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Hypogonadism

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Synonyms and keywords:Gonadal failure, Testosterone deficiency, Idiopathic hypogonadotropic hypogonadism

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Hypogonadism is a disorder of the reproductive system which results in lack of function of the gonads (ovaries or testes). Hypogonadism is caused by several conditions which may be congenital, acquired, genetic, or malignancies. Hypogonadism may be classified on the basis of etiology and the site causing the defect into primary or secondary hypogonadism. Primary hypogonadism results from defect in the gonads themselves and it is characterized by high level of the gonadotropin hormones (FSH and LH). Secondary hypogonadism indicates a defect in pituitary gland or hypothalamus and presents with a low level of gonadotropin releasing hormone, FSH, and LH. Genetic mutations that can cause hypogonadism include ANOS 1, SOX10, SEMA3A, IL17RD and FEZF1. Other genes include KISS, GNRNH, and PROK. Hypogonadism must be differentiated from diseases that may cause delayed puberty or infertility, such as Klinefelter syndrome, Kallmann syndrome and cryptorchidism. The prevalence of hypogonadism is estimated to be 38,700 per 100,000 individual aging 45 years. The incidence of hypogonadism is 1230 per 100,000 persons. Hypogonadism affects men more than women and its prevalence increases with age. Hypogonadism has many risk factors like dyslipidemia, obesity, malignancies and alcohol intake. If hypogonadism left untreated, patients will end up with infertility and rheumatic autoimmune diseases. Hypogonadism can cause complications like gynecomastia and delay of puberty in the prepubertal patients. It can also cause depression and cardiovascular stroke in the adults. Hypogonadism usually has a good prognosis with the proper treatment. Patients with hypogonadism usually present with loss of the secondary sexual characteristics. Male patients present with infertility, loss of libido and erectile dysfunction. Female patients present with amenorrhea and loss of pubic hair. Laboratory evaluation may reveal low testosterone levels and variable FSH and LH levels according to the cause of hypogonadism whether primary or secondary. The mainstay of treatment for hypogonadism is testosterone replacement therapy and it can be administrated through different regimens injected, transdermal or buccal. In females, estrogen replacement is helpful besides testosterone.

Historical Perspective

Hypogonadism was first reported by Dr. Maestre de San Juan in a case of small testes and loss of smelling sensation. Dr. Kallmann in 1944 identified this syndrome which was named on him after that. Dr. de Morsier reported various cases of hypogonadism with absent olfactory bulbs in the 1950s.

Classification

Hypogonadism may be classified according to the etiological site into three subtypes primary, secondary or combined. It can also be classified according to the age into two adult and child. Based on the causes, it can be classified into acquired or congenital.

Pathophysiology

Hypogonadism pathophysiology depends mainly on the deficiency of the testosterone hormone. Testosterone is secreted in response to stimulation from the brain to the hypothalamus which secretes the gonadotropin releasing hormones (GnRH). GnRH is responsible for secretion of FSH and LH. In males, LH stimulates the leydig cells in the testes which produce testosterone by converting the cholesterol to testosterone. In females, FSH and LH stimulate secretion of estrogen which helps in follicles maturation. Also, estrogen is involved in the ovulation process. GnRH deficiency may lead to decrease of testosterone levels and eventually causing hypogonadism. Genetic mutations have a major role in the development of hypogonadism as well as other factors. There are more than 25 gene mutations participate in the pathogenesis of hypogonadism. Genes that are responsible for Kallmann syndrome include ANOS 1, SOX10, SEMA3A, IL17RD and FEZF1. Other influencing genes are KISS, GNRNH, and PROK.  

Causes

Hypogonadism is commonly caused by congenital and acquired genetic and endocrinological conditions. Malignancies can be life threatening causes and should take priority when diagnosing the etiology.

Differentiating Hypopituitarism from Other Diseases

Hypogonadism must be differentiated from diseases that cause delayed puberty or infertility. These diseases include congenital diseases as Klinefelter syndrome, Kallmann syndrome and cryptorchidism. The diseases include also testicular torsion and orchitis in males, polycystic ovary syndrome, pelvic inflammatory disease, and endometriosis in females.

Epidemiology and Demographics

The prevalence of hypogonadism is estimated to be 38,700 per 100,000 individual aging 45 years. The incidence of hypogonadism is 1230 per 100,000 persons. Hypogonadism affects men more than women and its prevalence increases with age.

