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The Contegra conduit in the term follow-up of patients with the antibiotic-sterilized aor- right ventricular outfow tract is an independent risk factor for tic homograft valve inserted freehand in the aortic position viagra plus 400mg visa erectile dysfunction 5gs. Inhibition of aortic wall eration of aortic allografts in infants and young children discount viagra plus 400mg with visa erectile dysfunction 37 years old. J calcifcation in bioprosthetic heart valves by ethanol pretreat- Thorac Cardiovasc Surg 1994;107:1162–4. Circulation tics of porcine aortic valves cross-linked with glutaraldehyde 1991;84(Suppl. Percutaneous durability of pulmonary allograft conduits at systemic pres- insertion of the pulmonary valve. Stent fracture, degeneration of pulmonary homografts used as aortic valve valve dysfunction, and right ventricular outfow tract rein- substitute underlines early graft failure. Eur J Cardiothorac tervention after transcatheter pulmonary valve implantation: Surg 2002;22:802–7. Allogenous trans- catheter implantation of an aortic valve prosthesis for calcifc plantation of the mitral valve. Transcatheter aortic- carditis: a valve that can be repaired in the long-term (13 valve implantation for aortic stenosis in patients who cannot years). Congenital mitral ongrowth and tissue detachment in stent mounted heart valve stenosis resulting from anomalous arcade and obstructing allografts and xenografts. Early failure mitral valve replacement with the Bjork-Shiley prosthesis in of the autograft valve after the Ross procedure. Valve replacement in children for the teenager requiring aortic valve replacement. Experience with the Bjork-Shiley Thorac Cardiovasc Surg Pediatr Card Surg Annu 2005;176–80. Replacement of the aortic ment in 372 Marfan patients: evolution of operative repair valve or root with a pulmonary autograft in children. Midterm results of aortic root replacement in children: intermediate-term results. Vascular anasto- ment with the pulmonary autograft in children: a word of cau- moses in growing vessels: the use of absorbable sutures. Long-term results of arterial switch fndings and causes of failure in 24 explanted Ionescu– repair of transposition of the great vessels. Am J Cardiol Vicryl suture material and interrupted and continuous tech- 1980;46:429–38. In term infants, ductal closure usu- ous steal of blood from the systemic circulation during both ally occurs within the frst 24 hours after birth. Since coronary blood fow occurs dur- neonates, the immature ductal tissue is much less reactive ing diastole, there is a risk that coronary blood fow will be to oxygen and persistent patency of the ductus is therefore importantly compromised. Aortoventricular Relationship of the Ductus to the tunnel is a closely related anomaly that shares some of the Recurrent Laryngeal Nerve pathophysiologic features of these anomalies. Embryologically the ductus represents persistence of the distal component of the left sixth aortic arch. It is impor- Embryology tant to recall that the left sixth aortic arch originates in the A patent ductus arteriosus results from a failure of normal neck (branchial = gill). Therefore, the left recurrent laryngeal transition from the fetal to the postnatal circulation. Usually nerve is carried down into the thoracic cavity as the heart and ductal closure occurs initially by constriction of smooth proximal great vessels migrate from a more cervical to a tho- muscle within the wall of the ductus. On the right side, there is usually resorption tact between the opposing intimal cushions, which leads of the right sixth aortic arch, as well as the right ffth aortic to thrombosis. Thus, the right recurrent laryngeal nerve comes to pass weeks and months and the ductus evolves to become the around the remnant of the fourth aortic arch which persists as ligamentum arteriosum. During fetal life, the patency of the ductus is main- tained by both local and circulating prostaglandin. After Atypical Ductal Anatomy birth, increased pulmonary blood fow metabolizes prosta- When there is a right-sided aortic arch because of persistence glandin and absence of the placenta removes an important of the right-sided embryological arches rather than left-sided source of prostaglandin. Subsequently, there is a marked arches, the ductus usually arises from the left subclavian decrease in the circulating level of prostaglandin. It is also artery, which itself arises as the fnal branch of the aortic 267 268 Comprehensive Surgical Management of Congenital Heart Disease, Second Edition arch at the junction of the arch with the proximal descending AssociAtEd AnomAliEs aorta. In this anomaly, absence of the ductus may be a sequently passes anteriorly to join the origin of the left pul- contributing embryological factor in its development. However, a ductus is associated with another cardiac anomaly which the ductus does not always arise from the diverticulum of causes pulmonary hypertension, e. When there is diffcult to visualize the ductus by color Doppler mapping mirror image branching, that is, the frst branch of the right- because there is minimal pressure differential between the sided arch is an innominate artery which branches into a left aorta and pulmonary arteries and therefore little fow. On occasion, the ductus arteriosus may arise from the A patent ductus arteriosus results in a left to right shunt undersurface of a right-sided aortic arch and pass to the right between the aorta and pulmonary arteries. When the ductus is large, pulmonary artery pressure laryngeal