Diagnostics and therapy of AA amyloidosis

被引:6
作者
Blank, N. [1 ]
Lorenz, H. M. [1 ]
机构
[1] Univ Klinikum Heidelberg, Med Klin 5, Sekt Rheumatol, D-69120 Heidelberg, Germany
来源
PATHOLOGE | 2009年 / 30卷 / 03期
关键词
Amyloidosis; Rheumatic disease; TNF alpha; Familial Mediterranean fever; Colchicine; Periodic syndrome; FAMILIAL MEDITERRANEAN FEVER; PERIODIC SYNDROME TRAPS; GRANULOMATOUS ARTHRITIS; SYSTEMIC AMYLOIDOSIS; BLAU-SYNDROME; TNF RECEPTOR; MUTATIONS; DISEASE; URTICARIA; PROTEIN;
D O I
10.1007/s00292-009-1140-5
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
AA amyloidosis can be the consequence of any chronic inflammatory disorder. It is most commonly associated with chronic inflammatory rheumatic, pulmonary or gastrointestinal diseases, familial Mediterranean fever or other rare periodic syndromes. AA amyloidosis often affects the kidneys, gastrointestinal tract and the heart. Effective therapy of the underlying disease can normalize the inflammatory reaction and can slow or inhibit the deterioration of organ function if the diagnosis is made at an early stage of the disease. In rheumatoid diseases and in some periodic syndromes the use of antibodies against TNF alpha or IL-1 beta might be helpful. Patients with familial Mediterranean fever should regularly take colchicine to prevent attacks and to reduce the risk for development or progression of AA amyloidosis. Eprodisate is currently being investigated for AA amyloidosis and renal involvement.
引用
收藏
页码:219 / 225
页数:7
相关论文
共 29 条
[1]   De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with neonatal-onset multisystem inflammatory disease (NOMID) -: A new member of the expanding family of pyrin-associated autoinflammatory diseases [J].
Aksentijevich, I ;
Nowak, M ;
Mallah, M ;
Chae, JJ ;
Watford, WT ;
Hofmann, SR ;
Stein, L ;
Russo, R ;
Goldsmith, D ;
Dent, P ;
Rosenberg, HF ;
Austin, F ;
Remmers, EF ;
Balow, JE ;
Rosenzweig, S ;
Komarow, H ;
Shoham, NG ;
Wood, G ;
Jones, J ;
Mangra, N ;
Carrero, H ;
Adams, BS ;
Moore, TL ;
Schikler, K ;
Hoffman, H ;
Lovell, DJ ;
Lipnick, R ;
Barron, K ;
O'Shea, JJ ;
Kastner, DL ;
Goldbach-Mansky, R .
ARTHRITIS AND RHEUMATISM, 2002, 46 (12) :3340-3348
[2]   NOD2 gene-associated pediatric granulomatous arthritis -: Clinical diversity, novel and recurrent mutations, and evidence of clinical improvement with interleukin-1 blockade in a Spanish cohort [J].
Arostegui, Juan I. ;
Arnal, Cristina ;
Merino, Rosa ;
Modesto, Consuelo ;
Carballo, Maria Antonia ;
Moreno, Purificacion ;
Garcia-Consuegra, Julia ;
Naranjo, Antonio ;
Ramos, Eduardo ;
de Paz, Pilar ;
Rius, Josefa ;
Plaza, Susana ;
Yaguee, Jordi .
ARTHRITIS AND RHEUMATISM, 2007, 56 (11) :3805-3813
[3]   Familial Mediterranean fever [J].
Ben-Chetrit, E ;
Levy, M .
LANCET, 1998, 351 (9103) :659-664
[4]   Renal involvement in systemic amyloidosis [J].
Bergesio, F. ;
Ciciani, A. M. ;
Manganaro, M. ;
Palladini, G. ;
Santostefano, M. ;
Brugnano, R. ;
Di Palma, A. M. ;
Gallo, M. ;
Rosati, A. ;
Tosi, P. L. ;
Salvadori, M. .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2008, 23 (03) :941-951
[5]   FAMILIAL GRANULOMATOUS ARTHRITIS, IRITIS, AND RASH [J].
BLAU, EB .
JOURNAL OF PEDIATRICS, 1985, 107 (05) :689-693
[6]   Eprodisate for the treatment of renal disease in AA amyloidosis [J].
Dember, Laura M. ;
Hawkins, Philip N. ;
Hazenberg, Bouke P. C. ;
Gorevic, Peter D. ;
Merlini, Giampaolo ;
Butrimiene, Irena ;
Livneh, Avi ;
Lesnyak, Olga ;
Puechal, Xavier ;
Lachmann, Helen J. ;
Obici, Laura ;
Balshaw, Robert ;
Garceau, Denis ;
Hauck, Wendy ;
Skinner, Martha .
NEW ENGLAND JOURNAL OF MEDICINE, 2007, 356 (23) :2349-2360
[7]   Prospective study of anti-tumour necrosis factor receptor superfamily 1B fusion protein, and case study of anti-tumour necrosis factor receptor superfamily 1A fusion protein, in tumour necrosis factor receptor associated periodic syndrome (TRAPS): clinical and laboratory findings in a series of seven patients [J].
Drewe, E ;
McDermott, EM ;
Powell, PT ;
Isaacs, JD ;
Powell, RJ .
RHEUMATOLOGY, 2003, 42 (02) :235-239
[8]   Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes [J].
Feldmann, J ;
Prieur, AM ;
Quartier, P ;
Berquin, P ;
Certain, S ;
Cortis, E ;
Teillac-Hamel, D ;
Fischer, A ;
de Saint Basile, G .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 71 (01) :198-203
[9]   Mevalonate kinase deficiencies: from mevalonic aciduria to hyperimmunoglobulinemia D syndrome [J].
Haas, Dorothea ;
Hoffmann, Georg F. .
ORPHANET JOURNAL OF RARE DISEASES, 2006, 1 (1)
[10]   Diagnostic performance of amyloid A protein quantification in fat tissue of patients with clinical AA amyloidosis [J].
Hazenberg, Bouke P. C. ;
Bijzet, Johan ;
Limburg, Pieter C. ;
Skinner, Martha ;
Hawkins, Philip N. ;
Butrimiene, Irena ;
Livneh, Avi ;
Lesnyak, Olga ;
Nasonov, Evgeney L. ;
Filipowicz-Sosnowska, Anna ;
Guel, Ahmet ;
Merlini, Giampaolo ;
Wiland, Piotr ;
Oezdogan, Huri ;
Gorevic, Peter D. ;
Ben Maiz, Hedi ;
Benson, Merrill D. ;
Direskeneli, Haner ;
Kaarela, Kalevi ;
Garceau, Denis ;
Hauck, Wendy ;
van Rijswijk, Martin H. .
AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS, 2007, 14 (02) :133-140