Immunological Studies of the Placenta in Maternal Connective Tissue Disease

1999 ◽  
Vol 2 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Jeanne Ackerman ◽  
Erick F. Gonzalez ◽  
Enid Gilbert-Barness

Maternal connective tissue disease is an important cause of second-trimester fetal loss. In order to assess the pathological changes in the placenta in maternal connective tissue disease, we reviewed the clinical histories and performed histologic and immunofluorescence studies on nine placentas: five from mothers with systemic lupus erythematosus (SLE), two from mothers with mixed connective tissue disease (MCTD), one from a mother with rheumatoid arthritis (RA), and one from a mother without prior known connective tissue disease. Excessive intervillous fibrin deposition and infarction were noted in all cases. Immunofluorescent and immunoperoxidase studies showed deposits of fibrinogen, IgG, IgM, IgA, and complement 3 (C3) localized to the trophoblast basement membrane (TBM). Electron microscopy documented thickening of the trophoblast basal lamina in three SLE placentas examined. The use of immunofluorescence may be enhanced further if antitrophoblast antibodies can be linked to placental compromise.

2018 ◽  
Vol 30 (2) ◽  
pp. 76-78
Author(s):  
Razib Kumar Saha ◽  
Md Azizul Haque ◽  
Mohammad Hasan Tarik

Renal tubular acidosis (RTA) is caused by defect in renal tubular acid transport. Sjogren’s syndrome, rheumatoid arthritis, systemic lupus erythematosus and autoimmune hepatitis are the most common autoimmune causes of distal RTA. We are reporting a case of distal renal tubular acidosis associated with mixed connective tissue disease and hypothyroidism presenting as recurrent hypokalemic paralysis.TAJ 2017; 30(2): 76-78


1996 ◽  
Vol 184 (4) ◽  
pp. 1313-1318 ◽  
Author(s):  
E Feist ◽  
T Dörner ◽  
U Kuckelkorn ◽  
G Schmidtke ◽  
B Micheel ◽  
...  

Autoantibodies occur in low frequencies among patients with myositis characterizing only distinct subsets of this disease. Most of these known antibodies are directed to enzymatically active complexes. The 20S proteasome represents an essential cytoplasmatic protein complex for intracellular nonlysosomal protein degradation, and is involved in major histocompatibility complex class I restricted antigen processing. In this study we investigated whether the 20S proteasome complex is an antibody target in myositis and in other autoimmune diseases. 34 sera of poly/dermatomyositis patients were assayed for antiproteasomal antibodies using enzyme-linked immunosorbent assay, immunoblot, and two-dimensional non-equilibrium pH gradient electrophoresis (NEPHGE). Sera was from patients with systemic lupus erythematosus (SLE), mixed connective tissue disease, and rheumatoid arthritis; healthy volunteers served as controls. In 62% (21/34) of the cases sera from patients with myositis and in 58% (30/52) of the cases sera from patients with SLE reacted with the 20S proteasome. These frequencies exceeded those of sera from patients with mixed connective tissue disease, rheumatoid arthritis, and healthy controls. The alpha-type subunit C9 of the 20S proteasome was determined to be the predominant target of the autoimmune sera in myositis and SLE. Lacking other frequent autoantibodies in myositis, the antiproteasome antibodies are the most common humoral immune response so far detected in this disease entity.


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