Androgens in Health and Disease.pdf - E Library

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Chapter 3/Hypogonadism in Men 45 3 Hypogonadism in Men An Overview Stephen R. Plymate, MD CONTENTS INTRODUCTION CLINICAL CHARACTERISTICS OF HYPOGONADISM PRIMARY HYPOGONADISM CHEMOTHERAPY SECONDARY HYPOGONADISM COMBINED PRIMARY AND SECONDARY HYPOGONADISM SUMMARY REFERENCES INTRODUCTION Male hypogonadism may be defined as a failure of the testes to produce testosterone or sperm. This may be caused by a failure of the testes, anterior pituitary gland, or hypothalamus. Hypogonadism may also occur if a testicular product is unable to exert an effect, such as in the androgen-resistance syndromes. CLINICAL CHARACTERISTICS OF HYPOGONADISM The clinical presentation of hypogonadism depends on whether the onset was in utero, prepubertal, or postpubertal. If hypogonadism is present because of a defect that occurred in utero, the individual will have ambiguous genitalia. The clinical pictures of testicular androgen failure of prepubertal and postpubertal onset are presented in Tables 1 and 2. If the hypogonadism is manifest only as infertility, physical findings may be normal. With the development of sensitive assays for testosterone and free or unbound testosterone, an increasing number of circumstances have been described in which serum testosterone levels are lower than normal without any obvious end-organ deficiencies. Examples of this phenomenon are seen in aging or stressed men who have low levels of serum testosterone without definitive evidence of end-organ deficiency. In the case of stress, end-organ deficiency may not be seen, because the period of hypogonadism is transient. It may be difficult to decide whether these men really are androgen deficient or whether they simply are displaying a physiologic response to stress or age. These From: Contemporary Endocrinology: Androgens in Health and Disease Edited by: C. Bagatell and W. J. Bremner © Humana Press Inc., Totowa, NJ 45
46 Plymate Table 1 Classification of Male Hypogonadism Primary Hypogonadism Klinefelter syndrome XX males XY/XO mixed gonadal dysgenesis XYY syndrome Ullrich–Noonan syndrome Myotonia dystrophica Sertoli-cell-only syndrome Functional prepubertal castrate Enzymatic defects involving testosterone biosynthesis 5α-reductase deficiency Luteinizing hormone gonadotropin-resistant testis Persistent mullerian duct syndrome Male pseudohermaphroditism involving androgen receptor defects Testicular feminization Reifenstein syndrome Infertility resulting from a receptor defect After orchitis Cryptorchidism Leprosy Testicular trauma Testicular irradiation Autoimmune testicular failure Chemotherapy Secondary Hypogonadism Hypogonadotropic hypogonadism Isolated luteinizing hormone or follicle-stimulating hormone deficiency Acquired gonadotropin deficiencies Prolactin-secreting pituitary tumors Severe systemic illness Uremia Hemochromatosis Combined Primary and Secondary Etiology Aging Hepatic cirrhosis Sickle-cell disease situations pose further difficulties for clinicians who must decide whether androgen replacement is needed. In those situations in which obvious deficiency states are not present, the indication for replacement therapy may not be clear-cut. In some of these patients, the finding of an exaggerated gonadotropin response to gonadotropin-releasing hormone (GnRH) may help to define the presence of testicular failure. Functionally, the hypogonadal states may be classified according to the level at which the hypothalamic–pituitary–testicular axis is defective. Briefly, the control of testicular function begins with the release, in a pulsatile fashion, of GnRH from the hypothalamus. GnRH, transported by the hypothalamic pituitary portal system, then causes the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior
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CONTEMPORARY ENDOCRINOLOGY Androgen
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CONTEMPORARY ENDOCRINOLOGY P. Micha
Page 5 and 6: © 2003 Humana Press Inc. 999 River
Page 7 and 8: vi Preface We hope Androgens in Hea
Page 9 and 10: viii Contents 13 Androgens and Body
Page 11 and 12: x Contributors RICHARD S. LEGRO, MD
Page 13 and 14: 2 Winters and Clark
Page 15 and 16: 4 Winters and Clark chorionic gonad
Page 17 and 18: 6 Winters and Clark LH REGULATION O
Page 19 and 20: 8 Winters and Clark These enzymes a
Page 21 and 22: 10 Winters and Clark -subunit mRNA
Page 23 and 24: 12 Winters and Clark Fig. 3. A sche
Page 25 and 26: 14 Winters and Clark Table 1 Factor
Page 27 and 28: 16 Winters and Clark Table 2 Tissue