Risk Factors

Common risk factors in the development of hypogonadism in men are dyslipidemia, obesity, alcohol intake, malignancies and metabolic syndrome. Common risk factors in women include nulliparity and dysmenorrhea. Other risk factors include coronary heart disease, hypertension, heart failure, and smoking.

Screening

According to the endocrine society, screening for hypogonadism is not recommended as it is not cost-effective. Hypogonadism screening may be done in order to diagnose the disease early and provide the appropriate treatment. Screening may be done for men who present with erectile dysfunction, infertility, HIV, and young patients with osteoporosis.  

Natural History, Complications, and Prognosis

If left untreated, patients with hypogonadism will end up with infertility and rheumatic autoimmune diseases. The rheumatic autoimmune diseases include rheumatic arthritis and systemic lupus erythematosus. Complications of hypogonadism depend on age and include ambiguous genitalia in the new born, gynecomastia, and delay of puberty in the prepubertal phase. Complications include also depression and cardiovascular stroke in the adults. Prognosis of hypogonadism is good with treatment and patients can have a normal life alongside the appropriate medical therapy.

Diagnosis

History and Symptoms

The most common symptoms of hypogonadism in males include delayed puberty and loss of sexual characters as voice deepening and hair growth. Common symptoms include also erectile dysfunction, small testes, loss of libido and sweating. Common symptoms in females include no breast enlargement and no pubic hair. Less common symptoms include a headache, visual impairment, galactorrhea, and anorexia nervosa.

Physical Examination

Common physical examination findings of hypogonadism include the absence of secondary sexual characteristics in both male and females. In males, pubic hair loss, no beard hair, small testicular size and congenital anomalies may be observed. In females, no axillary hair and amenorrhea are common.

Laboratory Findings

Laboratory diagnosis consistent with cases of hypogonadism is measuring testosterone levels, gonadotropin hormones level and the semen analysis for the male patients. Testosterone level is low in cases of hypogonadism. Gonadotropin hormones level differs between the primary hypogonadism and secondary hypogonadism. The gonadotropin hormones are high in the primary causes and low in the secondary causes. 

X ray

X-ray may be performed in cases of hypogonadism only on bones to assess the bone age and the skeletal growth. A pelvic x-ray may be also needed to assess the internal genitalia and detect any masses. 

CT scan

There are no CT findings associated with hypogonadism.

MRI scan

MRI is performed in cases of hypogonadism to evaluate the pituitary gland and hypothalamus to detect any tumors that may cause hypogonadism. It is performed in specific patients who present with visual disturbances, neurological impairments and lab findings suggestive for hypopituitarism. Possible findings may include empty sella turcica and pituitary adenomas. 

Ultrasound

Ultrasound may be helpful in females presenting with hypogonadism to evaluate the uterus or to rule out cryptorchidism in males. 

Other Diagnostic Studies

There are no other diagnostic studies for hypogonadism.

Other imaging findings

There are no other imaging findings for hypogonadism.

Treatment

Medical Therapy

The mainstay of therapy for hypogonadism is the hormonal replacement therapy. Based on the endocrine society clinical guidelines, testosterone is important for the treatment of hypogonadism. Different regimens include injected, buccal and transdermal testosterone. For women, estrogen replacement therapy is important besides testosterone.

Surgery

Surgical intervention is not recommended for the management of hypogonadism. However, in some cases of the hypogonadism which present with high risk of malignancy, gonadal tissue should be surgically removed. This is more important in genetic diseases like Turner syndrome. In males, orchiectomy is indicated if the patient has completely nonfunctioning testes.

Prevention

There are no established methods for prevention of hypogonadism.

References

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Hypogonadism was first reported by Dr. Maestre de San Juan in a case of small testes and loss of smelling sensation. Dr. Kallmann in 1944 identified this syndrome which was named on him after that. Dr. de Morsier reported various cases of hypogonadism with absent olfactory bulbs in the 1950s.

Historical perspective

  • In 1856, Dr. Maestre de San Juan was the first one to report a case combining small testes (hypogonadism) and loss of smelling sense in a patient.
  • In 1944, Dr. Kallmann was the first to identify a case combining hypogonadism and anosmia as a syndrome which was named on him after then. He held a study showing the correlation between anosmia and hypogonadism in different families.[1]
  • In the 1950s, Dr. de Morsier reported various cases of patients with hypogonadism and with absent olfactory bulbs as well. After which, hypogonadism has been described as gonadotropin hormones deficiency.

