Re: Breast Cancer was Re: Elaine: Question

[Guest guest]

Hi Simon,

>>>Dr Derry, the suspended Canadian doctor, wrote extensively on

this topic (Google " Derry Breast Cancer Hypothyroidism " ). Whilst

Dr Derry's views are controversial, it should be noted that some

recent studies have tended to support him. If you want to obsess

I suggest you find citations of the studies given above, rather

than read Dr Derry's work, your doctors will prefer references

to peer reviewed journal over the writings of a suspended

thyroid doc's.<<<

Thanks for this! I happen to respect the way Dr. Derry thinks. His logic

regarding the use of TSH or overuse, is pure commonsense. I do appreciate

this link.

Jody

_________________________________________________________________

Chat with friends online, try MSN Messenger: http://messenger.msn.com

[Guest guest]

Ok, so there is a possible link. The thing is, how to avoid it? The best

prevention that I can come up with is whole organic foods, staying away from

pesticides, additives, stress etc. The same stuff we are doing to try to

beat this thyroid thing. And FLAX SEEDs! Ground flaxseeds on your oatmeal

or yogurt, flaxseed oil in your protein smoothies, salad dressing, pasta,

veggies, etc. The lignans in flaxseeds have been shown to prevent and

reduce the size of cancer tumors, breast cancer being one they specifically

mention.

And of course extra vigilance on those monthly self exams...

[Guest guest]

Oh yes, and avoiding hydrogenated oils like canola, corn and soy oils and

margarine. I keep forgetting those, thinking everyone knows about that

already...

http://www.westonaprice.org/know_your_fats/know_your_fats.html

[Guest guest]

Simon,

Could you cite where you heard about RAI

increasing small bowel cancer? As a celiac

patient this will be important for my thyroid doc

in my case, since celiac disease can be a prelude

to intestinal lymphoma. Wow, I had no idea.

Well, there goes RAI for me, no way I am taking

it.

Kit

--- Simon Waters

wrote:

> " L. Buck " wrote:

> >

> > Ooh - this is scary! I hope this is just a

> coincidence and not a connection

> > between the 2 conditions - yet another thing

> to obsess about!

>

> The jury is still out, but if I was a betting

> man <woman?>, I'd

> insist on adequate replacement hormone

> treatment after RAI or

> surgery.

>

> It comes back to the simple fact it is better

> to be euthyroid,

> everything works better.

>

>

http://www.thyroid-info.com/articles/breast-cancer.htm

>

> Dr Derry, the suspended Canadian doctor, wrote

> extensively on

> this topic (Google " Derry Breast Cancer

> Hypothyroidism " ). Whilst

> Dr Derry's views are controversial, it should

> be noted that some

> recent studies have tended to support him. If

> you want to obsess

> I suggest you find citations of the studies

> given above, rather

> than read Dr Derry's work, your doctors will

> prefer references

> to peer reviewed journal over the writings of a

> suspended

> thyroid doc's.

>

> The study of thyroid disease in breast cancer

> patients found 2

> Grave's disease cases out of 102, compared to a

> control group

> with 1. That particular difference is almost

> certainly not

> significant. This seems to be more associated

> with Hashimoto's

> thyroiditis, and I suspect it is undiagnosed

> hypothyroidism, or

> subclinical hypothyroidism that is responsible

> for the problems

> - which is what Dr Derry's theory suggests.

>

> Of course I can take heart from the fact that

> breast cancer is

> rare in men, but then so is autoimmune thyroid

> disease...

>

> Take care, and don't obsess on these things,

> just get euthyroid

> and stay there.

>

> Simon

>

> PS: As far as I know RAI only increases the

> incidence of thyroid

> cancer, and small bowel cancer, so presumably

> (since RAI being

> the most common cause of hypothyroidism in the

> US according to

> some sources) proper follow up treatment in RAI

> prevents any

> increased risks of breast cancer. Must remember

> to discuss this

> with my cousin who works in the UK bc screening

> programme, and

> is a walking encyclopedic reference on such

> things.

>

__________________________________________________

[Guest guest]

Why was this guy suspended?