Page 29 and 30: 18 Winters and Clark 11. Thomas JL,
Page 31 and 32: 20 Winters and Clark 61. Dufau ML,
Page 33 and 34: 22 Winters and Clark 112. Raivio T,
Page 35 and 36: 24 Brown Fig. 1. Mechanism for andr
Page 37 and 38: 26 Brown increase in intracellular
Page 39 and 40: 28 Brown Fig. 2. Structural and fun
Page 41 and 42: 30 Brown Fig. 3. Amino acid sequenc
Page 43 and 44: 32 Brown tions to shuttle the AR th
Page 45 and 46: 34 Brown Fig. 4. Amino acid primary
Page 47 and 48: 36 Brown part of an inactive chroma
Page 49 and 50: 38 Brown the external genitalia is
Page 51 and 52: 40 Brown tors, as well as the trans
Page 53 and 54: 42 Brown 49. Williams SP, Sigler PB
Page 55: 44 Brown 100. Gregory CW, He B, Joh
Page 59 and 60: 48 Plymate In addition to the direc
Page 61 and 62: 50 Plymate LABORATORY FINDINGS In p
Page 63 and 64: 52 Plymate those manifesting as phe
Page 65 and 66: 54 Plymate result in some improveme
Page 67 and 68: 56 Plymate If both testosterone and
Page 69 and 70: 58 Plymate Persistent Müllerian Du
Page 71 and 72: 60 Plymate INFERTILITY RESULTING FR
Page 73 and 74: 62 Plymate unaffected, contralatera
Page 75 and 76: 64 Plymate SECONDARY HYPOGONADISM H
Page 77 and 78: 66 Plymate Other syndromes manifest
Page 79 and 80: 68 Plymate period after the burn. I
Page 81 and 82: 70 Plymate These findings suggest t
Page 83 and 84: 72 Plymate 49. Goebelsmann U, Horto
Page 85 and 86: 74 Plymate 104. Yoshimoto Y, Moride
Page 87 and 88: 76 Plymate
Page 89 and 90: 78 Sutton, Amory, and Clark levels
Page 91 and 92: 80 Sutton, Amory, and Clark cebo in
Page 93 and 94: 82 Sutton, Amory, and Clark Finaste
Page 95 and 96: 84 Sutton, Amory, and Clark through
Page 97 and 98: 86 Sutton, Amory, and Clark 40. The
Page 99 and 100: 88 Sutton, Amory, and Clark 88. Rob
Page 101 and 102: 90 Lindzey and Korach Fig. 1. Cellu
Page 103 and 104: 92 Lindzey and Korach estrogen sign
Page 105 and 106: 94 Lindzey and Korach TESTIS AND DU
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96 Lindzey and Korach sufficient to
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98 Lindzey and Korach Seminal Vesic
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100 Lindzey and Korach 17. Krege JH
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102 Lindzey and Korach 68. Chang WY
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104 McPhaul on the Y chromosome det
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106 106 McPhaul
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108 McPhaul number of alleles, dele
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110 McPhaul The first mutation of t
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112 McPhaul gene. In vitro studies
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114 McPhaul risk of impaired sperma
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116 McPhaul carrying a single mutan
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118 McPhaul REFERENCES 1. Koopman P
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120 McPhaul 45. Weidemann W, Peters
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122 McPhaul 92. Koivisto P, Kononen
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124 Legro Fig. 1. The spectrum of p
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126 Legro Virilization presents wit
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128 Legro Fig. 3. The paradox of an
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130 Legro small high-density athero
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132 Legro Table 2 Syndromes or Dise
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134 Legro Insulin-Sensitizing Agent
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136 Legro is undetermined according
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138 Legro 39. Lee O, Farquhar C, To
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140 Legro
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142 Wang and Swerdloff PHARMACOLOGY
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144 Wang and Swerdloff The 17α-alk
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146 Wang and Swerdloff Table 2 Dose
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148 Wang and Swerdloff The steroid
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150 Wang and Swerdloff The inabilit
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152 Wang and Swerdloff 15. De Lorim
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154 Wang and Swerdloff
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156 Marcelli et al.