References

  1. ↑ Dodé C, Hardelin JP (2009). “Kallmann syndrome”. Eur J Hum Genet. 17 (2): 139–46. doi:10.1038/ejhg.2008.206. PMC 2986064. PMID 18985070.

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Hypogonadism may be classified according to the etiological site into three subtypes namely primary, secondary or combined. Hypogonadism can also be classified according to the age into two adult and child onset disease. Also, it could be classified based on the causes into acquired or congenital.[1]

Classification

  • Based on the location, hypogonadism can be classified into:
    • Primary: gonads (ovaries or testes) are the primary source of the pathology.
    • Secondary (central): If the cause of the disease is the hypothalamus or pituitary.
    • Combined
  • Based on the age, hypogonadism can be classified into:
  • Based on the causes of the disease, hypogonadism can be classified into:

References

  1. ↑ Rey RA, Grinspon RP, Gottlieb S, Pasqualini T, Knoblovits P, Aszpis S; et al. (2013). “Male hypogonadism: an extended classification based on a developmental, endocrine physiology-based approach”. Andrology. 1 (1): 3–16. doi:10.1111/j.2047-2927.2012.00008.x. PMID 23258624.

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Hypogonadism pathophysiology depends mainly on the deficiency of the testosterone hormone. Testosterone is secreted in response to stimulation from the brain to the hypothalamus which secretes the gonadotropin releasing hormones (GnRH). GnRH is responsible for secretion of FSH and LH. In males, LH stimulates the leydig cells in the testes which produce testosterone by converting the cholesterol to testosterone. In females, FSH and LH stimulate secretion of estrogen which helps in follicles maturation. Also, estrogen is involved in the ovulation process. GnRH deficiency may lead to decrease of testosterone levels and eventually causing hypogonadism. Genetic mutations have a major role in the development of hypogonadism as well as other factors. There are more than 25 gene mutations participate in the pathogenesis of hypogonadism. Genes that are responsible for Kallmann syndrome include ANOS 1, SOX10, SEMA3A, IL17RD and FEZF1. Other influencing genes are KISS, GNRNH, and PROK.

Pathophysiology

Pathogenesis

Hypogonadism in males

Genetic

  • Genetic mutations have a role in the development of the hypogonadism especially congenital hypogonadotropic hypogonadism. There are more than 25 genes responsible for the pathogenesis of hypogonadism.[3]
  • In this table number of genes with the associated diseases causing hypogonadism are enlisted:
Associated disease Genes Mutation Associated features with the mutated gene Comments
Kallmann syndrome (with loss of smelling sense – anosmia) ANOS 1[4]
SOX10
SEMA3A
  • Loss of function mutations
  • SEMA3A gene’s function is to encode the semaphorin 3A.
  • Semaphorin 3A is important for the GnRH neurons migration.
  • A defect in SEMA3A gene will end up with GnRH deficiency.[7]
IL17RD
FEZF1
Idiopathic hypogonadotropic hypogonadism (IHH) (normal smelling sensation – normosmia) KISS1R
  • Gain of function mutations
KISS1
GNRHR
  • Loss of function mutations
  • Patients with hypogonadism due to GNRHR mutations usually do not respond properly to the exogenous GnRH.
  • On big doses of GnRH, ovulation may be initiated in some patients.
GNRH1
  • GNRH1 is responsible for pre-pro GnRH encoding.[9]
TAC3
Mixed anosmic and nosmic IHH FGFR1
  • FGFR1 gene has an organizational function with ANOS1.
  • Products of ANOS1 act like a co receptor for FGFR1.[11]
FGF8[12]
PROK2

