
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
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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.
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FNA “POSITIVE” CONTRALATERAL
NODE FOLLOWING HEMITHYROIDECTOMY.
1 Apr 2008
QUESTION-I have a 21 year old who presented with a 3.6 cm Left thyroid mass,
TFT's were normal, TG and TPO antibodies were negative. The right lobe did not
show any nodules but she had a calcified LN measuring 1.8 cm with no fatty hilum.
She underwent left hemithyroidectomy and final pathology was reviewed at Mayo
clinic by Dr.Gary Keeney and signed out as as benign follicular adenoma with
background of Hashimoto's thyroiditis. The right LN was biopsied after the
surgery ( I ordered a repeat US post hemithyroidectomy 6 months later to
evaluate the contralateral lobe and the right LN with calcification was seen and
radiology suggested FNA) and the FNA result now showed follicular cells with
minimal nuclear pleomorphism, and cells with abundant cytoplasm consistent with
Hurthle cell differentiation.
Is it possible to have thyroid tissue in a LN in the absence of malignancy? I'm
thinking of sending her for excision of the LN but what about the right lobe?
Recent US now showed a 8 mm nodule on the right. Should I send her for
completion thyroidectomy "just in case" this developes into malignancy being
that she is only 21 years old. There is no family history of thyroid cancer and
no exposure to childhood head and neck irradiation. Please advise. Her mother
has been calling us everyday and I honestly am not sure how to proceed from
here. Marie Mercado,MD
Overland Park,KS
RESPONSE-
Thyroid tissue in a lateral node is usually considered a met, but I
would hesitate to say that it can never be benign. Since she has a probable met
on the R side, and a (?) new nodule by US, and had a good sized (3.6cm)
follicular lesion, R lobectomy and local node dissection might be the best
approach, followed by RAI, depending upon the pathology. L De Groot, MD.
rhTSH vs
HORMONE WITHDRAWAL IN RAI THERAPY 22 Mar 2008
QUESTION-An 18 year old girl with diffuse
miliary metastases of papillary thyroid cancer in lungs has had 200mc of I131
and we plan repeat doses every 6 months until no more uptake in lungs. This
first dose was given after withdrawal of thyroid hormone. Would future doses
after Thyrogen be as effective and less damaging to other tissues DW Ingram St
Clares Mercy Hospital St Johns Newfoundland Canada A1C5B8
RESPONSE-One study reports lower whole body radiation using rhTSH in comparison
to hormone withdrawal, but I do not believe the issue is settled as yet. Either
approach should provide adequate stimulation of any thyroid tumor tissue. My
personal preference is the "half-dose" method, outlined in
www.thyroidmanager.org, which raises TSH
effectively without inducing symptoms from hypothyroidism. L De Groot, MD
PET-SCAN POSITIVE MEDIASTINAL ? MET AFTER RAI AND PRIOR NEDIASTINAL OPERATION 3/21/2008
QUESTION- I would like your advice on the following case. A 28 year old female
underwent total thyroidectomy and central neck dissection in 2004, for a classic
papillary thyroid carcinoma (T2 (unifocal 2,5 cm), N1a, M0, EI). Afterwards she
received 150 mCi radioiodine (under low iodine diet). The post dose scan showed
uptake only in the thyroid bed. Antithyroglobulin antibodies were negative, but
her thyroglobulin level at that time (off t4,) was 802 ng/ml. Several studies
were performed, and a 18 FDG pet scan showed several foci of uptake in the
mediastinum and both sides of the lateral neck (the latter were also shown on
US). By then, about six months after the first surgery, off T4 her antibodies
were again negative, and the Tg was 540 ng/ml. She underwent bilateral neck and
mediastinum dissection, which was performed in an oncology center with a team of
specialized thoracic and head and neck surgeons. The pathologist report
confirmed metastatic lymph nodes for papillary thyroid cancer in all the three
areas. After that, her thyroglobulin off T4 dropped to 120 ng/ml, and she was
given additional 150 mCi radioiodine, with a negative post dose scan. Then, she
was followed with neck sonograms, MRI, CAT scan (all of them negative) and
thyroglobulin off T4 (her Ab were always negative) which gradually dropped to 64
and then 39 ng/ml over the next 18 months. No new doses of radioiodine were
given, as we assumed her tumor was not radioiodine avid. Then the tg off T4 rised
agan, this time to 153 ng/ml, and a new 18-FDG- PET scan with CAT was performed.
