Author Topic: books  (Read 4237 times)

Offline Finrod

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Does anyone know good books on the subject to start informing myself??? On both subjects, gynecomastia and hormonal disbalance that leads to gyne and other problems. I'd really love some suggestions for i'm just getting to know with the subject.
Thanks again.


(si se pueden conseguir en español mejor  :) )

Offline jc71

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  • Wilma, grab the lotion, we're going to the beach!
I don't think there's much written about gyne, with the exception of a plastic surgeons website. Also little written about the hormone factors involved in gyne, although Hypo can probably help point you in the right direction.

If you notice the first thread at the top of "gynecomastia talk" is says, Demystifying Male Gynecomastia. Evidently it's "coming soon." It's being billed as the first comprehensive document on gyne. You can sign up at the bottom of the first page of this site to be notified when it's ready.

These boards are also a great source of information for you.
« Last Edit: February 02, 2005, 04:57:15 PM by jc71 »

Offline hypo

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Putting me on the spot this is the best I can come up with.

Study hormones and hypogonadism and it leads via association to a very good understanding of the aetiology of gynecomastia.

So

Buy the Testosterone Syndrome by Eugene Shippen and Testosterone Revolution by Malcolm Carruthers and speak to people who deal day to day with the problem of testosterone replacent therapy (hypogonadism), because they tend to understand the endocrinology far better than people who abuse steroids.

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

http://journals.endocrinology.org/erc/006/0315/0060315.pdf#search='role%20of%20aromatase%20in%20steroid%20action'

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

see below

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




175 men with gynecomastia underwent pathology testing 18 patients were found to have serious underlying causes.

Unique Identifier
12662229
Record Owner
NLM
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.
Abbreviated Source
ANZ J Surg. 73(4):213-6, 2003 Apr.
Publication Notes
The publication year is for the print issue of this journal.
NLM Journal Code
dze, 101086634
Journal Subset
IM
Country of Publication
Australia
MeSH Subject Headings
Adolescent
Adult
Aged
Aged, 80 and over
Danazol / ad [Administration & Dosage]
*Danazol / st [Standards]
Danazol / tu [Therapeutic Use]
Estrogen Antagonists / ad [Administration & Dosage]
*Estrogen Antagonists / st [Standards]
Estrogen Antagonists / tu [Therapeutic Use]
*Gynecomastia / di [Diagnosis]
Gynecomastia / et [Etiology]
*Gynecomastia / th [Therapy]
Human
Male
Middle Aged
Patient Selection
*Physician's Practice Patterns / st [Standards]
*Practice Guidelines / st [Standards]
Retrospective Studies
Risk Factors
*Surgical Procedures, Operative / st [Standards]
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.
CAS Registry/EC Number
0 (Estrogen Antagonists). 17230-88-5 (Danazol).



Unique Identifier
53 men with gynecomastia underwent pathology testing, 24 patients were found to have serious underlying causes.


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.


60 boys with gynecomastia underwent pathology testing, 15 patients were found to have serious 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]

Unique Identifier
3088241
Authors
Eberle AJ. Sparrow JT. Keenan BS.
Title
Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate.
Source
Journal of Pediatrics. 109(1):144-9, 1986 Jul.
Abstract
Four boys with persistent pubertal gynecomastia were given intramuscular dihydrotestosterone heptanoate (DHT-hp) at 2 to 4-week intervals for 16 weeks. By the end of treatment, breast size in all four boys had decreased 67% to 78%. Initial plasma levels of gonadotropins, estradiol, testosterone, and dihydrotestosterone (DHT) were normal. Mean plasma DHT concentration rose with the injections of DHT-hp, and remained elevated throughout the treatment period. Estradiol, LH, FSH, and testosterone decreased during treatment, as did 24-hour urinary LH and FSH. No regrowth of breast tissue was observed 6 to 15 months after treatment, although hormone concentrations had returned to near pretreatment values by 2 months after the last injection. DHT-hp has potential to be an effective medical therapy for persistent pubertal gynecomastia