nerve passing around the ligamentum. There is increased pulmonary return to the left atrium resulting in dilation of the left atrium, as well as the AnAtomy left ventricle. As is the case for a ventricular septal defect, the degree of left to right shunt will increase in the frst As described above, the location of the ductus is usually left weeks and months of life as pulmonary resistance falls from sided arising from the junction of the aortic isthmus with the its elevated neonatal level. When the ductus is large, it can proximal descending aorta and passing to the origin of the cause a suffcient degree of elevation of pulmonary artery left pulmonary artery. However, the ductus may be situated pressure and fow that pulmonary vascular disease eventu- in a number of other locations, including originating from ally develops. Whatever the location of the ductus, patent ductus can result in retrograde fow from the abdomi- the size and shape can be quite variable. The preterm infant is at particu- frequently with the origin from a left innominate artery or lar risk for this problem if a large ductus is not closed early left subclavian artery. Patency of the ductus in the preterm infant results in a tus is larger than the pulmonary artery end. In the longer term, this “ampulla” of the ductus is helpful to the interventional cardi- can result in chronic lung disease in the form of bronchopul- monary dysplasia. If the It is important for the surgeon to appreciate that the tissue ductus is large, there may be tachypnea at rest. The child will integrity of the ductus varies enormously between the neo- be prone to frequent respiratory infections and will fail to nate and the older child. The pulse fragile structure particularly if the underlying adventitia is pressure is clearly widened both by palpation and blood pres- dissected off (which should be avoided). It must always be sure measurement when the ductus is large and pulmonary handled with the greatest respect. Auscultation of the chest demonstrates the through the ductus in an older child with aggressively frm characteristic systolic murmur extending into diastole or ligation. Consideration must always be given to division of even a continuous machinery murmur that may be best heard the short, wide ductus between clamps if it is anticipated that posteriorly. All of these same physical fndings may be pres- there is a chance that tissue integrity is inadequate to allow ent with aortopulmonary window, sinus of Valsalva fstula simple ligation. Patent Ductus Arteriosus, Aortopulmonary Window, Sinus of Valsalva Fistula, and Aortoventricular Tunnel 269 diAgnostic studiEs echocardiography both before and after the administration of indomethacin.

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The physical examination of the menopausal woman should be a cooperative effort of the doctor and patient order viagra plus 400mg line impotence australia. These problems occur more often in and touching it gently with a cotton-tipped applica- the winter months buy viagra plus 400 mg otc erectile dysfunction 25, with cold air outside and dry tor stick elicits a pain response. They take many area is prone to tear again with every attempt at forms (Figures 12. The diag- complaining of new growths in her private area was nosis can be made by a careful examination of the found to have a genital outbreak of condyloma acu- vulva with cotton-tipped applicators touching the minata (Figure 12. The diagnosis should be con- precancerous vulvar intraepithelial neoplasia 3 frmed by biopsy (Figure 12. The clinical diagnoses of vulvar multiplication, with resulting tissue infammation dystrophy, condyloma acuminatum, and precan- and patient symptomatology. One tion must be done in women with chronic vulvar patient complaining of perineal pain 1–3 days after changes, before any new long duration of therapy intercourse had a painful cluster of lesions, which is contemplated. This was her frst recognized followed by a thorough visual perusal and the use clinical outbreak, and it had been preceded by an of microscopic studies of vaginal secretions and asymptomatic primary infection. These fragile vascular structures are sometimes the source of an increased vaginal discharge. Women with a history of breast cancer who are tak- ing tamoxifen citrate have immature squamous cells present, with an increased number of white cells (Figure 12. Laboratory testing should be individualized to ft the diagnostic needs of each patient. During the suggested 3-year inter- vals between cytologic studies, precancerous cervi- cal changes can occur that will require colposcopy, biopsy, or conization procedures for these patients. Patients present with persis- tent vulvar burning and itching with an increase in their symptomatology every time they urinate. In women not taking estrogen systemically or These women are excellent candidates for local locally, the pH is usually alkaline. Then, the micro- estrogen therapy after a Candida infection is ruled scopic examination is performed. An estradiol cream ration often shows immature squamous cells and can be prescribed that patients apply to the infamed many white cells (Figure 12. Local adrenocor- cal examination, a variety of antiviral agents can ticoid creams or ointments are indicated if there is be immediately prescribed while waiting for the lab widespread infammation or lichen sclerosus is pres- report. The V-600 imaging system that enables the in the perineal area, which on biopsy are shown to observer to view tissue two cell layers under the sur- be condyloma acuminata (Figure 12. A