Hemolytic anemia following high dose intravenous immunoglobulin in patients with chronic neurological disorders

Markvardsen, Lars Kjøbsted; Christiansen, I; Harbo, Thomas; Jakobsen, Johannes

doi:10.1111/ene.12287

Cited by 38 publications

(48 citation statements)

References 13 publications

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“…All reported cases of IVIG‐associated hemolysis received IV product; subcutaneous administration of immunoglobulin does not appear to be associated with the same risk of hemolysis, possibly due to absorbance of anti‐A, anti‐B by ABH‐expressing tissues. The largest decrease of Hb observed in the case reports of IVIG‐associated hemolysis occurred in patients with AB+ blood group; this is similar to the largest decrease in Hb occurring in patients with AB blood group in a prospective study on IVIG‐associated hemolysis …”

Section: Discussionmentioning

confidence: 99%

“…Also there is no evidence that anti‐D currently plays any role in IVIG‐associated hemolysis with all of the case reports published after 1997 showing no evidence of anti‐D in the eluate or plasma of IVIG‐associated hemolysis cases. Furthermore in their prospective study, Markvardsen et al did not show a significant effect of Rh type on the decrease in Hb before and after receiving IVIG and hemolytic activity of various IVIG products has been demonstrated using D– RBCs . The absence of D– patients in the pediatric case reports might in part be attributable to the higher proportion of non‐Caucasian patients with Kawasaki disease; in these populations D negativity is much less common.…”

Section: Discussionmentioning

confidence: 99%

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Possible mechanisms for intravenous immunoglobulin–associated hemolysis: clues obtained from review of clinical case reports

Padmore

2015

Transfusion

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It is known that high-dose IVIG given to non-O blood group patients with underlying inflammatory and/or immune-mediated disorders is associated with increased risk of hemolysis. This review reveals additional patient characteristics in cases of IVIG-associated hemolysis, including underrepresentation of D- and group B cases, higher incidence in pediatric Kawasaki disease and unique at-risk patient groups including allogeneic stem cell transplant recipients with group A donor in a group O recipient, and patients in whom soluble AB substance is removed by plasma exchange at the same time as receiving IVIG.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Possible mechanisms for intravenous immunoglobulin–associated hemolysis: clues obtained from review of clinical case reports

Padmore

2015

Transfusion

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“…In one study, six of nine babies required treatment due to anti‐A,B hemolytic disease of the fetus and newborn, whereas in babies having only anti‐A or anti‐B on their RBCs, only five of 14 required treatment . Although the contribution of anti‐A,B to hemolysis after administration of IVIG to either group A or group B individuals has not been addressed, a significant number of ABO‐associated hemolysis cases have been reported after IVIG administration and can be severe …”

Section: Abo Isohemagglutinins: Relevance To Intravenous Immunoglobulinmentioning

confidence: 99%

Anti‐A and anti‐B: what are they and where do they come from?

Branch

2015

Transfusion

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Intravenous immunoglobulin (IVIG) is made from thousands of donors having a variety of blood groups. All of the donors being used for IVIG production, with the exception of group AB donors, have in their plasma antibodies of variable titer commonly known as isohemagglutinins or ABO antibodies. As blood groups O and A are the most commonly found in the world population, most of the plasma used in IVIG production is from donors having these blood groups, with group B and group AB donors being fewer in number. Consequently, all batches of IVIG contain antibodies that are reactive with individuals of group A, group B, and group AB. These antibodies were originally discovered by Dr Karl Landsteiner in the early 1900s and are now known to consist of immunoglobulin (Ig)M, IgG, and IgA classes. As the process for producing IVIG results in almost exclusively IgG, isohemagglutinins contained in IVIG are of this immunoglobulin class. ABO antibodies are highly clinically significant and, because of this, blood bank cross-matching is done to ensure that blood of the correct type is transfused into recipients to avoid a so-called major mismatch or major incompatibility that can cause significant morbidity and often death. Administration of IVIG, which contains ABO antibodies, is often infused into individuals who have the corresponding ABO antigens, commonly called a minor mismatch, and although not as significant as a major mismatch, the isohemagglutinins contained in the IVIG have some risk for a significant transfusion reaction due to the ABO incompatibility. Indeed, currently there is no way to match IVIG to recipients according to blood type, so when IVIG is administered to group A, B, or AB recipients, there is potential for transfusion reactions analogous to a blood transfusion mismatch. For this reason, strict guidelines have been put into place to restrict the titers of the ABO antibodies contained in IVIG. This review will provide background information about the discovery and biochemistry of the ABO antigens and discuss the various isohemagglutinins that are found in plasma of the different ABO blood types and their potential clinical significance. In addition, a brief discussion of the controversial topic of the origins of these antibodies will conclude this review.

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“…The titres of anti-A and anti-B blood group antigens varies between different batches of IVIg. The problem has been more widely reported in the haematology literature and also in relation to patients with neurological diseases such as Guillain-Barré syndrome, multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy, and dermatomyositis [5] [6]. The risk of haemolysis is greater in those patients receiving high dose IVIg (doses greater than or equal to 2 g/kg [7]).…”

Section: Discussionmentioning

confidence: 99%

Haemolytic Anaemia Following High Dose Intravenous Immunoglobulin Treatment for Epidermolysis Bullosa Acquisita

Brown¹,

Hampton²

2016

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Background: Epidermolysis bullosa aquisita (EBA) is a severe acquired blistering skin disease that is often resistant to prednisolone but can respond well to intravenous immunoglobulin infusion (IVIg). Main Observations: We describe the case of a 35 years old male patient with EBA who developed clinically significant haemolytic anaemia with a drop in Hb from 15.3 g/dL to a nadir of 8.4 g/dL within 5 days post IVIg infusion. The patient was blood group A and the IVIg batch was found to have a high titre of anti-A immunoglobulin. Conclusions: IVIg is an effective treatment for EBA. Haemolysis associated with IVIg has not previously been reported in the dermatology literature but review of data from other specialties shows that the problem is well recognised. Dermatologists using IVIg should be aware of this potential complication and patients should be consented appropriately and warned about this potential side effect.

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Hemolytic anemia following high dose intravenous immunoglobulin in patients with chronic neurological disorders

Abstract: Moderate hemolytic anemia is a concomitant complication of high dose IVIG in subjects with blood types A, B and AB.

Cited by 38 publications

References 13 publications

Possible mechanisms for intravenous immunoglobulin–associated hemolysis: clues obtained from review of clinical case reports

Possible mechanisms for intravenous immunoglobulin–associated hemolysis: clues obtained from review of clinical case reports

Anti‐A and anti‐B: what are they and where do they come from?

Haemolytic Anaemia Following High Dose Intravenous Immunoglobulin Treatment for Epidermolysis Bullosa Acquisita

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