PROKR2

References

  1. ↑ Kumar P, Kumar N, Thakur DS, Patidar A (2010). “Male hypogonadism: Symptoms and treatment”. J Adv Pharm Technol Res. 1 (3): 297–301. doi:10.4103/0110-5558.72420. PMC 3255409. PMID 22247861.
  2. ↑ Spratt DI, Carr DB, Merriam GR, Scully RE, Rao PN, Crowley WF (1987). “The spectrum of abnormal patterns of gonadotropin-releasing hormone secretion in men with idiopathic hypogonadotropic hypogonadism: clinical and laboratory correlations”. J Clin Endocrinol Metab. 64 (2): 283–91. doi:10.1210/jcem-64-2-283. PMID 3098771.
  3. ↑ Boehm U, Bouloux PM, Dattani MT, de Roux N, Dodé C, Dunkel L; et al. (2015). “Expert consensus document: European Consensus Statement on congenital hypogonadotropic hypogonadism–pathogenesis, diagnosis and treatment”. Nat Rev Endocrinol. 11 (9): 547–64. doi:10.1038/nrendo.2015.112. PMID 26194704.
  4. ↑ Franco B, Guioli S, Pragliola A, Incerti B, Bardoni B, Tonlorenzi R; et al. (1991). “A gene deleted in Kallmann’s syndrome shares homology with neural cell adhesion and axonal path-finding molecules”. Nature. 353 (6344): 529–36. doi:10.1038/353529a0. PMID 1922361.
  5. ↑ Schwanzel-Fukuda M, Bick D, Pfaff DW (1989). “Luteinizing hormone-releasing hormone (LHRH)-expressing cells do not migrate normally in an inherited hypogonadal (Kallmann) syndrome”. Brain Res Mol Brain Res. 6 (4): 311–26. PMID 2687610.
  6. ↑ Pingault V, Bodereau V, Baral V, Marcos S, Watanabe Y, Chaoui A; et al. (2013). “Loss-of-function mutations in SOX10 cause Kallmann syndrome with deafness”. Am J Hum Genet. 92 (5): 707–24. doi:10.1016/j.ajhg.2013.03.024. PMC 3644631. PMID 23643381.
  7. ↑ Cariboni A, Davidson K, Rakic S, Maggi R, Parnavelas JG, Ruhrberg C (2011). “Defective gonadotropin-releasing hormone neuron migration in mice lacking SEMA3A signalling through NRP1 and NRP2: implications for the aetiology of hypogonadotropic hypogonadism”. Hum Mol Genet. 20 (2): 336–44. doi:10.1093/hmg/ddq468. PMID 21059704.
  8. ↑ Teles MG, Bianco SD, Brito VN, Trarbach EB, Kuohung W, Xu S; et al. (2008). “A GPR54-activating mutation in a patient with central precocious puberty”. N Engl J Med. 358 (7): 709–15. doi:10.1056/NEJMoa073443. PMC 2859966. PMID 18272894.
  9. ↑ Bouligand J, Ghervan C, Tello JA, Brailly-Tabard S, Salenave S, Chanson P; et al. (2009). “Isolated familial hypogonadotropic hypogonadism and a GNRH1 mutation”. N Engl J Med. 360 (26): 2742–8. doi:10.1056/NEJMoa0900136. PMID 19535795.
  10. ↑ Gianetti E, Tusset C, Noel SD, Au MG, Dwyer AA, Hughes VA; et al. (2010). “TAC3/TACR3 mutations reveal preferential activation of gonadotropin-releasing hormone release by neurokinin B in neonatal life followed by reversal in adulthood”. J Clin Endocrinol Metab. 95 (6): 2857–67. doi:10.1210/jc.2009-2320. PMC 2902066. PMID 20332248.
  11. ↑ González-Martínez D, Kim SH, Hu Y, Guimond S, Schofield J, Winyard P; et al. (2004). “Anosmin-1 modulates fibroblast growth factor receptor 1 signaling in human gonadotropin-releasing hormone olfactory neuroblasts through a heparan sulfate-dependent mechanism”. J Neurosci. 24 (46): 10384–92. doi:10.1523/JNEUROSCI.3400-04.2004. PMID 15548653.
  12. ↑ Falardeau J, Chung WC, Beenken A, Raivio T, Plummer L, Sidis Y; et al. (2008). “Decreased FGF8 signaling causes deficiency of gonadotropin-releasing hormone in humans and mice”. J Clin Invest. 118 (8): 2822–31. doi:10.1172/JCI34538. PMC 2441855. PMID 18596921.
  13. ↑ Cole LW, Sidis Y, Zhang C, Quinton R, Plummer L, Pignatelli D; et al. (2008). “Mutations in prokineticin 2 and prokineticin receptor 2 genes in human gonadotrophin-releasing hormone deficiency: molecular genetics and clinical spectrum”. J Clin Endocrinol Metab. 93 (9): 3551–9. doi:10.1210/jc.2007-2654. PMC 2567850. PMID 18559922.

