[Anonymous]

#1050674

Since April I have been on large doses of PTU, I have developed a rash and am sleeping away my life. I caled my doctor and he was concerned about the rash. He lives in another city so had me go to a lab in my town and get a CBC, he says that he suspects agranulocytosis from the PTU. They gave me a copy of my blood tests and three of the portions are off, neutrophils are low, lympohcytes are high and eosinophils are high. I am waiting a call from y endo. Anyone know what this means I am scared to death!

[Anonymous]

#1149862

Did your endo say to stop taking the PTU while you wait for results? If not, call and check. A rash is one of the side effects to PTU. I had hives and itching. My endo had me stop the PTu, take nothing for 2 days, then start on Tapazole. So, I think you are right to check this out – you may have an allergy to PTU.
Good luck!
Casey

[Anonymous]

#1149863

Someone who has both Hashimoto and Graves????

[Anonymous]

#1149864

You should look at the URL:

http://www.sma.org/decsmj9// /text.htm

Its about some people that have both diseases.

[Anonymous]

#1149865

Sorry my computer could’nt find the URL again so maybe yours cant either so here it is:Hypothyroid Graves’ Disease

EMIL LESHO, DO, and ROBERT E. JONES, MD, Tacoma, Wash

Abstract

Background. Spontaneous conversion from hypothyroidism to hyperthyroidism has generally been considered uncommon.

Methods. Values obtained were serum thyroid-stimulating hormone (TSH), thyroxine, free thyroxine index, radioactive iodine uptake (RAIU), thyroid-stimulating immunoglobulins (TSI), and thyrotropin-binding inhibitory immunoglobulin (TBII).

Results. Five patients spontaneously had a minimum of two cycles in thyroid function with extremes of hypothyroxinemia to hyperthyroxinemia. One patient had four documented cyclic shifts in thyroid status. When measurements were obtained in the hyperthyroid phase, all patients had TSI, increased RAIU, and an undetectable TSH. When measurements were done in the hypothyroid phase, all patients had positive TBII but negative TSI.

Conclusions. Spontaneous reversal of thyroid function may be more common than previously thought. Clinical features associated with lability of thyroid function were abrupt change in goiter size, exaggerated response to therapy, or the presence of TSH-receptor antibodies.

GRAVESÍ DISEASE and Hashimoto’s thyroiditis are generally thought of as discrete clinical entities with completely different outcomes. Although there is increasing evidence that these diseases may represent a spectrum of autoimmune thyroid dysfunction,1-10 many physicians may view thyroid function at the time of initial presentation as constant. Primary care providers may assume that the hypothyroid patient will require lifelong hormone replacement, or perhaps that the patient with thyroid hyperfunction requires immediate ablative therapy. Our experience with the following cases, coupled with scattered reports in the literature, suggests that there is a group of patients with autoimmune thyroid disease (AITD) who have spontaneous and sometimes rapid changes in thyroid function.

We present the following case summaries to illustrate the dynamic and potentially variable course of AITD, to emphasize the importance of repeated assessment of thyroid function, and to acquaint primary care physicians with two potentially helpful but infrequently used antibody testsóthe thyroid-stimulating immunoglobulin (TSI) test and the thyrotropin-binding inhibitory immunoglobulin (TBII) test. We also describe clinical features that may be useful in predicting an imminent reversal of thyroid function.

Over the period of observation, which lasted from 6 months to several years, the five patients in our series spontaneously had at least two cycles in thyroid function, with extremes of hypothyroxinemia to hyperthyroxinemia. One patient had four documented cyclic shifts in thyroid status. When tested in the hyperthyroid phase, all patients were found to have TSI, increased radioactive iodine uptake (RAIU), and an undetectable TSH. When tested in the hypothyroid phase, all had thyrotropin-binding inhibitory immunoglobulins (TBII) but no TSI.

