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QUESTIONS ANSWERED IN 2006

Any physician may submit a question regarding a thyroid patient to <ldegroot@earthlink.net>  and one of our panel of expert thyroidologists will attempt to provide an answer as soon as possible by return Email. Physicians should provide adequate clinical information about the problem, and provide their name, office address, and telephone number. We will send an answer by Email to the address provided, and will publish the question and the response on this page. The name of the questioning physician WILL be published unless specific instruction not to do so is provided in the original Email. This service is available only to physicians.
Please note that Thyroidologists who hold opinions that differ from the advice we have offered are welcome to send in responses, and we will publish these comments. Commentators should kindly include name, office address, and Email address.
(TO REVIEW QUESTIONS ANSWERED IN 2004-2005, CLICK HERE)

FOLLOW-UP OF AN INCIDENTALLY FOUND PAPILLARY CA    3 December 2006
QUESTION- I have a 43 year-old asymptomatic white male with a multinodular goiter
 and a 3.1 cm dominant nodule on the right thyroid lobe diagnosed in
 11/2005. He has no family history of thyroid cancer and no history of head
 and neck radiation exposure. Thyroid function tests within normal limits.
 A subsequent FNA revealed a follicular lesion with the differential of a
 hyperplastic thyroid nodule vs. a neoplasm. The patient opted for a total
 thyroidectomy in 2/2006 and the subsequent pathology report revealed a 3
 cm microfollicular adenoma but there was an incidental finding of a 4 mm
 papillary microcarcinoma of the left lobe. He did not undergo RAI and his
 previous doctor just put him on suppressive doses of levothyroxine.
             He established himself with me after having moved to the area and he is
 presently on 150 mcg of levothyroxine daily and his latest TSH of
 11/21/2006 is 0.86. He denies any symptoms. A thyroid US of 10/2006
 revealed no thyroid tissue or mass in the thyroid bed area.
            There is excellent evidence in the existing literature that says that
 microcarcinomas have excellent prognosis. My question pertains to the
 appropriate follow up of these patients. I plan to do thyroglobulin and
 thyroglobulin antibody levels every six months and to continue suppressing
 his TSH  levels to <1 UIU/ML. Unfortunately, I have no previous
 thyroglobulin levels. I am also planning to do a thyrogen scan and
 metastatic search in 2/2007 a year from the original diagnosis.

Computed tomography (CT), magnetic resonance imaging (MRI), or FDG-PET  findings can help in the differentiation of benign from malignant tumors.  On CT imaging, struma ovarii is characteristically a complex mass with well‑defined cystic components and smooth surfaces.  The solid components of the tumor are heterogeneous and enhance following intravenous contrast administration, and contain scattered calcifications.  On MR imaging, the mass appears complex, and is composed of multiple cystic and solid components with multilobulated surfaces and thickened septa. Cystic areas have variable size and signal intensity within the tumor (15 - 17).  Solid components will enhance with Gadolinium‑DTPA because of their rich vascular supply and fibrous components. (16, 18).

