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1.
Andrology ; 7(6): 778-793, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31099174

RESUMO

BACKGROUND: Gynecomastia (GM) is a benign proliferation of the glandular tissue of the breast in men. It is a frequent condition with a reported prevalence of 32-65%, depending on the age and the criteria used for definition. GM of infancy and puberty are common, benign conditions resolving spontaneously in the majority of cases. GM of adulthood is more prevalent among the elderly and proper investigation may reveal an underlying pathology in 45-50% of cases. OBJECTIVES: The aim was to provide clinical practice guidelines for the evaluation and management of GM. MATERIALS AND METHODS: A literature search of articles in English for the term 'gynecomastia' was conducted. Evidence-based recommendations were developed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system. RESULTS: A set of five statements and fifteen clinical recommendations was formulated. CONCLUSIONS: The purpose of GM assessment should be the detection of underlying pathological conditions, reversible causes (administration/abuse of aggravating substances), and the discrimination from other breast lumps, particularly breast cancer. Assessment should comprise a thorough medical history and physical examination of the breast and genitalia (including testicular ultrasound). A set of laboratory investigations may integrate the evaluation: testosterone (T), estradiol (E2), sex hormone-binding globulin (SHBG), luteinizing hormone (LH), follicular stimulating hormone (FSH), thyroid stimulating hormone (TSH), prolactin, human chorionic gonadotropin (hCG), alpha-fetal protein (AFP), liver and renal function tests. Breast imaging may be used whenever the clinical examination is equivocal. In suspicious lesions, core needle biopsy should be sought directly instead. Watchful waiting is recommended after treatment of underlying pathology or discontinuation of substances associated with GM. T treatment should be offered to men with proven T deficiency. The use of selective estrogen receptor modulators (SERMs), aromatase inhibitors (AIs) and non-aromatizable androgens is not justified in general. Surgical treatment is the therapy of choice for patients with long-lasting GM. SUMMARY OF STATEMENTS (S) AND RECOMMENDATIONS (R): S1. Gynecomastia (GM) is a benign proliferation of glandular tissue of the breast in males. S2. GM of infancy is a common condition that usually resolves spontaneously, typically within the first year of life. S3. GM of puberty is a common condition, affecting approximately 50% of mid-pubertal boys; in more than 90% of cases, it resolves spontaneously within 24 months. S4. The prevalence of GM in adulthood increases with increasing age; proper investigation may reveal an underlying pathology in approximately 45-50% of the cases. S5. Male breast cancer is rare; GM should not be considered a premalignant condition. The following recommendations are divided into 'strong', denoted by the number 1 and associated with the terminology 'we recommend', and 'weak' denoted by the number 2 and associated with the phrase 'we suggest'. The grading of the quality of evidence is denoted as follows: ⊕○○○ for very low-quality evidence; ⊕⊕○○ for low quality; ⊕⊕⊕○ for moderate quality; and ⊕⊕⊕⊕ for high quality. R1. The presence of an underlying pathology should be considered in GM of adulthood. We recommend that the identification of an apparent reason for GM in adulthood, including the use of medication known to be associated with GM, should not preclude a detailed investigation (1 ⊕⊕⊕○). R2. We suggest that the initial screening to rule out lipomastia, obvious breast cancer, or testicular cancer might be performed by a general practitioner or another non-specialist (2 ⊕○○○). R3. We recommend that in those cases where a thorough diagnostic workup is warranted, it should be performed by a specialist (1 ⊕○○○). R4. We recommend that the medical history should include information on the onset and duration of GM, sexual development and function, and administration or abuse of substances associated with GM (1 ⊕⊕⊕○). R5. We recommend that the physical examination should detect signs of under-virilization or systemic disease (1 ⊕⊕⊕⊕). R6. We recommend that breast examination should confirm the presence of palpable glandular tissue to discriminate GM from lipomastia (pseudo-gynecomastia) and rule out the suspicion of malignant breast tumor (1 ⊕⊕⊕⊕). R7. We recommend that the physical examination should include the examination of the genitalia to rule out the presence of a palpable testicular tumor and to detect testicular atrophy (1 ⊕⊕⊕⊕). R8. We recommend that genitalia examination is aided by a testicular ultrasound, as the detection of a testicular tumor by palpation has low sensitivity (1 ⊕⊕○○). R9. We suggest that a set of evaluations may include T, E2 , SHBG, LH, FSH, TSH, prolactin, hCG, AFP, and liver and renal function tests (2 ⊕⊕○○). R10. We suggest that breast imaging may offer assistance, where the clinical examination is equivocal (2 ⊕⊕○○). R11. We suggest that, if the clinical picture is suspicious for a malignant lesion, core needle biopsy should be performed (2 ⊕⊕○○). R12. We recommend watchful waiting after treatment of underlying pathology or discontinuation of the administration/abuse of substances associated with GM (1 ⊕⊕○○). R13. We recommend that T treatment should be offered only to men with proven testosterone deficiency (1 ⊕⊕⊕○). R14. We do not recommend the use of selective estrogen receptor modulators (SERMs), aromatase inhibitors (AIs), or non-aromatizable androgens in the treatment of GM in general (1 ⊕⊕○○). R15. We suggest surgical treatment only for patients with long-lasting GM, which does not regress spontaneously or following medical therapy. The extent and type of surgery depend on the size of breast enlargement, and the amount of adipose tissue (2 ⊕⊕○○).


