Important information for gynecomastia

[hypo]

Infomation that some may wish to read.

I am adding this to the important info for gynecomastia thread as well.

Evidence that highlights the need for endocrine testing in gynecomastia sufferers.


http://www.leeds.ac.uk/acb/annals/annals_pdf/Nov01/596.pdf

http://www.ccjm.org/PDFFILES/Bembo604.pdf  

The above link kindly provided by Graham Ashe

Studies

20 out of 53 patients had underlying causes of gynecomastia

Unique Identifier
12270030
Record Owner
NLM
Authors
Ersoz H. Onde ME. Terekeci H. Kurtoglu S. Tor H.
Institution
Karadeniz Technical University, Faculty of Medicine, Department of Endocrinology and Metabolism, Trabzon, Turkey. hersoz@yahoo.com
Title
Causes of gynaecomastia in young adult males and factors associated with idiopathic gynaecomastia.
Source
International Journal of Andrology. 25(5):312-6, 2002 Oct.
Abbreviated Source
Int J Androl. 25(5):312-6, 2002 Oct.
Publication Notes
The publication year is for the print issue of this journal.
NLM Journal Code
gqk, 8000141
Journal Subset
IM
Country of Publication
England
MeSH Subject Headings
Adult
Anthropometry
Case-Control Studies
Comparative Study
Dehydroepiandrosterone Sulfate / bl [Blood]
Estradiol / bl [Blood]
Follicle Stimulating Hormone / bl [Blood]
*Gynecomastia / et [Etiology]
Human
Luteinizing Hormone / bl [Blood]
Male
Prolactin / bl [Blood]
Testosterone / bl [Blood]
Abstract
Gynaecomastia is a common clinical condition. Persistent pubertal or late onset idiopathic gynaecomastia is the leading cause of gynaecomastia in different series. The aim of this study was the assessment of the prevalence and characteristics of different causes of gynaecomastia in young adult males, and evaluation of the factors associated with idiopathic gynaecomastia. Fifty-three male patients (mean age 22.04 +/- 2.22, range 19-29), who had been admitted to our outpatient clinics with gynaecomastia as the main presenting symptom were enrolled in the study. Patients were evaluated with breast palpation, breast ultrasonography, anthropometric measurements and sex steroid levels. Secondary causes of gynaecomastia were ruled out. Thirty age-matched healthy individuals were also studied as healthy control group. Idiopathic gynaecomastia was diagnosed in 31 of 53 patients (58%), with 17 (32%) persistent pubertal and 14 (24%) late onset course. Other causes of gynaecomastia were hypogonadism in 13 cases (25%), hyperprolactinaemia in five (9%), chronic liver disease in two (4%), and drug induced (prolonged use of H2 antagonists) in two (4%). Patients with idiopathic gynaecomastia, either pubertal or late onset, were compared with the healthy control group in order to find out associated factors. Anthropometric measurements revealed a significant increase in body weight and body mass index (BMI) in the patient group compared with healthy controls (72.4 +/- 13.3 vs. 63.6 +/- 7.9 kg, p = 0.0086 and 25.2 +/- 4.0 vs. 21.5 +/- 2.7 kg/m2, p = 0.0001). Total skin fold thickness (SFT) of four different regions were also higher in the patient group (50.9 +/- 22.1 vs. 32.6 +/- 10.2 mm, p = 0.0006) indicating a higher body fat percentage. Total serum testosterone (4.76 +/- 1.31 vs. 5.70 +/- 1.06 microg/mL, p = 0.0038) and luteinizing hormone (LH) (4.80 +/- 1.92 vs. 7.32 +/- 1.90 mIU/mL, p < 0.0001) levels were significantly lower in the patient group while oestradiol levels were similar. There was a significant correlation between total testosterone and LH levels (r = 0.27, p = 0.0445). Total testosterone and LH levels were negatively correlated with BMI and total SFT. As a result most common form of gynaecomastia is idiopathic gynaecomastia either as persistent pubertal or late onset forms in young adult males. Idiopathic gynaecomastia is closely correlated with generalized obesity, reduced LH and testosterone levels which may be the result of increased conversion of testosterone to oestradiol in increased adipose tissue mass.
CAS Registry/EC Number
50-28-2 (Estradiol). 58-22-0 (Testosterone). 651-48-9 (Dehydroepiandrosterone Sulfate). 9002-62-4 (Prolactin). 9002-67-9 (Luteinizing Hormone). 9002-68-0 (Follicle Stimulating Hormone).
ISSN
0105-6263
Publication Type
Journal Article.
Language
English
Entry Date
20030304
Update Date
20031209