Histologic sections of a struma ovarii may appear indistinguishable from those of normal thyroid tissue.  Immunohistochemical staining for thyroglobulin will confirm the presence of thyroid tissue (5).  There is also a report of unique uptake of a technetium-99m-labeled monoclonal antibody (Tc-99m-MAB170H.82) in two patients with struma ovarii (19).  The label is directed against a panadenocarcinoma epitope (CA 170) and was picked up by very large tumors in these two patients which proved to be benign, although one had an elevation in CA125 levels. Approximately 3-10% (2, 20, 21) of struma ovarii appear to have malignant potential, but few of these will actually metastasize (20), with perhaps a score of such cases reported to date in the literature.  The cytopathologic features of malignant struma ovarii are identical to the characteristic features of well differentiated carcinoma of the thyroid gland (6). Leonard Warofsky, MD
1.  Boettlin R   1889   Ueber Zahnentwicklung in Dermoidzysten des ovariums.  Virchows Arch Path Anat 115:493-504
2.  Ayhan A, Yanik F, Tuncer R, Tuncer ZS, Ruacan S 1993 Struma Ovarii.  Int J Gynecol Obstet 42: 143‑146.
3.  Joja I, Asakawa T, Mitsumori A et al. 1998 I 123 Uptake in Nonfunctional Struma Ovarii. Clin Nucl Med 23:  10‑12.
4.  Szyfelbein WM, Young RH Scully RE 1994 Cystic Struma Ovarii: A Frequently Unrecognized Tumor.  Amer J Surg Path 18: 785‑788.
5.  Szyfelbein WM, Young RH, Scully RE 1995 Struma Ovarii Simulating Ovarian Tumors of Other Types. Amer J Surg Path 19: 21‑29.
6.  Devaney K, Snyder R, Norris HJ, Tavassoli FA.  1993   Proliferative and histologically malignant struma ovarii: a clinicopathologic study of 54 cases.  Int J Gynecol Path 12:333-43.
7.  Bethune M, Quinn M, Rome R.  1996   Struma ovarii presenting as acute pseudo-Meigs syndrome with an elevated CA125 level.  Austral N Zeal J Obstet Gyn 36:372-3.
8.  Alfie-Cohen  I, Castillo-Aguilar E, Sereno-Gomez B, Marinez-Rodrigues O.   1999 Struma ovarii: a variety of monodermic teratoma of the ovary.  Report of 8 cases.   Ginecol y Obstet Mex 67:153-7. 
9.  Rosenblum NG, LiVolsi VA, Edmonds PR, et al.    1989    Malignant struma ovarii.  Gynecol Oncol 32:224-227.
10.  Berghella V, Ngadiman S, Rosenberg H, Hoda S, Zuna RE.  1997   Malignant struma ovarii.  A case report and review of the literature.  Gynecol Obstet Investig 43:68-72.
11.  Vadmal MS, Smilari TF, Lovecchio JL, Klein IL, Hajdu SI.  1997   Diagnosis and treatment of disseminated struma ovarii with malignant transformation.  Gynecol Oncol 64:541-6.
12.  Rose PG, Arafah B, Abdul-Karim FW   1998   Malignant struma ovarii: recurrence and response to treatment monitored by thyroglobulin levels.  Gynecol Oncol 70:425-7.
13.  Brenner W, Bohuslavizki KH, wolf H, Sippel C, Clausen M, Henze E.  1997   Radiotherapy with iodine-131 in recurrent malignant struma ovarii.  Europ J Nucl Med 23:91-4.
14.  Mango L   1997   Radiotherapy with iodine-131 in recurrent malignant sruma ovarii.   Europ J Nucl Med 24:233 (letter)
15.  Matsumoto F, Yoshioka H, Hamada T et al. 1990 Struma Ovarii: CT and MR Findings.  J Comp Assist Tomog 14: 310‑312.
16.  Dohke M, Watanabe Y, Takahashi A et al. 1997  Struma Ovarii:  MR Findings.  J  Comp Assist Tomog 21: 265‑267.
17.  Joja I, Asakawa T, Mitsumori A et al.1998  Struma Ovarii: appearance on MR Images. Abdom Imag: 23; 652‑656.
18.  Yamashita Y, Hatanaka Y Takahashi M 1997 Struma Ovarii:  MR appearances. Abdom Imag 22: 100‑102.
19.  Lieberman G, Buscombe JR, Hilson AJ, Thakrar D, MacLean A.   1998   The detection of struma ovarii in two patients by radioimmunoscintigraphy.   Amer J Obstet Gynecol 179:262-3.
20.  Kempers RD, Dockerty MB, Hoffman DL , Bartholomew LG 1970 Struma Ovariiascitic, hyperthyroid and asymptomatic syndromes. Ann Int Med 72: 883‑893.
21.  Barrande G, Munz C, deRochambeau B, Dazza F, LeMarois E, et al.  1997 Struma ovarii or malignant ovarian goiter.  Presse Medicale 26:900-902.

MILD HYPERTHYROIDISM, QUESTIONABLE CAUSE     25 OCTOBER 2006 QUESTION-F 40+yrs, history of hypothyroidism on variable combination of T4 and T3 replacement (prescribed by GP, not seen by us or any endocrine specialist) for >10 years. The only retrievable TFT around that time (5/1999) : fT4 10.1 pmol/L (10-24), TSH 5.62 mU/L(0.4-4). Early 2005, given herbal treatment for tiredness for 1-2mths then stopped. Mid 2005, started to have mild hyperthyroid symptoms and T3 related hyperthyroid state on TFT: In the past 15months, TFT picture remain very stable with fT4 16-19, fT3 6.2-11 (2.5-5.5pmol/L), TSH <0.08. Thyroid just bearly palpable, no goitre. Thyroglobulin <1ug/L (<55)(DPC Immulite 2000) with antithyroglobulin antibody 259 IU/ml (EIA) (<100), antithyroid peroxidase 300 IU/ml (EIA) (<100). Thyroid 99m Tc pertechnetate scan - Asymmetry R > L, right large hot nodule with left lobe diffusely warm, i.e. no suppressionm. At 20mins - increased uptake at 3.4%. Deny ongoing use of T4 or T3 replacement since mid 2005. Despite tremor and tachycardia found and explanation of cardiac/osteoporosis risk - patient feels good in hyperthyroid state and refuse any kinds of treatment offer. Questions:
1. The differential at the top of the list is toxic adenoma with predominant T3 secretion. However, is it unusual to see toxic adenoma arising from a previously hypothyroid state for some many years ( from whatever reason like Hashimoto thyroiditis to start off with ) ?
2. Is it true that I should expect thyroglobulin to be raised (even if it is mild ) in most patients with toxic adenoma ?
3. Can the undetectable level of thyroglobulin as measured on the Immulite platform be explainable by this relatively low titre of raised antithyroglobulin antibody ?4. Another differential raised was factitious hyperthyroidism - esp with the undetectable thyroglobulin and patient's apparent comfort in the hyperthyroid state and refusal of any kind of treatment but very willling for regular biochemical monitoring. However, the thyroid scintiscan finding seems to be not typical of factitious hyperthyroidism ( expect reduced uptake ). Thus, does this finding from thyroid scintiscan totally refute this diagnosis ?  Dr. Weldon Chiu  FRACP, FRCPA 
RESPONSE-  I think a more likely diagnosis is autoimmune thyroid disease, which began with hypothyroidism, but now manifests itself as very mild hyperthyroidism. The low TG is  unreliable in the presence of the antibodies. A toxic nodule should be obvious on physical or US, since it typically would need to be 3 cm in size to produce hyperthyroidism. Having both AITD and a toxic nodule is possible, but a unitary diagnosis is usually better than two. The elevated T3 and normal T4 fits with the output of an auto-immune-damaged gland, and could not easily be duplicated by a pill unless the patient took a special mixture of T4 and T3. (This last statement is conditioned on what would happen to T4 and T3 when taking such pills in the presence of a normal gland, and I can not be sure what would occur in the presence of a nodule or thyroiditis.) The scan and uptake also argue against a toxic nodule, and fit with AITD  (Hashitoxicosis?)     L  De Groot, MD