Assuntos
Mama/fisiopatologia , Ginecomastia/diagnóstico , Ginecomastia/terapia , Testosterona/uso terapêutico , Adolescente , Adulto , Androgênios/uso terapêutico , Inibidores da Aromatase/uso terapêutico , Mama/diagnóstico por imagem , Neoplasias da Mama Masculina/diagnóstico , Ginecomastia/fisiopatologia , Humanos , Lactente , Recém-Nascido , Lipoma/diagnóstico , Masculino , Guias de Prática Clínica como Assunto , Moduladores Seletivos de Receptor Estrogênico/uso terapêutico , Neoplasias Testiculares/diagnóstico , Testosterona/deficiência
2.
Artigo em Inglês | MEDLINE | ID: mdl-28260521

RESUMO

BACKGROUND: Gynecomastia may occur physiologically in the neonatal period, during puberty, and in old age. It may also develop in association with various pathologic states. The challenge for the physician is to distinguish physiological gynecomastia from those with an underlying pathology. OBJECTIVE: To review in depth the pathophysiology, clinical manifestations, and treatment of gynecomastia. METHOD: A PubMed search was completed in Clinical Queries using the key term "gynecomastia". Patents were searched using the key term "gynecomastia" from www.google.com/patents, www.uspto.gov, and www.freepatentsonline.com. RESULTS: Gynecomastia is caused by an imbalance between the stimulatory effect of estrogen and the inhibitory effect of androgen at the breast tissue level. Clinically, gynecomastia is characterized by the presence of a firm or rubbery, discrete, subareolar ridge of glandular tissue that is symmetrical in shape, freely movable, and nonadherent to skin or underlying tissue. Since most cases of physiological gynecomastia regress spontaneously with time, reassurance is all that is necessary. For pathological gynecomastia, treatment should be directed at the underlying cause, if possible. If gynecomastia persists in spite of the above measures, pharmacologic therapy and reduction mammoplasty may be considered. Recent patents related to the management of gynecomastia are discussed. CONCLUSION: The majority of cases are physiological and do not require treatment other than reassurance. For pathological cases, the underlying cause should be treated if possible. If gynecomastia persists in spite of the above measures and treatment becomes necessary, tamoxifen is the treatment of choice. Reduction mammoplasty may be considered for resistant cases.


Assuntos
Androgênios/metabolismo , Estrogênios/metabolismo , Ginecomastia/diagnóstico , Adolescente , Criança , Antagonistas de Estrogênios/uso terapêutico , Ginecomastia/fisiopatologia , Ginecomastia/terapia , Humanos , Lactente , Recém-Nascido , Masculino , Mamoplastia/métodos , Patentes como Assunto , Puberdade/fisiologia , Tamoxifeno/uso terapêutico
3.
Horm Res Paediatr ; 87(5): 354-358, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-27951541

