Clinical Endocrinology (1977) 6, 11-15.
LUTEINIZING HORMONE, FOLLICLE STIMULATING HORMONE AND TESTOSTERONE IN NORMAL AND IMPOTENT MEN FOLLOWING LHRH AND HCG STIMULATION G . DELITALA, A. MASALA, S . ALAGNA A N D G. LOTTI
Cattedra di Medicina Costituzionale ed Endocrinologia, University of Sassari, Italy
(Received 25 May 1976; revised 21 July 1976; accepted 2 August 1976) SUMMARY
The effect of synthetic LHRH on plasma concentrations of LH, FSH, testosterone and testosterone response to i.v. HCG was studied in fifteen normal men and in fifteen men with impotence. The mean basal concentrations of LH, FSH and testosterone in the men with impotence were not significantly different from those of the normal group. A normal response of gonadotrophins and testosterone was also observed. It is concluded that a normal pituitary sensitivity to synthetic LHRH and a normal response to endogenous and exogenous gonadotrophins exist in this particular disorder.
Impotence may result from organic hypothalamic-pituitary and testicular disfunction or may complicate severe chronic disease; moreover, it may be due to treatment with certain drugs such as certain antihypertensive agents or phenothiazines. When none of these factors is involved impotence is usually assumed to be of psychogenic origin (Anon., 1970). It is indeed accepted that at least 90% of all cases of impotence are psychogenic. Most authors now believe that organic disorders are relatively rare and that in the majority of patients psychogenic factors are dominant (Cooper, 1970). There are few published data on plasma testosterone levels in psychological impotence which show similarity in the plasma sex steroid concentration both in normal and impotent males (Racey et al., 1973; Lawrence & Swyer, 1974). However, an impaired response in testosterone excretion to human chorionic gonadotrophin (HCG) and low plasma testosterone levels with high levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) have been reported (Ismail etal., 1970; Magrini et al., 1973). In the present study we determined the plasma FSH, LH and testosterone response to synthetic luteinizing hormone releasing hormone (LHRH) in impotent men in order to elucidate further the possible mechanism of this particular disorder. In addition, the testicular response to i.v. HCG administration was studied. Correspondence: Dr G. Delitala, Cattedra di Medicina Costituzionale ed Endocrinologia, University of Sassari, Vide S. Pietro 12,07100 Sassari, Italy.
11
12
G. Delitala et al. MATERIALS AND METHODS
Fifteen normal adult men aged 22-40 and fifteen male patients aged between 21 and 46 with a primary complaint of impotence were investigated. None of these patients was taking any drug likely to cause impotence. On clinical examination external genitalia and secondary sex characteristics were normal and no evidence of major organic disorders was found. Ejaculation was possible and a specimen of semen was obtained from each subject: all had normal seminal fluid examination. Laboratory data including an oral glucose tolerance test and studies of hepatic and renal function gave normal results. No gross abnormality in endocrine function was present clinically or as judged from plasma 1 1-hydroxy-corticosteroids (Mattingly, 1962), urinary 17-oxogenic steroids (Appleby et al., 1971) and 17-oxosteroids (Vestergaard, 197 l), serum thyroxine (T4(D),Tetralute) labelled triiodothyronine uptake by Sephadex G-25 (RT$J%, Trilute), and X-rays of the pituitary fossa. The LHRH test was performed according to Besser et al. (1972) with a 100 pg dose of the substance (Relisorm-Serono) rapidly injected intravenously: results in normal subjects have previously