25 out of 175 men had underlying conditions


Unique Identifier
12662229
Authors
Daniels IR. Layer GT.
Institution
St Peter's Breast Centre, St Peter's Hospital, Surrey, UK. irdaniels@dorkingrh4.freeserve.co.uk
Title
How should gynaecomastia be managed?.
Source
ANZ Journal of Surgery. 73(4):213-6, 2003 Apr.
Abstract
BACKGROUND: The purpose of the present paper was to review the management of men referred to a breast clinic with presumed gynaecomastia. METHODS: A retrospective analysis was carried out of 175 men over the age of 16 years who presented with breast enlargement and/or 'lumps', during a 7-year period to a single-surgeon. All patients had complete biochemical assessment (liver function tests, gamma-glutamyl transferase, prolactin, alpha-fetoprotein, beta-human chorionic gonadotropin), and mammography and/or ultrasound with fine-needle biopsy if indicated. RESULTS: One hundred and seventy-five men, median age 44 years (range: 18-89 years), were assessed. Thirty-nine had bilateral true gynaecomastia and 88 had unilateral gynaecomastia (53% left). Carcinoma of the breast was diagnosed in eight, pseudo-gynaecomastia in 18, 13 had physiological pubertal changes only and nine had other diagnoses. Adverse drug reactions were possibly implicated in the aetiology of 47 patients, alcohol in seven patients, cannabis in one patient, testicular malignancy in four patients and hepatocellular carcinoma in one patient. Five patients were found to have hyperprolactinaemia. Twenty-four per cent of patients were reassured without intervention; 18% failed to attend follow up. Sixteen per cent were treated with danazol, 15% underwent surgery and 28 were referred for management of their cause. Danazol was effective in 81%, and three patients required surgery when danazol was ineffective. One further patient developed testicular cancer 9 months after presentation. CONCLUSION: Men presenting to a breast clinic require clinical assessment to exclude diagnoses other than gynaecomastia. True gynaecomastia can be managed with exclusion of causative factors by non-invasive investigation and examination. Many patients can be reassured as to the idiopathic nature of the condition and many will fail to attend follow up. Danazol is successful in some patients and surgery should be reserved for resistant cases.





Relevant issues again detailed

Unique Identifier
2659478
Record Owner
NLM
Authors
von Werder K.

Title
[The significance of gynecomastia in general practice]. [Review] [16 refs] [German]
Original Title
Bedeutung der Gynakomastie in der Allgemeinpraxis.
Source
Fortschritte der Medizin. 107(12):271-3, 1989 Apr 20.
Abbreviated Source
Fortschr Med. 107(12):271-3, 1989 Apr 20.
Publication Notes
The publication year is for the print issue of this journal.
NLM Journal Code
f62, 2984763r
Journal Subset
IM
Country of Publication
Germany, East
MeSH Subject Headings
Diagnosis, Differential
English Abstract
Estradiol / bl [Blood]
*Gynecomastia / et [Etiology]
Human
Male
Testosterone / bl [Blood]
Abstract
Gynecomastia in the male is usually due to a change of the estradiol/testosterone ratio in favor of the estrogens. There is usually no need for therapy of the gynecomastia which frequently occurs during puberty and old age. However, it is important not to overlook hormone-secreting tumors, often testicular malignancies, as the underlying cause of gynecomastia. A careful history and clinical investigations including thorough palpation of the testes (sonography) are complemented by a laboratory workup including blood chemistry (liver function) and hormone determinations (estradiol, beta-HCG, FSH, LH, prolactin, testosterone, thyroid hormones). Treatment of gynecomastia includes elimination of the cause of the condition. In cases with fibrous and voluminous gynecomastia breast tissue must be removed surgically. Antiestrogenic treatment with tamoxifen is indicated only in patients with recently developed, tender gynecomastia. [References: 16]
CAS Registry/EC Number
50-28-2 (Estradiol). 58-22-0 (Testosterone).
ISSN
0015-8178
Publication Type
Journal Article. Review. Review, Tutorial.
Language
German
Entry Date
19890725
Revision Date
20001218
Update Date
20031209


7 out of 60 had underlying causes.