RESUMO

BACKGROUND: 17ß-hydroxysteroid dehydrogenase (17ß-HSD) type 3 deficiency is an autosomal recessive disorder with diminished testosterone synthesis and consequently underandrogenisation. 46,XY patients with 17ß-HSD type 3 deficiency are often assigned a female sex at birth but have a high virilisation potential at the time of puberty. METHODS: We studied four 46,XY patients with 17ß-HSD type 3 deficiency at puberty with regard to the underlying mutations, the hormone values, and the clinical findings. RESULTS: Three patients were initially assigned a female sex and 1 was assigned a male sex. All had relevant mutations in the HSD17B3 gene. The 2 patients with deleterious mutations had lower testosterone values at the time of puberty than the patients with possible residual activity of 17ß-HSD type 3. One of the latter patients changed to male gender. CONCLUSION: All 4 patients with 17ß-HSD type 3 deficiency synthesized relevant amounts (>0.7 µg/L) of testosterone at puberty, which lead to variable androgenisation. In patients with presumable residual activity of the mutated enzyme, testosterone values in the male reference range can be achieved, thereby inducing male pubertal development. These patients should possibly be assigned a male sex. Any surgical intervention should be avoided until the patients are old enough to consider their options of medical and surgical intervention.
.


Assuntos
17-Hidroxiesteroide Desidrogenases/deficiência , Transtorno 46,XY do Desenvolvimento Sexual , Ginecomastia , Mutação , Puberdade , Erros Inatos do Metabolismo de Esteroides , Virilismo , 17-Hidroxiesteroide Desidrogenases/genética , Adolescente , Transtorno 46,XY do Desenvolvimento Sexual/genética , Transtorno 46,XY do Desenvolvimento Sexual/patologia , Transtorno 46,XY do Desenvolvimento Sexual/fisiopatologia , Feminino , Ginecomastia/genética , Ginecomastia/patologia , Ginecomastia/fisiopatologia , Humanos , Masculino , Erros Inatos do Metabolismo de Esteroides/genética , Erros Inatos do Metabolismo de Esteroides/patologia , Erros Inatos do Metabolismo de Esteroides/fisiopatologia , Virilismo/genética , Virilismo/patologia , Virilismo/fisiopatologia
4.
J Pediatr Endocrinol Metab ; 29(1): 77-83, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26353169

RESUMO

During puberty, estrogen has a biphasic effect on epiphyses; at low levels, it leads to an increase in height and bone mass, whereas at high levels, it leads to closure of the epiphysis. Tamoxifen is a selective estrogen receptor modulator that has been used in the treatment of pubertal gynecomastia. Although it has not been approved for this indication, studies have shown it to be both successful and safe. In males, the peak of pubertal bone development occurs during Tanner stage 3-4, which is also when pubertal gynecomastia reaches its highest prevalence. Thus tamoxifen treatment could potentially effect pubertal bone development. The aim of this study was to assess the effects of tamoxifen on bone mineral density (BMD) and skeletal maturation when used for pubertal gynecomastia. We evaluated 20 boys with pubertal gynecomastia receiving tamoxifen for at least 4 months. BMD was measured with dual-energy X-ray absorptiometry. Z-score and absolute BMD (g/cm(2)) was determined at baseline and 2 months after completing tamoxifen treatment. Bone age and height was evaluated before treatment and again one year later. Using absolute BMD (g/cm(2)), the mean difference from baseline was significant between the two groups both at spine (p=0.002) and femur (p=0.001), but not with the Z-score. This result was attributed to the expected increase during puberty according to sex and age. No significant effect on skeletal maturation was found (p=1.112). We conclude that when pubertal bone development is concerned, tamoxifen is safe for the treatment of pubertal gynecomastia as neither bone mineralization nor growth potential was affected.


Assuntos
Densidade Óssea/efeitos dos fármacos , Desenvolvimento Ósseo/efeitos dos fármacos , Ginecomastia/tratamento farmacológico , Ginecomastia/fisiopatologia , Maturidade Sexual/efeitos dos fármacos , Tamoxifeno/uso terapêutico , Adolescente , Conservadores da Densidade Óssea/uso terapêutico , Criança , Humanos , Estudos Longitudinais , Masculino
5.
Femina ; 43(5): 197-202, set.-out. 2015. ilus
Artigo em Português | LILACS | ID: lil-771214

RESUMO

O objetivo deste trabalho foi observar na literatura dados referentes à etiologia da ginecomastia, seu diagnóstico e aspectos radiológicos. A metodologia adotada foi a pesquisa bibliográfica sistematizada para a produção de um artigo de revisão, de modo a responder ao objetivo proposto. A ginecomastia pode ser dividida em fisiológica (neonatal, puberal e senil) e patológica (resultante da diminuição da ação da testosterona, ou do aumento da ação estrogênica, por mecanismo de indução por drogas, idiopática ou secundária a outras causas). O diagnóstico deve ser realizado através do exame físico, investigação endócrina e exames radiológicos, como a mamografia e a ultrassonografia. O tratamento está baseado na orientação, medicamentos e, em último caso, cirúrgico.(AU)