THYROIDITIS, HYPOTHYROIDISM, PREGNANCY 7 SEP 2006
QUESTION-Thank you for giving us such quality input at such convenience. This is a 37 yr old white female who had a normal TSH in Aug 2005. In Jan'06 her TSH was noted to be elevated at 7.92 with normal FT4 of 0.88 and free T3 of 3.52(2.3-4.2). She was started on Synthroid 50mcg by her Ob, but chose to discontinue it on her own in 3 weeks due to sx of hypothyroidism worsening. Her repeat TFT in Mar'06 now showed her TSH to be further elevated at 10.16 with FT4 of 0.82, FT3 of 2.78 and she was referred to me.
She saw me in April'06 and was 6 weeks IUP. She had no goiter on exam and was otherwise healthy.No antibody testing done so far.No sx of URTI in the last 6months and her gland was nontender.I initiated her on 100mcg of levothyroxine, with F/U in 4 wks with TFT and Ab titers.
5wks later she informed me she had a miscarriage at 8wks IUP. Her TPO, TG and TSI ab were all in the normal range. TSH was low at 0.11, Ft4 elevated at 1.9 and T3 at 171. I discontinued her levothyroxine, counselled her on preg and thyroid and asked her to F/U in 2m with labs, emphasising not to get preg till thyroid is sorted out.
She is back after 3m, 5 weeks IUP. Off LT4 her TSH is 5.30(0.30-4.5 for 1st trim), Free T4 is 0.8 and T3 is 111. Her TPO and Tg Ab are undectectable. Her thyroid appears slightly bulky on exam without nodularity.
Do I reinitiate LT4 and at what dose? Pls advice. thanks for your prompt response. Radha ReddyMD
RESPONSE-This young woman has undoubtedly subclinical hypothyroidism, considered idiopathic since no cause was evidenced.I believe it to be due to autoimmune thyroiditis (most likely) since the gland seemed somewhat "bulky" on palpation.
I would do a thyroid ultrasound and repeat antibody detection 2-3 times/year.
To answer your specific query, I would restart the patient on l-T4 administration, probably 50 µg/day, and monitor thyroid function carefully, especially if pregnant again.  Daniel Glinoer, MD
 

TWIN PREGNANCY, LOW TSH, NORMAL T4 AND T3 (2 JUNE 2006)
QUESTION-I am taking care of a 32 year old lady, first pregnancy, at 18 weeks with a twin gestation who comes in with the following thyroid numbers:
TSH=0.02 (NV=.30-5.00), Total T4=15.7 (NV=4.5-12.0), Free T4=1.5
(NV=0.71-1.85), free T3=4.1 (NV=2.4-4.2)
I repeated the blood work 10 days after the first set of numbers:
TSH=0.02, Total T4=15.5, Free T4=1.3, free T3=3.6, Total T3=339 (NV=100-200)
She is complaining of occasional palpitations and SOB that sometimes wakes her from sleep. She had been having hyperemesis gravidarum since about the second week of pregnancy and is still having occasional bouts of vomiting. No diarrhea and no heat intolerance. She is gaining weight appropriately.
Thyroid stimulating immunoglobulin is pending.
My question is: If the TSI comes back within normal limits, could this be HCG-mediated thyrotoxicosis or gestational transient thyrotoxicosis? What would the appropriate treatment for this condition be and would it be reasonable to just repeat bloodwork after a month? I thank you in advance for any advice you could give me.  Patrick Litonjua, MD, Binghamton, NY
RESPONSE-Although the TSH is quite low, it is not out of the range seen in the Hyperemesis Syndrome, in this case presumably due to high hCG associated with twins.. The normal free hormone levels are reassuring,  as are the total hormone levels which do not exceed 150% of the upper non-pregnant range, and the patient is doing well clinically. I agree with your plan to wait and re-check levels in a month unless there is a clinical change. L De Groot, MD

