TreatmentAnticonvulsant Pathology


BMJ 2002;325:1213,23 November. (Case Report)


Full Text

Antibody deficiency associated with carbamazepine

G HaymanA 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 gamma  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

1.

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].

2.

Spickett GP, Gompels MM, Saunders PW. Hypogammaglobulinaemia with absent B lymphocytes and agranulocytosis after carbamazepine treatment. J Neurol Neurosurg Psychiatry 1996; 60(4): 459.

3.

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].

4.

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.

© BMJ 2002

Source: http://bmj.com/cgi/content/full/325/7374/1213?etoc


 

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