It showed two small foci of 8,7 SUV: one in the upper right neck (near the
mandible, maybe level II-I) and the other in the mediastinum. Despite the
intense metabolic activity, the size of the lesiones is about 1,2-1,5 cm. The
surgeons agree with the idea that surgery is the treatment of choice, but there
is a concern of missing the lesions (mostly the mediastinal), since considerable
scarring is expected, and the risk of complications is considered high (the
previous surgeries were fortunately uneventful, besides a small neumothorax that
evolved favourably). Is there anything you would recommend in this case? Thank
you very much, Ines Califano MD, Argentina.
RESPONSE- A second mediastinal exploration is certainly depressing idea for all
concerned. It makes sense to remove the lesion in the neck since you see it on
US and it is PET positive. However neck nodes usually produce low levels of TG-
such as 8-20. So presumably the lesion in the chest, or other lesions that may
be present but unseen, is (are) likely to be the source of the TG. You can not
destroy a 1.5 cm thyroid metastasis with RAI when the uptake is so low that it
is not seen on a post-therapy scan. However that scan was ?? a few years ago? If
it was some time ago, I would consider doing another scan and then possible RAI
treatment, on the remote and unlikely, (but hopeful) idea that significant
uptake may be present, and there is nothing to loose except a bit of time.
After that comes the idea of surgery and all of its possible problems, and the
significant possibility that not all of the lesions present would be seen. But
the patient has an increasing TG, Xray is of uncertain value, and she is not a
candidate for chemo. In a certain sense, the second operation is the only real
chance for a cure. So I would side with the surgeons if the patient is up to the
procedure. Best regards, Leslie J De Groot, MD
PREGNANT (POST RAI ON T4) WOMAN WITH ELEVATED TSAb
13 MAR 2008
QUESTION-I have a pregnant lady with history
of Grave's dse s/p RAI before her first pregnancy. This is her second
pregnancy and she is on her 2nd trimester. I have her on Synthroid and
her TSH levels have been at 1-1.5uiu/ml. I ordered a TSI and it is
mildly elevated at 146 %(<=125% Quest lab) . On her first pregnancy,
her TSI was normal at 81%. Clinically she is ok but I'm not sure if I
have to start her on PTU plus synthroid because her TSI is high and I
worry about fetal hyperthyroidism. What do you think?Thank you. Maria
Mercado, MD
Overland Park, KS 66213
RESPONSE-Dr Mercado-You are correct in being concerned since the TSAb
level is significantly elevated. However, the exact TSI level at which
the fetus would be in danger is not certain. I think a consensus
position at this point would be to not institute PTU therapy, but to
follow the patient and TSI closely, and check the fetus by US for signs
of hyperthyroidism, growth abnormalities, and goiter. It would be
interesting to hear from you again as the pregnancy progresses. L De
Groot, MD
REPEATED MISCARRIAGES IN A YOUNG WOMAN WITH HASHIMOTO’S THYROIDITIS AND
ANTIBODIES-
5 Mar 2008
QUESTION- This is a 32 yr old female who first saw me 3/7/7 when she was
8 weeks IUP, G4M3. First pregnacy was 5yrs ago FTND. Subsequent 3
miscarriages at 6-8wks IUP.
Hypothyroidism diagnosed 3yrs ago, not treated for reasons unclear. 6/06 she
was started on LT4 50 mcg, gradually increased to 100mcg by 2/07. When I saw
her 3/7/7 - TSH was 6.9 (1st trim N- 0.3-4.5), FT4-1.3, TPO> 1000, TGAb>3000,
TSI - 132 (N<125), TBII -30%(n<16%). I increased her LT4 to 112mcg, but she
went on to have a miscarriage 5/07 at 12 weeks IUP. Her TSH on f/u post
miscarriage was - 0.03, FT41.8, T3 185, TPO> 1000, TGAb1050. I reduced her
LT4 back to 100mcg/day.
She also had a tennis ball sized fibroid which was subsequently removed. She
has also had extensive testing by her reproductive endo, for etiology for
her miscarriages, all which seem negative.
She wants to conceive again.
Since 11/07 her TFT have been normal on LT4 88mcg/day.