--- Jody Spitale wrote:

> Hi Simon,

> >>>Dr Derry, the suspended Canadian doctor,

> wrote extensively on

> this topic (Google " Derry Breast Cancer

> Hypothyroidism " ). Whilst

> Dr Derry's views are controversial, it should

> be noted that some

> recent studies have tended to support him. If

> you want to obsess

> I suggest you find citations of the studies

> given above, rather

> than read Dr Derry's work, your doctors will

> prefer references

> to peer reviewed journal over the writings of a

> suspended

> thyroid doc's.<<<

>

> Thanks for this! I happen to respect the way

> Dr. Derry thinks. His logic

> regarding the use of TSH or overuse, is pure

> commonsense. I do appreciate

> this link.

> Jody

>

>

>

>

_________________________________________________________________

> Chat with friends online, try MSN Messenger:

> http://messenger.msn.com

>

>

__________________________________________________

[Guest guest]

Kit Kellison wrote:

>

> Why was this guy suspended?

A patient of another endo left him for Dr Derry, got better and

complained about the original endo.

The original endo complained about Dr Derry's unorthodox

treatment regime, and it was Dr Derry who ended up suspended.

So it seems Dr Derry got suspended for helping a patient.

It would be amusing if it wasn't the reputation and livelihood

of a person at stake.

The whole saga is ongoing, and I don't know enough to comment on

the right or wrongs.

Although the failure of the College of Physicians and Surgeons

of British Colombia to carry out it's investigations to the

timetable they promised to the court, doesn't reflect well on

them as an organisation.

http://www.bites-medical.org/dderry/history.html

[Guest guest]

Simon,

Thanks so much for the link on Derry!

Jody

_________________________________________________________________

Join the world’s largest e-mail service with MSN Hotmail.

http://www.hotmail.com

[Guest guest]

I thought this might be a good time to post this again. I work with a

breast cancer dragon boat team. There are a number of women with hypo

and Hashis and only one that seemed to have had Graves, makes me

conclude that hypo thyroidism is indeed a risk factor associated with

breast cancer. Although there is little literature or documentation to

that fact. I am also specutalating that along with bone marrow and the

thymus the thyroid must be involved with the immune system.

Endocrine and non endocrine diseases associated with thyroid

disorders.

Claudio Giani*, nna Bonacci, Paola Fierabracci

Istitute of Endocrinology, University of Pisa, Italy

*Visiting professor of town University

ABSTRACT

We have examined 102 BC patients previously submitted to

modified radical mastectomy for

infiltrating ductal carcinoma of the breast and 100

age-matched control healty women living in the

same lodine border-line sufficient geographic area. There

is an higher prevalence of thyroid disease in

breast cancer and clearly have shown that Hashimoto's

thyroiditis account to a large extent for this

finding. Our results indicate the usefulness of screening

for thyroid disease and patients with breast

cancer.

(Electr J Surg 1996; 1:5-7)

Key words: Thyroid, Breast Cancer, Hashimoto

The problem of the relationship between thyroid disease and other

endocrine or non endocrine disorders is a field of several

clinical and experimental studies.

The association between Hashimoto's thyroiditis, Graves' disease and

other several autoimmune disorders has been reported

by various authors (1-4). The most important autoimmune endocrine

disorders which coexist with Graves' and Hashimoto's

disease include type 1 (insulin dependent) diabetes mellitus, autoimmune

adrenalitis ('s disease), autoimmune

oophoritis and, most rarely, autoimmune hypoparathyroidism and

hypophysitis . In addition,a relation between autoimmune

thyroid disease and various non endocrine autoimmune disorders has been

described, including pernicious anemia, vitiligo,

myasthenia gravis , Sjogren'ssyndrome, cronic active hepatitis,

thrombocytopenic purpura and alopecia.(5) In the context of

autoimmune disorders involving thiroid gland and other endocrine system,

several observations provided for a significant

association with histocompatibility antigen HLA-DR3 (6)

Extensive clinical observations have resulted in the identification of

endocrine neoplastic syndromes involving multiple

endocrine glands, including thiroid gland. Generally, the cell types

involved in these tumors are considered to have a

common embryologic precursor in the neuroectoderm: these cells may have

a well characterized metabolic pathway for amine

precursor uptake and decarboxilation (APUD cells) (7,8). In particular,

the medullary thyroid carcinoma arises in cell (C

Cells) given origin from embryonicneuronal crest. (7).

