Cardiac Specific Auto-Antibody Levels are not Increased after Bypass Surgery

Abstract Data have been collected from 47 centers in Europe and North America on the treatment with porcine factor VIII concentrate of 74 acute bleeding episodes in 65 patients with acquired hemophilia. The median initial anti-human factor VIII auto-antibody inhibitor level was 38 Bethesda unit (BU)/mL (range 1.2 to 1,024) whereas that against porcine was 1 BU/mL (range 0 to 15). The mean initial dose of porcine factor VIII infused was 84 IU/kg, which increased the plasma factor VIII:C activity by 0.85 IU/mL. Therapy was continued for a mean of 8.5 days during which time the average number of infusions was 11. Objective clinical responses were rated as good or excellent in 78% of recipients. Side effects were uncommon; only one patient experienced a severe anaphylactic reaction necessitating the discontinuation of porcine FVIII therapy. After therapy, no increase in the median level of anti- human FVIII or anti-porcine antibody was noted in the group as a whole, although 13 patients showed individual increases in either anti-human or anti-porcine antibody levels or both of more than 10 BU/mL. Of the 7 patients who subsequently rebled, 5 were successfully re-treated and 2 did not respond to further porcine factor VIII treatment. Porcine factor VIII is safe and clinically effective treatment for bleeding episodes associated with acquired hemophilia and should be considered as first-line therapy for patients whose acquired anti-factor VIII:C antibody cross-reacts with porcine factor VIII:C at low levels.

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PARP inhibition in atherosclerosis and its effects on dendritic cells, T cells and auto-antibody levels

European Journal of Medical Research ◽

10.1186/2047-783x-16-8-367 ◽

2011 ◽

Vol 16 (8) ◽

pp. 367 ◽

Cited By ~ 8

Author(s):

C Erbel ◽

J Achenbach ◽

M Akhavanpoor ◽

TJ Dengler ◽

F Lasitschka ◽

...

Keyword(s):

T Cells ◽

Dendritic Cells ◽

Parp Inhibition ◽

Antibody Levels ◽

Auto Antibody

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Use of porcine factor VIII in the treatment of patients with acquired hemophilia

Blood ◽

10.1182/blood.v81.6.1513.bloodjournal8161513 ◽

1993 ◽

Vol 81 (6) ◽

pp. 1513-1520 ◽

Cited By ~ 9

Author(s):

AE Morrison ◽

CA Ludlam ◽

C Kessler

Keyword(s):

Factor Viii ◽

Acquired Hemophilia ◽

First Line Therapy ◽

Human Factor Viii ◽

Plasma Factor ◽

Inhibitor Level ◽

Clinical Responses ◽

Bleeding Episodes ◽

Antibody Levels ◽

Auto Antibody

Data have been collected from 47 centers in Europe and North America on the treatment with porcine factor VIII concentrate of 74 acute bleeding episodes in 65 patients with acquired hemophilia. The median initial anti-human factor VIII auto-antibody inhibitor level was 38 Bethesda unit (BU)/mL (range 1.2 to 1,024) whereas that against porcine was 1 BU/mL (range 0 to 15). The mean initial dose of porcine factor VIII infused was 84 IU/kg, which increased the plasma factor VIII:C activity by 0.85 IU/mL. Therapy was continued for a mean of 8.5 days during which time the average number of infusions was 11. Objective clinical responses were rated as good or excellent in 78% of recipients. Side effects were uncommon; only one patient experienced a severe anaphylactic reaction necessitating the discontinuation of porcine FVIII therapy. After therapy, no increase in the median level of anti- human FVIII or anti-porcine antibody was noted in the group as a whole, although 13 patients showed individual increases in either anti-human or anti-porcine antibody levels or both of more than 10 BU/mL. Of the 7 patients who subsequently rebled, 5 were successfully re-treated and 2 did not respond to further porcine factor VIII treatment. Porcine factor VIII is safe and clinically effective treatment for bleeding episodes associated with acquired hemophilia and should be considered as first-line therapy for patients whose acquired anti-factor VIII:C antibody cross-reacts with porcine factor VIII:C at low levels.

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Partial Protection From Lupus-Like Disease by B-Cell Specific Type I Interferon Receptor Deficiency

Frontiers in Immunology ◽

10.3389/fimmu.2020.616064 ◽

2021 ◽

Vol 11 ◽

Author(s):

Emma J. Keller ◽

Neeva B. Patel ◽

Madeline Patt ◽

Jane K. Nguyen ◽

Trine N. Jørgensen

Keyword(s):

B Cells ◽

B Cell ◽

Lupus Erythematosus ◽

Immune Cell ◽

Type I ◽

Type I Ifns ◽

B Cell Survival ◽

Complex Deposition ◽

Antibody Levels ◽

Auto Antibody

Systemic lupus erythematosus (SLE) is an autoimmune disease that can present with many different permutations of symptom presentation. A large subset of SLE patients have been shown to present with elevated interferon stimulated gene (ISG) expression, and Type I IFNs (IFNαβ) have been shown to drive disease in murine models through global IFNα Receptor (IFNAR) knockouts. However, the disease contribution of distinct immune cell subsets in response to constitutively increased levels of IFNαβ is not fully understood. We utilized a B-cell specific IFNAR knockout (BΔIFNAR) on the B6.Nba2 spontaneous-lupus background to determine the contribution of IFNαβ stimulated B cells in disease. We found that IFNαβ signaling in B cells is driving increased splenomegaly, increased populations of activated B cells, and increased populations of germinal center (GC) B cells, memory B cells, and plasma blasts/cells, but did not affect the development of glomerulonephritis and immune-complex deposition. IFNAR expression by B cells also drove production of anti-chromatin IgG, and anti-dsDNA and -nRNP IgG and IgG2C auto-antibody levels, as well as increased Bcl2 expression, affecting GC B cell survival in B6.Nba2 mice.

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