2/07 - TSH- 2.87, FT4 1.4, T3-122, TPO>1000, TGAb> 3000.
She weighs 123lbs, and was hyperthyroid on 100mcg LT4.So, I have not changed
her current dose.
Is she a candidate for IVIG? Is there anything else I can do from endo
standpoint to reduce her risk for miscarriage? What would you advice her?
Radha ReddyMD, Rancho Cucamonga CA
RESPONSE-I am not too familiar with the medical phraseology used in
the U.S. when presenting case histories, but I think I understood correctly
that this patient has been pregnant 4 times, with three previous
miscarriages, and a fourth - and last miscarriage - during her most recent
pregnancy in 2007. Obviously, she also has chronic autoimmune thyroiditis,
with hypothyroidism diagnosed a couple of years ago. It is not clear to me
whether the 3 previous miscarriages took place while she was an untreated
hypothyroid patient or whether the obstetrical history occurred before that
period (where, by the way, she may also have already been hypothyroid,
without a diagnosis). In her most recent pregnancy, the patient received
L-thyroxine 'almost' from the onset of gestation. However, and despite
increasing her l-T4 dosage, the "best" TSH obtained was still clearly
suboptimal in the first trimester (6.9 mU/L). After that, she miscarried
once again. Finally, the antibody data indicate high titers of anti-Tg
(>1000-3000) and anti-TPO (>1000) Abs and a positive TBII value (30% TSH
binding inhibition).
Comments:
1) This is the sad - but not unusual - story of those patients who miscarry
early (in the first trimester) and repeatedly, who have autoimmune
thyroiditis and a not well-controlled thyroid function. Most studies on
recurrent abortion in such 'thyroid' cases indicate that the best that can
be done to help them is to make sure that their thyroid function is
perfectly equilibrated before they become pregnant (serum TSH below 2.5 mU/L
is probably the best target). In my own practice, I tend to titrate them
even 'higher', to obtain a serum TSH around 1 mU/L. As soon as they become
pregnant (spontaneously or medically-assisted), their thyroid function tests
need to be monitored extremely closely to make sure that thyroid function
remains entirely normal. This can only be achieved by sequential monitoring
(every three-four weeks) of serum free T4 and TSH, with rapid (or even
anticipated, as I like to do) increments in L-T4 dosage, and a close follow
up until 24 weeks gestation, at least.
2) If this Hashimoto patient also has TSH-receptor antibodies (again from my
understanding of the data presented), she may well be one of those rare
cases with blocking-type TSHR-Abs. In principle, this should not affect the
mother other than enhancing the risk of hypothyroidism, but could constitute
a risk for fetal thyroid function during the second half of pregnancy (if
she ever gets to that point !).
3) She may well be a candidate for IVIG (in addition to L-T4?). This
decision is usually taken by our Ob-Gyn colleagues. The rate of pregnancy
success with IVIG in the study by E. Vaquero (Amer J Reproductive Immunology
in 2000) was improved (54.5%) but less than with l-T4 administration
(81.2%). However, that study was not randomized nor controlled and the
number of cases in each branch was small (see my Editorial with this article
on pages 202-203).
4) I have followed personally a small number of women with the similar
difficult medical conditions. Some have undergone medically-assisted
procreation, some have even eventually adopted children, and despite these
heavy antecedents, we have witnessed a few (but remarkable) successes since
some women finally achieved natural conception and successful outcome of
pregnancy (after many failed attempts) by treating adequately their
Hashimoto's disease. Thus, there is still hope since the patient is only 32
years of age, but this of course is not to say that success is obtained in
all those cases !!
I hope my comments will be helpful to you.Prof Daniel GLINOER
(University of Brussels)
RESIDUAL PAPILLARY CANCER- RAI vs SURGERY??
QUESTION-I would appreciate your input. This is a 51 year-old lady who was
diagnosed with papillary cancer of the thyroid (4 cm , right lobe), s/p
total thyroidectomy on 2/2005. Her primary MD gave her a 30 mCi RAI ablative
dose. The metastatic search showed increase uptake in the thyroid bed. The
baseline thyroglobulin was 87.1 ng/ml (NV=0.5-43) with a TSH of 27.0 uiu/ml
(NV=0.3-5.0). She was then treated with Synthroid and her subsequent TSH was
maintained < 0.5 uiu/ml. The follow-up thyroglobulin on 7/2005 was 7.5 ng/ml.