been reported (Delitala et aE., 1973). Ten patients in the group and ten normal subjects underwent an i.v. HCG test: HCG (Profasi-Serono) at a dose of 5000 iu was dissolved in 150 ml isotonic saline and infused over a period of half an hour: blood samples were drawn at times 0, 15,30,45,60,90, 120, 150, 180,240 and 300 min from the beginning of the infusion. An interval of at least 10 days elapsed between the LHRH and the HCG tests. All tests were performed in the morning at 09.00 hours after an overnight fast and the subjects remained in bed or sitting. Serum LH and FSH concentrations were measured in duplicate by a double-antibody radioimmunoassay (Midgley, 1966, 1967) in all samples drawn: the results are expressed as miu of the 2nd IRP-HMG/ml serum. Standards, labelled hormones and antisera (human pituitary LH antiserum and human pituitary FSH antiserum) were furnished by Serono Immunochemicals, Rome, Italy. In our laboratory 1 miu LH is equivalent to 5 ng of LER 907, and 1 miu FSH is equivalent to 35 ng of LER 907. The intra-assay coefficient of variation as calculated from the duplicate was 5% and 4% for LH and FSH respectively. The interassay coefficient of variation as calculated from the results obtained by the two different assay procedures, amounted t o 9.8% for LH and 7.8% for FSH. The sensitivity of the method is about 0.8 miu/ml: the normal value range in our laboratory varies from 5 to 20 miu/ml for LH and FSH. Serum testosterone was determined by a double-antibody radio-immunoassay (Collins, 1972), using standards, antiserum and te~tosterone-3-TME-'~~I provided by Serono Immunochemicals. The method's sensitivity is 3.5 nmol/l: the intra-assay error of the method, measured as the coefficient of variation, amounted to 0.9%. The inter-assay coefficient of variation was 9.7%. In our laboratory normal values for adult male subjects are 17.3-34.7 nmolll. Student's t test was used for statistical analysis. RESULTS The plasma testosterone levels in the normal males ranged from 20.5 to 3 1.2 nmol/l (mean f SE 24.0 k 1.26). The range for plasma LH and FSH varied between 5.0 and 11.0 miu/ml (mean +. SE 6.95 f 0.46) and between 5.5 and 8.5 miu/ml (mean k SE 6.75 k 0.24) res-
13
Plasma gonadotrophins and testosterone in impotent men Table 1. Plasma testosterone (nmol/l) response t o i.v. HCG in impotent and normal men (mean f SE)
0 min
15
30
45
60
90
120
150
180
240
300
rnin
min
rnin
min
rnin
min
min
min
min
min
19.8 1.45
19.9 1.61
22.8 3.16
27.7 2.37
31.9 2.78
32.0 3.98
34.8 3.19
36.3 5.15
37.0 6.51
29.0 3.82
22.2 1.45
21.8 1.23
28.4 3.48
34.2 3.76
39.9 2.91
46.4 4.52
46.7 4.14
43.7 3.82
31.2 4.68
31.4 3.70
Jmpotent men
w
21.0 1.23 SE
Normal men
X SE
24.0 1.26
pectively. The men with impotence had values ranging from 19.0 to 27.7 nmol/l (mean It SE 21.0 k 1.23) for testosterone, 5.5-16 miu/ml (mean -+ SE 7.34 k 0.75) for LH and 5.0-8.5 (mean t SE 6.57 -+ 0.29) for FSH. Concentrations of plasma testosterone and gonadotrophin after an i.v. injection of 100 pg synthetic LHRH are shown in Fig. 1. The mean values of LH, FSH and testosterone in the men with impotence were not significantly different from those in the normal group (P > 0.05). Administration of LHRH induced a significant rise in plasma LH (P< 0.001), FSH (P< 0.001) and testosterone (P < 0.01) concentrations, both in normal and impotent men. CHRH
IIIIIIII
0
15 30
I
I
I
I
I
I
60
90
120
IIIIIIII
I
11111II
I
0
15
30
I
I
1
I
I
I
60
90
120
Time (min)
Fig. 1. Concentrations of plasma LH, FSH and testosterone after an i.v. 100 pg synthetic LHRH injection in impotent and normal men. Means k SE are reported. Open circles denote impotent men, filled circles denote normal men.
