Hashimoto’s, Transient Hypothyroidism, and an Elevated RAIU


Question

May I get your opinion on the following case:

22 year old woman with presents to her primary provider with complaints of amenorrhea times 6 months. Additional concerns include cold intolerance, dry skin, hair loss and an 18lb weight gain over the past year. In March of this year TSH 2.54.. On 8/14/02 TSH 52.43, Free T4 0.62 (nl .68-1.76).

On 9/9/02 TSH 30.61, free T4 0.69, T3 118, TPO ab 972.

Primary provider orders thyroid uptake and scan which are completed on 9/12/02, prior to her evaluation in the endocrine clinic 9/16/02. The scan shows a diffuse goiter. The 6 hour uptake is 32%. In endocrine clinic the above history is obtained.

Physical examination is notable only for a diffuse goiter about 2 times normal size, which is non-tender.

Can we explain this mixture of findings based on an acquired defect > of iodide organification secondary to TPO ab inhibition of thyroid peroxidase? If not, what might be the cause of the high uptake at the same time as the high TSH and low free T4 levels. Would you not just go ahead and put her on L-T4 replacement therapy?

Thank-you so much for your assistance,

Karen Kartun, M.D., Kaiser Permanente

Division of Endocrinology, 9985 Sierra Avenue’> Fontana, CA 92335

email: kkartun@pol.net

Response

This patient clearly has autoimmune thyroid disease as shown by the positive TPO antibodies. There has been a very rapid change in thyroid function, from a normal TSH to a value of 50 in 6 months and then a rapid fall, with only barely reduced T4 levels at the peak of TSH and a normal T4 on the last value we are given.

Although TPO antibodies may inhibit TPO enzyme activity in vitro, these data are controversial and there is no in vivo evidence to support this type of action. For instance TPO antibodies are transferred across the placenta yet the babies of such mothers with high TPO antibodies have normal thyroid function.

Goitrous autoimmune hypothyroidism with an elevated TSH is a known cause of increased radioiodine uptake (1). I suspect that this is the diagnosis here and the pattern of thyroid function fits with a recovering phase of silent thyoiditis in such a gland. Whether the increased uptake is solely mediated by the elevated TSH or is due to coincidental thyroid stimulating antibodies, which occur in some patients, could only be assessed by measuring these antibodies but I do not think this test is strictly necessary. I would simply ensure that the patient is not taking iodine supplements intermittently, and monitor thyroid function regularly, say every 3- 4 weeks; the latest T4 level is normal and therefore there is no need to start thyroxine until the pattern of illness shows this is needed. If normal thyroid function resumes, regular followup will be required.

1. McDougall IR, Cavalieri RR. In vivo radionuclide tests and imaging. In Werner and Ingbar's The Thyroid. 8th edition Eds Braverman LE, Utiger RD, Lippincott, Philadelphia pp355-375

P.S.-May another contributor note that the last values fit with subclinical hypothyroidism, and some practitioners - (including this one) would feel safer starting replacement T4 at this time. L De Groot,MD

When is a Pentagastrin Test Advised in Following MTC?


Question

I would like to see more information about the use of pentagastrin-stimulated CT secretion as a test to determine whether thyroidectomy is to be recommended in persons with the C609Y (or other relevant location) mutant RET proto-oncogene on chromosome 10. It appears that some physicians recommend thyroidectomy in such a case without ordering the test. The only place where I see it briefly mentioned in the ThyroidManager web site is <http://www.thyroidmanager.org/Chapter18/18-medullar.htm> Yours, L. David Roper: roperld@vt.edu

Response

Dear Dr. Roper- I received your question about the utility of pentagastrin test in patients with C609Y ret mutation. This mutation has been reported in association with familial isolated medullary thyroid cancer (FMTC). As is the case with mutations in other codons associated with FMTC, the consensus agreement proposed in several congress of the MEN 2 study group is that pentagastrin test it is always advise in gene carriers of FMTC to ascertain whether some minimal disease is already present. If a significant response of calcitonin to pentagastrin stimulation is present (or if some other clinical features are suspicious) thyroidectomy is advise. If not, thyroidectomy may be delayed, although some authors prefer to propose surgery even if pentagastrin test is negative. I hope that this clarification may answer your question.

Sincerely, Dr Furio Pacini

How to Treat Sub-Clinical Hypothyroidism?


Question

Hello. One of my patients is a lady aged 48 years. She has most signs and symptoms that correlate with hypothyroidism. Her TSH is 9.7 mlu/L ( range 0.27-4.2), T4 is 13 pmol/L (range 12-22), T3 is 4.7 pmol/L (range 2.8-7.1) . There is no relevant history. She is having menorrhagia (severe) , shortness of breath, iron deficiency anemia, obesity, lemon yellow color, flushing of checks, BP= 170/90, diabetic since one year (type 2) , had rough skin, complain always of somnolence , general weakness and sweating. Please send for me your opinion and plan for management and should we consider it as a case of overt hypothyroidism or a subclinical one. T hanks for your cooperation. Dr.Moh'd Attallah, Mohammed_attallah@yahoo.com

Response

Dear Dr Attallah, your patient has still a T4 and T3 within the normal range and should therefore be classified as subclinically hypothyroid. It is difficult to assess if her complaints are due to hypothyroidism and/or to her diabetes in combination with obesity. On the other hand the level of TSH and free T4 are at the border of overt hypothyroidism and my advise to you is to determine her thyroid auto-antibodies and to treat her with thyroid hormone such that her final TSH finally drops between 0.27 and maximally 2.0 mU/l. If antibodies are present in the serum, than it is almost certain that she will eventually develop full blown hypothyroidism and in that case treatment should be continued irrespective of any immediate effect. If antibodies are absent and T4 substitution has no effect discontinuation of T4 could be considered but the patient should be frequently seen in follow up.

Georg Hennemann, MD, PhD, FRCP, FRCP(E)

E mail: g@hennemann.demon.nl