The objective of this study was to observe data in the literature regarding the etiology, diagnosis and radiological aspects of gynecomastia. The methodology included a systematic literature search to produce a review article in order to meet the objective. Gynecomastia can be divided into physiologic (neonatal, pubertal and senile) and pathological (due to decreased action of testosterone, increased estrogen action, drug?induced, idiopathic or due to other causes). The diagnosis could be made by physical examination, endocrine and radiological investigation, as mammography and ultrasound. The treatment is based on the guidance, medication and, ultimately, surgery.(AU)


Assuntos
Humanos , Masculino , Ginecomastia/diagnóstico , Ginecomastia/etiologia , Ginecomastia/fisiopatologia , Ginecomastia/diagnóstico por imagem , Tamoxifeno/uso terapêutico , Bases de Dados Bibliográficas , Ginecomastia/tratamento farmacológico
6.
J Clin Endocrinol Metab ; 100(10): 3752-9, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26287961

RESUMO

CONTEXT: Physiological gynecomastia is common and affects a large proportion of otherwise healthy adolescent boys. It is thought to be caused by an imbalance between estrogen and testosterone, although this is rarely evident in analyses of serum. OBJECTIVE: This study aimed to describe the frequency of physiological gynecomastia and to determine possible etiological factors (eg, auxology and serum hormone levels) in a longitudinal setup. DESIGN, SETTINGS, AND PARTICIPANTS: A prospective cohort study of 106 healthy Danish boys (5.8-16.4 years) participated in the longitudinal part of the COPENHAGEN Puberty Study. The boys were examined every 6 months during an 8-year follow-up. Median number of examinations was 10 (2-15). MAIN OUTCOME MEASUREMENTS: Blood samples were analyzed for FSH, LH, testosterone, estradiol, SHBG, inhibin B, anti-Müllerian hormone, IGF-1, and IGF binding protein-3 by immunoassays. Auxological parameters, pubertal development, and the presence of gynecomastia were evaluated at each visit. RESULTS: Fifty-two of 106 boys (49%) developed gynecomastia, of which 10 (19%) presented with intermittent gynecomastia. Boys with physiological gynecomastia reached peak height velocity at a significantly younger age than boys who did not develop gynecomastia (13.5 versus 13.9 years, P = .027), and they had significantly higher serum levels of IGF-1 (P = .000), estradiol (P = .013), free testosterone (P < .001), and FSH (P = .030) during pubertal transition. However, no differences in serum LH or in the estradiol to testosterone ratio were found. CONCLUSIONS: Gynecomastia is frequent in pubertal boys. Increased IGF-1 levels and pubertal growth appear to be associated, whereas changes in estrogen to testosterone ratio seem negligible.


Assuntos
Estatura/fisiologia , Estradiol/sangue , Ginecomastia/fisiopatologia , Fator de Crescimento Insulin-Like I/metabolismo , Testosterona/sangue , Adolescente , Hormônio Antimülleriano/sangue , Criança , Pré-Escolar , Hormônio Foliculoestimulante/sangue , Ginecomastia/sangue , Humanos , Inibinas/sangue , Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/sangue , Estudos Longitudinais , Hormônio Luteinizante/sangue , Masculino , Estudos Prospectivos , Puberdade/sangue , Puberdade/fisiologia , Globulina de Ligação a Hormônio Sexual/metabolismo
7.
Saudi Med J ; 36(9): 1115-7, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-26318471

RESUMO

Gynecomastia is an enlargement of male breast resulting from a proliferation of its glandular component, and it is usually due to an altered estrogen-androgen balance. It should be differentiated from pseudogynecomastia, which is characterized by fat deposition without glandular proliferation and from breast carcinoma. Gynecomastia could be physiological in neonates and pubertal or pathological due to drug intake, chronic liver, or renal disease, hyperthyroidism, testicular or adrenal neoplasms, and hypogonadism whether primary, or secondary. Properly organized work-up is needed to reach the cause of gynecomastia. Here, we reported a case of a young Omani man with gynecomastia with the aim of creating awareness of the occurrence of Klinefelter's syndrome (KS) in patients with gynecomastia, to observe any differences in clinical presentation of KS from those reported in the literature, and highlight the needed diagnostic work-up and treatment.