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2] Luke Rusowicz-Orazem, B.S.

Overview

Hypogonadism is commonly caused by congenital, acquired genetic and endocrinological conditions. Life threatening causes may include malignancies and must take in to consideration during patient approach.[1][2]

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. The following diseases are life threatening causes of hypogonadism:

Common Causes

Causes by Organ System

Cardiovascular Alström syndrome, Amyloidosis, Cardiofaciocutaneous syndrome, Vascular abnormalities of the cns
Chemical/Poisoning Alcohol, Alkylating agents, Cytotoxic therapeutic agents, Environmental toxins, Ethanol, Toxins
Dental Jaffe-campanacci syndrome, Lepromatous leprosy
Dermatologic No underlying causes
Drug Side Effect Antiandrogens, Ketoconazole, Marijuana use, Opioids
Ear Nose Throat No underlying causes
Endocrine Adiposogenital dystrophy, Adrenal hypoplasia, Autoimmune polyendocrine syndrome type 2, Combined pituitary hormone deficiency , Disorders of androgen synthesis, Functional gonadotropin deficiency, Glucocorticoids, Glycoprotein syndrome type 1, Gonadal dysgenesis , Growth hormone secreting pituitary adenoma, Hyperprolactinemia, Hypogonadic hypogonadism, Hypopituitarism, Hypothalamic glioma, Panhypopituitarism, Pituitary tumor, Poems syndrome, Polycystic ovarian disease, Proprotein convertase 1/3 deficiency, Pseudohypoparathyroidism type 1a, Swyer’s syndrome, Testicular biosynthetic defects
Environmental No underlying causes
Gastroenterologic Hepatic cirrhosis
Genetic 17α-hydroxylase deficiency, 17β-hydroxysteroid dehydrogenase iii deficiency, 20-lyase deficiency, 48, xxxy aneuploidy, 48, xxyy aneuploidy, 4h syndrome, Acrocephalopolysyndactyly type 2, Alström syndrome, Aromatase deficiency, Autoimmune oophoritis, Bardet-biedl syndrome, Belgian type mental retardation, Blepharophimosis syndrome, Borjeson-forssman-lehmann syndrome, Boucher-neuhäuser syndrome, Cardiofaciocutaneous syndrome, Ccfdn syndrome, Charge syndrome, Congenital adrenal hypoplasia, Craniofacial anomalies, Craniopharyngioma, Cryptorchidism, Didmoad syndrome, Dystrophia myotonica type 2, Fsh receptor deficiency, Fsh beta subunit mutation (follicle stimulating hormone), Fsh receptor mutation, Galactose-1-phosphate uridyltransferase deficiency, Galactosemia, Gaucher disease, Gordon holmes syndrome, Hartsfield syndrome, Image syndrome, Isolated fsh deficiency, Isolated lh deficiency, Jaffe-campanacci syndrome, Kallmann syndrome, Klinefelter syndrome, Laurence-moon syndrome, Leptin deficiency, Lh (luteinizing hormone) beta subunit mutation, Lh receptor mutation, Lh resistance, Lipoid congenital adrenal hyperplasia, Malouf syndrome, Marinesco-sjogren-garland syndrome, Martsolf syndrome, Mobius syndrome, Mosaicism, Myotonic dystrophy, Noonan syndrome, Prader-willi syndrome, Proprotein convertase 1/3 deficiency, Resistant ovary, Rud syndrome, Sertoli-cell-only syndrome, Turner syndrome, Woodhouse-sakati syndrome, X-linked mental retardation-hypotonic facies syndrome, Xx gonadal dysgenesis
Hematologic Glycoprotein syndrome type 1, Hemochromatosis, Langerhans histiocytosis, Leukoencephalopathy , Zinc deficiency
Iatrogenic Chemotherapy, Opioids, Orchitis, Radiation therapy, Surgery
Infectious Disease Aids, Infections, Mumps
Musculoskeletal/Orthopedic No underlying causes
Neurologic Astrocytoma, Belgian type mental retardation, Craniopharyngioma, Gordon holmes syndrome, Poems syndrome, Postinfectious lesions of the central nervous system (cns), Vascular abnormalities of the cns
Nutritional/Metabolic Zinc deficiency
Obstetric/Gynecologic Exercise-induced amenorrhea, Ovarian resistance syndrome, Ovarian torsion, Polycystic ovarian disease, Premature ovarian failure, Premature menopause, Resistant ovary, Rud syndrome, Suramin, Swyer’s syndrome
Oncologic Astrocytoma, Germinoma, Growth hormone secreting pituitary adenoma, Hypothalamic glioma, Langerhans histiocytosis, Optic glioma, Other germ cell tumors, Pituitary tumor
Ophthalmologic Optic glioma
Overdose/Toxicity Alcohol
Psychiatric Anorexia nervosa
Pulmonary No underlying causes
Renal/Electrolyte Chronic renal failure, Renal failure
Rheumatology/Immunology/Allergy Amyloidosis, Autoimmune damage, Autoimmunity, Chronic systemic illnesses, Lepromatous leprosy
Sexual Aids, Epididymo-orchitis, Germinoma, Orchidectomy, Suramin
Trauma Head trauma, Hepatic cirrhosis, Ovarian torsion, Testicular torsion, Trauma
Urologic Anorchia, Anorchidism, Congenital hypogonadotropic hypogonadism, Cryptorchidism, Disorders of androgen synthesis, Epididymo-orchitis, Gonadal dysgenesis , Hypogonadic hypogonadism, Orchitis, Testicular torsion, Varicocele
Miscellaneous No underlying causes