variety face is a great aid in determining the extent of vulvar of ablative techniques or the use of locally applied infammation before and during steroid therapy. If a local yeast infection is confrmed, a In addition to the readiness to culture any infam- local nystatin cream can be ordered. If this causes matory lesions, the physicians must be prepared to a local contact dermatitis, oral fuconazole therapy biopsy any new suspicious growths on the vulva. After this treatment, local steroids can be a variety of treatment options are available to the prescribed. The usual course is close Postmenopausal women with infections of the observation over time with repeated biopsies to be vulva should be managed with specifc care directed sure there has been no progression of the lesions toward the pathogen identifed by laboratory stud- in this area. If any of these women complain of the sudden of the vulva is confrmed by biopsy (Figures 12. These gynecologic oncologist so that vulvar resection and may be clinically obvious lesions (Figure 12. These ing of a vaginal discharge or vaginal burning requires cases demonstrate the importance of obtaining a an accurate diagnosis for there can be a variety of Vulvovaginal Infections 134 etiologies for these symptoms. Symptoms due to the A large group of postmenopausal patients com- presence of an endometrial polyp (Figure 12. On examination, they have other, uncommon, benign causes of an increase in an alkaline vaginal pH, a negative whiff test, and on vaginal symptoms in these women. Rarely, a foreign microscopic examination, immature squamous cells, body is found, and when it is removed, the patient an increased number of white cells, and a diminu- becomes asymptomatic. If the cultures grow no Candida Vaginal infections in these menopausal women and no bacterial pathogens, a local form of estrogen should be based upon laboratory fndings. If the iso- this estrogen therapy improved the bacterial fora of late is Candida krusei or Candida glabrata, local these women, it was not as effective as a daily dose or oral azoles are not indicated, and a regimen with of oral nitrofurantoin in preventing urinary tract local boric acid is begun for a 2-week treatment infections in this population. The microscopic examination intravaginal estradiol cream given daily for 2 weeks of the saline preparation shows immature squa- is usually effective. If the patient has had a reaction mous cells and an infammatory response with an to the cream in the past or has a reaction with cur- increased number of white cells (Figure 12. Local estrogen, which should reverse this pro- who cannot or will not take estrogen, vaginal acid cess, is usually not indicated. The periodic use of gels can be employed, supplemented with the vaginal an acidic vaginal gel helps some patients, but relief use of vaginal boric acid once or twice a week. This always comes when the tamoxifen citrate therapy is maintains the normal acid state of the vagina for a terminated. The introduction of new, more effective time and does result in a diminution of the vaginal agents, such as exemestane, should reduce the over- symptoms in many of these women. If either is positive, then biopsy to determine whether there are more severe appropriate antibiotic therapy should be prescribed. Writing Group for the Women’s Health Initia- nants of the increased prevalence of high- tive Investigators. Incidence vaginal estriol in postmenopausal women with and clearance of genital human papillomavi- recurrent urinary tract infection. Exploratory comparison on vaginal glycogen Antibody response to infuenza vaccination and lactobacillus levels in premenopausal and in the elderly: A quantitative review. Vaginal microfora in post- in proinfammatory cytokine activity after menopausal women who have not received menopause. Investigation among postmenopausal women in the of the sensitivity of a cross-polarized light United States. J Gerontol B Psychol Sci Soc Sci visualization system to detect subclinical 2014;69(Suppl 2):S205–S214. The years of tamoxifen therapy in postmenopausal relationship of bacterial vaginosis, Candida women with primary breast cancer. Chronic saries and nitrofurantoin microcrystal therapy vulvovaginitis in women older than 50 years: in the prevention of recurrent urinary tract Analysis of a prospective database. Her minute-to-minute awareness is that her vul- This heightened awareness by physicians was fol- var pain, whether constant or only with contact, is lowed by attempts of clinical investigators to divide so severe that intercourse becomes a trial of pain; and categorize the different clinical presentations even the insertion of a tampon is avoided because of this syndrome, i. The practitioners, these women are an unwanted intru- pain was described as provoked vulvodynia, where sion, smack-dab in the middle of an overcrowded the patient remains free of pain until vaginal entry offce schedule. These sufferers do not ft nicely is attempted, and unprovoked vulvodynia, in which into any of the recognizable categories of pathol- vulvar pain is constant. The pain has been further ogy for which doctors have a straightforward plan subdivided as localized, limited to a discrete por- of care. These women remain a cipher for the busy tion of the vulva, the vestibular glands, or the cli- physician and are dismissed from any future con- toris, or generalized, affecting the whole anatomic sideration with such hurtful postexamination com- vulvar site. It’s all in your which permits evaluation of the tissue at a depth of head” or “Just drink a glass of wine and relax.