Assuntos
Ginecomastia/diagnóstico , Adulto , Ginecomastia/fisiopatologia , Ginecomastia/terapia , Humanos , Masculino
10.
J Clin Endocrinol Metab ; 98(12): E2013-21, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24064691

RESUMO

CONTEXT: Genomic rearrangements at 15q21 have been shown to cause overexpression of CYP19A1 and resultant aromatase excess syndrome (AEXS). However, mutation spectrum, clinical consequences, and underlying mechanisms of these rearrangements remain to be elucidated. OBJECTIVE: The aim of the study was to clarify such unsolved matters. DESIGN, SETTING, AND METHODS: We characterized six new rearrangements and investigated clinical outcome and local genomic environments of these rearrangements and of three previously reported duplications/deletions. RESULTS: Novel rearrangements included simple duplication involving exons 1-10 of CYP19A1 and simple and complex rearrangements that presumably generated chimeric genes consisting of the coding region of CYP19A1 and promoter-associated exons of neighboring genes. Clinical severities were primarily determined by the copy number of CYP19A1 and the property of the fused promoters. Sequences at the fusion junctions suggested nonallelic homologous recombination, nonhomologous end-joining, and replication-based errors as the underlying mechanisms. The breakpoint-flanking regions were not enriched with GC content, palindromes, noncanonical DNA structures, or known rearrangement-associated motifs. The rearrangements resided in early-replicating segments. CONCLUSIONS: These results indicate that AEXS is caused by duplications involving CYP19A1 and simple and complex rearrangements that presumably lead to the usage of cryptic promoters of several neighboring genes. Our data support the notion that phenotypes depend on the dosage of CYP19A1 and the characteristics of the fused promoters. Furthermore, we show that the rearrangements in AEXS are generated by both recombination- and replication-mediated mechanisms, independent of the known rearrangement-inducing DNA features or late-replication timing. Thus, AEXS represents a unique model for human genomic disorders.


Assuntos
Transtornos 46, XX do Desenvolvimento Sexual/genética , Aromatase/deficiência , Rearranjo Gênico , Ginecomastia/genética , Infertilidade Masculina/genética , Erros Inatos do Metabolismo/genética , Transtornos 46, XX do Desenvolvimento Sexual/metabolismo , Transtornos 46, XX do Desenvolvimento Sexual/fisiopatologia , Adolescente , Adulto , Aromatase/biossíntese , Aromatase/genética , Aromatase/metabolismo , Criança , Replicação do DNA , Deleção de Genes , Dosagem de Genes , Duplicação Gênica , Fusão Gênica , Ginecomastia/metabolismo , Ginecomastia/fisiopatologia , Humanos , Infertilidade Masculina/metabolismo , Infertilidade Masculina/fisiopatologia , Masculino , Erros Inatos do Metabolismo/metabolismo , Erros Inatos do Metabolismo/fisiopatologia , Regiões Promotoras Genéticas , Recombinação Genética , Índice de Gravidade de Doença
11.
Ann Dermatol Venereol ; 140(6-7): 436-43, 2013.
Artigo em Francês | MEDLINE | ID: mdl-23773741

RESUMO

Because andrology is relatively undeveloped in France, the dermatologist is often the doctor first consulted for diseases of the nipple in men. All dermatological diseases can in fact occur at this site. There are some specific nipple diseases such as gynaecomastia, congenital abnormalities, hyperplasia, benign tumours and breast cancer. All clinical examinations and laboratory examinations should focus on diagnosis of this type of cancer and its elimination.


Assuntos
Doenças Mamárias/patologia , Piercing Corporal/efeitos adversos , Doença de Bowen/patologia , Mama/anormalidades , Neoplasias da Mama Masculina/diagnóstico , Neoplasias da Mama Masculina/patologia , Carcinoma/patologia , Dermatite Atópica/patologia , Eczema/patologia , Eritema/etiologia , Eritema/patologia , Ginecomastia/etiologia , Ginecomastia/patologia , Ginecomastia/fisiopatologia , Humanos , Hiperprolactinemia/patologia , Hiperprolactinemia/fisiopatologia , Leiomioma/patologia , Masculino , Mastite/patologia , Melanoma/patologia , Mamilos/anormalidades , Mamilos/patologia , Doença de Paget Mamária/patologia , Siringoma/patologia
13.
Pharmacotherapy ; 32(12): 1123-40, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23165798

