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Antibody deficiency
associated with carbamazepine
G Hayman, A Bansal
Epsom
and St Helier NHS Trust, Carshalton, Surrey SM5 1AA. Correspondence to: G Hayman
Grant.Hayman@epsom-sthelier.nhs.uk
A 45 year old woman was referred to our
immunology department with antibody deficiency and an eight month history of
recurrent upper respiratory tract infections that required antibiotic
therapy.
Four years previously she was diagnosed as having epilepsy and was
treated with carbamazepine.
Serum immunoglobulins were measured repeatedly and showed antibody
deficiency (IgG 4.5 g/l (range 6-16 g/l), IgM 0.3 g/l
(0.5-2 g/l), and IgA 0.67 g/l (0.8-2.8 g/l)).
Lymphocyte immunophenotyping and specific antibody production to
tetanus toxoid, Haemophilus influenzae type B, and Pneumovax II
vaccines were normal.
In view of her recurrent infections she was treated with prophylactic
oral antibiotics and her condition was monitored over several
months.
She stopped taking carbamazepine and three months later her IgG had
increased to within the reference range (IgG 6.1 g/l, IgM
0.22 g/l, and IgA 0.74 g/l).
By seven months the serum immunoglobulins were virtually normal (IgG
7.5 g/l, IgM 0.33 g/l, and IgA 0.89 g/l).
At this point she had improved clinically with no active infections,
and prophylactic antibiotics were discontinued without incident.
Antibody deficiency is a recognised, but rare, adverse effect associated
with the use of carbamazepine, although the prevalence of this
complication is unknown. The Committee on Safety of Medicines ADROIT
database lists nine cases of hypogammaglobulinaemia or globulin
abnormality related to the use of carbamazepine (R. Granados,
personal communication) and a handful of case reports have been
published on the subject.1-3
The British National Formulary does not, however, mention antibody
deficiency as an adverse effect of carbamazepine.
Many of the other
cases report associated skin rashes.
It is not known how many
patients using carbamazepine develop symptomatic or asymptomatic
antibody deficiency, compared with the total number using the drug,
or how long it takes for antibody deficiency to develop or resolve.
Similar antibody deficiency has been reported in association with the
use of phenytoin, although isolated IgA deficiency is far more common
with this drug.4
Patients requiring carbamazepine should have
serum immunoglobulins measured if they experience recurrent or persistent
infections.
At present, the apparent rarity of carbamazepine related antibody deficiency
precludes routine serum immunoglobulin assessment.
Footnotes
Funding: None.
Competing interests: None declared.
References
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1.
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Van
Ginnekin EE, van der Meer JW, Netten PM. A man with a mysterious hypogammaglobulinaemia and skin rash. Neth J
Med 1999; 54: 158-162[ISI][Medline].
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2.
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Spickett
GP, Gompels MM, Saunders PW. Hypogammaglobulinaemia with absent B
lymphocytes and agranulocytosis after carbamazepine treatment. J Neurol
Neurosurg Psychiatry 1996; 60(4): 459.
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3.
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Garcia
Rodriguez MC, de la Concha EG, Fontan G, Pascal-Salcedo D, Fernandez J,
Ojeda JA, et al. Transient hypogammaglobulinaemia in the adult. Functional
assessment of T and B lymphocytes. J Clin Lab Immunol
1983; 11(1): 55-58[ISI][Medline].
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4.
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Hammarstrom
L, Smith CIE. Genetic
approach to common variable immunodeficiency and IgA deficiency. In: Ochs
HD, Smith CI, Puck JM, eds. Primary immunodeficiency diseases. New
York: Oxford University Press, 1999:250-262.
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© BMJ 2002
Source: http://bmj.com/cgi/content/full/325/7374/1213?etoc
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