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Routine steroid prophylaxis is not yet justified
EDITOR Walsh et al go further and advocate that high dose prednisone, as used
in Bartalena et al's trial, should be used routinely in all patients
with mild ophthalmopathy who are to receive radioiodine, to reduce the
risk of deterioration in eye disease. Surely this is not yet justified.
No account has been taken of the appreciable adverse effects of giving
prednisone for three months (typically 30-40 mg/day for the first month
and then reducing over the next two months). In Bartalena et al's
study under a tenth of patients (7/72) with mild pre-existing
ophthalmopathy who received radioiodine had a deterioration that was
more than transient and required treatment.
Routine use of glucocorticoids exposes all patients who receive
them to important adverse effects, while the benefit is limited to a
few. Certain clinical features (for example, mild but active or
progressive ophthalmopathy) are likely to mark out those who are at
risk. Further studies are needed to examine this and to determine the
minimum dose and duration of glucocorticoid treatment that protects
against deterioration of eye disease.
At present there is a case for limiting treatment with
glucocorticoids to those who have an appreciable symptomatic worsening of ophthalmopathy rather than treating all routinely. Bartalena et al
did not go so far as to advocate routine glucocorticoid treatment for
all patients with mild ophthalmopathy who receive radioiodine, and with
good reason. Clinical trials showing that a treatment is effective are
immensely useful but need to be supported by further, balanced
evaluation of the risks and benefits of treatment before the original
demonstration of efficacy is translated directly into routine clinical
practice
The relation between treatment with radioiodine and thyroid eye
disease, discussed in Walsh et al's editorial, troubles many
endocrinologists and patients.1 There have been concerns that the use of radioiodine for thyrotoxicosis due to Graves' disease
may be associated with a deterioration in ophthalmopathy, raising the
question of whether radioiodine is safe for patients with mild
ophthalmic Graves' disease. This question has been addressed recently
by Bartalena et al, who showed that there is a small but significant
risk of deterioration in mild ophthalmopathy after the use of
radioiodine and that this risk may be reduced by simultaneous administration of systemic glucocorticoids.2
a message for all clinicians, not just endocrinologists.
First do no harm.
Endocrine Unit, Southend Hospital SS0 0RY
a dr.ahlquist{at}southend-hospital.thenhs.com
| 1. |
Walsh JP, Dayan CM, Potts MJ.
Radioiodine and thyroid disease.
BMJ
1999;
319:
68-69 |
| 2. |
Bartalena L, Marcocci C, Bogazzi F, Manetti L, Tanda ML, Dell'Unto E, et al.
Relationship between therapy for hyperthyroidism and the course of Graves' ophthalmopathy.
N Engl J Med
1998;
338:
73-78 |
Authors' reply
EDITOR Of 72 patients with mild ophthalmopathy at baseline (defined as
mild conjunctival oedema and periorbital inflammation) who were not
treated with steroids, however, 17 (24%) showed a deterioration in
their eye disease after radioiodine treatment. Although in many cases
this was transient (lasting two to three months), it is nevertheless
likely to have caused distress to those who were affected. Even more
importantly, seven (10%) patients had an exacerbation requiring
orbital radiotherapy and high dose steroid treatment. Adjuvant steroid
treatment at a substantially lower dose reduced the risk of
exacerbation of thyroid eye disease to <1%.
We believe that a 24% risk of a short term deterioration in
thyroid eye disease and a 10% risk of a more prolonged and severe exacerbation justify the risks of adjuvant, moderated dose
corticosteroid treatment. We do not underestimate the problems that
some patients experience from prednisolone treatment at a mean dose of
20 mg daily for three months, but similar doses are widely used to
treat conditions such as polymyalgia rheumatica and asthma, with few long term adverse effects over this period.
Limiting treatment to patients with mild eye disease (and avoiding
radioiodine treatment in patients with moderate, severe, or active eye
disease) means that only one patient with Graves' disease in five who
are referred for radioiodine will require corticosteroid treatment. At
the very least, the 24% risk of exacerbation of thyroid eye disease
needs to be fully discussed with the patient. Trials to see if lower
steroid doses are effective would be desirable but, in view of the
number of patients required, would prove a major undertaking.
We suggest that using appropriate treatment to prevent iatrogenic
exacerbation of a disease that is distressing, disfiguring, and
difficult to treat is entirely consistent with Ahlquist's philosophy
of first do no harm.
Ahlquist suggests that the adverse effects of corticosteroid
treatment outweigh the beneficial effect on the course of thyroid eye
disease after radioiodine treatment. With regard to patients without
pre-existing ophthalmopathy we agree, as the study of Bartalena et al
showed a low risk (1%) of severe eye disease developing de
novo.1
Sir Charles Gairdner Hospital, Nedlands, Western
Australia 6009, Australia
Colin M Dayan
University Division of Medicine, Bristol Royal Infirmary,
Bristol BS2 8HW
1.
Bartelena L, Marcocci C, Bogazzi F, Manetti L, Tanda ML, Dell'Unto E, et al.
Relation between therapy for hyperthyroidism and the course of Graves' ophthalmopathy.
N Engl J Med
1998;
338:
73-78.
© BMJ 1999