Intended for healthcare professionals

Letters

Products with low IgA content may be used in patients with total IgA deficiency

BMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7069.1400 (Published 30 November 1996) Cite this as: BMJ 1996;313:1400
  1. Siraj Misbah
  1. Consultant clinical immunologist Department of Chemical Pathology and Immunology, Institute of Pathology, Leeds General Infirmary, Leeds LS1 3EX

    EDITOR,—R A C Hughes emphasises that, on the basis of the results of recent randomised studies, intravenous immunoglobulin is as efficacious as plasmapheresis in the treatment of the Guillain-Barre syndrome.1 In view of the practical difficulties associated with plasmapheresis, intravenous immunoglobulin is increasingly likely to be preferred as first line treatment.

    In this context Hughes states that intravenous immunoglobulin should be avoided in patients with IgA deficiency. This may mislead clinicians who are unfamiliar with immunoglobulin treatment and may result in them needlessly withholding treatment from all IgA deficient patients. Although it is true that anaphylaxis remains an important risk in some patients with selective IgA deficiency, this is virtually confined to those with the combination of severe or absolute IgA deficiency (<0.05 g/l) and high levels of antibodies to IgA.2 Even in these patients the risk of anaphylaxis can be greatly reduced by the cautious use of an IgA depleted immunoglobulin product. Immunodeficient patients with high levels of antibodies to IgA (1 in 200 to 1 in 7000) have been maintained on regular replacement with an IgA depleted product with no serious adverse effects over a six year period.3

    Table 1 shows the IgA content of immunoglobulin preparations currently available in Britain. Because measurement of the level of antibodies to IgA is available in only a few immunology laboratories in Britain it would be unwise to delay emergency treatment of the Guillain-Barre syndrome until the results of such measurement are available. It would be sensible to treat patients known to be totally IgA deficient, and those in whom any doubt exists, with an immunoglobulin product with a low IgA content.

    Table 1

    Approximate IgA content of immunoglobulin preparations

    View this table:

    Hughes's statement that intravenous immunoglobulin should be avoided in patients with renal failure also requires clarification. Temporary reversible deterioration in renal function (ranging from an asymptomatic increase in the serum creatinine concentration to anuric renal failure) associated with the use of high dose intravenous immunoglobulin (2 g/kg) is likely to be related to the toxic effect of a high sugar load on renal tubules.5 While the use of a single dose of 2 g/kg should be avoided in patients with preexisting renal impairment, it may be possible to infuse lower doses at a slower rate safely in such patients.5 Hence, rather than renal failure being viewed as an absolute contraindication to intravenous immunoglobulin therapy, each case should be assessed on its individual merits.

    References

    1. 1.
    2. 2.
    3. 3.
    4. 4.
    5. 5.