Microscopic Polyangiitis - General Practice Notebook microscopic polyangiitis. microscopic polyangiitis affects the smallerarteries and is the most common form of arteritis. There may http://www.gpnotebook.co.uk/cache/362414118.htm
Extractions: microscopic polyangiitis Microscopic polyangiitis affects the smaller arteries and is the most common form of arteritis. There may be a history of hypersensitivity to drugs or foreign proteins, and the natural history is a short duration of vasculitis in the small veins, arteries and capillaries. Treatment is as for Wegener's granulomatosis.
Microscopic Polyangiitis : Meddie Health Search ITEMS LINKS microscopic polyangiitis in a Pediatric Patient From Archives ofFamily Medicine, a description of this disorder, followed by a case study. http://www.meddie.com/search/Health/Conditions_and_Diseases/Immune_Disorders/Aut
Extractions: hbv_research archives mailto:martins@zoomnet.net http://www.geocities.com/Mamablondie/hblist.html Prev by Date: Hepatitis B Core Antibody-Positive Liver Donors May Transmit Hepatitis B Next by Date: Dual topology of the hepatitis B virus large envelope protein: Determinants influencing posttranslational translocation Return to Table of Contents:
Mayo Clinic - Clinical Trials In PCRC to top microscopic polyangiitis Pilot Trial of Rituximab (Rituxan) in ANCAAssociatedVasculitis (Wegener's Granulomatosis and microscopic polyangiitis). http://www.mayo.edu/research/pcrc/trials_by_condition.html
Extractions: A clinical trial currently recruiting participants. Why is this research study being done? This research study is being done to find out if Mycophenolate Mofetil (CellCept) given with prednisone, causes and maintains remission in patients with p-ANCA Microscopic polyangiitis, with mild to moderate kidney dysfunction. What will happen in the research study? For the first three days of study, patients will receive Methylprednisone through a vein in the arm. Participants will then receive steroids by mouth for at least 24 weeks, and Mycophenolate mofetil (18 months) throughout the study period. There will be a lowering of the dose of steroids at 4 weeks depending on the responses to therapy. Follow-up visits will take place at baseline, weeks 2, 4 and 8 and months 3, 6, 9, 12, and 18, that include a physical exam, blood tests (a sample of two tablespoons), urinalysis and chest x-ray.
Microscopic Polyarteritis Background. This small vessel vasculitis is also known as microscopicpolyangiitis. SYNONYMS, microscopic polyangiitis. INCIDENCE, 1100,000. http://www.thedoctorsdoctor.com/diseases/microscopic_polyarteritis.htm
Extractions: Background This small vessel vasculitis is also known as microscopic polyangiitis . It is a disease of middle aged males and mainly affects the kidneys, skin, and lungs. Like polyarteritis nodosa , the disease presents with constitutional symptoms of fever, malaise, myalgia, and weight loss. Skin lesions occur in 30-50% presenting with purpura and rarely nodules and ulcers. One of the diagnostic hallmarks is the presence of antineutrophil cytoplasmic antibodies (p-ANCA). The kidney shows a focal and segmental glomerulonephritis. The skin shows a leukocytoclastic vasculitis. In nodular skin lesions, the vessels of the dermis and subcutaneous fat may be involved. SYNONYMS Microscopic polyangiitis INCIDENCE AGE RANGE-MEDIAN Mean 50 years SEX (M:F) Male slight predominance LABORATORY/RADIOLOGIC/OTHER TESTS CHARACTERIZATION Laboratory Markers ANCA PR3 ANCA and MPO-ANCA are present in 40% and 50% of cases with 10% negative GROSS APPEARANCE/CLINICAL VARIANTS CHARACTERIZATION General VARIANTS Pulmonary-Renal syndrome Arch Intern Med 1996;156:440-445
Vasculitis PATIENTS AND METHODS Fortythree patients with histologically proven vasculitis(21 with Wegener's granulomatosis, 17 with microscopic polyangiitis, and 5 http://www.thedoctorsdoctor.com/diseases/vasculitis.htm
Extractions: Background A vasculitis is an inflammation of a blood vessel. These blood vessels may be as small as capillaries to as large as the aorta. Surprisingly, many vasculitides affect only a certain caliber of vessels, although there are conditions which affect all. Because any vessel can be affected the diagnosis is often not suspected clinically and requires a biopsy to establish the diagnosis. ANCA Takuo Tsuji, MD Nagoya, Japan J Am Acad Dermatol 2001;45:S215-7 Abstract quote Generalized morphea is rarely associated with systemic overlap. We report an unusual case with generalized morphea involving cutaneous large vessel vasculitis, mononeuritis multiplex, and lupus anticoagulant without any evidence of the coexistent systemic lupus erythematosus. LABORATORY TESTING CHARACTERIZATION Serial measurements of antineutrophil cytoplasmic autoantibodies in patients with systemic vasculitis.