Causes in Alphabetical Order

References

  1. ↑ Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  2. ↑ Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X

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Differentiating Hypogonadism from other Diseases

Differentiating Hypogonadism from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Hypogonadism must be differentiated from diseases that cause delayed puberty or infertility. These diseases include congenital diseases as Klinefelter syndrome, Kallmann syndrome and cryptorchidism. The diseases also include testicular torsion and orchitis in males, polycystic ovary syndrome, pelvic inflammatory disease, and endometriosis in females.

Differentiating Hypogonadism from other Diseases

Hypogonadism must be differentiated from diseases that cause delayed puberty or infertility. These diseases include congenital diseases as Klinefelter syndrome, Kallmann syndrome and cryptorchidism. The diseases also include testicular torsion and orchitis in males, polycystic ovary syndrome, pelvic inflammatory disease, and endometriosis in females.[1][2][3][4][5][6][7][8][9][10]

Diseases Clinical findings Diagnosis Manangement
Congenital diseases Klinefelter syndrome
  • Language learning impairment
Kallmann syndrome
Cryptorchidism
  • Treatment of cryptorchidism is mainly surgical in order to reduce the risk of malignancy
  • Orchiopexy surgery is recommended in order to reposition the undecsended testes.
Male diseases Testicular torsion Management is mainly surgical through detorsion and fixation of the affected testes.
Orchitis
Female diseases Polycystic ovarian syndrome (PCOS)
Pelvic inflammatory disease
Endometriosis Medical therapy:

Surgery:

References

  1. ↑ Denschlag, Dominik, MD; Clemens, Tempfer, MD; Kunze, Myriam, MD; Wolff, Gerhard, MD; Keck, Christoph, MD (October 2004), “Assisted reproductive techniques in patients with Klinefelter syndrome: A critical review”, Fertility and Sterility, 82 (4): 775–779, doi:10.1016/j.fertnstert.2003.09.085
  2. ↑ Virtanen HE, Bjerknes R, Cortes D, Jørgensen N, Rajpert-De Meyts E, Thorsson AV; et al. (2007). “Cryptorchidism: classification, prevalence and long-term consequences”. Acta Paediatr. 96 (5): 611–6. doi:10.1111/j.1651-2227.2007.00241.x. PMID 17462053.
  3. ↑ Schmitz D, Safranek S (2009). “Clinical inquiries. How useful is a physical exam in diagnosing testicular torsion?”. J Fam Pract. 58 (8): 433–4. PMID 19679025.
  4. ↑ Trojian TH, Lishnak TS, Heiman D (2009). “Epididymitis and orchitis: an overview”. Am Fam Physician. 79 (7): 583–7. PMID 19378875.
  5. ↑ Stewart A, Ubee SS, Davies H (2011). “Epididymo-orchitis”. BMJ. 342: d1543. PMID 21490048.
  6. ↑ Christine Cortet-Rudelli, Didier Dewailly (2006). “Diagnosis of Hyperandrogenism in Female Adolescents”. Hyperandrogenism in Adolescent Girls. Armenian Health Network, Health.am. Unknown parameter |month= ignored (help)
  7. ↑ Legro RS, Barnhart HX, Schlaff WD (2007). “Clomiphene, Metformin, or Both for Infertility in the Polycystic Ovary Syndrome”. N Engl J Med. 356 (6): 551–566. PMID 17287476.
  8. ↑ Brunham RC, Gottlieb SL, Paavonen J (2015). “Pelvic inflammatory disease”. N. Engl. J. Med. 372 (21): 2039–48. doi:10.1056/NEJMra1411426. PMID 25992748.
  9. ↑ Ford GW, Decker CF (2016). “Pelvic inflammatory disease”. Dis Mon. 62 (8): 301–5. doi:10.1016/j.disamonth.2016.03.015. PMID 27107781.
  10. ↑ Murphy AA (2002). “Clinical aspects of endometriosis”. Ann N Y Acad Sci. 955: 1–10, discussion 34-6, 396–406. PMID 11949938.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