HYPERTHYROIDISM, LOW  UPTAKE, NEGATIVE AB (5/24/06)

QUESTION-Thanks for you site.I will greatly appreciate your --.Clinical problems 

PATIENT 1.Young female.Symtoms of thyrotoxicosis , no eye signs ,no grossly enlarged thyroid gland  , or bruit,T4 = 50  ;TSH =  < 0.03

Referred for   I-131.Thyroid scan done = Uniform uptake  of  TC. Calculated uptake  = 2 % , Gland not grossly enlarged. Not convinced that patient is actually Graves disease , I put patient on neomercazole. Repeat testing  approximately 6 weeks later .T4 = 18.6    T3 = 9.9  TSH < 0.03   ANTIBODIES  -VE

 Referring doctor  incist on I-131 

1. Should  I  administer the I-131
2. Is there a cutoff level on the TC uptake scan that defines Graves disease from other, if so what is it , some text claims 5 % , some says 20 %.
   If I look at the diagram in the website it appears that   the the scan does not play much of a role .
3. Strictly speaking , should the scan  have been done .
4.   How should patients be managed with prolonged symptoms of hyper-tyroxemia ,clearly of thyroid origin , (as the thyroid does show up on the scan), but the level of uptake does not appear clearly to be of a thyroditis( I am under the impression that a thyroid does not show up in the more common thyroditis , -but the level of uptake does not appear that clearcut of a Graves disease .  
5. What  is the role of antibody testing in this general scenario , and for that matter a Thyroid FNA or biopsy (no nodules palpable )maxwell@axxess.co.za

RESPONSE-The three diagnoses that come to mind are 1) Graves' disease with an iodide load suppressing thyroid uptake, 2)"painless thyroiditis" of the Hashimoto's variety, and 3) subacute thyroiditis, which can also be painless. You could measure urinary iodide. Obviously there are other possibilities but less likely. If both TG and TPO antibodies were negative, that is against #1 or #2, but not conclusive. Possibly measuring anti TSH-Receptor antibodies would be helpful. High ESR or CRP might have been helpful to suggest SAT. A biopsy might be diagnostic, but usually is not needed.  You have time on your side, and the patient is not now in danger. I personally would not give RAI at this time. By the way, it is difficult to judge the tests in the absence of normal values.

    It is not sure whether you describe 2% TeCO4 uptake, or iodide uptake. I am only familiar with RAIU in this siuation, and would not want to treat a patient with a low uptake since the diagnosis is obscure, and you would need to give a very large dose to "treat" the thyroid. The scan is usually not helpful in this situation. A scan can easily identify the thyroid even if the isotope uptake is miniscule, because of the sensitivity of the machinery.

    What to do? One approach would be, when the T4 is normal, stop the neomercazole, and follow the patient. If hyperthyroidism recurs, check antibodies in aonther lab. Do another RAIU. Test urinary iodide if uptake of I-131 or I-123 is low. Check TRAb and ESR. Get a good dietary history. Was the patient recently pregnant? Find out if the patient had a previous normal thyroid test at some time.Make sure that the patient is not on some drug such as amiodarone. Usually the process wioll become more clear in time, and both #2 and #3 tend to be self-limiting.. A list of possible causes of this problem can be found in WWW.THYROIDMANAGER.ORG. L De Groot,MD

 

QUESTION-PATIENT 2.I had a similar 70 year old female.Ab,s ? , referred for I-131. With biochemical and clinical typer thyroxemia  for 3  - 4  months, gland not grossly ,significantly enlarged ,with a calculated TC(20 MIN ) uptake of 2 %, Not convinced that she required the I-131 , I opted for neomercazole , the elevated hormone levels dropped  , as well as after  I stopped the medication . (Was this correct , if the levels did not normalize what should have been done .

    RESPONSE- Most of the above applies here as well. Your approach seems to be logical so far. L De Groot,MD

MICROCARCINOMA  IN  TEENAGER  WITH DYSHORMONOGENESIS  12 MAY 06

QUESTION-  I’d like to tap into the expertise of this forum (Thyroid Manager) regarding an unusual situation in a pediatric patient.  Patient was a non-adherent young, obese 14 yo teen with an original diagnosis of congenital hypothyroidism secondary to dyshormonogenesis.  He’d been lost to follow-up for more than a year.  Upon return, he presented with an asymptomatic 2.5 cm nodule.  Biopsy results suggested follicular adenoma with pre-malignant features (I don’t recall at this time.).  Subsequent total thyroidectomy led to the finding of a 6mm papillary carcinoma on the contralateral side of the original lesion.  He was ablated with I131 following surgery. Thyroglobulin levels were unmeasurably low when his TSH was 130 uU/mL about 2 months following the ablation.  He has since become adherent to treatment with Synthroid and TSH has been maintained around 0.02 uU/mL.  Microcarcinoma is a well-described phenomenon in adults, but not in children.  Is this a patient (now 15 yo) who will need to have regular scans to look for metastases?  Does he need to be this suppressed?  Any input will be greatly appreciated.  Thanks,Vered Lewy, M.D. VLE@the-institute.org

RESPONSE-Your case raises many issues. I suppose that in the presence of dys-hormonogenesis, and "non-adherence", that his tumor could be related to excessive TSH stimulation in the past. However, going forward, I do not think there is any proven connection between human thyroid dyshormonogenesis, and cancer, except via TSH action, although one wonders whether there could be some other genetic link. I also believe, in the absence of any compelling data, that one should be more aggressive about a <1cm lesion, in this youth, than in an adult.

