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DEVELOPMENT OF HYPERTHYROIDISM FOLLOWING PRIMARY HYPOTHYROIDISM

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... antibodies have been reported in about 10 percent of patients with goitrous ... atrophic thyroiditis and from 0% to 20% of patients with goitrous thyroiditis ... – PowerPoint PPT presentation

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Title: DEVELOPMENT OF HYPERTHYROIDISM FOLLOWING PRIMARY HYPOTHYROIDISM


1
DEVELOPMENT OF HYPERTHYROIDISM FOLLOWING PRIMARY
HYPOTHYROIDISM
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2
Case Report
  • A 60-year-old male was presented with conscious
    disturbance in Mar 1992. Hyponatremia was noted
    at ER. The diagnosis of primary hypothyroidism
    due to Hashimotos disease was made on the basis
    of low serum T4 (1.1 µg/dL) and T3 (32.6 ng/dL),
    high TSH (153.429 µU/mL) , and positive AMiA
    (16400). Thyroxine was started.

3
Case Report
  • He received I-131 thyroid uptake and scan in
    April 1992, and the result was 2hr 1.7 (4-12)
    and 24hr 0.78 (15-40). Both thyroid lobes are
    hardly visualized due to very low uptake of
    radioiodine, and the findings suggest
    hypothyroidism.
  • With the thyroxine therapy, the T3, T4 and TSH
    levels became normal.

4
Case Report
  • During the thyroxine therapy, in February 1998,
    he presented with body weight loss. The serum T4
    (13.9 ug/dL), T3 (240.7 ng/dL) were high, and TSH
    (0.024 uU/mL) was low. The thyroxine therapy was
    tapered and discontinued since September, 1998
  • I-131 thyroid uptake and scan 2hr 1.31, 24hr
    40.9. Bilateral thyroid lobes are not enlarged
    with diffuse radioactivity.

5
Case Report
  • Six months later, he was still thyrotoxic with
    elevated serum T4 and T3 levels. Therapy with
    Tapazole was started. He has been euthyroid with
    Tapazole therapy till now.

6
Discussion
  • Development of hypothyroidism spontaneously or
    after ATD treatment in patients with Graves
    disease is well known and is believed to result
    from concomitant autoimmune thyroiditis ( Wood
    Ingbar 1979 Hirota et al. 1986) or emergence of
    blocking type TSH receptor antibodies (Kasagi et
    al. 1986)

7
Discussion
  • Development of hyperthyroidism following primary
    hypothyroidism is uncommon and only a few
    documented cases have been reported (Bell et al.,
    1985 Kasagi et al., 1986b Takeda et al., 1988
    Cho et al., 1989 Takasu et al., 1990)

8
Discussion
  • It is difficult to explain how a patient with
    hypothyroidism, conventionally thought to result
    from thyroid destruction, could subsequently
    develop hyperthyroidism
  • Hypothyroidism previous to hyperthyroidism may be
    due to TSH receptor blocking antibodies causing
    reversible hypothyroidism secondary to their
    effects at the TSH receptor, without the
    necessary of there being severe gland destruction

9
Discussion
  • TSH receptor blocking antibodies have been
    reported in about 10 percent of patients with
    goitrous autoimmune thyroiditis and in about 20
    percent of those with atrophic autoimmune
    thyroiditis
  • Among adults in whom these antibodies
    spontaneously disappear during treatment with
    thyroxine, only 40 percent remain euthyroid after
    therapy has been discontinued - (Takasu et al.
    NEJM, 1992)

10
Discussion
  • TSH receptor blocking antibodies contribute to
    hypothyroidism in about 5 to 10 percent of
    patients with chronic autoimmune thyroiditis
  • Alterations of thyroid-related immunoglobulins in
    serum could be considered to explain in thyroid
    status ---- Steel et al.(1985)