This rose to 11.3 ng/ml on 10/2005. The patient underwent a thyrogen scan
showing increase activity in the neck area, and a thyroglobulin level
was 26.8 ng/ml on 11/2005. Her primary MD then gave a 200 mCi ablative dose
on 1/2006. The subsequent metastatic search revealed area of increased
accumulation in the neck with physiologic distribution throughout the body.
She was then referred to me on 5/2006. She was on 150 mcg of Synthroid
and her TSH was 0.22 uiu/ml. Throglobulin level at 3.6 ng/ml. ng/ml. On
11/2006, I did a thyrogen scan and metastatic search with no abnormal
activity in the neck identified. Unfortunately, my lab did not do the
thyroglobulin as requested. After 6 months, on 5/2007, TSH = 0.04 with a
Thyroglobulin of 1.5 ng/ml. On 11/2007, a thyrogen scan and metastatic
search revealed no uptake in the neck area with physiologic uptake
throughout the rest of the body. TSH of 19.2 uiu/ml and thyroglobulin of 9.0
ng/ml. Since the 2 previous metastatic searches were negative and with a
significant rise in the thyroglobulin, I did a neck ultrasound rather than a
radionuclide study and this revealed on the right a hypoechoic 0.7x0.9x0.4
cm nodule, isoechoic lesion in right thyroid bed 0.7x0.3x0.5 cm., mildly
hypo/isoechoic tissue in left thyroid bed 0.5x0.7x0.5 cm. I ordered an FNA
of the three masses but the radiologist could ony sample the right-sided
masses: 0.9 cm mass negative for malignancy, 0.7 cm mass positive for
metastatic papillary carcinoma.
I am in a quandary as to my next step. Would it be better for the
patient to undergo surgical removal of all three masses or again subject her
to a 200 mCi RAI ablative dose? The surgeon is understandably reluctant to
go after the sub-centimeter masses, and she already received 230 mCi over
the past 2 years and this may potentially increase her risk of
radiation-induced carcinoma. I thank you in advance for your insight.
Patrick Litonjua, MD Lourdes Hospital
RESPONSE- I will
offer my view, and note that there may be differing opinions. Concern about
leukemia is appropriate, but the total projected RAI dose would be <600mCi
even if re-treated, so probably safe. However the prior dose of 200mCi
failed to ablate this tumor. Thus I would be strongly in favor of careful
reoperation and node removal, and re-evaluation with US, TG and scans at a
later date. Treatment with RAI might still be tried if TG remains elevated.
Possibly this is a difficult tumor, and even radiotherapy may be indicated
at some point in the future. As noted, it would be of interest for readers
to write in if they have differing view-points on this case. Best regards,
L De Groot, MD
POSSIBLE
THYROID HORMONE RESISTANCE
1 Jan 2008
QUESTION-Your thoughts regarding this generally healthy 65 yo man would be
most appreciated. He presented with non-specific but suspicious symptoms:
hyperkinetic, emotional irritability, weight loss despite intentional high
calorie intake (nickname of "Joe Donuts" by his family).
Exam:
Equivocal tremor, normal reflexes, no lid lad. Thyroid exam enlarged,
consistent with the ultrasound.
Lab (all serum results confirmed on multiple determinations over several
years):
FreeT4=3.3 ng/dl (ARUP) (.8-1.7 ng/dl)
FreeT4=2.6 ng/dl (Quest) (.8-1.8 ng/dl)
FreeT4 by equilibrium dialysis=3.6 ng/dl (.8-2.7 ng/dl)
TotalT3=268 ng/dl (70-175 ng/dl)
ESR=15
TSH=1.5-2.5 (.3-5.0 UIU/ml)
Thyroid Scan: Mildly enlarged gland; 27% uptake at 24
hours; cold defect.
Ultrasound: 2cm nodule; gland 5.4-5.7 cm. bilat.
FNA: colloid nodule
Bone Density: T score
Spine 2004 = -1.6
2007 = -1.5
Rt. Femur 2004 = -1.2
2007 = -1.7
Lt. Femur 2004 = -1.0
2007 = -1.4
The elevated circulating levels of thyroid hormone with a normal TSH
appears to support a diagnosis resistance to thyroid hormone. The bone
density studies suggest the possibility of accelerated bone loss and the
question of whether there could be an organ specific variability in this
resistance. Specifically, pituitary resistance and thus the normal TSH, but
intact peripheral action and the consequent symptoms and accelerated bone
loss.