The prevalence of hypogonadism in men is estimated to be 38,700 per 100,000 individual aging 45 years. The incidence of hypogonadism is 1230 per 100,000 persons. Hypogonadism affects men more than women and its prevalence increases with age.[1]

Epidemiology and demographics

Prevalence

  • The prevalence of hypogonadism in men is 38,700 per 100,000 persons aged 45 years.[2]
  • The prevalence of androgen deficiency ranges from a low of 6,000 per 100,000 persons aged 40 years to a high of 12,000 per 100,000 persons aging 70 years.[1]
  • There are no sufficient prevalence results for hypogonadism in women.

Incidence

  • The incidence of hypogonadism is 1230 per 100,000 persons.[1] The rate may be increasing[3][4].

Gender

  • Hypogonadism is more common in the males than females.

Age

  • The prevalence of hypogonadism increases with age.

Race

  • There is no racial predilection of hypogonadism.

References

  1. ↑ 1.0 1.1 1.2 Araujo AB, O’Donnell AB, Brambilla DJ, Simpson WB, Longcope C, Matsumoto AM; et al. (2004). “Prevalence and incidence of androgen deficiency in middle-aged and older men: estimates from the Massachusetts Male Aging Study”. J Clin Endocrinol Metab. 89 (12): 5920–6. doi:10.1210/jc.2003-031719. PMID 15579737.
  2. ↑ Mulligan T, Frick MF, Zuraw QC, Stemhagen A, McWhirter C (2006). “Prevalence of hypogonadism in males aged at least 45 years: the HIM study”. Int J Clin Pract. 60 (7): 762–9. doi:10.1111/j.1742-1241.2006.00992.x. PMC 1569444. PMID 16846397.
  3. ↑ Bhasin S (2007). “Secular decline in male reproductive function: Is manliness threatened?”. J Clin Endocrinol Metab. 92 (1): 44–5. doi:10.1210/jc.2006-2438. PMID 17209224.
  4. ↑ Lokeshwar SD, Patel P, Fantus RJ, Halpern J, Chang C, Kargi AY; et al. (2021). “Decline in Serum Testosterone Levels Among Adolescent and Young Adult Men in the USA”. Eur Urol Focus. 7 (4): 886–889. doi:10.1016/j.euf.2020.02.006. PMID 32081788 Check |pmid= value (help).

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Common risk factors in the development of hypogonadism in men are dyslipidemia, obesity, alcohol intake, malignancies and metabolic syndrome. Common risk factors in women include nulliparity and dysmenorrhea. Other risk factors include coronary heart disease, hypertension, heart failure, and smoking.[1]

Risk Factors

Men

Based on several studies done in different populations, many risk factors for hypogonadism have been suggested. The studies ended up into common and less common risk factors which are discussed below.[1][2][3]

Common risk factors in men

Common risk factors of hypogonadism include the following:

Less common risk factors in men

Less common risk factors of hypogonadism include the following:

Women

Based on a study done among women in menopause, various risk factors of hypogonadism or premature ovarian failure were suggested. These risk factors are enlisted below.[7][8]

