TF bearing NETs. TF implication in MP dependent thrombin generation was demonstrated by antibody neutralisation studies. CONCLUSIONS: Expression of TF in NETs and neutrophil derived MPs proposes a novel mechanism for the induction of thrombosis and inflammation in active AAV.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1136/annrheumdis-2013-203430

  6 / 32350 MEDLINE  
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[PMID]: 23606708
[Au] Autor:Saadoun D; Resche Rigon M; Thibault V; Longuet M; Pol S; Blanc F; Pialoux G; Karras A; Bazin-Karra D; Cazorla C; Vittecoq D; Musset L; Decaux O; Ziza JM; Lambotte O; Cacoub P
[Ad] Address:Department of Internal Medicine, Service de Médecine Interne, AP-HP, Groupe Hospitalier Pitié-Salpétrière, , Paris, France.
[Ti] Title:Peg-IFNα/ribavirin/protease inhibitor combination in hepatitis C virus associated mixed cryoglobulinemia vasculitis: results at week 24.
[So] Source:Ann Rheum Dis;73(5):831-7, 2014 May.
[Is] ISSN:1468-2060
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The standard-of-care treatment of patients with hepatitis C virus (HCV)-mixed cryoglobulinemia (MC) vasculitis includes pegylated interferon α (PegIFN)-α plus ribavirin and/or rituximab. About 30-40% of patients are non-responders or relapsers to such combination. OBJECTIVE: To analyse the safety and efficacy of Peg-IFNα/ribavirin/protease inhibitor combination in HCV-MC vasculitis. PATIENTS AND METHODS: Open-label, prospective, cohort study including 23 patients with HCV-MC vasculitis. Peg-IFNα/ribavirin was associated to telaprevir (375 mg three times daily, for 12 weeks, (n=15)) or boceprevir (800 mg three times daily, for 44 weeks, (n=8)) for 48 weeks. RESULTS: The median age was 59 (52.5-66) years, with 48.8% women. Thirteen patients (56.5%) were complete clinical responders, and 10 (43.5%) were partial responders at week 24. The virological response (ie, HCV RNA negativation) was of 69.6% at week 24 (p=0.005). The cryoglobulin level decreased from 0.44 to 0.06 g/l (p=0.0006) and the C4 level increased from 0.09 to 0.15 g/l (p=0.045). Grades 3 and 4 adverse events (mainly anaemia, neutropenia and thrombocytopenia) were observed in 10 cases (43.5%). Twenty patients (87%) received erythropoietin, 9 (39.1%) had red cell transfusion, and 2 (8.7%) had granulocyte stimulating agents. Antiviral therapy discontinuation was required in 8 (34.7%) patients for virological non-response (n=5), virological relapse (n=2) and depression (n=1). CONCLUSIONS: Peg-IFNα/ribavirin/protease inhibitor combination seems highly effective in HCV-MC. Such therapeutic regimen should be administered cautiously considering the high rate of side effects.
[Mh] MeSH terms primary: Antiviral Agents/administration & dosage
Cryoglobulinemia/drug therapy
Hepatitis C, Chronic/drug therapy
Interferon-alpha/administration & dosage
Polyethylene Glycols/administration & dosage
Protease Inhibitors/administration & dosage
Ribavirin/administration & dosage
[Mh] MeSH terms secundary: Aged
Antiviral Agents/adverse effects
Cohort Studies
Cryoglobulinemia/virology
Drug Therapy, Combination
Female
Hepacivirus
Hepatitis C, Chronic/complications
Humans
Interferon-alpha/adverse effects
Male
Middle Aged
Oligopeptides/administration & dosage
Oligopeptides/adverse effects
Polyethylene Glycols/adverse effects
Proline/administration & dosage
Proline/adverse effects
Proline/analogs & derivatives
Protease Inhibitors/adverse effects
Recombinant Proteins/administration & dosage
Recombinant Proteins/adverse effects
Ribavirin/adverse effects
Treatment Outcome
Vasculitis/drug therapy
Vasculitis/virology
[Pt] Publication type:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antiviral Agents); 0 (Interferon-alpha); 0 (N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide); 0 (Oligopeptides); 0 (Polyethylene Glycols); 0 (Protease Inhibitors); 0 (Recombinant Proteins); 0 (peginterferon alfa-2a); 0 (telaprevir); 49717AWG6K (Ribavirin); 9DLQ4CIU6V (Proline)
[Em] Entry month:1405
[Cu] Class update date: 141018
[Lr] Last revision date:141018
[Js] Journal subset:IM
[Da] Date of entry for processing:140407
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2012-202770

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[PMID]: 24505587
[Au] Autor:Haddad F; Helm TN
[Ad] Address:SUNY Upstate Medical School, 4 Fiore Cir, Latham, NY 12110, USA. Haddadf@upstate.edu.
[Ti] Title:Wells syndrome.
[So] Source:Cutis;93(1):17, 38-9, 2014 Jan.
[Is] ISSN:2326-6929
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Cellulitis/diagnosis
Eosinophilia/diagnosis
[Mh] MeSH terms secundary: Cellulitis/pathology
Diagnosis, Differential
Eosinophilia/pathology
Granuloma/diagnosis
Granuloma/pathology
Humans
Urticaria/diagnosis
Urticaria/pathology
Vasculitis, Leukocytoclastic, Cutaneous/diagnosis
Vasculitis, Leukocytoclastic, Cutaneous/pathology
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[Da] Date of entry for processing:140207
[St] Status:MEDLINE