Is this a plausible interpretation of this information? Is there any
other study that would confirm or refute the impression of thyroid hormone
resistance? Is there any role for anti-thyroid therapy in his care?
Tim Howland , thowland@lourdes.com
RESPONSE- Indeed you are correct that the elevated TH levels and
non-suppressed TSH are consistent with Resistance to Thyroid Hormone.
Differential Diagnoses of TSH mediated hyperthyroxinemia include
RTH
TSH secreting pituitary tumor
antibodies interfering with measurement of the thyroid hormone levels or
TSH.
Transient elevations in the TH levels are also seen following certain viral
syndromes.
Is there any family history of thyroid abnormalities?
Additional testing to confirm the diagnosis would be:
-Measurement of the alpha subunit (elevated alpha SU:TSH ratios are seen in
the TSHomas)
-Measurement of antithyroid antibodies, if negative would make interfering
substances less likely
-Determination of thyroid hormone function in parents, children, siblings
(where possible). If there are other affected individuals it makes the
diagnosis of RTH more likely
-Obtain an MRI of the pituitary
-Measure SHBG in serum (if elevated it would be consistent with a TSHoma)
-Send blood for DNA analysis of Thyroid Hormone Receptor beta mutation to
Quest Diagnostics
Additional Comments:
The presence of decreased BMD is commonly seen in generalized RTH (GRTH).
The reason being that the primary thyroid hormone receptor in bone is the
TR alpha. Since it is the TR beta gene which is abnormal in most patients
with GRTH, the TR alpha gene is normal and responds to the high thyroid
hormone levels dictated by the pituitary. Hence the bone loss.
The colloid nodule is likely incidental, as there is no evidence of increase
thyroid nodules or thyroid cancer in RTH.
Before recommending a specific treatment, it would be best to have a
definitive diagnosis which explain the thyroid tests. My recommendations
above should help sort this out.
Please let me know the results of the testing and if you have any further
questions, please feel free to contact me directly. Roy E. Weiss,
MD,University of Chicago,
rweiss@medicine.bsd.uchicago.edu
PRIOR RADIATION TO BONE AND USE OF TERIPARATIDE
20 Jan 08
Is the amount of irradiation received by the underlying rib cage in a
woman who receives radiation to the breast/axilla after a lumpectomy for
breast carcinoma enough to make the use of teriparatide
contraindicated.? Edward Biederman, MD,FACE
RESPONSE-Yes,
any amount of radiation would be considered a contraindication. Pam
Taxel, MD
HURTHLE
CELLS IN AN FNA OF A HASHIMOTO’S GLAND
20 Jan 08
QUESTION-A patient of mine with euthyroid Hashimoto's thyroiditis was noted to
have a single nodule on sonogram; FNAB showed follicular cells with Hurthle
cell change and colloid, consistent with Hurthle cell metaplasia within a
nodular goiter. As a pediatric endocrinologist, I am not particularly
experienced with analyzing these results. Is this just Hashimoto's or something
else that I should be concerned about? Ian Marshall, MD,
marshaia@umdnj.edu
RESPONSE- I hesitate to be too specific, since I am not a pathologist, and have
not seen the slides. But--- nodular areas with Hurthle cells, normal follicular
cells, colloid and lymphocytes are common in Hashimoto's thyroiditis, and may
present as nodules on exam and by US. I believe an FNA with only Hurthle cells
from a lesion that is a very distinct single nodule on US, would be suggestive
of a growth. But one with all of the other components, including lymphocytes,
especially if there are other slightly nodular areas in the gland, would be
typical of Hashimoto's, and not alarming. Leslie J De Groot, MD
TREATMENT OF 2.3 CM UNIFOCAL FOLLICULAR VARIANT OF PAPILLARY CANCER 1/5/08
QUESTION-I would like to ask you about encapsulated follicular variant of papillary thyroid cancer. I have a young female 28 yo recently diagnosed with a 2.3 cm nodule left lobe with the above pathology confirmed by Dr. LiVolsi. She will have completion thyroidectomy and my question is how aggressive one should be with this form of PTC ; since some reports from Dr. Tuttle mention that this may be a different and less aggressive cancer. Do you recommend radio iodine therapy if she has cancer confined to one lobe and no lymph nodes? Thank you very much for your time. Mandana Ahmadian, MD
RESPONSE- Certainly the patient's youth and the histology suggest a high probability of cure by surgery alone. However, 131-I ablation is neither difficult nor arduous for the patient, and has several advantages. It may slightly improve her chance of recurrence free survival, and it definitely makes the results of isotope scanning and TG assay more easily interpreted during follow-up. So I would be for it. L De Groot, MD
POSSIBLE
THYROID HORMONE RESISTANCE
1 Jan 2008
QUESTION-Your thoughts regarding this generally healthy 65 yo man would be
most appreciated. He presented with non-specific but suspicious symptoms:
hyperkinetic, emotional irritability, weight loss despite intentional high
calorie intake (nickname of "Joe Donuts" by his family).
