Posterior reversible encephalopathy induced by intravenous immunoglobulin

Belmouaz, Simohamed; Desport, Éstelle; Leroy, Fannie; Teynie, J.; Hannequin, Jérôme; Ayache, Ramzi Abou; Bridoux, Frank; Touchard, Guy

doi:10.1093/ndt/gfm594

Cited by 24 publications

(17 citation statements)

References 4 publications

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“…[2] It is a clinico-radiological entity characterized by neurological signs (headache, seizures, vomiting, altered mental status, visual disturbances especially cortical blindness, focal neurological deficits) and radiological abnormalities of occipital white matter, usually bilateral, characterized by cerebral edema with hypodense signals on CT scan; and hyperintense signals on T2 weighted images by MRI. [3] The most common presenting symptoms were headache, seizure, altered consciousness, and cortical blindness.…”

Section: Discussionmentioning

confidence: 99%

Cortical blindness in a child with acute glomerulonephritis

Kaarthigeyan¹,

Vijayalakshmi²

2012

Indian J Nephrol

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The association between hypertensive encephalopathy and cortical blindness in children with acute glomerulonephritis is extremely rare. We report the case of a 9-year old girl who presented with headache, seizures, altered sensorium, hematuria, and transient cortical blindness as a complication of hypertensive encephalopathy which showed complete reversal following normalization of blood pressure and an underlying post-infectious acute glomerulonephritis was revealed.

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Section: Discussionmentioning

confidence: 99%

Cortical blindness in a child with acute glomerulonephritis

Kaarthigeyan¹,

Vijayalakshmi²

2012

Indian J Nephrol

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“…This condition should be suspected in patients developing visual disturbances, confusion, and seizures following IVIg infusion, and the diagnosis can be confirmed by MRI. In such cases, improvement was reported with PE therapy [75,76]. Other possible side effects include vasospasm, vasculitis, enterocolitis, eczema, hyperproteinemia, hyponatremia, and mild leukopenia [72].…”

Section: Safety Considerationsmentioning

confidence: 99%

Intravenous immunoglobulin: pharmacological properties and use in polyneuropathies

Dézsi

Horváth

Vécsei

2016

Expert Opinion on Drug Metabolism & Toxicology

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1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 This review includes a description of the composition, pharmacokinetics, and mechanisms of action of IVIg. The second part of the paper provides an overview of the immune-mediated polyneuropathies in which IVIg is a first-line therapy, with special focus on the pathomechanism of the diseases, the mechanisms of action of IVIg, and of the main results of clinical trials supporting the evidence of its efficacy. Composition of IVIgIVIg is a complex preparation pooled from a minimum of 1000 and up to 60,000 donors, [6,7]. The anti-idiotypes can block the antigen-binding site of the pathological antibody.IVIg preparations contain many idiotypes and antibodies against several receptors as well. See Table 2 for details [8,9].At first, IVIg was used in a concentration of 5%, but subsequently, formulations with higher concentrations of 10-12% were also developed, which permitted the lowering of the volume load and the shortening of the time of administration. Formulations for subcutaneous use (SCIg) are available since the 1980s, which permit steadier IgG levels and a more favorable systemic side effect profile, except for the higher incidence of local reactions. Several brands of IVIg are available, with each considered to be a distinct product with a unique composition and different excipients. The products differ with regard to the production process, viral inactivation, purification, IgA content, sodium content, and the applied stabilizers, and are associated with different risks of adverse effects, depending predominantly on the IgA content, the osmolarity, and the stabilizers used.In recent years, significant advances have been achieved in the production process of IVIg preparations with regard to purity, pathogen inactivation, and stabilization. Cold alcohol fractionation is used to isolate the immunoglobulin-containing plasma fraction, which is further purified through multiple steps of precipitation and can also be combined with ionexchange chromatography, processes resulting in a highly purified polyvalent IgG product 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 PharmacokineticsThe dose of IVIg used for the treatment of immunodeficient conditions is 0.4-0.6 g/kg, administered every 3 to 4 weeks. Once the diagnosis is set, a continuous replacement therapy is to be initiated, which should not be interrupted. Some patients require higher doses of up to 0.8 g/kg. Doses exceeding this level have not been evaluated [13]. The total dose used in autoimmune/inflammatory diseases is 2 g/kg, administered in 2-5 consecutive days. This dose was introduced to clinical practice after the observation of a dramatic increase ...

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“…Bevacizumab [20] Sunitinib [21] Raf kinase inhibiteur BAY 43-9006 [22] Cytokines immunomodulatrices Interféron alpha [5,23] Interleukine 2 [24] Anticorps Monoclonaux Rituximab (anti-CD20) [25] Infliximab (anti-TNFα) [26] Immunoglobulines intraveineuses [27] Protéine Anti-TNFα Étanercept [28] Globuline antilymphocyte [29] Immunosuppresseurs Anticalcineurine [8] Cyclosporine A [4,5,7,10,12] Tacrolimus (FK 506) [5,10,12] Sirolimus [30] Corticothérapie forte dose (dexaméthasone et méthylprednisolone) Transfusion sanguine [31] Autres agents Facteurs de croissance leurocytaires [32] Antirétroviraux [33] Linezolid [34] Érythropoïétine [35] Cocaïne [10] Ephedra sinica (médecine traditionnelle chinoise) [36] Produits de contraste intraveineux [10] Lysergic acid amide [37] Carbamazépine [38] Caféine intraveineuse [39] Maladies auto-immunes…”

Section: Prééclampsie-éclampsieunclassified