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Bone mineral density usually improves following curative surgery in patients with Cushing’s syndrome because of the preserved bone microarchitecture (tra- becular pattern) purchase viagra plus 400mg erectile dysfunction treatment los angeles. Patients of Cushing’s syndrome who are elderly buy generic viagra plus canada impotence home remedies, have osteo- porosis/fracture or have a low probability of cure should be offered anti-osteoporotic therapy, whereas younger individuals who have osteopenia without fractures and have a high probability of cure do not need anti-osteopo- rotic therapy. Teriparatide may be preferred over bisphosphonates for the treatment of osteo- porosis in patients with both endogenous as well as exogenous Cushing’s syndrome. The diagnosis of Cushing’s syndrome: an endocrine society clinical practice guideline. She had menarche at the age of 12 years, and soon after she started having menorrhagia. She had progres- sive increase in hair growth all over the body along with weight gain of 10 kg for the past 3 years. There was no history of galactorrhea, striae, easy bruisibility, or proxi- mal myopathy. She resorted to cosmetic measures including laser for her hirsutism without significant improvement. There was no acne, temporal recession, or low-pitch voice, but she had clitoromegaly and male torso without any features of defeminiza- tion. She did not have features of protein catabolism like striae, bruise, and proxi- mal myopathy or any stigma of acromegaly. In addition, there were bilateral bulky ovaries with multiple tiny cystic areas suggestive of polycystic ovaries. At 6 weeks of follow-up, her hirsute score was same, but the frequency of cosmetic mea- sures was reduced. Unfortunately our patient never had a thorough evaluation for the etiological diagnosis. The differential diagnosis in this scenario includes androgen-secreting adrenal or ovarian tumors, ovarian hyperthecosis, Cushing’s syndrome, and use of androgens or androgenic progestins. Slow and pro- gressive development of features of virilization without any defeminization and lack of palpable abdominal or pelvic mass virtually excludes the possibility of androgen- secreting ovarian or adrenal malignant tumors. Virilization with defeminization is usu- ally seen with severe and rapid-onset hyperandrogenism and denotes the presence of androgen-secreting ovarian or adrenal malignant tumors. Ovarian hyperthecosis is unlikely as these patients commonly present in the postmenopausal period with severe manifestations of hyperandrogenism. Possibility of Cushing’s syndrome in our patient was low as she did not have any mani- festations of protein catabolism. Size of the adrenal tumor was >4 cm in the index patient, and the probability of malignancy with a tumor size between 4. The biochemical improvement precedes clinical improvement by weeks to months as shed- ding of preexisting hair depends on the duration of hair cycle, as seen in our patient. Androgens are normally produced by the ovary and adrenals in women, but when it is associated with clinical features and/or biochemical evidence of androgen excess, they constitute “disorders of androgen excess. The clinical manifestations of androgen excess are hirsutism, acne, androgenic alopecia, low-pitch voice, male torso, and clitoromegaly. The features of virilization in a woman include androgenic alopecia, acne, low- pitch voice, male torso, and clitoromegaly. These are the manifestations of severe androgen excess and are due to ovarian/adrenocortical malignancy or ovarian hyperthecosis. The features of defeminization include breast atrophy, oligomenorrhea/amenor- rhea, and loss of gluteofemoral adiposity. These are the features of estrogen defi- ciency; however, they may be present with severe virilization, as androgen excess interferes with the binding of estrogen to its nuclear receptor. In a rapidly grow- ing androgen-secreting tumor, features of defeminization precede virilization. Hirsutism is defined as excessive terminal hair growth in “male pattern” in an androgen-dependent area in a woman. The “male pattern” hair should not be considered synonymous with “hair in androgen-dependent areas” as axillary and pubic hair common to both men and women are also present in an androgen- dependent area but are not included in the “male pattern. The terminal hair are thick, coarse, and pigmented and are present in androgen-dependent areas as opposed to vellus hair which are fine, thin, and unpigmented and are distributed all over the body. Hair present in almost all areas of the body is androgen dependent except eye- brows, eyelashes, nostrils, and lateral and occipital scalp hair (asexual hair). The axillary and pubic hair are common to both gender