Monoamine oxidase inhibitors for IgA nephropathy

被引：3

作者：

Altschuler, EL ^{[1
]}

机构：

[1] Univ Calif San Diego, Brain & Percept Lab, La Jolla, CA 92093 USA

来源：

MEDICAL HYPOTHESES | 2001年 / 56卷 / 02期

关键词：

D O I：

10.1054/mehy.2000.1158

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

IgA nephropathy (IgAN), characterized by renal mesangial deposits of antibodies (of the IgA subtype), is the most common glomerulonephritis worldwide. The cause of IgAN is not known. IgAN can often lead to end stage renal disease (ESRD), and there is no known treatment proven to prevent ESRD in IgAN. Long term use of steroids or other immunosuppressant drugs carry severe toxicities and other risks. IgAN patients have high serum levels of tumor necrosis factor-alpha (TNF). Increased monoamine levels, via increased cellular cyclic AMP, can decrease TNF elaboration. Monoamine oxidase inhibitors (MAO-ls) have been found effective in case studies for a number of diseases, e.g. rheumatoid arthritis and Crohn's disease, characterized by high TNF levels. Here I suggest that MAO-is might be of utility in IgAN by decreasing TNF levels. (C) 2001 Harcourt Publishers Ltd.

引用

页码：225 / 226

页数：2

共 15 条

[1] Elevated levels of interferon gamma, tumor necrosis factor α, interleukins 2, 4, and 5, but not interleukin 10, are present in recurrent aphthous stomatitis [J].

Buño, IJ ;

Huff, C ;

Weston, WL ;

Cook, DT ;

Brice, SL .

ARCHIVES OF DERMATOLOGY, 1998, 134 (07) :827-831

[2] Catecholamines increase monocyte TNF receptors and inhibit TNF through β2-adrenoreceptor activation [J].

Guirao, X ;

Kumar, A ;

Katz, J ;

Smith, M ;

Lin, E ;

Keogh, C ;

Calvano, SE ;

Lowry, SF .

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1997, 273 (06) :E1203-E1208

[3]

Hunley Tracy E., 1999, Current Opinion in Pediatrics, V11, P152, DOI 10.1097/00008480-199904000-00009

[4] Crohn's disease remission with phenelzine treatment [J].

Kast, RE .

GASTROENTEROLOGY, 1998, 115 (04) :1034-1035

[5] REMISSION OF RHEUMATOID-ARTHRITIS AND OTHER DISORDERS OF IMMUNITY IN PATIENTS TAKING MONOAMINE-OXIDASE INHIBITORS [J].

LIEB, J .

INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY, 1983, 5 (04) :353-357

[6] Infliximab (chimeric anti-tumour necrosis factor α monoclonal antibody) versus placebo in rheumatoid arthritis patients receiving concomitant methotrexate:: a randomised phase III trial [J].

Maini, R ;

St Clair, EW ;

Breedveld, F ;

Furst, D ;

Kalden, J ;

Weisman, M ;

Smolen, J ;

Emery, P ;

Harriman, G ;

Feldmann, M ;

Lipsky, P .

LANCET, 1999, 354 (9194) :1932-1939

[7] Release of tumor necrosis factor-α from coronary smooth muscle:: Activation of NF-κB and inhibition by elevated cyclic AMP [J].

Newman, WH ;

Zhang, LM ;

Lee, DH ;

Dalton, ML ;

Warejcka, DJ ;

Castresana, MR ;

Leeper-Woodford, SK .

JOURNAL OF SURGICAL RESEARCH, 1998, 80 (02) :129-135

[8] Amelioration of collagen II-induced arthritis in rats by the type IV phosphodiesterase inhibitor Rolipram [J].

Nyman, U ;

Mussener, A ;

Larsson, E ;

Lorentzen, J ;

Klareskog, L .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1997, 108 (03) :415-419

[9] CHARACTERIZATION OF CAMP-DEPENDENT INHIBITION OF LPS-INDUCED TNF-ALPHA PRODUCTION BY ROLIPRAM, A SPECIFIC PHOSPHODIESTERASE-IV (PDE-IV) INHIBITOR [J].

PRABHAKAR, U ;

LIPSHUTZ, D ;

BARTUS, JO ;

SLIVJAK, MJ ;

SMITH, EF ;

LEE, JC ;

ESSER, KM .

INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY, 1994, 16 (10) :805-816

[10]

ROSENTHAL SH, 1984, NEW ENGL J MED, V311, P1442

← 1 2 →