    Surely he is at low risk in view of ablation and negative TG with TSH high. (I presume he had detectable TG at some point??) I think a common opinion would be that his TSH could be moderated toward 0.4uU/ml, and that he could be followed by yearly stimulated TGs. My own personal preference (being from the old school) would be,  one year after ablation, to do another 131-I scan and TG.  Assuming both are .totally negative, I would at that point be satisfied to follow with stimulated TGs on an annual basis. Regards, L  De Groot, MD

HOT NODULE  WITH INDETERMINATE  HISTOLOGY  (9 May 2006)

NORMAL T4 RANGES IN PREGNANCY

QUESTION-All along, I thought  that free hormone levels (ft4/ft3) are better  initial parameters (vs t4)  in monitoring treatment in pregnant patients with toxic goiter.  In the march 2006 issue of Endocrinology and met clinics of NA, the authors, recommend measuring total t4 concentration for dose titration of anti thyroid drug. Can you comment on this. Thanks again. Lynn F. W. Bilar, MD

MANAGEMENT OF A MEDIASTINAL MASS -  5 APRIL 2006

QUESTION-I would like your opinion regarding a 63 year old lady with well differentiated follicular variant papillary carcinoma (3.7cm) with mediastinal metastases.

She presented in August 2005 with thyrotoxicosis (TSH <0.04, FT3 6.3, normal FT4) and subsequent tests demonstrated a dominant left thyroid nodule (3 cm) and nondominant nodule in the right lobe (<3mm) with increased tracer uptake in the left hemi-thyroid. Anti-TP0 were present in low titers at 81 IU/ml ( 0-60). As needle cytology of the left nodule favoured oncocytic proliferation she had left hemi-thyroidectomy in September. Unfortunately, the pathology revealed a 37mm well differentiated thyroid carcinoma displaying mixed follicular and papillary features, with focal full thickness capsular penetration. A completion thyroidectomy was performed in early December with no evidence of residual malignancy in the right thyroid lobe.

She received ablative RAI (3.55GBq of Iodine-131 orally) 7 weeks after completion thyroidectomy, however, the TSH on the day of dosing was sub therapeutic (21.9 mIU/L). Thyroglobulin was <0.02ug/l and thyroglobulin antibody was <40 kIU/L. Whole body survey, 3 days after the RAI dose showed a focal moderately intense abnormal radioiodine accumulation in the anterior mediastinum in the midline just below the transaxial level of the carina. When correlated with the low-dose CT scan, this appeared to correspond to a small soft tissue mass in the anterior mediastinum. There was no definite evidence of iodine avid thyroid tissue in the region of thyroid bed or elsewhere. She was started on levothyroxine after RAI.

How do I best manage this patient?

1. Repeat diagnostic scan in 6 months and consider second RAI treatment if positive diagnostic scan?
2. Consider thoracotomy for removal of metastases if positive diagnostic scan as mediastinal nodes/metastates may not ablate with RAI therapy?
3. Monitor thyroglobulins / surveillance neck ultrasound/ CT scan chest for recurrent disease whilst maintaining TSH suppressive therapy ( 0.1- 0.4), if diagnostic scan in 6 months is negative?
4. Should Radiotherapy be considered? Any other recommendations?

Thank you in advance for your advice. K.Guttikonda FRACP, NSW Australia

RESPONSE-In summary this is a patient with uptake in the anterior mediastinum
corresponding to a small mass at CT scan with an undetectable
thyroglobulin and negative anti-Tg while TSH was elevated. The Tg result
may be interpreted as false negative, which is possible in case of small
lymph node metastases. As an alternative, one can think of unspecific
uptale of radioiodine in a non-thyroidal mass (i.e. thymus, or something
else) which has rarely been described in that area of the mediastinum. I
would perform a stimulation of serum Tg  using rhTSH and CT scan (and/or
FDG-PET) in six months. In case of negative Tg and FDG-PET, even if the
mediastical mass is still visible at CT, I would not recommend therapy
but only follow-up. In case of evolution at CT or positive PET and/or
stimulated Tg I would  recommend RAI therapy followed by post-therapy
WBS. No need in my opinion for a diagnostic RAI WBS.  F. Pacini MD

RAI  TREATMENT  WHILE  PREGNANT- 16 MARCH 2006

QUESTION-I am an endocrinologist in Maryland. I have a 35 y/o woman with hx Grave's  just had RAI in mid Jan 2006, had negative pretreatment pregnancy test and now came in today and is pregnant.  I had previously counseled the couple multiple times about avoiding this issue.  Anyway, what would be your advice as to the potential risks to the fetus.  The couple is thinking of terminating the fetus. Thanks,R.N.

