Risedronate therapy is effective for patients presenting with secondary osteoporosis with cerebral palsy. Moreover, it is desirable to treat patients more aggressively from the early stage because risedronate is not affected by the patients' other factors.

Anticarbamazepine antibody was detected in a patient who had clinical signs of serum sickness induced by carbamazepine. Skin rash, fever, oedema, and lymphadenopathy are classic signs of severe adverse reaction, but although immunological hypersensitivity is thought to be a contributory factor, the presence of anticarbamazepine antibody has not previously been reported to our knowledge.Carbamazepine is widely used in the treatment of various forms of epileptic disorders.' 2 Although different side effects have been reported, skin rash is the most common adverse reaction. Exfoliative dermatitis, urticaria, toxic epidermal necrolysis, Stevens-Johnson syndrome, and a reaction similar to systemic lupus erythematosus have been reported.2 3 In some cases the skin rash is part of a severe illness affecting several organs, and immunological hypersensitivity is thought to contribute to the skin reaction.3 4 So far, however, we know of no report of the presence of anticarbamazepine antibody in any patient with severe skin reactions.We present a patient with the typical clinical manifestations of serum sickness, fever, eruption with oedema (particularly around the face and neck), and lymphadenopathy. The laboratory findings showed a decrease in complement C4 and an increase in C3a and C4a activity. Anticarbamazepine antibody was detected in the serum using an enzyme linked immunosorbent assay (ELISA). Methods BALB/C mice were given carbamazepine (1 g/kg) orally, and bled six hours later. The serum was used as the antigen.The anticarbamazepine antibody of serum from the patient was analysed by ELISA, a procedure that has been described elsewhere.5 Briefly, the mouse serum diluted (1:100) with 10 mM carbonate buffer was added to 96 well polyvinylchloride microtitre plates, and left for two hours at room temperature. The nonbinding sites were blocked with phosphate buffered saline containing 0 05% Tween 20 and 2% ovalbumin. Diluted human serum was added to the wells and incubated for one hour at 4°C. After three washings, 100 >t of appropriately diluted horseradish peroxidase conjugated goat antimouse Ig antiserum was added to each well. The plates were then incubated for one hour at 4°C and washed three times, and 200 tl of freshly prepared substrate solution containing 0-05% o-phenylendiamine and 0 0075% hydrogen peroxide in McIlvain buffer, pH 6-0, was added to each well. After 30 minutes of incubation at room temperature, absorbance was read at 405 nm with a Titertek Multiskan plate reader.Case report An 8 year old girl was admitted with fever and skin rash. Thirty seven days before admission carbamazepine 200 mg (10 mg/kg) had been prescribed because of a complex partial seizure. Twenty seven days before admission the first skin rash had appeared on her cheeks, but this disappeared within a few days. Twenty three days before admission, the dose of carbamazepine had been increased to 300 mg. The day before admission she had again developed maculopapular erythema on her face and neck, this time accompanied by fever...

We report on a patient with severe serum sickness induced by carbamazepine in whom anticarbamazepine IgG antibodies were detected in the serum. The T cells of the patient showed impairment of phytohemagglutinin-induced proliferation, and hypergammaglobulinemia was evident. The clinical features and immunological abnormalities were compatible with immunoblastic lymphadenopathy. Immunosuppressive factors were also detected in the patient. Their molecular weights ranged from 20,000 to 30,000 as evaluated by Sephadex G-200 gel filtration. Such immunosuppressive cytokines were not detected in other patients with carbamazepine allergy who did not develop the clinical manifestations of immunoblastic lymphadenopathy. These results suggest that the T cell functional deficiency of immunoblastic lymphadenopathy is induced by these immunosuppressive cytokines.

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