Common risk factors in women

  • Nulliparous women
  • History of irregular menstrual periods

References

  1. ↑ 1.0 1.1 Zarotsky V, Huang MY, Carman W, Morgentaler A, Singhal PK, Coffin D; et al. (2014). “Systematic literature review of the risk factors, comorbidities, and consequences of hypogonadism in men”. Andrology. 2 (6): 819–34. doi:10.1111/andr.274. PMID 25269643.
  2. ↑ Template:Citejournal
  3. ↑ Laaksonen DE, Niskanen L, Punnonen K, Nyyssönen K, Tuomainen TP, Valkonen VP; et al. (2005). “The metabolic syndrome and smoking in relation to hypogonadism in middle-aged men: a prospective cohort study”. J Clin Endocrinol Metab. 90 (2): 712–9. doi:10.1210/jc.2004-0970. PMID 15536158.
  4. ↑ Li FP, Wang CZ, Huang JM, Yang WT, Lan BY, Ding CZ; et al. (2020). “Obesity-associated secondary hypogonadism in young and middle-aged men in Guangzhou: A single-centre cross-sectional study”. Int J Clin Pract. 74 (8): e13513. doi:10.1111/ijcp.13513. PMID 32304616 Check |pmid= value (help).
  5. ↑ Lokeshwar SD, Patel P, Fantus RJ, Halpern J, Chang C, Kargi AY; et al. (2021). “Decline in Serum Testosterone Levels Among Adolescent and Young Adult Men in the USA”. Eur Urol Focus. 7 (4): 886–889. doi:10.1016/j.euf.2020.02.006. PMID 32081788 Check |pmid= value (help).
  6. ↑ Kolodny, Robert C.; Masters, William H.; Kolodner, Robert M.; Toro, Gelson (18 April 1974). “Depression of Plasma Testosterone Levels after Chronic Intensive Marihuana Use”. New England Journal of Medicine. 290 (16): 872–874. doi:10.1056/NEJM197404182901602. eISSN 1533-4406. ISSN 0028-4793. PMID 4816961.
  7. ↑ Progetto Menopausa Italia Study Group (2003). “Premature ovarian failure: frequency and risk factors among women attending a network of menopause clinics in Italy”. BJOG. 110 (1): 59–63. PMID 12504937.
  8. ↑ Testa G, Chiaffarino F, Vegetti W, Nicolosi A, Caliari I, Alagna F; et al. (2001). “Case-control study on risk factors for premature ovarian failure”. Gynecol Obstet Invest. 51 (1): 40–3. doi:52889 Check |doi= value (help). PMID 11150874.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

If left untreated, patients with hypogonadism will end up with infertility and rheumatic autoimmune diseas. These autoimmune disease include rheumatic arthritis and systemic lupus erythematosus. Complications of hypogonadism depend on age and include ambiguous genitalia in the newborn, gynecomastia, and delay of puberty in the prepubertal phase. Complications also include depression and cardiovascular stroke in the adults. Prognosis of hypogonadism is regarded as good for patients who receive treatment and can have a normal life with appropriate medical therapy.

Natural History

Complications

Complications of hypogonadism depend on the age of the patient. Complications that can develop are enlisted as the following:[2]

Prognosis

  • The prognosis of hypogonadism is good with treatment and patients can have a normal life with the appropriate medical therapy.[3]

References

  1. ↑ Baillargeon J, Al Snih S, Raji MA, Urban RJ, Sharma G, Sheffield-Moore M; et al. (2016). “Hypogonadism and the risk of rheumatic autoimmune disease”. Clin Rheumatol. 35 (12): 2983–2987. doi:10.1007/s10067-016-3330-x. PMID 27325124.
  2. ↑ Arver S, Luong B, Fraschke A, Ghatnekar O, Stanisic S, Gultyev D; et al. (2014). “Is testosterone replacement therapy in males with hypogonadism cost-effective? An analysis in Sweden”. J Sex Med. 11 (1): 262–72. doi:10.1111/jsm.12277. PMID 23937088.
  3. ↑ Rahnema CD, Lipshultz LI, Crosnoe LE, Kovac JR, Kim ED (2014). “Anabolic steroid-induced hypogonadism: diagnosis and treatment”. Fertil Steril. 101 (5): 1271–9. doi:10.1016/j.fertnstert.2014.02.002. PMID 24636400.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therpies

Case Studies

Case Studies

Case #1

External links



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