THYROIDITIS, OR GRTH? –6 March 2006

QUESTION-I  would like to ask your opinion regarding 10,5 years old Caucasian girl. She was referred to me after series of doctors.  

Anamnesis and complaints. 6 mo ago she lost a lot of hair on the head, shortly after her parents told her about the family moving to another country. Very similar episodes had happened twice before - 6 and 4 years ago, each time related to moving to another country. The hair would grow gradually back within 4 to 6 months. Local application of steroids did not help to facilitate the re-growth of the hair.  

Second major complaint is tiredness, which does not dramatically interfere with the daily life performances. Otherwise she is a happy girl, starting running into teenagers' problems (moody, sometimes quarrels with younger sister). Her school performance is good (according to her mom).

Denies constipation, rather mild diarrhea occasionally. Allergy test revealed allergy to wheat, corn, oat and sea fruits. 

Family history. Two sisters from father's side were diagnosed with celiac disease and thyoid problems last year (in adulthood). Grandmother from mom's side had been taken Thyroxin 'her whole life'. Two younger sisters and parents are healthy.
Objective findings. Girl's length lies within 50percentile, and her weight - within 75 percentile. Skin warm, not too dry. Bold areas on the head around 10 over 15 cm diameter, not in regular circle shape. Denies heat or cold inteolerance. No tremor, nystagm, eyes normal. Skin clear, no pigemntation or depigmentation, no signs of infection. RR 18/min, HR 60/min, BP 86/56 mm Hg. Thyroid gland I-II, firm, symmetrical. Tanner development score: B2 P3 A0.  

Laboratory results. Please, find enclosed the sheet below. Tests done for celiac disease diagnosis where related to parents' concern and family history.

2005 11 04 she received Ba contrast for small bowel Xray series.

 2005 08 29 Thyroid US: R 39x13x12 mm L 35x10x12 mm.Both uneven, but no nodular mass observed.

 2005 08 30  Pituitary MRI: Normal

 Antigliadin and antiendomisial AB positive. Biopsy not performed.

Series of gastrointestinal X-rays with Ba contrast – no abnormal bowel movements.

 My questions:how further could we and should we differentiate between autoimmune thyroiditis and resistance to thyroid hormones? (is T3 test necessary?) May it be a part of some polyglandular syndrome?( should she be tested for adrenal hormones?) Treatment? L-THyroxine? With kind regards, V.Kuehne, MD, PhD Shanghai Worldlink Medical Center,

SUBCLINICAL HYPERTHYROIDISM AND CONCEPTION (1 FEB 06)
QUESTION- I am following a 39 y/o woman with 1ry infertility found by her fertility
 GYN to have a low tsh and diagnosed by myself as having a subclinically
 hyperthyroid multinodular goiter[-ve fna]. Her TSH has  fluctuated between .04 and .15 or so with normal free T4 and T3total. She  has no overt hyperthyroid symptoms. She is anxious to try fertility  treatments asap due to her age. She has had a fluctuating asymptomatic low  WBC count for years[2000s-5000s]. Can you help us quantify the risks of:

THYROXIN DOSE AFTER THYROIDECTOMY FOR PAPILLARY CANCER
QUESTION- Following a complete thyroidectomy 18mo ago (papillary CA) I am now on 250ug thyroxine. Key question is: If I am exercising more, (trying to run 7kms, 3x/w) should I be raising my thyroxine dose. I would imagine that under normal circumstances, metabolic needs would rise hence a greater need for thyroxine. Compared to pre-thyroidectomy running, I now need 2-4 days recovery time after a run - previously running every 2nd day. If I don't run, my energy levels are certainly better. When I do run, there is a definite accumulated lag time in my recovering energy, and subsequently need to take 7-10 days off exercise. I am 6"2', weighing 94kg. Appreciate your thoughts. Dr. Christopher Hume-Phillips
 RESPONSE- Your dose of T4 may be making you hyperthyroid, and possibly more so than needed. Hyperthyroidism certainly could affect your running. Check the TSH.  Then discuss with your MD the desired level. This could be "well suppressed" (+/- 0.1uU/ml), or more likely, as in most patients thought to be cured, 0.5-1uU/ml. It is a decision that is based on all of the facts in the circumstances. L De Groot,MD