Medullary carcinoma of the thyroid gland occurs in one of four distinct

setting: 1) as sporadic form. 2) as part of multiple

endocrine neoplasia (MEN 2A) 3)as part of MEN 2B 4) as familial

medullary thyroid carcinoma (9-11). In MEN 2A, MEN

2B,and familial type of the medullary thyroid carcinoma the distribution

of malignancy is bilateral and sporadic form

unilateral (11); the familial pattern has been found in all but one

(sporadic form) type (10). In MEN 2A the abnormalities

associated with medullary thyroid carcinoma include pheochromocytomas

and hyperparathyroidism and in MEN 2B

pheochromocytomas, mucosal neuromas, ganglioneuromas and characteristic

phenotype associated with a typical neural

hyperthrophy.

The biologic virulence of medullary thyroid cancer changes in the

different four types, being more aggressive in MEN 2B

and progressively less in sporadic form, MEN 2A and familial type.

Genetic linkage studies have mapped the genes for

MEN 2A, MEN 2B and familial form in the pericentric region of chromosome

10 (12,13), where RET had also been mapped

and this protooncogene is therefore an obvious candidate gene for each

of these familial cancer syndromes (14). RET is a

member of the receptor tyrosine kinase gene family involved in the

control of cell proliferation: a germline inherited

mutations in the RET protoncogene was found to be associated with MEN 2A

and FMTC (15) and unique different germline

mutation with MEN 2B. No germline mutation of RET or other

protooncogenes has been detected in sporadic type of

medullary thyroid cancer (16). We can conclude for a prevalent role of

genetic factors in the development of the poliglandular

autoimmune syndrome involving thyroid gland, of the two types of

multiple endocrine neoplasia and of familial form of

medullary thyroid carcinoma.

So far, beyond the genetic form described above, no evidence has been

provided for the significant association between

thyroid disorders and non endocrine tumors arising from different

organs. It is known that mammary gland epitelium chares

with the thyroid epithelial cells the property of concentraing the

iodine by a membrane active transport mechanism. A

possibile role of iodine deficiency in the development of breast disease

has been suggested by epidemiologic studies

performed in endemic area showing an increased prevalence of fibrocystic

disease (17). So far, no data are available of the

incidence of breast cancer and thyroid disease is debated. To carify

this point we have carried out a prospective study on the

incidence of thyroid disease in a group of patients submitted to

surgical treatment for breast cancer (BC). Our results indicate

a higher overall incidence of thyroid disorders in BC patients and in

particular a high frequency of autoimmune thyroid

disorders.

Materials and methods

We have examined 102 BC patients previously submitted to modified

radical mastectomy for infiltrating ductal carcinoma of

the breast and 100 age-matched control healty women living in the same

lodine border-line sufficient geographic area.

All subjects were submitted to sonographic evaluation of thyroid gland

and serum FT3,FT4,THS, antithyroglobuling

antibiodies (TgAb) and thyroperoxidase autoantibodies (TPOAb)

measurement.

Results

The overall incidence of thyroid disease was 47/102 (46%) in BC patients

and 14% in controls (p<0.0001). Non toxic goiter

was found in 27.4%BC patients and in 11% of control group (p= " 0.003) "

and Hashimoto's thyroidtis was shown in 13.7%

of breast cancer and only in 2% of the controls. In addition in BC group

we have found 2 Graves' disease 1 subacute

thyroiditis and 2 thyroid carcinoma: in control group only 1 Graves'

disease. Serum TPOAb was significantly more

represented in BC patients (23.5%) than in control (8%) (p<0.05), while

the incidence of TgAb was similar.

Discussion

This is the first prospective study on the incidence of thyroid

disorders in breast cancer. Our results indicate a higher

prevalence of non toxic goiter in breast cancer. Our BC patients and

controls were living in the same border-line iodine

sufficient area: thus, the iodine deficiency was not able to explain

this difference. We can suppose that a common, albeit

unknown, factor may responsible for both the increased susceptibility to

goiter and mammary gland disorders. In addition,

we have demonstrated a very high frequency of thyroid autoimmune

phenomena in BC patients. Particularly, our results

indicate a higher incidence of Hashimoto's thiroiditis and an increased

prevalence of TPOAb. Interestingly, in BC the

antithyroid antibodies (TAb) were widely distributed in the group of

patients with Hashimoto's tyroiditis, in contrast in

control subjects the higher incidence of TAb was detected in the absence

of detectable thyroid disorders. This original

observation suggests a prevalence of cytotoxic antibodies in breast

malignancy.