11
Discussion
  • Two cases were reported Takeda et al.(1988), Cho
    et al.(1989) in which TSH receptor antibodies
    from blocking to stimulating type resulted in the
    development of hyperthyroidism after primary
    hypothyroidism

12
Takeda et al. Clinical Endocrinology,1988, 28,
341-344
13
Cho et al. Acta Endocrinologica, 1985, 120,
447-450
14
Discussion
  • Takasu et al.(1990) report seven patients with
    hypothyroidism due to Hashimotos disease, who
    developed Graves disease with hyperthyroidism.
    They also report one patient with hypothyroidism
    due to Hashimotos disease, who continued to be
    hypothyroid even in the presence of TSAb

15
Conclusion
  • Hyperthyroidism following primary hypothyroidism
    is a rare phenomenon and only 36 cases having
    been reported
  • Only three cases were documented to have the
    changes of TSH receptor antibodies from blocking
    to stimulating type resulted in the development
    of hyperthyroidism after primary hypothyroidism

16
Conclusion
  • This phenomenon may be due to alterations of TSH
    receptor antibodies in serum, but the exact
    mechanism is still remained to be elucidated
  • We should keep in mind that primary
    hypothyroidism due to autoimmune thyroiditis is
    not always life-long , and even thyrotoxicosis
    may eventually develop

17
Antibodies to The TSH Receptor
  • TSH receptor-stimulating antibodies stimulate
    cAMP production in thyroid cells and are
    responsible for hyperthyroidism in patients with
    Graves disease
  • TSH receptor-blocking antibodies inhibit
    TSH-mediated activation of the receptor and may
    contribute to the development of thyroid atrophy
    and hypothyroidism in some patients with chronic
    autoimmune thyroiditis

18
Assays for TSH receptor Antibodies
  • Radioreceptor assay, which is based on the
    ability of serum of IgG to inhibit the binding of
    radiolabeled TSH to its receptor (TSH-binding
    inhibitory immunoglobulin, TBII)
  • Bioassay, which can be used to measure either
    stimulating or blocking activity

19
Assays for TSH receptor Antibodies
  • Measurement of TSH receptor-stimulating
    antibodies is based on the ability of serum (of
    IgG) to stimulate adenylyl cyclase and therefore
    increase the production of cAMP by thyroid tissue
    or cultured thyroid cells
  • Measurement of TSH receptor-blocking antibodies
    is based on the ability of serum (or IgG) to
    inhibit TSH Stimulation of adenylyl cyclase

20
TSH receptor antibodies
  • Among patients with Graves thyrotoxicosis, TBII
    tests are positive in 76 to 95
  • TSH receptor-stimulating antibodies can be
    detected in the serum of more than 90 of
    patients with Graves thyrotoxicosis
  • TSH receptor-blocking antibodies can be detected
    in 10 to 75 of patients with atrophic
    thyroiditis and from 0 to 20 of patients with
    goitrous thyroiditis

21
Indications for measurement of serum TSH receptor
antibodies
  • Difficult diagnostic conditions
  • Thyrotoxicosis in pregnancy
  • Subclinical thyrotoxicosis with diffuse goiter
  • Euthyroid ophthalmopathy
  • Toxic multinodular goiter with cold nodules
  • Prediction of relapse of Grave thyrotoxicosis
    when antithyroid drug therapy is to be
    discontinued

22
Indications for measurement of serum TSH receptor
antibodies
  • Prediction of neonatal thyrotoxicosis in mother
    with Graves disease
  • Previous child with neonatal thyrotoxicosis
  • Receiving high-dose antithyroid drug therapy in
    third trimester
  • Euthryoid, after radioiodine or surgical therapy
  • Euthyroid with T4 therapy, after radioiodine or
    surgical therapy

23
Indications for measurement of serum TSH receptor
antibodies
  • Prediction of transient neonatal hypothyroidism
    in mother with chronic autoimmune thyroiditis
  • Previous child with transient neonatal
    hypothyroidism
  • Euthyroid receiving T4 therapy
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