RESUMO

Drugs account for about 20% of gynecomastia cases in men. As a number of factors can alter the estrogen:androgen ratio, several pathophysiologic mechanisms are associated with drugs causing this disorder. Antiandrogens, protease inhibitors, and nucleoside reverse transcriptase inhibitors are the most common drug causes of gynecomastia, whereas first-generation antipsychotics, spironolactone, verapamil, and cimetidine are less common causes. Other drugs have been reported rarely as causes. Treatment may involve switching to an alternative agent or may require surgery or irradiation if the causative agent cannot be discontinued. We reviewed the literature on drug-induced gynecomastia and provided another perspective by reviewing data from the United States Food and Drug Administration's Adverse Event Reporting System. Epidemiologic studies are needed to provide a more accurate description of the frequency of drug-induced gynecomastia.


Assuntos
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos , Ginecomastia/induzido quimicamente , Sistemas de Notificação de Reações Adversas a Medicamentos , Antagonistas de Androgênios/efeitos adversos , Androgênios/metabolismo , Estrogênios/metabolismo , Ginecomastia/fisiopatologia , Ginecomastia/terapia , Humanos , Masculino , Inibidores de Proteases/efeitos adversos , Inibidores da Transcriptase Reversa/efeitos adversos
14.
Horm Res Paediatr ; 78(4): 261-8, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22964562

RESUMO

BACKGROUND: The adequate replacement dose of estrogens during infancy and childhood is still not known in girls. Aromatase deficiency offers an excellent model to study how much estrogens are needed during infancy, childhood and adulthood. OBJECTIVES: We studied the impact of oral 17ß-estradiol treatment, on longitudinal growth, bone age maturation, pituitary gonadotropin feedback, multicystic ovaries and bone mass in the long-term follow-up of a girl compound heterozygote for two point mutations of the CYP19A1 gene. RESULTS: Low doses of 17ß-estradiol were needed to achieve normal height velocity and adequate bone age maturation from early childhood on. Serum estradiol levels needed for breast development and for the appearance of an endometrial reflex were not sufficient to achieve physiological gonadotropin levels. Without 17ß-estradiol treatment the ovaries of the patient showed a multicystic appearance, which reversed on 17ß-estradiol replacement. Bone mass was within normal ranges during the whole follow-up period. CONCLUSION: In summary, we have shown that estradiol is needed not only in puberty but also in childhood for normal growth, bone maturation and achievement of normal bone mass. Particularly, this observation underscores the importance of early low-dose estrogen replacement also in other estrogen-deficient conditions as for instance in Turner's syndrome.


Assuntos
Transtornos 46, XX do Desenvolvimento Sexual , Desenvolvimento Infantil/efeitos dos fármacos , Estradiol/farmacologia , Estradiol/uso terapêutico , Gônadas/efeitos dos fármacos , Ginecomastia , Infertilidade Masculina , Erros Inatos do Metabolismo , Hipófise/efeitos dos fármacos , Transtornos 46, XX do Desenvolvimento Sexual/tratamento farmacológico , Transtornos 46, XX do Desenvolvimento Sexual/metabolismo , Transtornos 46, XX do Desenvolvimento Sexual/fisiopatologia , Adolescente , Aromatase/deficiência , Aromatase/efeitos dos fármacos , Aromatase/genética , Aromatase/metabolismo , Desenvolvimento Ósseo/efeitos dos fármacos , Osso e Ossos/efeitos dos fármacos , Osso e Ossos/fisiologia , Criança , Pré-Escolar , Estradiol/administração & dosagem , Terapia de Reposição de Estrogênios , Feminino , Seguimentos , Gônadas/metabolismo , Ginecomastia/metabolismo , Ginecomastia/fisiopatologia , Humanos , Infertilidade Masculina/metabolismo , Infertilidade Masculina/fisiopatologia , Erros Inatos do Metabolismo/metabolismo , Erros Inatos do Metabolismo/fisiopatologia , Hipófise/metabolismo , Transdução de Sinais/efeitos dos fármacos
15.
Expert Opin Drug Saf ; 11(5): 779-95, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22862307