NEJM -- Sign In have been distinguished from polyarteritis nodosa, such as Wegener's granulomatosis,ChurgStrauss syndrome, microscopic polyangiitis, and Kawasaki's disease http://content.nejm.org/cgi/content/full/338/14/994
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Autoimmunity In Glomerulonephritis; Serological Diagnosis And Autoimmunity in glomerulonephritis; serological diagnosis and clinical outcome withspecial reference to Wegener´s granulomatosis and microscopic polyangiitis. http://eprints.lub.lu.se/archive/00009750/
JN - Vol 10 No 1-1997, Pp 30-32 Arteritis Temporalis in a patient with microscopic polyangiitis. KEY WORDS Microscopicpolyangiitis, Temporal arteritis, Vasculitis, ANCA. Introduction. http://www.sin-italia.org/jnonline/vol10n1/hergesel/hergesel.htm
Extractions: Table of Contents JOURNAL OF NEPHROLOGY Vol. 10 no. 1 - 1997 / pp 30-32 Short preliminary report Arteritis Temporalis in a patient with microscopic Polyangiitis Olaf W. Hergesell , Konrad Andrassy , Rüdiger Waldherr , Markus Blum Division of Nephrology, Division of Pathology, Division of ophthalmology, University of Heidelberg - Germany ABSTRACT: Coexistence of temporal arteritis with other types of systemic vasculitis has already been reported We describe the case history of a 72-year-old woman who first presented with biopsy-proven, ANCA-positive microscopic polyangiitis, and while on clinical and serological remission of microscopic polyangiitis, developed a biopsy proven temporal arteritis. KEY WORDS: Microscopic polyangiitis, Temporal arteritis, Vasculitis, ANCA Introduction Case Report Laboratory investigation disclosed a moderately elevated erythrocyte sedimentation rate (ESR) with 40 mm/h, a hemoglobin concentration of 125 g/l and normal leukocyte and platelet counts. Electrolytes, liver and thyroid function tests, glucose and muscle enzymes were within the normal range. The serum creatinine was 1.5 mg/dl and the urea concentration was 65 mg/dl. Urinalysis revealed a microhematuria and proteinuria of 1.6 g/24 h. The urinary sediment showed dysmorphic erythrocytes, red cell-and granular casts. Serological tests for Hepatitis B were negative. A collagen-vascular work-up including ANA, ds-DNA, cryglobulins, rheumatoid facter, SSA/SSB-antibodies was negative except for a borderline positive ANA (IgG-ANA titer 1:40). Complement and immunglobulin levels were within the normal range. Immunoelectrophoresis of serum and urine was normal. An infectious cause of the disease was thus excluded
Lund University, Doctoral Dissertation in glomerulonephritis; serological diagnosis and clinical outcome with specialreference to Wegener´s granulomatosis and microscopic polyangiitis . http://www.lub.lu.se/cgi-bin/show_diss.pl?db=global&fname=med_185.html
Journal References For Drug Information al. microscopic polyangiitis clinical and laboratory findings in eightyfivepatients. Arthritis Rheum 1999;4242130. Guillevin http://www.user.fast.net/~rcb1/mpa/MPA_Information/Drugs/References/references.h
Extractions: Allison AC, Eugui EM. Immunosuppressive and other effects of mycophenolic acid and an ester prodrug, mycophenolate mofetil. Immunol Rev 1993;136:528. Brijker F, Magee CC, Cohen Tervaert JW, ONeill S, Walshe JJ. Outcome analysis of patients with vasculitis associated with antineutrophil cytoplasmic antibodies. Clin Nephrol 1999;52:34451. Falk RJ, Hogan S, Carey TS, Jennette JC. Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis: the Glomerular Disease Collaborative Network. Ann Intern Med 1990;113:65663. Falk RJ, Jennette JC. Anti-neutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis. N Engl J Med 1988;318:165157. Jennette JC, Falk RJ. Small-vessel vasculitis. N Engl J Med 1997;337:151223. Jennette JC, Falk RJ, Andrassy K, et al. Nomenclature of systemic vasculitides: proposal of an international consensus conference. Arthritis Rheum 1994;37:18792. Guillevin L, Druand Gasselin D, Cevallos R, et al. Microscopic polyangiitis: clinical and laboratory findings in eighty-five patients. Arthritis Rheum 1999;42:42130.