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158 Marcelli et al. Differentiated
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160 Marcelli et al. These coactivat
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162 Marcelli et al. tigators have e
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164 Marcelli et al. AR in Prostate
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166 Marcelli et al. Table 1 Androge
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168 Marcelli et al. A molecular exp
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170 Marcelli et al. The above data
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172 Marcelli et al. up to 9 yr late
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174 Marcelli et al. Three major pha
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176 Marcelli et al. vitro model of
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178 Marcelli et al. yr, survival wa
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180 Marcelli et al. 26. McKenna NJ,
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182 Marcelli et al. 78. Isaacs J, C
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184 Marcelli et al. 126. Watanabe M
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186 Marcelli et al. 177. Kousteni S
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188 Marcelli et al. 231. Colombel M
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190 Marcelli et al.
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192 Wu and von Eckardstein contrace
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194 Wu and von Eckardstein beam com
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196 Wu and von Eckardstein excess o
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198 Wu and von Eckardstein Endogeno
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Table 3 Change in Lipids in Hypogon
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Table 3 (continued) ∆LDL ∆HDL
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204 Wu and von Eckardstein THE HEMO
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206 Wu and von Eckardstein In vivo
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208 Wu and von Eckardstein (uptake
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210 Wu and von Eckardstein 4. Bhasi
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212 Wu and von Eckardstein 57. Barr
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214 Wu and von Eckardstein 107. Fra
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216 Wu and von Eckardstein 152. Zmu
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218 Wu and von Eckardstein 201. Cho
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220 Wu and von Eckardstein 250. Eic
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222 Kenny and Raisz with a cartilag
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224 Kenny and Raisz METABOLISM OF A
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226 Kenny and Raisz The level of th
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228 Kenny and Raisz REFERENCES 1. G
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230 Kenny and Raisz 51. Morishima A
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232 Kenny and Raisz 103. Snyder PJ,
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234 Basaria and Dobs losses in wome
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236 Basaria and Dobs 15 dialysis pa
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238 Basaria and Dobs duced remissio
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240 Basaria and Dobs hematocrit lev
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242 Basaria and Dobs 40. Sanchez-Me
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244 Katznelson in men with testoste
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246 Katznelson Fig. 1. Body weight,
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248 Katznelson change during treatm
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250 Katznelson testosterone or free
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252 Katznelson disproportionate dec
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254 Katznelson have been additional
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256 Katznelson 18. Marin P, Lonn L,
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258 Katznelson 71. Davis SR, McClou
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260 Bancroft Androgen Deficiency an
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262 Bancroft studies had presented
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264 Bancroft Bagatell et al. (36) g
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266 Bancroft much larger group of a
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268 Bancroft In a report of a serie
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270 Bancroft onset was related to a
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272 Bancroft Particularly confusing
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274 Bancroft 4. Studies using place
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276 Bancroft either E and T or plac
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278 Bancroft cytotoxic therapy supp
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280 Bancroft Women with Endocrine A
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282 Bancroft in response to the fil
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284 Bancroft Men are much more awar
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286 Bancroft 22. Morales A, Johnsto
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288 Bancroft 78. Hyde JS, DeLamater
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290 Bancroft 129. Appelt H, Strauss
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292 Cherrier and Craft Fig. 1. Path
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294 Cherrier and Craft ment of the
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296 Cherrier and Craft information
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298 Cherrier and Craft Fig. 3. Wech
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300 Cherrier and Craft gen excess r
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302 Cherrier and Craft occurring wi