and are sensitive to low levels of androgen (ambosexual hair). However, hair on the upper lip, chin, chest, upper arms, abdomen, back, and thighs require a higher level of androgens and characterize the “male pattern” (sexual hair). On the contrary, scalp hair are the only exception where androgen excess results in regression. This is due to short- ened anagen phase and possibly androgen receptor downregulation. Most of the hair in women are androgen dependent, but some hair are estrogen dependent, e. This is evident by maximal scalp hair growth seen during pregnancy, and it occurs due to prolongation of the anagen phase because of estrogen. Further, despite normal adrenarche, pubarche is absent in patients with hypogonadotropic hypogonadism and Turner’s syndrome as adrenal andro- gens act in concert with estrogen for the appearance of pubic and axillary hair. This is evidenced by the absence of hair in these areas in patients with 5α-reductase deficiency. However, there is a poor correlation between hair growth and serum androgen 130 6 Disorders of Androgen Excess levels as hair growth also depends on local growth factors and end-organ sensi- tivity. Hair follicular growth is a continuous process characterized by a period of growth (anagen), transition (catagen), and rest (telogen). The anagen phase for scalp hair usually lasts for 2–6 years followed by the catagen phase lasting for 1–2 weeks and finally ends into the telogen phase for 4–6 weeks. Estrogen regulates the anagen phase of the scalp hair and is responsible for longer hair in women. Ovary and adrenal are the primary source of androgens, and adipose tissue is involved in the peripheral conversion of weaker androgens (e. Therefore, pathogenic abnormalities causing hirsutism involve ovary, adrenal gland or adipose tissue. Other endocrine disorders associated with hirsutism include Cushing’s syndrome, acromegaly, and hyper- prolactinemia. Drugs causing hirsutism are phenytoin, minoxidil, cyclosporine, diazoxide, and androgens or androgenic progestins. Idiopathic hirsutism is the diagnosis of exclusion and is characterized by regular menstruation, normal androgen profile, and no ovarian or adrenal abnormalities. Modified Ferriman–Gallaway score is an objective score to define hirsutism, and a score >8 is considered as significant.

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How to decide whether bone age is signifcantly advanced over chronological age or not? The table given below shows standard deviation for bone age at various chronological ages in boys and girls from age of 1 year to 17 years buy 400 mg viagra plus fast delivery erectile dysfunction doctors fort lauderdale. The recommended dose of leup- rolide acetate depot is 140–300 μg/Kg/month intramuscularly buy viagra plus 400mg on line erectile dysfunction causes yahoo, while that of triptorelin acetate depot is 60 μg/Kg/month intramuscularly. Three monthly formulations of these agonists are also available and are equally effective as compared to monthly preparations. However, fnal adult height may not improve in children aged >6 years at initiation of therapy, possibly because of signifcant advancement of bone age at presentation. This occurs as a result of reduced feedback inhibition at hypothalamus due to decrease in gonadal steroids. Hormonal evaluation should be performed after 8–12 weeks of initia- tion of therapy and every 3–6 monthly, thereafter. In boys, there is a decrease in testicular volume, thinning of pubic hair, resolution of acne and seborrhea, and improvement in aggressive behavior. These clinical improve- ments are evident within 6 months of initiation of therapy. Height velocity steadily decreases in the initial years of therapy, accompanied with retarded progression of bone age. In a study, it was shown that mean height velocity decreased from pretreatment value of 8. In children with precocity who are treated for psychosocial concerns, therapy can be stopped at an age appropriate for the pubertal development for that par- ticular race (e. In girls, pro- gression of pubertal signs starts within 3–6 months after discontinuation of 6 Precocious Puberty 209 therapy, menses resumes within 1–1. Ovarian follicular cyst spontaneously regresses and does not require surgical treatment in majority of children. Optimal therapy with glucocorticoids and fudrocortisone results in regression of secondary sexual characteristics in children with congenital adrenal hyperplasia. Ketoconazole acts by inhibiting cytochrome P450-dependent enzymes involved in steroidogenesis. Fulvestrant, a pure antiestrogen, has been shown to be effective in some of these children. Patients with isolated premature pubarche are at a higher risk for the development of polycystic ovarian disease due to coexisting hyperinsulinemia