Rachael's MPA Support Site Support and information for people fighting microscopic polyangiitis. Frequently asked questions and Category Health Conditions and Diseases microscopic polyangiitisWelcome to my microscopic polyangiitis Support Site. Rachael. Last ModifiedSaturday, May 19, 2001. . What is microscopic polyangiitis? http://www.user.fast.net/~rcb1/mpa/
Extractions: Welcome to my Microscopic Polyangiitis Support Site. I created this site to offer people with this disease a place to come for information about the condition and also a place to share their experiences with someone who understands. I have been searching for an MPA support Web site for the past few years and I havent found one, so I thought Id create my own. Since I started this site in Fall 2000, Ive heard from a few others who have MPA. Were not alone! (Were rare, but were not alone.) Microscopic Polyangiitis, or MPA, is a disease that causes inflammation of small blood vessels and capillaries in the body. It is an autoimmune disease, which means that the inflammation comes from the bodys immune system and not from an outside bacteria or virus. For more information about MPA, go to the
References Jayne DRW Conventional treatment and outcome of Wegener's granulomatosis andmicroscopic polyangiitis. Cleve Clin J Med 2002, 69 (suppl 2) SII110115. http://www.medscape.com/content/2003/00/44/74/447497/447497_ref.html
Extractions: ** This retrospective, single-center analysis assessed the outcome of 59 AASV patients (both WG and MPA) during hemodialysis therapy and after renal transplantation (performed in 22 cases). In contrast to other case series, very low relapse rates were observed (0.09 and 0.02 per patient per year for patients on chronic dialysis and after transplantation, respectively), possibly due to prolonged immunosuppressive therapy. Relapse rates were not affected by ANCA positivity at the time of transplantation, duration of dialysis therapy, the nature of the AASV (WG or MPA), and the type of ANCA (proteinase 3 or myeloperoxidase). Nachman PH, Segelmark M, Westaman K, et al.: Recurrent ANCA-associated small vessel vasculitis after transplantation: a pooled analysis. Kid Int 1999, 56:1544-1550. ** This retrospective analysis on the recurrence of AASV following renal transplantation pooled published case series of AASV patients who received a renal transplant with patients treated at the authors' institutions. Recurrence was observed in 17.3% of 127 cases. Treatment with cyclosporine A, circulating ANCAs at the time of transplantation, and diagnosis (WG or MPA) did not seem to influence relapse rate. Most relapses responded to the reinstitution of cyclophosphamide treatment.
