Growth in juvenile idiopathic arthritis: the role of inflammation

被引:0
作者
Gaspari, S. [1 ]
Marcovecchio, M. L. [1 ]
Breda, L. [1 ]
Chiarelli, F. [1 ]
机构
[1] Univ G dAnnunzio, Dipartimento Pediat, I-66100 Chieti, Italy
关键词
growth; juvenile idiopathic arthritis; cytokines; inflammation; NECROSIS-FACTOR-ALPHA; I GENE-EXPRESSION; RHEUMATOID-ARTHRITIS; ARTICULAR CHONDROCYTES; TRANSGENIC MICE; GH RECEPTOR; TNF-ALPHA; IGF-I; BONE-GROWTH; INTERLEUKIN-6;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Growth disorders are common among patients with juvenile idiopathic arthritis (JIA). These disorders range from general growth retardation to local acceleration of growth in the affected limb, and are associated with an increased production of pro-inflammatory cytokines, such as interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Proinflammatory cytokines may act individually or in combination to impair child growth through systemic mechanisms and/or a local action. Whereas IL-6 affects growth mainly via systemic mechanisms altering growth hormone secretion. IL-1 beta and TNF-alpha can directly affect growth plate chondrocyte dynamics as well as longitudinal bone growth. There are emerging data suggesting that interleukin-15 and interleukin-5 may be new cytokines implicated in inflammatory diseases, but further well-designed longitudinal studies in larger groups of children are required to establish a causal relationship. Other factors, which might contribute to growth suppression associated with childhood arthritis, include the degree, extent, and duration of disease activity, age at onset, immobility, sub-optimal nutrition and corticosteroid therapy.
引用
收藏
页码:104 / 110
页数:7
相关论文
共 68 条
[1]   Induction of apoptosis in chondrocytes by tumor necrosis factor-alpha [J].
Aizawa, T ;
Kon, T ;
Einhorn, TA ;
Gerstenfeld, LC .
JOURNAL OF ORTHOPAEDIC RESEARCH, 2001, 19 (05) :785-796
[2]   TNFα and IFNγ potentiate IL-1β induced mitogen activated protein kinase activity in rat pancreatic islets of Langerhans [J].
Andersen, NA ;
Larsen, CM ;
Mandrup-Poulsen, T .
DIABETOLOGIA, 2000, 43 (11) :1389-1396
[3]   GROWTH IN STILLS DISEASE [J].
ANSELL, BM ;
BYWATERS, EGL .
ANNALS OF THE RHEUMATIC DISEASES, 1956, 15 (04) :295-319
[4]   DIFFERENTIAL CELLULAR SYNTHESIS OF INSULIN-LIKE GROWTH-FACTOR BINDING PROTEIN-1 (IGFBP-1) AND IGFBP-3 WITHIN HUMAN LIVER [J].
ARANY, E ;
AFFORD, S ;
STRAIN, AJ ;
WINWOOD, PJ ;
ARTHUR, MJP ;
HILL, DJ .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1994, 79 (06) :1871-1876
[5]   Soluble IL-6Rα upregulates IL-6, MMP-1 and MMP-2 secretion in bone marrow stromal cells [J].
Barillé, S ;
Collette, M ;
Thabard, W ;
Bleunven, C ;
Bataille, R ;
Amiot, M .
CYTOKINE, 2000, 12 (09) :1426-1429
[6]   Targeting interleukin-15 in patients with rheumatoid arthritis - A proof-of-concept study [J].
Baslund, B ;
Tvede, N ;
Danneskiold-Samsoe, B ;
Larsson, P ;
Panayi, G ;
Petersen, J ;
Petersen, LJ ;
Beurskens, FJM ;
Schuurman, J ;
van de Winkel, JGJ ;
Parren, PWHI ;
Gracie, JA ;
Jongbloed, S ;
Liew, FY ;
McInnes, IB .
ARTHRITIS AND RHEUMATISM, 2005, 52 (09) :2686-2692
[7]  
Bateman J.F., 1996, Extracellular Matrix, P22
[8]  
Bierbaum S, 2006, CLIN EXP RHEUMATOL, V24, P219
[9]   REGULATION OF IGF-1 RECEPTORS ON RABBIT ARTICULAR CHONDROCYTES BY INFLAMMATORY MEDIATORS [J].
BLOUNT, S ;
CRAWFORD, A .
AGENTS AND ACTIONS, 1994, 41 :C177-C179
[10]   IL-1β impairs insulin-like growth factor I-induced differentiation and downstream activation signals of the insulin-like growth factor I receptor in myoblasts [J].
Broussard, SR ;
McCusker, RH ;
Novakofski, JE ;
Strle, K ;
Shen, WH ;
Johnson, RW ;
Dantzer, R ;
Kelley, KW .
JOURNAL OF IMMUNOLOGY, 2004, 172 (12) :7713-7720