THYROID TISSUE IN A LATERAL MASS, WITH THYROIDITIS--- IS IT CANCER? 16 Jan 2006

QUESTION-I am taking the liberty to write to you because of a management dilemma which I am having difficulty to solve using the available published data. A 34-year-old woman was referred to our Institution after she had undergone total thyroidectomy and right modified neck dissection. The surgery was performed because FNA of a lateral neck mass (presumed to be a lymph node) revealed thyroid tissue. The pathology of the thyroid gland consisted of nodular Hashimoto's thyroiditis with no evidence for  neoplasia. 12 lymph nodes were excised, 11 of which were normal or "reactive". The remaining mass, the one that has been originally biopsied (region 2 of the neck, next to the jugular vein), initially was interpreted as "thyroid inclusion in lymph node" , the follicular cells appeared normal.   The slides were re-examined in the pathology department of our institution and their conclusion was that the lesion is a "parasitic thyroid nodule, in the context of Hashimoto's thyroiditis". They explained to me that the whole mass looked like Hashimoto, and did not fit the diagnosis of inclusion, where one should be able to identify normal lymph node structure, with a small subcapsular area of thyroid tissue. Looking through the literature, I was not able to make up my mind as to whether these lesions should be considered potentially as metastasis from well differentiated thyroid carcinoma, and thus be treated accordingly (we usually administer 150 mCu I131 in cases of metastasis to lymph nodes) or interpret it and treat it as a benign finding. What is your position? I thank you very much for  your time. Sincerely, Yona Greenman MD, Tel Aviv-Sourasky Medical Center, Tel Aviv
RESPONSE-My understanding is that the idea of "lateral aberrant thyroid" has been largely laid to rest, and thyroid tissue outside the thyroid or in a node is now generally thought to be a met. Obviously this is difficult to prove. It is not hard to imagine that thyroiditis could involve the aberrant tissue as well as the thyroid. Inability to find a primary in a patient with a nodal met is always distressing, but not rare.   Thus I feel, with no published support that I am aware of, that the case is best handled as if the process was a low grade tumor  with a met, and would agree with 131-I ablation.  I think I would use a somewhat lower dose.

It would be of great interest to hear from others who read this case if they have reason for a different approach. Best regards. L De Groot, MD
ADDENDUM 2/28/06-

HYPERTHYROIDISM  IN  THE  TRULY  ELDERLY  12 Jan 2006
QUESTION- I would appreciate your input on the following case: a 103 yrs old white female, was first  diagnosed with hyperthyroidism 6 month ago, but she was followed up w/t therapy. There is no known thyroid disorder in the  family.  Thyroid was normal in size. Since the beginning of January are clinically present diarrhea, nervousness, palpitations, breathlessness. Geriatric physician gave her beta blockers with a partial resolution of symptoms.

Thyroid tests are as follow: FT3 -----4.14 pg/ml (1.45-3.48),   FT4------2.45 ng/dl (0.71-1.85) ,    TSH  0.007 micro IU/L (0.4-2.8 ), Anti TPO antibody 41 IU/ml ( 0.0-12), Anti TG antibody   15.1 IU/ml (0.0-34).  How do I best manage the patient? Do I start methimazole? Prof. Daniele Danese, Università "La Sapienza" Roma

RESPONSE-You do not mention the thyroid, or eye symptoms, but everything seems to fit with Graves' disease of moderate severity. I can not speak based on a string of cases in 103 year old patients! However, I may offer the following. In general her life would be simpler with definitive treatment, rather than continued antithyroid drugs. Thus if she seems fairly well, and to have expectancy to live on another year(s), I would choose therapy with RAI over continued ATD.  Usually therapy is intended to effectively ablate the thyroid. If she has no eye symptoms, it might be sensible to use a lower dose intended to reduce function to normal, but not ablate. That might, or might not work, but little would be lost in the effort, except the possible need to retreat at a later date. Regards,  L De Groot, MD

THYROXIN ABSORPTION TEST

QUESTION-In patients with suspected T-4 malabsorption, is there a "standardized" T-4 absorption test during which time patients are given their T-4 dose supervised in the office, and have their labs monitored at intervals?  I have done this in the past, and have derived useful information; however, I am uncertain as to the best time to draw samples following the dose, and exactly what tests will provide the most information.  i.e. to order TSH, T-4, and/or free T-4 levels, at what intervals for how long? Thanks
Victor E. Silverman, M.D.  vsss@bellsouth.net

RESPONSE- The problem to test T4 absorption using 'cold'-, i.e. non-radioactive T4 is the fact that T4 disappearance from blood is relatively slow (10%/day). This means that the peak of T4 after absorption does not give any quantitative information. The best way to measure T4 absorption is to administer the patient intravenously a known amount of 131I labeled T4 and simultaneously differently labeled i.e. 125I T4 orally. The differences in the serum kinetics of the 2 labels shows the fraction that is absorbed from the intestines. Regards Georg Hennemann, MD, PhD, FRCP, FRCPE
Note added—The FDA and others use a standard “AREA under the curve” measurement with 100ug tablets, but it is fairly insensitive.. The test can be done with a 1000ug dose, safely, but I could not find an available reference to this in my quick search in MEDLINE.  L De Groot, MD

Blouin RA, Clifton GD, Adams MA, Foster TS, Flueck J. Biopharmaceutical comparison of two levothyroxine sodium products. Clin Pharm. 1989 Aug;8(8):588-92