Further Readings 1. Final height after long-term treatment with triptorelin slow-release for central precocious puberty: importance of statural growth after interruption of treatment. Final height after long-term treatment with triptorelin slow release for central precocious puberty: importance of statural growth after interruption of treatment. Reexamination of the age limit for defning when puberty is preco- cious in girls in the United States: implications for evaluation and treatment. Leuprolide stimulation testing for the evaluation of early female sexual maturation. He was born at term through normal vaginal delivery, and his devel- opmental milestones were normal. He noticed appear- ance of pubic and axillary hair by 15 years of age, but failed to develop facial or body hair or increase in penile length or size of the testes. There was no history of head trauma, surgery for midline defects, chronic systemic illness, testicular trauma, mumps, or drug abuse. He had no history of abnormality in smell, visual defcits, headache, seizure disorder, or other neurological defcits. Tanner stage of pubertal development was A+, P2, and both testes were present within poorly devel- oped scrotal sac and soft in consistency and measured 1 ml each. He had genu valgum but no midline defects, synkinesia, nystagmus, ataxia, and visual defcits. On investigations, com- plete blood count and liver and renal function tests were normal. The doses of testosterone were increased gradually to 200 mg every fortnightly over a period of 2 years. He is planned for gonadotropin therapy for induction of spermatogenesis after the attainment of virilization (Fig. Delayed puberty in boys is defned as lack of pubertal development by the age of 14 years which is in correspondence with 2. Our patient presented at the age of 19 years with poor development of secondary sexual characteristics; therefore, the diagnosis of hypogonadism as a cause of delayed puberty was considered. Development of secondary sexual characteristics results from both adrenarche and gonadarche which may overlap or come in succession. Patients with hypogonadism usually have normal onset of adrenarche, but pubarche is delayed as was seen in our patient who had appearance of pubic hair at the age of 15 years without evidence of gonadarche. This is because the weaker adrenal androgens require conversion to potent andro- gens in functional testes for induction of pubarche. Long- leggedness, gynecomastia, small frm testes, learning disabilities/behavioral abnor- malities, and some degree of virilization favor the diagnosis of Klinefelter’s syndrome which is considered as prototype of hypergonadotropic hypogonadism. Our patient had eunuchoidal proportions, skeletal deformities (genu valgum), and small soft testes which support the diagnosis of hypogonadotropic hypogonadism. Hypogonadotropic hypogonadism can be due to hypothalamic or pituitary lesion or due to familial or sporadic genetic mutations. Defective migration of olfactory neurons from olfactory placode to bulb results in impaired development of olfactory bulb and consequent anosmia. For induction of sec- ondary sexual characteristics, testosterone therapy is initiated with a low dose of testosterone esters (testosterone enanthate 50–100 mg) intramuscularly every month which is gradually built up to 200–250 mg every fortnightly over a period of 2–3 years. Improvement in libido, mood, and quality of life is observed over a period of 3–6 months, whereas increase in body hair, muscle mass and strength, and deepening of voice take longer time over a period of 1–2 years. Serum testos- terone should be measured midway between the two injections after 3 months of initiation of treatment to assess the adequacy of therapy; however, it may also be required to measure serum testosterone just prior to the next injection to decide about the dosing interval. The adverse effects associated with testosterone therapy include gynecomastia, aggressive behaviour, priapism, mood swings, acne, and androgenic alopecia. In addition, limited data is available regarding the use of gonadotropins as a primary therapy in induction of secondary sexual characteristics. The index patient was initiated with 100 mg tes- tosterone every monthly for 3 months, and later the dose frequency was increased to fortnightly. At 6 months of follow-up, his serum testosterone was 5 nmol/L and he had improvement in generalized well-being. Once the serum testosterone level is maintained >9 nmol/L, semen analy- sis should be performed at monthly interval. The predictors of response to gonadotropin therapy include initial larger testicular volume, prior history of gonadotropin therapy, and absence of prior androgen therapy.

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