In conclusion, our results have found an higher prevalence of thyroid

disease in breast cancer and clearly have shown that

Hashimoto's thyroiditis account to a large extent for this finding. Our

results indicate the usefulness of screening for thyroid

disease and patients with breast cancer.

Correspondence to:

Claudio Giani, MD

Institute of Endocrinology

University of Pisa

Viale del Tirreno, 64

56018 Tirrenia

Pisa, Italy

References

1.Bloodworth JM, Kirkendall WM, Curr TL. 's disease

associated with thyroid insufficiency and atrophy

(Schimdt's syndrome). J Clin Endocrinol 1951; 14: 540.

2.Bottazzo GF, Doniach D. Poliendocrine Autoimmunity and

endocrine disease. Volpè R., Ed, Marcell Dekker, New

York, 1985, 375.

3.Bottazzo GF, Mirakjan R, De Lazzari F et al. Autoimmune

endocrine organ specific disorders: clinical diagnostic

relevance and novel approaches to patogenesis. In:Hormones

and Immunity Berczi I and Kovacs K (Eds.), MTP

Press, Norvell, MA, 1987, 296.

4.Doniach D, Bottazzo GF. Polyendocrine autoimmunity.

In:Clinical Immunology Update 1981, lin ED. (Ed),

Elseiver North-Holland, New York, 1981, 96.

5.Volpè R. Autoimmune thyroid disease In:Autoimmunity and

endocrine disease, Volpè R (Ed), Marcell Dekker, New

York, 1985, 109.

6.Betterle C, Presotto F, Caretto A, et al. Studies of Class 1

and Class II antigen expression and lymphocitic infiltrate

to thyroid tumors. In: Thyroid Autoimmunity, Pinchera A,

Ingbar SH, McKenzie JM, and Fenzi GF (eds),Plenum

Press, New York, 1987, 567.

7.The neurocrestopaties. A unifying concept of disease arising

from neural crest maldevelopment. Hum. Pathl. 1974;

5:409.

8.Pearse HGE. The APUD concept and hormone production. Clin

Endocrinol Metab 1980; 9: 211.

9.Hazard JB, Havk WA, Ceile G Jr. Medullary (solid) carcinoma of

the thyroid: a clinicalpathologic entity. Clin

Endocrinol Metab. 1959; 19:152.

10.Block MA, CE, Greenavald KA et al. Clinical

characteristics distinguishing hereditary from sporadic

medullary thyroid carcinoma: treatment implications. Arch

Surg 1980; 115:142.

11.Wells SA. New approaches to the patients with medullary

carcinoma of the thiroid gland. Thyroid Today 1994;

1:17.

12.Simpson NE, Kidd KK, Goodfellow PJ et al. Assignement of

multiple endocrine neoplasia type 2A to chromosoma

10 by linkage. Nature 1988; 328:528.

13.Lairmore TC, Howe JR, Kort e JA et al. Familial medullary

thyroid carcinoma and multiple endocrine neoplasia

type 2B map to the same region of chromosome 10 as

multiple andocrine neoplasia type 2A. Genomics 1981; 9:181.

14.Lairmore TC, Dou S, Howe JR et al. A 1.5 megabase yeast

artificial chromosome 10q11.2 connecting three genetic

loci (RET, D10s94 and D10S02) closely linked to the MEN 2A

locus. Proc Natl Acad ScI USA 1993; 90:492.

15.Donis-Keler H, Dou S, Chi Det al. Mutations in the RET

protooncogene are associated with MEN 2A and FMTC.

Human Molec Genet 1993; 2:851.

16.Carlsol KM, Dou S, Chi D et al.:Single missense mutation in the

thirosine catalytic domin of the RRET

protooncogene is associated with multiple endocrine

neoplasia type 2B. Proc Natl Acad Scl USA 1994; 91:1579.

17.Ghent WR, Eskin BA. Iodine deficiency breast syndrome. In:

Medeiros Neto, Gaitan R. (Eds), Frontiers in

Thyroidology. New York: Raven Press, 1986, 1021.

Endocrine and non

endocrine diseases associated with thyroid disorders.

Claudio Giani, nna Bonacci, Paola Fierabracci

EJS No. 1 - Contents

[Guest guest]

Hi Simon, breast cancer is no becoming not so rare in men. We now have

two men young men 35, on the team and men now make up 1% of all breast

cancers.