Walter-Sack I, Clanget C, Ding R, Goeggelmann C, Hinke V, Lang M, Pfeilschifter J, Tayrouz Y, Wegscheider K. Assessment of levothyroxine sodium bioavailability: recommendations for an improved methodology based on the pooled analysis of eight identically designed trials with 396 drug exposures. Clin Pharmacokinet. 2004;43(14):1037-53

ADVERSE EFFECT OF IODINE TREATMENT OF DRINKING WATER     28 Oct 2005
QUESTION-I've read your article regarding iodine and the thyroid gland.  I hope you can advise us regarding our problem.  I am a 37 years old man. My entire family (father,mother, sister, wife and myself) developed thyroid illness because we have been using a pentaiodide water purification device that had been producing water with toxic level of iodine (6mg. per liter).  Weâ?Tve been using this device for three years, and the symptoms (loss of weight, weakening) appeared on the third year.  We were diagnosed with hyperthyroid due to goitrous thyroiditis.  Our FT4 and TSH values are beginning to have normal levels after taking Strumazole for four months.  Attached are my own lab test results through a 6-month  period. 

My questions are:
1.) Are we going to recover fully now that weâ?Tve stopped drinking the toxic water?  Are our thyroid
glands going to get normal again, producing adequate thyroid hormones, even without medication?  Are we going to have blood tests and regular visits to the endocrinologist for the rest of our lives?
2.) Is the excess iodine in our body going to disappear?
3.) Are there foods to be avoided, like foods rich in iodine or goitrogens?
Any advice or referral that you could give us regarding our condition will be deeply appreciated.
Thank you. Jess Ko, Philippines jsk88888@yahoo.com
RESPONSE-: Your thyroid volume and function will most probably return entirely and permanently to normal. In this case, you will not need any longer follow up by endocrinologists, blood tests and medication. The minor restriction I make is that you indicate that the diagnosis of thyroiditis was made and this possible side effect of iodine excess is not necessarily entirely reversible.  I cannot be more precise about this possibility because you do not provide enough data and blood tests results to evaluate properly what  means  "thyroiditis" in your particular case.
Practically speaking, I suggest that you remain under control by endocrinologists with blood tests for at least 6-12 months because iodine-induced hyperthyroidism can last for long. After that time interval, if thyroid function is normal out of any medication and if blood tests do not confirm persistent thyroiditis, you will be all right and should forget this difficult period. (but see also my reply to your question 3).
2.) Is the excess iodine in our body going to disappear?:  Yes, definitely, within weeks or a few months, depending on the duration of the iodine overload.
3.) Are there foods to be avoided, like foods rich in >> iodine or goitrogens?: Yes, you should avoid any cause of iodine excess. The main cause is drugs, especially drugs usually used for the therapy of cardiac arrhythmia (amiodarone),  iodinated skin disinfectants (Povidone iodine) and some x-ray contrast media (ask the question to the radiologist if you need an x ray with contrast media). Regarding food, avoid sea weeds, whic are extremely rich in iodine (in case you are attracted by japanese-like foods). The other sea foods are allowed (fish, shells). You are also among the very very few people who should avoid the use of  salt enriched in iodine (iodized salt) for the family table and kitchen.  On the contrary, iodized salt is firmly recommended for the inhabitants of your country, which still contains large parts deficient in iodine (I used to be a consultant of your Ministry of Health on this issue). I am entirely optimistic about the outcome of your very unpleasant experience The test to be used for the evaluation of iodine excess and its disappearance is urinary iodine rather than thyroidal uptake of radioiodine, which is not very precise in this case and should be avoided as much as possible.

For my personal information, I should be interested to hear more about the water purification device you have used (producer, use in your country and elsewhere). I do hope that this answers your questions. Please, do not hesitate to come back to Dr De Groot and/or me for any further information.

INVASIVE PAPILLARY CANCER AND ENLARGED NODE  24 Oct 2005
QUESTION-35 yo male patient  with 8.5 cm tumor of the right lobe of thyroid. Pathology reports poorly  differentiated papillary, Hurthle, and Follicular cell types. Extensive  lymphovascular invasion, 9 out of 15 nodes positive. Modified radical neck  dissection was performed and 7/54 nodes positive. Patient received 151mc  dose of RAI, scan showed no uptake. Follow up Thyrogen stimulated scan  showed no uptake either. PET scan was neg. Hashimotos antibodies are  present therefore Tg is not valuable. Follow up CTs show suspicious nodes  on the left side of the neck, submandibular. Recent USOctober 2005 showed  the submandibular node to be 2.5cm in diameter.  TSH is suppressed at .01.  The patient is 2 years post initial diagnosis.
         My question is what is  the likely hood that the nodes on the left side are residual cancer?   At time of TT nodes on the left were sampled and found to be  negative. Should the node be removed out of caution? If the node  is positive should I131 be repeated even though the variants do not seem to  absorb iodine or follow with EBRT. What is the long term prognosis for the  variants that do not respond to I131 and are there other therapies that may  be of value. Lungs are clear at this time. Are any of the clinical trials  regarding THYCA promising? Dr. Joshua J.  J