Changes in biochemical, hematological and immunological profiles after low-dose intravenous immunoglobulin administration in patients with hypogammaglobulinemia

Berlana, David; Vidaller, Antonio; Jódar, R.; Fort, E.; Domingo, Alícia; Pastó, Lourdes

doi:10.1016/j.tracli.2006.02.023

Cited by 6 publications

(3 citation statements)

References 43 publications

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“…Additionally, RALB increased both the serum ALB and GLB levels, and then some of the above changes may be caused by GLB. Intravenously injected Ig has been reported to transiently decrease LYM, MON, and/or PLT counts in patients 39,40 and to induce apoptosis in LYM and MON of humans 41 . The same mechanism may be involved in the decreased LYM, and MON counts in the present animals.…”

Section: Discussionmentioning

confidence: 99%

Aggravation of Galactosamine Hepatotoxicity by Albumin in Rats

et al. 2008

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Abstract:The effect of rat albumin (RALB) on D-galactosamine (GalN) hepatotoxicity was investigated in male Crl:CD(SD) rats aged 6 weeks. The animals were divided into control, RALB, GalN, and RALB + GalN groups. GalN (800 mg/kg) was intraperitoneally administered immediately after an intravenous injection of RALB (100 mg/kg). The animals were euthanized 6 or 24 h later and subjected to laboratory investigations and histological examinations of the liver. Furthermore, in order to determine the contributing factors of the effect on the hepatotoxicity, intra-and intergroup comparisons were made between liver-injured and normal animals for parameters showing marked fluctuations at 6 h post-dosing. As a result, RALB induced fluctuations in many parameters, but no histological changes were observed in the liver at both 6 and 24 h. GalN induced mild or moderate hepatocyte necrosis (necrosis and/or apoptosis of hepatocytes) at 6 and 24 h, respectively, accompanied by increases in the serum ALT and AST levels. Concurrent administration of RALB with GalN markedly aggravated the GalN-induced hepatotoxicity, as shown by severe hepatocyte necrosis accompanied by further increases in the serum ALT, AST, and T-BIL levels in the surviving animals at 6 and 24 h, and by very severe hepatocyte necrosis with congestion in the dead animals. Moreover, serum tumor necrosis factor-α (TNF-α) level was also increased at 6 h in the RALB + GalN group, but not in the RALB or GalN alone groups. In conclusion, RALB was shown to aggravate GalN hepatotoxicity in rats, and the increased serum TNF-α level is considered to be a contributing factor of the aggravation. (J Toxicol Pathol 2008; 21: 175-183)

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Section: Discussionmentioning

confidence: 99%

Aggravation of Galactosamine Hepatotoxicity by Albumin in Rats

et al. 2008

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“…Previous studies have demonstrated the acute and long-term effects of IVIG in lymphocyte subsets and cytokine synthesis in patients with CVID [12][13][14][15]. However, it is unclear how IVIG affects the Fas expression and activation markers in T cells in patients with CVID.…”

Section: Introductionmentioning

confidence: 99%

In vivo modulation of the expressions of Fas and CD25 by intravenous immunoglobulin in common variable immunodeficiency

2009

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Although the presence of physiologic anti-CD95 (Fas, APO-1) autoantibodies in intravenous immunoglobulin (IVIG) preparations is known, the effects of these antibodies in patients with common variable immunodeficiency are unclear (CVID). The aim of the study was to assess the effects of IVIG in Fas expression, activation markers and the subsets of T cells in patients with CVID. We studied 15 cases with CVID and 10 healthy controls with no signs of immunodeficiency. The Fas expression of T cells, activation markers (CD25, CD69 and HLA-DR) and T-cell subsets were analyzed by four-color flow cytometry. We found that the Fas expression of CD3+ T cells in patients was significantly higher than in controls. In addition, there was a significant increase in the Fas expression of CD3+ T cells and CD4+ T cells, and the CD25 expression of CD3+ and CD4+ T cells after IVIG supplementation (P < 0.05). The CD69 and HLA-DR expressions of T cells and CD8+ T cells were not affected by IVIG infusion. Our observation showed that IVIG replacement causes an increase in the Fas and CD25 expressions in patients with CVID. These data suggest that the Fas protein may have an important role in the effects of IVIG for the control of autoimmunity in patients with CVID, as well as in the generation of autoimmune disease.

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“…[1][2][3] IVIg has been approved by the US Food and Drug Administration (FDA) as a safe and effective treatment for a variety of autoimmune and inflammatory diseases, such as idiopathic thrombocytopenic purpura (ITP), paediatric human immunodeficiency infections, graftversus-host disease and Kawasaki's syndrome. 4 Unfortunately, it is associated with a wide range of adverse events, which have an incidence ranging from 1% to 42% 5 and a somewhat variable frequency. These adverse events are categorized as: (i) minor self-limiting side-effects, such as headache, chills, myalgia and fever; (ii) moderate, such as skin reactions; (iii) severe, such as anaphylactic shock or fatal renal complications.…”

Section: Introductionmentioning

confidence: 99%