Unique Identifier
9637901
Authors
Sher ES. Migeon CJ. Berkovitz GD.
Institution
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Title
Evaluation of boys with marked breast development at puberty. [Review] [24 refs]
Source
Clinical Pediatrics. 37(6):367-71, 1998 Jun.
Abstract
During the 10-year period from 1979 to 1988 we evaluated 60 boys who were more than 9 years old and who had significant breast development (greater than 4 cm in diameter) around the time of puberty. An endocrine abnormality was identified in seven subjects. The pathology included Klinefelter's syndrome; 46,XX maleness; primary testicular failure; partial androgen insensitivity; fibrolamellar hepatocarcinoma; and increased aromatase activity. Eight of the remaining 53 subjects had underlying medical problems, five of them having neurologic disorders. The 45 remaining subjects were considered to have significant idiopathic gynecomastia, a condition sometimes referred to as macromastia. These boys tended to be both taller and heavier than average, the mean Z score for height being 1.4 SDs above the mean and the mean weight score being 2.7 SDs above the mean. This study underscores the observation that pathologic causes of marked pubertal gynecomastia are unusual. However, the potential for significant health problems among boys with marked breast development supports the need for an endocrine evaluation of all affected subjects. Our data also indicate that boys with marked idiopathic breast development have greater body mass than other boys of similar age. This may contribute in part to the greater breast development in these subjects. [References: 24]

Again the need for testing highlighted.

Unique Identifier
12704923
Authors
Pfeilschifter J.

Institution
Berufsgenossenschaftliche Kliniken Bergmannsheil, Universitatsklinik, Medizinische Klinik und Poliklinik, Burkle-de-la-Camp-Platz 1, 44789 Bochum. Johannes.Pfeilschifter@ruhr-uni-bochum.de
Title
[Disordered hormone regulation in gynecomastia]. [German]
Source
Kongressband/Deutsche Gesellschaft fur Chirurgie. 119:743-7, 2002.
Abstract
Gynecomastia develops when there is an increase in the ratio of estrogen to androgens. Whereas mild forms of gynecomastia are frequently encountered in the male population, any breast enlargement that is prominent, painful, progressive or of recent onset always requires a careful evaluation, as it may be an important clue to disease elsewhere. Underlying causes are plenty and include drugs, congenital and acquired disorders of androgen and estrogen production, various tumors, renal failure, cirrhosis of the liver, and thyrotoxicosis. Evaluation includes a careful patient's history, physical examination of sexual characteristics and the breast tissue, and measurements of serum LH, FSH, testosterone, estradiol, hCG-beta, TSH and tests of liver and kidney function.


25% of cases found to have hypogonadism

Unique Identifier
12270030
Authors
Ersoz H. Onde ME. Terekeci H. Kurtoglu S. Tor H.
Institution
Karadeniz Technical University, Faculty of Medicine, Department of Endocrinology and Metabolism, Trabzon, Turkey. hersoz@yahoo.com
Title
Causes of gynaecomastia in young adult males and factors associated with idiopathic gynaecomastia.
Source
International Journal of Andrology. 25(5):312-6, 2002 Oct.
Abstract
Gynaecomastia is a common clinical condition. Persistent pubertal or late onset idiopathic gynaecomastia is the leading cause of gynaecomastia in different series. The aim of this study was the assessment of the prevalence and characteristics of different causes of gynaecomastia in young adult males, and evaluation of the factors associated with idiopathic gynaecomastia. Fifty-three male patients (mean age 22.04 +/- 2.22, range 19-29), who had been admitted to our outpatient clinics with gynaecomastia as the main presenting symptom were enrolled in the study. Patients were evaluated with breast palpation, breast ultrasonography, anthropometric measurements and sex steroid levels. Secondary causes of gynaecomastia were ruled out. Thirty age-matched healthy individuals were also studied as healthy control group. Idiopathic gynaecomastia was diagnosed in 31 of 53 patients (58%), with 17 (32%) persistent pubertal and 14 (24%) late onset course. Other causes of gynaecomastia were hypogonadism in 13 cases (25%), hyperprolactinaemia in five (9%), chronic liver disease in two (4%), and drug induced (prolonged use of H2 antagonists) in two (4%). Patients with idiopathic gynaecomastia, either pubertal or late onset, were compared with the healthy control group in order to find out associated factors. Anthropometric measurements revealed a significant increase in body weight and body mass index (BMI) in the patient group compared with healthy controls (72.4 +/- 13.3 vs. 63.6 +/- 7.9 kg, p = 0.0086 and 25.2 +/- 4.0 vs. 21.5 +/- 2.7 kg/m2, p = 0.0001). Total skin fold thickness (SFT) of four different regions were also higher in the patient group (50.9 +/- 22.1 vs. 32.6 +/- 10.2 mm, p = 0.0006) indicating a higher body fat percentage. Total serum testosterone (4.76 +/- 1.31 vs. 5.70 +/- 1.06 microg/mL, p = 0.0038) and luteinizing hormone (LH) (4.80 +/- 1.92 vs. 7.32 +/- 1.90 mIU/mL, p < 0.0001) levels were significantly lower in the patient group while oestradiol levels were similar. There was a significant correlation between total testosterone and LH levels (r = 0.27, p = 0.0445). Total testosterone and LH levels were negatively correlated with BMI and total SFT. As a result most common form of gynaecomastia is idiopathic gynaecomastia either as persistent pubertal or late onset forms in young adult males. Idiopathic gynaecomastia is closely correlated with generalized obesity, reduced LH and testosterone levels which may be the result of increased conversion of testosterone to oestradiol in increased adipose tissue mass.