Exam:
Equivocal tremor, normal reflexes, no lid lad. Thyroid exam enlarged,
consistent with the ultrasound.
Lab (all serum results confirmed on multiple determinations over several
years):
FreeT4=3.3 ng/dl (ARUP) (.8-1.7 ng/dl)
FreeT4=2.6 ng/dl (Quest) (.8-1.8 ng/dl)
FreeT4 by equilibrium dialysis=3.6 ng/dl (.8-2.7 ng/dl)
TotalT3=268 ng/dl (70-175 ng/dl)
ESR=15
TSH=1.5-2.5 (.3-5.0 UIU/ml)
Thyroid Scan: Mildly enlarged gland; 27% uptake at 24
hours; cold defect.
Ultrasound: 2cm nodule; gland 5.4-5.7 cm. bilat.
FNA: colloid nodule
Bone Density: T score
Spine 2004 = -1.6
2007 = -1.5
Rt. Femur 2004 = -1.2
2007 = -1.7
Lt. Femur 2004 = -1.0
2007 = -1.4
The elevated circulating levels of thyroid hormone with a normal TSH
appears to support a diagnosis resistance to thyroid hormone. The bone
density studies suggest the possibility of accelerated bone loss and the
question of whether there could be an organ specific variability in this
resistance. Specifically, pituitary resistance and thus the normal TSH, but
intact peripheral action and the consequent symptoms and accelerated bone
loss.
Is this a plausible interpretation of this information? Is there any
other study that would confirm or refute the impression of thyroid hormone
resistance? Is there any role for anti-thyroid therapy in his care?
Tim Howland , thowland@lourdes.com
RESPONSE- Indeed you are correct that the elevated TH levels and
non-suppressed TSH are consistent with Resistance to Thyroid Hormone.
Differential Diagnoses of TSH mediated hyperthyroxinemia include
RTH
TSH secreting pituitary tumor
antibodies interfering with measurement of the thyroid hormone levels or
TSH.
Transient elevations in the TH levels are also seen following certain viral
syndromes.
Is there any family history of thyroid abnormalities?
Additional testing to confirm the diagnosis would be:
-Measurement of the alpha subunit (elevated alpha SU:TSH ratios are seen in
the TSHomas)
-Measurement of antithyroid antibodies, if negative would make interfering
substances less likely
-Determination of thyroid hormone function in parents, children, siblings
(where possible). If there are other affected individuals it makes the
diagnosis of RTH more likely
-Obtain an MRI of the pituitary
-Measure SHBG in serum (if elevated it would be consistent with a TSHoma)
-Send blood for DNA analysis of Thyroid Hormone Receptor beta mutation to
Quest Diagnostics
Additional Comments:
The presence of decreased BMD is commonly seen in generalized RTH (GRTH).
The reason being that the primary thyroid hormone receptor in bone is the
TR alpha. Since it is the TR beta gene which is abnormal in most patients
with GRTH, the TR alpha gene is normal and responds to the high thyroid
hormone levels dictated by the pituitary. Hence the bone loss.
The colloid nodule is likely incidental, as there is no evidence of increase
thyroid nodules or thyroid cancer in RTH.
Before recommending a specific treatment, it would be best to have a
definitive diagnosis which explain the thyroid tests. My recommendations
above should help sort this out.
Please let me know the results of the testing and if you have any further
questions, please feel free to contact me directly. Roy E. Weiss,
MD,University of Chicago,
rweiss@medicine.bsd.uchicago.edu