CASE SummarieS

Case 1. A 26-year-old woman had a small goiter, antimicrosomal antibodies, and a TSH value of 30 mIU/mL. With levothyroxine therapy, the TSH value became normal. After 5 years of replacement therapy, the patient was found to be thyrotoxic with a suppressed TSH level (<0.1 mIU/mL) and a 24-hour radioiodine uptake of 52%. Levothyroxine therapy was discontinued, and without specific therapy, the total serum thyroxine (T4) fell over the next 3 months from 12 mg/dL to 4.3 mg/dL. During the thyrotoxic phase, tests for both TSI and TBII were positive. After a 3-year euthyroid interval, she was found to have a TSH value of 82.4 mIU/mL in conjunction with positive TBII titers. She was given levothyroxine but moved to a different part of the country and was lost to follow-up.

Case 2. A 28-year-old woman was referred for treatment of hypothyroidism. Before referral, she had a radioiodine uptake of <1% at 24 hours, a positive test for antithyroid peroxidase antibodies (1:409,600 titer), and a TSH value of >100 mIU/mL. No palpable thyroid tissue was found on examination. The patient was treated with levothyroxine. During a follow-up visit 4 months later, she had a small goiter, as well as signs and symptoms of hyperthyroidism. Laboratory evaluation showed TSH suppression (<0.1 mIU/mL), mild hyperthyroxinemia (T4 12 mg/dL), and TSI. Radioactive iodine uptake was not done because of a positive test for serum b-HCG (human chorionic gonadotropin, b subunit). Levothyroxine therapy was discontinued, and the patient was monitored closely. After a second brief episode of hypothyroidism (TSH 78 mIU/mL), she had florid hyperthyroidism and a diffusely enlarged thyroid (four times normal size) and was treated initially with propylthiouracil and later with a combination of propylthiouracil and levothyroxine. Finally, radioiodine ablation was done.

Case 3. A 22-year-old woman with a history of a bipolar disorder was referred for evaluation of hypothyroidism (TSH 73 mIU/mL; T4 2.5 mg/dL). Values obtained 6 months earlier included TSH, <0.2 mIU/mL; T4, 14.0 mg/dL; and free thyroxine index (FTI), 18.8. She recalled symptoms consistent with hyperthyroidism during the time TSH was suppressed but denied receiving any therapy for this problem. She reported a strong family history of thyroid disease. Examination revealed a firm, enlarged thyroid (twice normal size). She had been treated with lithium for more than 1 year (lithium levels were 0.7 mEq/L to 0.8 mEq/L). At follow-up after 3 months of levothyroxine therapy, she was overtly hyperthyroid, with suppressed TSH (<0.1 mIU/mL) and elevated T4 (14.0 mg/dL). On examination, the thyroid had further enlarged to three times normal size, with a soft bruit audible over both lobes. Radioactive iodine uptake (during levothyroxine therapy) was 62% at 24 hours. Levothyroxine was immediately withdrawn, and the patient was eventually treated with radioiodine ablation.

Case 4. A 25-year-old woman was referred for treatment of hypothyroidism (TSH >100 mIU/mL). She was given levothyroxine and returned for follow-up 6 months later with symptoms of progressive weight loss, insomnia, and tremor. Routine thyroid tests showed hyperthyroidism, and radioiodine uptake was 50%. Thyroid hormone replacement was discontinued, and the patient quickly became euthyroid. During close follow-up over the next 5 years, she had three distinct spontaneous fluctuations from hyperthyroidism to hypothyroidism. Tests for TSI during her hyperthyroid periods were clearly positive. She declined therapy and was eventually lost to follow-up.

Case 5. An 18-year-old man was referred for evaluation of a goiter and elevated thyroid hormone levels. Radioiodine uptake at 24 hours was 63%, and the patient was treated with propylthiouracil and propranolol. Two months later, he returned for follow-up with a complaint of progressively worsening fatigue. The TSH was slightly elevated (8.1 mIU/mL), and the T4 level was low (3.2 mg/dL). Propylthiouracil was discontinued after tests were negative for TSI but positive for TBII titers (47.8%; normal <10%). Three months later, the patient was again thyrotoxic (24-hour radioiodine uptake, 59%), and he was definitively treated with radioiodine.