The need for pathology highlighted again.

Unique Identifier
2659478
Authors
von Werder K.

Title
[The significance of gynecomastia in general practice]. [Review] [16 refs] [German]
Source
Fortschritte der Medizin. 107(12):271-3, 1989 Apr 20.
Abstract
Gynecomastia in the male is usually due to a change of the estradiol/testosterone ratio in favor of the estrogens. There is usually no need for therapy of the gynecomastia which frequently occurs during puberty and old age. However, it is important not to overlook hormone-secreting tumors, often testicular malignancies, as the underlying cause of gynecomastia. A careful history and clinical investigations including thorough palpation of the testes (sonography) are complemented by a laboratory workup including blood chemistry (liver function) and hormone determinations (estradiol, beta-HCG, FSH, LH, prolactin, testosterone, thyroid hormones). Treatment of gynecomastia includes elimination of the cause of the condition. In cases with fibrous and voluminous gynecomastia breast tissue must be removed surgically. Antiestrogenic treatment with tamoxifen is indicated only in patients with recently developed, tender gynecomastia. [References: 16]



Effect of steroid abuse explained on the body explained

http://www.attract.wales.nhs.uk/question_answers.cfm?question_id=806

http://bmj.bmjjournals.com/cgi/content/full/313/7049/100?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=gynaecomastia&andorexactfulltext=and&searchid=1087738340024_3267&stored_search=&FIRSTINDEX=20&sortspec=relevance&resourcetype=1

http://www.hormone.org/pdf/Horm_Abuse_Fact_Sheet.pdf

http://www.hormone.org/learn/abuse_3.html


An individuals case and an explanation a various factors

http://www.surgery-news.com/news/1203/other12302.htm

Tetsosterone levels for young men?- explained

http://www.wellmanclinic.org/paper2.htm

[Blarneystoner]

i got some info for ya, GYNECOMASTIA SUCKS!

[hypo]

My information is in accordance with the views of;

The Testosterone Deficiency Society,

The American Association of Clinical Endocrinologists,

Hypogonadism Patients support groups in the US and the UK,

The Pituitary Foundation,

World leading endocrinologists/andrologists in the US and the UK- notably Dr Eugene Shippen (author of the Testosterone Syndrome) and Dr Malcolm Carruthers (author of the Testosterone Revolution).

I could run and run and run with the authoratitive sources that I am in accordance with.

I see one of the top endocrinologists in the world in the above Dr Malcolm Carruthers and I also see the head of the north west section of the society of endocrinology in the UK.

Information I provide in this area is fairly straightforward and includes little subjective opinion.

But your not asking these questions because you are suddenly concerned about these issues.

Your asking these question because I do not stand for your outrageous antics/behavior on this website so you are trying to mucky your feet in matters where I genuinely help people.

You can go ahead and comment on what I represent- just make sure you post in another thread.

This thread has been stickied for a specific reason, to help people with endocrine issues.







 

[hypo]

You have no genuine concerns, we both know what this and you are about.

The information stands up to scrutiny and is in alignment with the top endocrinologists in the world and the AACE  and is of great help to those who have genuine issues.

P.S

You have absolutely nothing positive to offer this site, have helped no one and I do not have to answer to the likes of you.

This discourse is at an end.

[aux513s]

However, I think asking and commenting about all these details (and we will) might antagonize the endochrinologist, especially if his understanding of the problem is somewhat different.

If a patient asking and commenting about their own treatment annoys a doctor, who they are paying money to see, then they need to find a different doctor.

I doubt a specialized endocrinologist would be incorrect in their interpretations of someone's hormone results/symptoms. When has anyone on this board expressed mistrust in their endocrinologist?

[Gine2D]

Many endo are not up on the field.  The one I HAD gone to for 4 years did not know what E2 was when I asked him to test for it.  I told him it was estrogen estradiol.  He said that was a female hormone & if I had it I would have breasts.  

He had examined me nude several times & had not acknowledged that I had breasts. They are 40-C & very hard to not see nude.  I never went back to him, I got another endo that has more knowledge the field of male hormones.  The new endo did a breast exam the first time I went to him & ordered an E2 test & mammogram.

G