Demystifying autoimmune thyroid disease
J
The full articles is on the website below. I don't agree with everything.
It mentions annual monitoring (once the thyroid level is "normal"), but I
think every 6 months is better.
And that depends on whose "normal" they're talking about. Some doctors
I've seen just shrug when the thyroid levels are too high. I'ts not their
bodies, not their thyroid.
You'll see in the article, that tthey seem to imply that some people are
non-compliant on purpose.
Maybe some are. That's no reason to treat everyone (who has a thyroid
condition) like they're "thyroid hormone criminals" .
Anyway, FWIW
J
http://www.postgradmed.com/issues/2000/01_00/fatourechi.htm
Diagnosis
A diagnosis of Hashimoto's thyroiditis is usually made when positive
antithyroid antibodies are present or spontaneous hypothyroidism develops.
The presence of serum antithyroid antibodies with or without thyroid
dysfunction or goiter is usually adequate. Fine-needle aspiration biopsy
is needed to confirm the diagnosis in suspected cases of goitrous
euthyroid Hashimoto's thyroiditis (ie, the presence of questionable
nodules in patients who have a goiter and a negative result on antibody
testing).
The antithyroidperoxidase (TPO) antibody test is more sensitive than the
antithyroglobulin antibody assay. Results of scintigraphy and
ultrasonography are highly variable in goitrous Hashimoto's thyroiditis
and usually not helpful. In some cases, ultrasound-guided biopsy of small,
clinically suspicious nodules may be required (9). Open biopsy may be
needed to differentiate between a rapidly growing goiter and lymphoma.
In Graves' disease, the combination of suppressed levels on "sensitive"
thyrotropin testing, high thyroidal uptake of radioiodine, and elevated
serum levels of thyroid hormones in patients with a diffuse goiter is
diagnostic. Measurement of radioiodine uptake is essential for
differentiating between Graves' disease and conditions involving very low
radioiodine uptake. Such conditions include subacute, or granulomatous,
thyroiditis (a painful condition, most likely of viral origin); silent and
postpartum thyroiditis; factitious thyrotoxicosis; and iodine-induced
hyperthyroidism. In toxic multi-nodular goiter and toxic adenoma, the
uptake may be normal. Measurement of TSH receptor antibodies is indicated
only in patients with euthyroid Graves' ophthalmopathy and in pregnant
women with a past history of Graves' disease who have had thyroid
ablation. During pregnancy, TSH receptor antibodies may cross the placenta
and cause fetal thyrotoxicosis.
Clinical presentations of Hashimoto's thyroiditis
Patients with Hashimoto's thyroiditis may be asymptomatic or may present
with goiter, hypothyroidism or, in rare cases, transient hyperthyroidism.
The goiter may be described as bosselated, rubbery, hard, fibrotic, firm,
or atrophic and may have a pseudonodular consistency. It is usually
nontender, and pressure symptoms and pain are rare.
In patients with juvenile Hashimoto's thyroiditis and hypothyroidism,
retarded growth is a typical presenting characteristic. Although rare,
precocious puberty may occur. Another common feature is a decline in
school performance (10). Extrathyroidal manifestations of Graves' disease
(eg, ophthalmopathy, dermopathy) are seen in 5% to 10% of cases of typical
Hashimoto's thyroiditis and hypothyroidism.
Remission of hypothyroidism occurs in 5% to 11% of patients with
Hashimoto's thyroiditis (11). There are no convincing data to indicate
that thyroxine (T4) replacement therapy alters the course of progression
to hypothyroidism, but it may reduce goiter size. Remission is less likely
in atrophic thyroiditis than in the goitrous form. For practical purposes,
clinical hypothyroidism should be considered permanent once it has become
fully established.