DISCUSSION

A confusing variety of terms have been applied to thyrotropin-receptor antibodies, depending on which assay is used for their detection. Until recently, results obtained in various laboratories could not be compared because of lack of uniform standards. With the advent of newer assays that are less operator-dependent and more sensitive and specific, this should no longer be a problem.9,11 Radioreceptor assays are generally used as a screening test for the presence of TSH-receptor antibodies. They measure both stimulating and blocking antibodies but do not provide information about function. Thyroxine-binding inhibitory immunoglobulins fall into this category. On the other hand, thyroid-stimulating immunoglobulins are detected by bioassay, a method that measures the ability of antibodies in the patients’ serum to stimulate the production of adenyl cyclase. A positive TBII test indicates that antibodies are present. If a simultaneously done TSI test is negative, the antibodies are blocking. If the TSI test is positive, the antibodies are stimulating. TSH-receptor antibodies can be detected in 80% to 100% of patients with Graves’ disease and only 10% of patients with Hashimoto’s thyroiditis.9,11 Blocking antibodies are thought to be partly responsible for both the hypothyroidism and the lack of goiter in some patients with primary myxedema, whereas stimulating antibodies are thought to be partly responsible for the goitrogenesis and hyperthyroidism of Graves’ disease.9,11

Currently, there is no widely accepted classification of autoimmune thyroid disease (AITD).9 The types of autoimmune thyroiditis include lymphocytic, postpartum, subacute or de Quervain’s, silent or painless, and Hashimoto’s. Hashimoto’s thyroiditis is a type of chronic autoimmune thyroiditis characterized by thyroid gland atrophy, fibrosis, and eosinophilic infiltration.9 Graves’ disease is a related type of autoimmune thyroid disease but is not considered a type of autoimmune thyroiditis.9

Graves’ disease and Hashimoto’s thyroiditis are often viewed as discrete clinical entities.9,10 As such, Graves’ disease is typically associated with thyroid gland hyperactivity due to TSI. Hashimoto’s disease is associated with thyroid hypofunction due to immunologic destruction. In 1968, Alexander et al12 were probably the first to describe spontaneous shifts in thyroid function (which they attributed to emotion or non-specific infections.) Subsequent scattered reports in the literature have described a small number of patients in whom a hypothyroid state evolved into overt hyperthyroidism.1-8,10 Graves’ disease and Hashimoto’s thyroiditis represent just two of many possible points on a continuum of AITD from thyrotoxicosis to myxedema. It is becoming clear that they may share the same pathogenic mechanisms.9,10

Although lithium directly inhibits thyroid hormone secretion and may produce hypothyroidism, the patient in Case 3 had had a shift to hyperthyroidism while still on lithium, suggesting that lithium was not the cause of the initial hypothyroidism. Lithium is generally associated with hypothyroidism, but there have been small series and isolated case reports documenting hyperthyroidism.13-16

This case series and other reports of spontaneous alterations in thyroid function suggest that certain clinical features or tests may be useful in predicting potential lability of thyroid function. In one series, all patients with an elevated serum thyroglobulin value and concurrent primary hypothyroidism had spontaneous remission of hypothyroidism, whereas none of the hypothyroid patients with normal thyroglobulin levels recovered spontaneously.17 (This has not been a widely accepted observation, however.) Clinical findings that were associated with an impending change in thyroid function in our cases were a rapid change in thyroid gland size, an exaggerated response to either levothyroxine or antithyroid therapy, an unexpected change in TSH level, or a shift in thyrotropin receptor antibody pattern. These findings were similar to those in another case series in which the presence of a goiter, thyroid antibodies, and TSI were more common in patients who had spontaneous fluctuations of thyroid function.10

Clinicians should not consider thyroid status at the time of the initial diagnosis of a thyroid disorder as being constant or final but rather subject to a sometimes abrupt change, in accordance with shifts in the prevailing thyrotropin receptor antibody. The frequency of these antibody shifts is unknown; however, considering our small clinical series and other scattered reports,1-10,12 these alterations in clinical status may be more common than primary care physicians realize. Repeated assessment of thyroid function, or a change in thyrotropin receptor antibody pattern, along with a strong clinical suspicion may reveal a trend in the patient’s course that could portend an imminent shift in function and possibly obviate the need for expensive interventions.

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