Studies on the treatment of idiopathic gynaecomastia with percutaneous dihydrotestosterone.
Source
Clinical Endocrinology. 19(4):513-20, 1983 Oct.
Abstract
We have studied clinical and endocrine parameters in a group (group A) of forth men referred to us because of persistent idiopathic gynaecomastia (of more than 18 months duration), before and during the administration of percutaneous dihydrotestosterone (DHT). The endocrine parameters (testosterone (T), 17 beta-oestradiol (E2), DHT, gonadotrophins (FSH and LH) and prolactin (PRL), were compared to those of control groups of 12 healthy men on DHT therapy (group B) and 10 on placebo (group C). Local administration of DHT was followed by the complete disappearance of gynaecomastia in 10 patients, partial regression in 19 and no change in 11 patients after 4 to 20 weeks of percutaneous DHT (125 mg twice daily). Before treatment the T + DHT/E2 ratio was significantly (P less than 0.001) lower in group A 244 +/- 21 (SEM) than in groups B and C (361 +/- 21) while T, DHT and E2 concentrations were all within the normal range. During DHT treatment plasma hormone levels were measured in 26 patients from group A: DHT levels increases significantly (day 0: 1.63 +/- 0.14 nmol/l; day 15: 12.8 +/- 1.6 nmol/l, P less than 0.001) while T and E2 levels fell significantly (T: day 0: 22.6 +/- 1.2 nmol/l; day 15: 11.0 +/- 1.5 nmol/l, P less than 0.001; E2: day 0: 110.5 +/- 7.12 pmol/l; day 15: 86.79 +/- 9.4 pmol/l, P less than 0.01). The T/E2 ratio decreased from 231 +/- 20 to 164 +/- 27 (P less than 0.05) while the T + DHT/E2 ratio increased significantly (P less than 0.02) to a normal mean value (day 15: 354 +/- 57).(ABSTRACT TRUNCATED AT 250 WORDS)


Unique Identifier
6489180
Authors
Eversmann T. Moito J. von Werder K.
Title
[Testosterone and estradiol levels in male gynecomastia. Clinical and endocrine findings during treatment with tamoxifen]. [German]
Source
Deutsche Medizinische Wochenschrift. 109(44):1678-82, 1984 Nov 2.
Abstract
Oestradiol-(E2) levels in serum were significantly higher in a group of 91 males with gynaecomastia than in a control group. The levels were highest in patients with testicular tumour, hyperprolactinaemia and idiopathic gynaecomastia. In gynaecomastia of puberty and primary or secondary hypogonadism, the E2 level was within normal limits, but the testosterone/oestradiol ratio was significantly reduced. Tamoxifen, at a daily dose of 20 mg, was administered over 2-4 months to 16 patients with gynaecomastia. Of twelve patients with painful gynaecomastia ten became painfree. Gynaecomastia regressed partially or completely in 14 patients, in only 2 was it unchanged. There was no recurrence of gynaecomastia after discontinuing tamoxifen. Side-effects did not occur. It is concluded that tamoxifen is a promising alternative to the surgical treatment of gynaecomastia.

Unique Identifier
7705318
Authors
Plymate S.

Institution
Seattle/American Lake Geriatric Research Education and Clinical Center, Washington.
Title
Hypogonadism. [Review] [101 refs]
Source
Endocrinology & Metabolism Clinics of North America. 23(4):749-72, 1994 Dec.
Abstract
Hypogonadism is a common finding in men, involving up to 5% of the population. Diagnosis of hypogonadism is dependent on clinical examination. Laboratory studies will confirm the cause. Treatment of testosterone deficiency is readily achieved; however, correction of spermatogenesis depends on the cause of the testicular failure. [References: 101]




« Last Edit: February 02, 2005, 04:26:53 PM by hypo »

Offline hypo

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See my new thread

Offline Finrod

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Great info hypo, i'll be more than glad to read it and also the extracts you will post in the other thread.

Offline hypo

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They will not be extracts they will be complete papers.







 

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