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304 Cherrier and Craft gesting that
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306 Cherrier and Craft 39. Gouchie
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308 Cherrier and Craft 94. Kelso WM
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310 Cherrier and Craft
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312 Matsumoto
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314 Matsumoto long-term benefits an
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316 Matsumoto manifestations (7). F
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318 Formulation Usual adult dosage
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320 Matsumoto Fig. 1. Mean serum T
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322 Matsumoto dosage is increased g
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324 Matsumoto Androgel 5 g (50 mg o
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326 Matsumoto gen receptor and tiss
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328 Matsumoto such as hepatic cirrh
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330 Matsumoto occasionally, more se
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332 Matsumoto 27. Bhasin S, Bremner
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334 Matsumoto 77. Dobs AS, Meikle A
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336 Richmond and Rogol PHYSIOLOGY O
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338 Richmond and Rogol activity (28
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340 Richmond and Rogol increase lin
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342 Richmond and Rogol curve, the h
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344 Richmond and Rogol Permanent hy
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346 Richmond and Rogol 46. Stanhope
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348 Tenover In aging men, the combi
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350 Tenover Table 1 Changes in Andr
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352 Tenover studies in which eugona
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354 Tenover Table 3 Testosterone Th
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356 Tenover Table 5 ART in Older Me
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358 Tenover be overcome with either
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360 Tenover Laboratory tests should
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362 Tenover 40. Kohrt WM, Malley MT
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364 Tenover 95. Mooradian AD, Morle
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366 Davis Table 1 Proposed Androgen
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368 Davis transdermal testosterone
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370 Davis increase in circulating t
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372 Davis (93). Most recently, Zhou
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374 Davis Table 4 Androgen Replacem
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376 Davis 8. Vierhapper H, Nowotny
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378 Davis 60. Simberg N, Titinen A,
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380 Davis
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382 Bhasin, Woodhouse, and Storer h
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384 Table 2 Effects of Testosterone
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386 Bhasin, Woodhouse, and Storer e
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388 Bhasin, Woodhouse, and Storer F
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390 Bhasin, Woodhouse, and Storer t
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Table 3 Effects of Testosterone Sup
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Table 4 Effects of Testosterone Sup
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396 Bhasin, Woodhouse, and Storer c
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398 Bhasin, Woodhouse, and Storer C
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400 Bhasin, Woodhouse, and Storer w
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402 Bhasin, Woodhouse, and Storer 4
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404 Bhasin, Woodhouse, and Storer
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406 Amory Fig. 1. The endocrinology
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408 Amory pregnancies fathered by t
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410 Amory antagonists can suppress
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412 Amory 100-mg doses of weekly TE
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414 Amory FUTURE DIRECTIONS Given t
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416 Amory 22. Oral contraception. I
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418 Amory
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420 Anawalt inadequate androgen eff
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422 Anawalt few specialty commercia
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424 Anawalt Fig. 1. (C) Secondary h
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426 Anawalt Fig. 2. Evaluation and
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428 Anawalt All men with secondary
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430 Anawalt anemia (38). With the a
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432 Anawalt osterone levels achieve
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434 Anawalt SIDE EFFECTS OF ANDROGE
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436 Anawalt 7. Rosner W. Errors in
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438 Anawalt 59. Mackey MA, Conway A
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440 Index polycystic ovaries, 131 A
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442 Index lipoid congenital adrenal
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444 Index women, 254 dihydrotestost
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446 Index Pituitary adenoma, male h
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448 Index lipoid congenital adrenal
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