[Guest guest]

Thanks, ,

I remember that study causing great controversy on one of the other boards. I

hope these researchers are continuing to study this relationship because it

certainly seems that there is a link. Take care, Elaine

[Guest guest]

We're seeing more breast cancer in men where I work too. One of my

co-worker's husband's was also recently diagnosed with it and has just

started chemo.

[Guest guest]

Just to confirm this:

When I was first diagnosed, I saw a naturopath who said that WITHOUT

questions, in the view of naturopathy, there was a connection between

hypothyroidism and breast cancer: both the thyroid and breast are part of

the endocrine system and there appeared (at least in this discipline's

paradigm) to be a link between remaining hypo and becoming more likely to

develop breast cancer. As said, this doctor felt that hyperthyroidism

did not put one at risk, but hypothyroidism (whether due to over or under

medication or hashis) over a chunk of time, did.

B

Re: Breast Cancer was Re: Elaine: Question

> I thought this might be a good time to post this again. I work with a

> breast cancer dragon boat team. There are a number of women with hypo

> and Hashis and only one that seemed to have had Graves, makes me

> conclude that hypo thyroidism is indeed a risk factor associated with

> breast cancer. Although there is little literature or documentation to

> that fact. I am also specutalating that along with bone marrow and the

> thymus the thyroid must be involved with the immune system.

>

> Endocrine and non endocrine diseases associated with thyroid

> disorders.

>

> Claudio Giani*, nna Bonacci, Paola Fierabracci

>

> Istitute of Endocrinology, University of Pisa, Italy

>

> *Visiting professor of town University

>

> ABSTRACT

>

> We have examined 102 BC patients previously submitted to

> modified radical mastectomy for

> infiltrating ductal carcinoma of the breast and 100

> age-matched control healty women living in the

> same lodine border-line sufficient geographic area. There

> is an higher prevalence of thyroid disease in

> breast cancer and clearly have shown that Hashimoto's

> thyroiditis account to a large extent for this

> finding. Our results indicate the usefulness of screening

> for thyroid disease and patients with breast

> cancer.

> (Electr J Surg 1996; 1:5-7)

>

>

> Key words: Thyroid, Breast Cancer, Hashimoto

>

>

> The problem of the relationship between thyroid disease and other

> endocrine or non endocrine disorders is a field of several

> clinical and experimental studies.

> The association between Hashimoto's thyroiditis, Graves' disease and

> other several autoimmune disorders has been reported

> by various authors (1-4). The most important autoimmune endocrine

> disorders which coexist with Graves' and Hashimoto's

> disease include type 1 (insulin dependent) diabetes mellitus, autoimmune

> adrenalitis ('s disease), autoimmune

> oophoritis and, most rarely, autoimmune hypoparathyroidism and

> hypophysitis . In addition,a relation between autoimmune

> thyroid disease and various non endocrine autoimmune disorders has been

> described, including pernicious anemia, vitiligo,

> myasthenia gravis , Sjogren'ssyndrome, cronic active hepatitis,

> thrombocytopenic purpura and alopecia.(5) In the context of

> autoimmune disorders involving thiroid gland and other endocrine system,

> several observations provided for a significant

> association with histocompatibility antigen HLA-DR3 (6)

> Extensive clinical observations have resulted in the identification of

> endocrine neoplastic syndromes involving multiple

> endocrine glands, including thiroid gland. Generally, the cell types

> involved in these tumors are considered to have a

> common embryologic precursor in the neuroectoderm: these cells may have

> a well characterized metabolic pathway for amine

> precursor uptake and decarboxilation (APUD cells) (7,8). In particular,

> the medullary thyroid carcinoma arises in cell (C

> Cells) given origin from embryonicneuronal crest. (7).

> Medullary carcinoma of the thyroid gland occurs in one of four distinct

> setting: 1) as sporadic form. 2) as part of multiple

> endocrine neoplasia (MEN 2A) 3)as part of MEN 2B 4) as familial

> medullary thyroid carcinoma (9-11). In MEN 2A, MEN

> 2B,and familial type of the medullary thyroid carcinoma the distribution

> of malignancy is bilateral and sporadic form

> unilateral (11); the familial pattern has been found in all but one

> (sporadic form) type (10). In MEN 2A the abnormalities

> associated with medullary thyroid carcinoma include pheochromocytomas

> and hyperparathyroidism and in MEN 2B

> pheochromocytomas, mucosal neuromas, ganglioneuromas and characteristic

> phenotype associated with a typical neural

> hyperthrophy.