Arch Dermatol -- Page Not Found associated vasculitis includes a group of socalled pauci-immune vasculitis (Wegenergranulomatosis, Churg-Strauss disease, microscopic polyangiitis) in which http://archderm.ama-assn.org/issues/v135n6/ffull/dlt0699-2.html
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Arch Dermatol -- Page Not Found 1 in a recent issue of the ARCHIVES that describes a cutaneouslimited variant ofmicroscopic polyangiitis associated with antimyeloperoxidase autoantibody. . http://archderm.ama-assn.org/issues/v134n2/ffull/dlt0298-1.html
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Extractions: Get Five DVDs for $.49 each. Join now. Tell me when this page is updated VASCULITIS DERMATOLOGY LECTURE NOTES Debabrata Bandyopadhyay, Associate Head, Department of Dermatology, R.G.Kar Medical College Kolkata INDIA VASCULITIS Aetiology and pathogenesis Pathology Classification Clinical features ... Management T he vasculitides are a heterogeneous group of clinicopathological entities that share the common feature of vascular inflammation and injury. There is no universally acceptable classification of these group of disorders. While a number of underlying causes can be identified in some disorders, the aetiology is unknown in many. The pathogenetic mechanisms involved are mainly immunological, immune complex mediated tissue injury being the most commonly incriminated factor. Aetiology and pathogenesis While some forms of vasculitides may be ascribed to underlying factors like infections, malignancy, drug reactions or connective tissue disorders, the cause may remain undetermined in many vasculitic syndromes. Immunologic damage by immune-complex deposition or cell-mediated hypersensitivity is responsible in the majority of cases. The possible immunopathologic mechanism in the causation of vasculitis are . Deposition of circulating antigen-antibody complex or in -situ formation of immune complex within the vessel wall. This leads to complement activation and chemotactic attraction of neutrophils by complement components. Subsequent phagocytosis of such complexes with liberation of neutrophil granular products leads to vascular damage.
VASCULITIC SYNDROMES Once the disease is silent for about a year withdrawal of drugs may betried. Top of the Document. microscopic polyangiitis Microscopic http://dermind.tripod.com/vascsalient.htm
Extractions: Get Five DVDs for $.49 each. Join now. Tell me when this page is updated VASCULITIC SYNDROMES DERMATOLOGY LECTURE NOTES Debabrata Bandyopadhyay, Associate Head, Department of Dermatology, R.G.Kar Medical College Kolkata INDIA CUTANEOUS SMALL VESSEL VASCULITIS (LEUKOCYTOCLASTIC VASCULITIS ) Also known as allergic angiitis hypersensitivity vasculitis and cutaneous necrotizing venulitis , this is a clinicopathologic entity characterized by segmental vasculitis of small vessels (particularly post-capillary venules) with endothelial swelling, fibrinoid necrosis of vessel wall and a prominent neutrophilic infiltrate with fragmentation of their nuclei (leukocytoclasia). The clinical hallmark of cutaneous small vessel vasculitis is palpable purpura. The disease is most often induced by immune complex deposition and subsequent complement activation. LCV may be idiopathic or may be caused by a number of underlying diseases or drugs Clinical data Constitutional: Fever, anorexia, myalgia, arthralgia Cutaneous: Palpable purpura Persistent urticaria Papulonodular lesions Vesicles and bulla Hemorrhagic pustules Infarcts Ulcers Extra-cutaneous: Joint pain particularly of the lower limbs Renal dysfunction Abdominal symptoms: nausea, vomiting, pain abdomen. Rarely GI bleeds
Atlas Of Renal Pathology No. 8 Pauciimmune Necrotizing Crescentic Glomerulonephritides Wegener's Granulomatosis/MicroscopicPolyangiitis. granulomatosis or microscopic polyangiitis. http://www3.us.elsevierhealth.com/ajkd/atlas/32/2/atlas32_2.htm
Extractions: Each month the Atlas of Renal Pathology presents a compilation of figures on a specific pathologic entity. You should read the Terms and Conditions of Use before using this site. If you agree to the terms, you may download the figures to create your own personal, noncommercial library of images or to create slides for teaching purposes. To view a larger version of each figure, select View larger version below each figure. To make a slide, select download slide-quality image file . Download times may be somewhat lengthy. For tips on preparing slides from the files, please see Downloading Images for Slide Preparation Pathology Editor: Agnes Fogo, MD Download slide-quality image Fig 1. Segmental fibrinoid necrosis with nuclear debris and glomerular basement membrane disruption, typical of early stage of pauci-immune crescentic glomerulonephritis, diagnosed clinically as Wegener's granulomatosis in this case. The morphological differential includes microscopic polyangiitis and Wegener's granulomatosis, which cannot be distinguished morphologically from the kidney biopsy. Immunofluorescence studies are negative in both of these diseases, and few if any, electron dense areas are found by electron microscopy (Jones silver stain; original magnification x400).