RESUMO

INTRODUCTION: Drugs are estimated to cause about 10 - 25% of all cases of gynecomastia. Over the course of several decades, multiple medications have been implicated in the development of gynecomastia mostly in the form of case reports and case series. However, these reports suffer from a multitude of deficiencies, including poor quality of evidence. AREAS COVERED: Studies were selected for this review by performing an extensive electronic and hand-search using BIOSIS, EMBASE and Medline, from 1940 to present, for all reported drug associations of gynecomastia and their possible pathophysiology. Quality of evidence was assessed on a three-point scale: good, fair and poor, and each of the drugs reported to cause gynecomastia was assigned a level of strength. The pathophysiology of gynecomastia is also discussed in detail for each of the drugs found to have a good or fair evidence of association with gynecomastia. EXPERT OPINION: Most of the reported drug-gynecomastia associations were based on poor quality evidence. The drugs definitely associated with the onset of gynecomastia are spironolactone, cimetidine, ketoconazole, hGH, estrogens, hCG, anti-androgens, GnRH analogs and 5-α reductase inhibitors. Medications probably associated with gynecomastia include risperidone, verapamil, nifedipine, omeprazole, alkylating agents, HIV medications (efavirenz), anabolic steroids, alcohol and opioids.


Assuntos
Inibidores de 14-alfa Desmetilase/efeitos adversos , Ginecomastia/induzido quimicamente , Antagonistas de Receptores de Andrógenos/efeitos adversos , Medicina Baseada em Evidências , Ginecomastia/tratamento farmacológico , Ginecomastia/fisiopatologia , Humanos , Masculino , Antagonistas de Receptores de Mineralocorticoides/efeitos adversos , Farmacovigilância , Moduladores Seletivos de Receptor Estrogênico/uso terapêutico , Tamoxifeno/uso terapêutico
16.
Sao Paulo Med J ; 130(3): 187-97, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22790552

RESUMO

Gynecomastia (GM) is characterized by enlargement of the male breast, caused by glandular proliferation and fat deposition. GM is common and occurs in adolescents, adults and in old age. The aim of this review is to discuss the pathophysiology, etiology, evaluation and therapy of GM. A hormonal imbalance between estrogens and androgens is the key hallmark of GM generation. The etiology of GM is attributable to physiological factors, endocrine tumors or dysfunctions, non-endocrine diseases, drug use or idiopathic causes. Clinical evaluation must address diagnostic confirmation, search for an etiological factor and classify GM into severity grades to guide the treatment. A proposal for tailored therapy is presented. Weight loss, reassurance, pharmacotherapy with tamoxifen and surgical correction are the therapeutic options. For long-standing GM, the best results are generally achieved through surgery, combining liposuction and mammary adenectomy.


Assuntos
Ginecomastia , Doenças do Sistema Endócrino/fisiopatologia , Ginecomastia/etiologia , Ginecomastia/fisiopatologia , Ginecomastia/terapia , Humanos , Masculino , Índice de Gravidade de Doença
18.
Adv Exp Med Biol ; 769: 153-68, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23560310

RESUMO

Kennedy's disease (KD) or spinobulbar muscular atrophy is a hereditary X-linked, progressive neurodegenerative condition caused by an expansion of the CAG triplet repeat in the first exon of the androgen receptor gene. The phenotype in its full form is only expressed in males and presents as weakness and wasting of the upper and lower limbs and bulbar muscles associated with absent reflexes. Sensory disturbances are present. Various endocrine abnormalities including decreased fertility and gynecomastia are common and amongst the first features of KD. Animal models of KD have demonstrated improvement on withdrawal of testosterone, indicating that this agonist of the androgen receptor is required for the toxic effect. Potential therapies based on testosterone withdrawal in humans have shown some promise, but efficacy remains to be proven. Potential clinical factors, pathogenesis and future approaches to therapy are reviewed in this chapter.