> The biologic virulence of medullary thyroid cancer changes in the

> different four types, being more aggressive in MEN 2B

> and progressively less in sporadic form, MEN 2A and familial type.

> Genetic linkage studies have mapped the genes for

> MEN 2A, MEN 2B and familial form in the pericentric region of chromosome

> 10 (12,13), where RET had also been mapped

> and this protooncogene is therefore an obvious candidate gene for each

> of these familial cancer syndromes (14). RET is a

> member of the receptor tyrosine kinase gene family involved in the

> control of cell proliferation: a germline inherited

> mutations in the RET protoncogene was found to be associated with MEN 2A

> and FMTC (15) and unique different germline

> mutation with MEN 2B. No germline mutation of RET or other

> protooncogenes has been detected in sporadic type of

> medullary thyroid cancer (16). We can conclude for a prevalent role of

> genetic factors in the development of the poliglandular

> autoimmune syndrome involving thyroid gland, of the two types of

> multiple endocrine neoplasia and of familial form of

> medullary thyroid carcinoma.

> So far, beyond the genetic form described above, no evidence has been

> provided for the significant association between

> thyroid disorders and non endocrine tumors arising from different

> organs. It is known that mammary gland epitelium chares

> with the thyroid epithelial cells the property of concentraing the

> iodine by a membrane active transport mechanism. A

> possibile role of iodine deficiency in the development of breast disease

> has been suggested by epidemiologic studies

> performed in endemic area showing an increased prevalence of fibrocystic

> disease (17). So far, no data are available of the

> incidence of breast cancer and thyroid disease is debated. To carify

> this point we have carried out a prospective study on the

> incidence of thyroid disease in a group of patients submitted to

> surgical treatment for breast cancer (BC). Our results indicate

> a higher overall incidence of thyroid disorders in BC patients and in

> particular a high frequency of autoimmune thyroid

> disorders.

>

> Materials and methods

>

> We have examined 102 BC patients previously submitted to modified

> radical mastectomy for infiltrating ductal carcinoma of

> the breast and 100 age-matched control healty women living in the same

> lodine border-line sufficient geographic area.

> All subjects were submitted to sonographic evaluation of thyroid gland

> and serum FT3,FT4,THS, antithyroglobuling

> antibiodies (TgAb) and thyroperoxidase autoantibodies (TPOAb)

> measurement.

>

> Results

>

> The overall incidence of thyroid disease was 47/102 (46%) in BC patients

> and 14% in controls (p<0.0001). Non toxic goiter

> was found in 27.4%BC patients and in 11% of control group (p= " 0.003) "

> and Hashimoto's thyroidtis was shown in 13.7%

> of breast cancer and only in 2% of the controls. In addition in BC group

> we have found 2 Graves' disease 1 subacute

> thyroiditis and 2 thyroid carcinoma: in control group only 1 Graves'

> disease. Serum TPOAb was significantly more

> represented in BC patients (23.5%) than in control (8%) (p<0.05), while

> the incidence of TgAb was similar.

>

> Discussion

>

> This is the first prospective study on the incidence of thyroid

> disorders in breast cancer. Our results indicate a higher

> prevalence of non toxic goiter in breast cancer. Our BC patients and

> controls were living in the same border-line iodine

> sufficient area: thus, the iodine deficiency was not able to explain

> this difference. We can suppose that a common, albeit

> unknown, factor may responsible for both the increased susceptibility to

> goiter and mammary gland disorders. In addition,

> we have demonstrated a very high frequency of thyroid autoimmune

> phenomena in BC patients. Particularly, our results

> indicate a higher incidence of Hashimoto's thiroiditis and an increased

> prevalence of TPOAb. Interestingly, in BC the

> antithyroid antibodies (TAb) were widely distributed in the group of

> patients with Hashimoto's tyroiditis, in contrast in

> control subjects the higher incidence of TAb was detected in the absence

> of detectable thyroid disorders. This original

> observation suggests a prevalence of cytotoxic antibodies in breast

> malignancy.

> In conclusion, our results have found an higher prevalence of thyroid

> disease in breast cancer and clearly have shown that

> Hashimoto's thyroiditis account to a large extent for this finding. Our

> results indicate the usefulness of screening for thyroid

> disease and patients with breast cancer.

