Hurthle Cell Nodule and Hyperthyroidism in Hashimoto’s Gland


W is a 44 yo woman referred 3/02 for a thyroid nodule 1.2 cm bx “c/w Hash thyroiditis with Hurthle cell proliferation” cannot r/o Hurthle cell neoplasm Hx: h/o ? partial Lt thyroidectomy in 1991 on Synthroid since. Saw PMD to have BW checked, fullness noted Rt. Lobe. Had u/s and BX of rt. Nodule. No compressive sx. Despite TSH 0.01 no sx of over relacement. PMH 1991 ?Partail lt thyroidectomy for a nodule

SHX smoker FHX : strong for throid dz in mo, aunt, cousins

PE: P: 90 Mild bilat thyr enlarg

Data : TSH: 0.01, fT4: 1.57 Thyroid U/S: (1/02) inhomog, mild bilat enlarg. 1.2 X 1.0 cm echogenic nod Rt. Lobe prob within thyroid, poss parathyr adenoma.

Path: as above. Most c/w chronic thyroiditis but more Hurhtle cellls than usual. Less likely and definitely not favored could be Hurthle cell neoplasm. Path recommended following without surg if sero positive for Hash.

Course: Synthroid decreased and d/ced based on bw and mild sx of hyperthyr. Anti-TPOAbs 3345(0-34) T3:376 fT4: 1.77 TSH: 0.01 (off Synthroid). PTHi profile WNLRAUI/scan: 6 hr: 70%, 24 hr 57%, scan: cold defect Lt. Lobe., nonhomog in Lt. Lobe, homog in Rt. Lobe. Repeat u/s: 7 mm nod Lt lobe felt to be too small to rep cold area on scan. Rest of gland “c/w MNG” Treated with 29mci I-131 8/27/02. Became hypo 10/02 ,started Syhtroid 88 mcg. F/u with PMD for adjustments in dose. Repeat thyroid u/s 3/26/03: 6 mm nodule in lt.lobe not seen. Rt. Nodule 1.3 X 0.8 cm (uchanged from 8/02 1.4 X 1.1 cm). Rt lobe 3 X 1.4 X .07, LT lobe 3.6 X1.2X1.0 cm. Somewhat smaller gland.

Questions: 1. Would recommend follow up (serial u/s), repeat bx , or surgery? If repeat u/s, when and how often?

2. Is it worrisome that nodule and gland are still present after I-131 rx with subsequent hypothyroidism.

3. Does patient have Grave’s disease. If so, wouldn’t expect gland to have been destroyed by I –131 RX?

Thanks again, Lisa Wisniewski, MD, MACV 2215 Landover Place Lynchburg, VA 24501, -


May I offer several comments? Firstly, it would have been a good case for surgical therapy of the hyperthyroidism. Secondly, Graves’ Disease and Hashimoto’s Disease overlap in most ways except for the metabolic status. With an elevated RAIU and autonomous hyperthyroidism, she must have thyroid stimulating antibodies, so I would tend to call this a variety of Graves Disease. The gland remains palpable in part because it must contain a lot of lymphs and fibrous reaction. Lastly, for sure you are going to keep a close watch on the “nodule” in the right lobe, which has too many Hurthle cells and now has received about 1000 rads of gamma rays from the 131-I. Hurthle cell rich nodules in Hashimoto’s glands, and variable “pseudo-nodules “ seen on US, are a frequent problem. If on serial US the R nodule enlarges, or if a repeat biopsy in a year shows a more worrisome histology, it will need resection. Otherwise it is probably safe to watch it, but I think you can never offer complete complete reassurance to the patient in this setting. Leslie J De Groot,MD

Thyroid Hormone and TSH Levels During Pregnancy


I am a reproductive endocrinology and infertility specialist in Quito Ecuador. First of all congratulation for your thyroid website. It is very good and a great help. Knowing your great experience in thyroid problems I want to know if you could please be so kind to comment about the new TSH reference range. Last year the Th e National Academy of Clinical Biochemistry published a Laboratory Medicine Practice Guidelines LABORATORY SUPPORT FOR THE DIAGNOSIS AND MONITORING OF THYROID DISEASE where is stated that a TSH greater than 4.0 is considered abnormal. However, the American Association of Clinical Endocrinologist published some guidelines stating that treatment should be considered when the TSH level is greater than 3.0. In our infertility practice we have many patients with TSH levels between 3.0 and 5.0. We have adopted a policy of testing for anti-thyroid antibodies in these patients and recommend re-testing 6 month later if the antibodies are negative. However, if the patient is positive for the antibodies we are recommending treatment with low dose thyroid hormone. Almost 50% of our patients are testing positive. The problem is that there is no information in the literature to support our practice, yet, so we are feeling a little concern that maybe we are overtreating and stressing our patients.

Could you please comment a little about the TSH range. Are you recommending treatment when the TSH is greater than 3.0.? Do you think we should treat our infertile patients only if the TSH level is greater than 5.0? Do you think in recurrent miscarriage patients with a TSH level between 3 a 5 are worth to treat with levothyroxine? What do you think about our current practice?Thank you very much for your time and your comment will be greatly appreciate.

Ivan Valencia MD, Centro Medico de Fertilidad y Esterilidad CEMEFES, Quito, Ecuado, Ph 2468068


In the first place my sincere congratulations that you, "avant la lettre", were already aware of possible problems when the TSH value was between 3.0 and 4.0. You may have learned form the publication you refer to that many persons with a TSH level in that range have circulation thyroid auto-antibodies as well, like your patients, suggestive of developing subclinical hypothyroidism . My personal strategy with regard to the serum TSH is perhaps even more radical than yours, in that I mistrust TSH values already if they are above 2.5. I would suggest that if you find a TSH above 3.0 (and may be even above 2.5) at least twice in your special category of patients, that you treat with thyroxine even in the absence of antibodies and titrate the TSH to a level of not higher than 1.5 or maximally 2.0. The reason for this low normal range in patients substituted with T4 is that, as the T3 contribution to the plasma by the thyroid (being 20% of total plasma T3) is lacking, one need to give more T4 to reach about normal T3 plasma values. In doing so TSH decreases to a plasma level not higher than 2.0 or even 1.5.

When no antibodies are present you can discontinue the T4 substitution in your patients, after a successful pregnancy if that happens or after attempts to have fertilization are stopped and then see what happens to the TSH. My position is that in patients with TSH levels in the range that we discuss PLUS the presence of antibodies one should seriously consider permanent T4 substitution as these subjects have a risk of 70 times the normal risk to develop overt hypothyroidism in the (near) future.

I hope that this reaction is of some help and please do not hesitate to contact me if I have not been clear or for any other reason. Kind regards, Georg Hennemann