Assuntos
Atrofia Bulboespinal Ligada ao X/genética , Peptídeos/genética , Receptores Androgênicos/genética , Expansão das Repetições de Trinucleotídeos , Transtornos 46, XX do Desenvolvimento Sexual/fisiopatologia , Aromatase/deficiência , Atrofia Bulboespinal Ligada ao X/tratamento farmacológico , Atrofia Bulboespinal Ligada ao X/metabolismo , Atrofia Bulboespinal Ligada ao X/fisiopatologia , Drogas em Investigação/farmacologia , Drogas em Investigação/uso terapêutico , Éxons , Ginecomastia/fisiopatologia , Humanos , Infertilidade Masculina/fisiopatologia , Masculino , Erros Inatos do Metabolismo/fisiopatologia , Receptores Androgênicos/metabolismo , Fatores Sexuais , Testosterona/antagonistas & inibidores , Testosterona/metabolismo
19.
São Paulo med. j ; 130(3): 187-197, 2012. ilus, tab
Artigo em Inglês | LILACS | ID: lil-640911

RESUMO

Gynecomastia (GM) is characterized by enlargement of the male breast, caused by glandular proliferation and fat deposition. GM is common and occurs in adolescents, adults and in old age. The aim of this review is to discuss the pathophysiology, etiology, evaluation and therapy of GM. A hormonal imbalance between estrogens and androgens is the key hallmark of GM generation. The etiology of GM is attributable to physiological factors, endocrine tumors or dysfunctions, non-endocrine diseases, drug use or idiopathic causes. Clinical evaluation must address diagnostic confirmation, search for an etiological factor and classify GM into severity grades to guide the treatment. A proposal for tailored therapy is presented. Weight loss, reassurance, pharmacotherapy with tamoxifen and surgical correction are the therapeutic options. For long-standing GM, the best results are generally achieved through surgery, combining liposuction and mammary adenectomy.


A ginecomastia (GM) é caracterizada pelo aumento do volume mamário em homens, provocada por proliferação glandular e depósito de gordura. É comum e pode ocorrer em adolescentes, adultos e idosos. O objetivo desta revisão é discutir a fisiopatologia, etiologia, avaliação clínica e terapia da GM. Um desequilíbrio entre estrogênios e androgênios é reconhecido como a condição fundamental para a determinação do quadro, podendo ser atribuído a fatores fisiológicos, tumores ou distúrbios endócrinos, doenças não-endócrinas, uso de drogas ou ser de causa idiopática. A avaliação clínica deve enfocar a confirmação diagnóstica, a procura de uma causa específica e a classificação em graus de gravidade para orientar o tratamento. Um roteiro de conduta individualizada é apresentado, variando entre perda de peso e explicações verbais, tratamento com tamoxifeno e correção cirúrgica. Para casos de GM persistente, os melhores resultados são obtidos em geral mediante abordagem cirúrgica, combinando lipoaspiração e adenectomia mamária.


Assuntos
Humanos , Masculino , Ginecomastia , Doenças do Sistema Endócrino/fisiopatologia , Ginecomastia/etiologia , Ginecomastia/fisiopatologia , Ginecomastia/terapia , Índice de Gravidade de Doença
20.
Endokrynol Pol ; 62(2): 190-202, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-21528484

RESUMO

Gynecomastia is a benign, abnormal, growth of the male breast gland which can occur unilaterally or bilaterally, resulting from a proliferation of glandular, fibrous and adipose tissue. Gynecomastia is characterised by the presence of soft, 2-4 cm in diameter, usually discusshaped enlargement of tissues under the nipple. It is estimated that this pathology occurs in 32-65% of men over the age of 17. Gynecomastia is a psychosocial problem and may lead to a perceived lowering of quality of life. The main cause of gynecomastia is a loss of equilibrium between oestrogens and androgens. Increased sensitivity for oestrogens of the breast gland, or local factors (e.g. an excessive synthesis of oestrogens in breast tissues or changes in oestrogen and androgen receptors) may cause gynecomastia. Also, prolactin, thyroxine, cortisol, human chorionic gonadotropin, leptin and receptors for human chorionic gonadotropin, prolactin and luteinizing hormone localised in tissues of the male breast may participate in the etiopathogenesis of gynecomastia. Usually three types of gynecomastia are distinguished: physiological, idiopathic and pathological gynecomastia. The latter is the consequence of relative or absolute excess of oestrogens. In this paper, frequent as well as casuistic causes of gynecomastia will be described. A diagnosis of gynecomastia is usually possible after a palpation examination. Ultrasonographic, mammographic or histopathological examinations are useful in aiding diagnosis. The five degree scale devised by Tanner and Marshall is useful in estimating disease progression.


Assuntos
Ginecomastia/diagnóstico , Ginecomastia/etiologia , Adolescente , Adulto , Androgênios/fisiologia , Diagnóstico Diferencial , Estrogênios/fisiologia , Ginecomastia/fisiopatologia , Humanos , Masculino
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