>

> Correspondence to:

> Claudio Giani, MD

> Institute of Endocrinology

> University of Pisa

> Viale del Tirreno, 64

> 56018 Tirrenia

> Pisa, Italy

>

> References

>

> 1.Bloodworth JM, Kirkendall WM, Curr TL. 's disease

> associated with thyroid insufficiency and atrophy

> (Schimdt's syndrome). J Clin Endocrinol 1951; 14: 540.

> 2.Bottazzo GF, Doniach D. Poliendocrine Autoimmunity and

> endocrine disease. Volpè R., Ed, Marcell Dekker, New

> York, 1985, 375.

> 3.Bottazzo GF, Mirakjan R, De Lazzari F et al. Autoimmune

> endocrine organ specific disorders: clinical diagnostic

> relevance and novel approaches to patogenesis. In:Hormones

> and Immunity Berczi I and Kovacs K (Eds.), MTP

> Press, Norvell, MA, 1987, 296.

> 4.Doniach D, Bottazzo GF. Polyendocrine autoimmunity.

> In:Clinical Immunology Update 1981, lin ED. (Ed),

> Elseiver North-Holland, New York, 1981, 96.

> 5.Volpè R. Autoimmune thyroid disease In:Autoimmunity and

> endocrine disease, Volpè R (Ed), Marcell Dekker, New

> York, 1985, 109.

> 6.Betterle C, Presotto F, Caretto A, et al. Studies of Class 1

> and Class II antigen expression and lymphocitic infiltrate

> to thyroid tumors. In: Thyroid Autoimmunity, Pinchera A,

> Ingbar SH, McKenzie JM, and Fenzi GF (eds),Plenum

> Press, New York, 1987, 567.

> 7.The neurocrestopaties. A unifying concept of disease arising

> from neural crest maldevelopment. Hum. Pathl. 1974;

> 5:409.

> 8.Pearse HGE. The APUD concept and hormone production. Clin

> Endocrinol Metab 1980; 9: 211.

> 9.Hazard JB, Havk WA, Ceile G Jr. Medullary (solid) carcinoma of

> the thyroid: a clinicalpathologic entity. Clin

> Endocrinol Metab. 1959; 19:152.

> 10.Block MA, CE, Greenavald KA et al. Clinical

> characteristics distinguishing hereditary from sporadic

> medullary thyroid carcinoma: treatment implications. Arch

> Surg 1980; 115:142.

> 11.Wells SA. New approaches to the patients with medullary

> carcinoma of the thiroid gland. Thyroid Today 1994;

> 1:17.

> 12.Simpson NE, Kidd KK, Goodfellow PJ et al. Assignement of

> multiple endocrine neoplasia type 2A to chromosoma

> 10 by linkage. Nature 1988; 328:528.

> 13.Lairmore TC, Howe JR, Kort e JA et al. Familial medullary

> thyroid carcinoma and multiple endocrine neoplasia

> type 2B map to the same region of chromosome 10 as

> multiple andocrine neoplasia type 2A. Genomics 1981; 9:181.

> 14.Lairmore TC, Dou S, Howe JR et al. A 1.5 megabase yeast

> artificial chromosome 10q11.2 connecting three genetic

> loci (RET, D10s94 and D10S02) closely linked to the MEN 2A

> locus. Proc Natl Acad ScI USA 1993; 90:492.

> 15.Donis-Keler H, Dou S, Chi Det al. Mutations in the RET

> protooncogene are associated with MEN 2A and FMTC.

> Human Molec Genet 1993; 2:851.

> 16.Carlsol KM, Dou S, Chi D et al.:Single missense mutation in the

> thirosine catalytic domin of the RRET

> protooncogene is associated with multiple endocrine

> neoplasia type 2B. Proc Natl Acad Scl USA 1994; 91:1579.

> 17.Ghent WR, Eskin BA. Iodine deficiency breast syndrome. In:

> Medeiros Neto, Gaitan R. (Eds), Frontiers in

> Thyroidology. New York: Raven Press, 1986, 1021.

>

>

>

> Endocrine and non

> endocrine diseases associated with thyroid disorders.

>

> Claudio Giani, nna Bonacci, Paola Fierabracci

>

> EJS No. 1 - Contents

>

>

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