  8 / 32350 MEDLINE  
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[PMID]: 23344748
[Au] Autor:Aboukhoudir F; Pansieri M; Rekik S
[Ad] Address:Department of Cardiology, Avignon Hospital Center, Avignon, France.
[Ti] Title:Chronic calcific constrictive pericarditis complicating churg-strauss syndrome: first reported case.
[So] Source:Thorac Cardiovasc Surg;62(7):631-3, 2014 Oct.
[Is] ISSN:1439-1902
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Churg-Strauss syndrome is a necrotizing systemic vasculitis characterized by extravascular granulomas and eosinophilic infiltrates of small vessels. Although cardiac complications are considered to be relatively common, no case of constrictive calcified pericarditis has ever been previously described in this setting. In this report, we present the case of a 46-year-old man with Churg-Strauss syndrome, in whom we were able to document the development of symptomatic calcific constrictive pericarditis during a 10-year period despite long-term corticosteroid therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1055/s-0032-1331579

  9 / 32350 MEDLINE  
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[PMID]: 25207681
[Au] Autor:Hamedi M; Bergmeier LA; Hagi-Pavli E; Vartoukian SR; Fortune F
[Ad] Address:Centre Clinical and Diagnostic Oral Sciences, Institute of dentistry, Bart's and The London School of Medicine and Dentistry, London, UK.
[Ti] Title:Differential Expression of Suppressor of Cytokine Signalling Proteins in Behçet's Disease.
[So] Source:Scand J Immunol;80(5):369-76, 2014 Nov.
[Is] ISSN:1365-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Behçet's disease (BD) is a chronic, multisystemic, recurrent vasculitis disease of unknown aetiology. Proinflammatory cytokines are a key feature of the disease, but the triggers for their induction are not well understood and/or controversial. Suppressor of cytokine signalling (SOCS) proteins which negatively regulate the JAK-STAT signalling pathway of cytokine induction may be dysregulated in BD. The expression of SOCS1 and 3 mRNA and protein was studied in peripheral blood mononuclear cells (PBMCs) and neutrophils of patients with BD and compared with healthy controls (HCs) and patients with recurrent aphthous stomatitis (RAS) using RT-PCR, Western blot and immunohistochemistry. SOCS1 and 3 mRNA was also measured in buccal mucosal cells (BMC) of patients with BD and HCs. SOCS1 and 3 mRNA was significantly upregulated in PBMCs of patients with BD compared with HCs (P = 0.0149; P = 0.0007). In addition, there were subtle differences between expression in active and symptom-free BD (quiescent BD). SOCS1 and SOCS 3 were also significantly upregulated in BMC from oral ulcers of BD compared with HCs (both at P = 0.0001). A differential expression of both SOCS1 and 3 was observed between PBMCs and neutrophils in patients with BD. Immunohistochemical analysis revealed differential expression of SOCS proteins in the buccal mucosa with an increased expression at the ulcer surface of ulcers than in the non-ulcerated tissue. These observations suggest a dysregulation of the expression of these important regulators not only between patients with BD and healthy controls but also between mucosal and systemic tissues, which may reflect the nature of the aetiopathology of the disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/sji.12211

  10 / 32350 MEDLINE  
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[PMID]: 23262231
[Au] Autor:Joseph EK; Levine JD
[Ad] Address:Department of Medicine, Division of Neuroscience, University of California at San Francisco, San Francisco, CA 94143-0440, USA; Department of Oral Surgery, Division of Neuroscience, University of California at San Francisco, San Francisco, CA 94143-0440, USA.
[Ti] Title:Role of endothelial cells in antihyperalgesia induced by a triptan and ß-blocker.
[So] Source:Neuroscience;232:83-9, 2013 Mar 1.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:While blood vessels have long been implicated in diverse pain syndromes (e.g., migraine headache, angina pectoris, vasculitis, and Raynaud's syndrome), underlying mechanisms remain to be elucidated. Recent evidence supports a contribution of the vascular endothelium in endothelin-1-induced hyperalgesia, and its enhancement by repeated mechanical stimulation; a phenomenon referred to as stimulus-induced enhancement of (endothelin) hyperalgesia (SIEH). SIEH is thought to be mediated by release of ATP from endothelial cells, to act on P2X3 receptors on nociceptors. In the present study we evaluated the ability of another vasoactive hyperalgesic agent, epinephrine, to induce endothelial cell-dependent hyperalgesia and SIEH. We found that epinephrine also produces hyperalgesia and SIEH. Both P2X3 receptor antagonists, A317491 and octoxynol-9, which attenuate endothelial cell function, eliminated SIEH without affecting epinephrine hyperalgesia. We further evaluated the hypothesis that members of two important classes of drugs used to treat migraine headache, whose receptors are present in endothelial cells - the triptans and ß blockers - have a vascular component to their anti-hyperalgesic action. For this, we tested the effect of ICI-118,551, a ß2-adrenergic receptor antagonist and sumatriptan, an agonist at 5-HT1B and 5-HT1D receptors, on nociceptive effects of endothelin and epinephrine. ICI-118,551 inhibited endothelin SIEH, and attenuated epinephrine hyperalgesia and SIEH. Sumatriptan inhibited epinephrine SIEH and inhibited endothelin hyperalgesia and SIEH, while having no effect on epinephrine hyperalgesia or the hyperalgesia induced by a prototypical direct-acting inflammatory mediator, prostaglandin E2. These results support the suggestion that triptans and ß-blockers interact with the endothelial cell component of the blood vessel to produce anti-hyperalgesia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review


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