14
G. Delitala et al.
The LH,FSH and testosterone response to LHRH in impotent men were comparable to that of the controls (P>0.05).; Following stimulation with HCG there was an increase in testosterone from 24.0 to 46.7 nmol/l in normals, from 21.0 t o 37.0 nmol/l in patients (Table 1). No statistical differences were found between the two groups (P> 0.05). DISCUSSION In clinical practice psychogenic impotence is commonly treated with androgen preparations, administered either orally or by injection, usually with no resultant clinical improvement. This attempt at therapy is justified by some authors’ findings showing the overall mean urinary testosterone excretion t o be lower in impotent men than in normal subjects (Cooper, 1970; Ismail et al., 1970). Previous data on impotence have in fact shown high discrepancies between plasma and urinary testosterone levels, the latter being markedly lower in impotent men. Our findings show a normal hypophyseal-gonadal response to synthetic LHRH in impotent men and no deficiency in either plasma testosterone or gonadotropins. Changes in plasma testosterone levels after treatment with HCG and in testosterone and LH-FSH patterns after synthetic LHRH reported here confirm previously published results for normal men (Maurer et al., 1971, 1973; Masala et al., 1974; Judd et al., 1974; Kley et al., 1974, 1976). The present study shows that the pituitary-gonadal response to LHRH and the testosterone response to i.v. HCG administration in impotent men is comparable to that of normals. The acute gonadotrophin rise induced by i.v. LHRH administration exerted a stimulatory action on Leydig cell function as assessed by changes in circulating levels of testosterone concentrations both in normals and patients: these statistically significant testosterone rises were always greater than any spontaneous fluctuation during the baseline study. Synthetic LHRH seems to stimulate Leydig cell function in man indirectly via the stimulation of increased pituitary gonadotrophin release (Kley et al., 1974, 1976): previous studies in animals were unable to show any direct effect of LHRH on Leydig cell function. We did not detect any differences in the testosterone response of normal and impotent men to an i.v. HCG injection. For the moment we are unable to explain the discrepancy between our finding of a normal plasma testosterone response to i.v. HCG administration and the low urinary testosterone excretion reported by other workers. Data reported by Ismail ef a/. (1970) indicate that i.m. HCG stimulation had little or no effect on testosterone excretion in four impotent men: our results, based on a greater number of patients and on a different route of HCG administration, do not show this difference. We can conclude that in impotence of psychological origin the secretory capacity of the pituitary, as well as that of the gonads, is apparently normal and does not appear to bear any direct relationship to the underlying mechanism of the disease. REFERENCES ANON. ( 1 970) Androgenic function and impotence. British Medical Journal, iii, 3-4. APPLEBY, G.L., GIBSON, G . , NORYMBERSKY, I.K. & STUBBS, E.D. (1971) In: Hormone Assays and their Clinical Application (ed. by J . A. Loraine and E. T. Bell), pp. 442-443. Livingstone, Edinburgh. BESSER, G.M., McNEILLY, A S . , ANDERSON, D.C., MARSHALL, J.C., HARSOULIS, P., HALL, R., ORMSTON, B.J., ALEXANDER, L. & COLLINS, W.P. (1972) Hormonal response to synthetic luteinizing hormone and follicle stimulating hormone-releasing hormone in man. British Medical Journal, iii, 267-271.
Plasma gonadotrophins and testosterone in impotent men
15
COLLINS, W.P. (1972) Radioimmunoassay of plasma testosterone. Journal of Steroid Biochemistry, 3,333-338. COOPER, A.J. (1970) Guide to treatment and short-term prognosis of male potency disorders in hospital and general practice. British Medical Journal, i, 157-159. DELITALA, G., MASALA, A. & LOTTI, G . (1973) Plasma gonadotropin behaviour after an i.v. 100 fig synthetic Gn-RF injection in normal subjects. Studi Sassaresi, 51, 191-206. ISMAII,, A.A.A., DAVIDSON, D.W. & LORAINE, J.A. (1970) Assessment of gonadal function in hpotent men. Reproductive Endocrinology (ed. by W. J . Irvine),pp. 138-147. Livingstone, Edinburgh. JUDD, H.L., REBAR, R., VANDENBERC, G . & YEN, S.S.C. (1974) Effect of luteinizing hormonereleasing factor on Leydig cell function. Journal of Clinical Endocrinology and Metabolism, 38,8-13. KLEY, H.K., WIEGELMAN, W., NIESCHLAG, E., SOLBACH, H.G., ZIMMERMANN, H. & KRUSKEMPTER, H.L. (1974) LH, FSH and testosterone in plasma following LH-RH infusion: a combined test for pituitary and Leydig cell function. Acta Endocrinologica, 75,417-427. KLEY, H.K., NIESCHLAG, E., WIEGELMANN, W. & KRUSKEMPER, H.L. (1976) Oestrone, oestradiol and testosterone in normal and hypogonadal men following LH-RH or HCG stimulation. Acta Endocrinologica, 81,616-622. LAWRENCE, D.M. & SWYER, G.I.M. (1974) Plasma testosterone and testosterone binding affinities in men with impotence, oligospermia, azoospermia and hypogonadism. British Medical Journal, i, 349351. MAGRINI, G., LEMARCHAND-BERAUD, T., REUDI, B., FELBER, J.P. & VANNOTTI, A. (1973) Plasma levels of sex steroids and gonadotropins in male infertility and impotence. Acta Endocrinologica, Suppl. 177,56. MASALA, A., DELITALA, G., ALAGNA, S., ROVASIO, P.P. & DEVILLA, L. (1974) Effect of intravenously administered human chorionic gonadotropin (HCG) on plasma testosterone and oestrogens levels in man. Studi Sassaresi, 52,347-355. MATTINGLY, D. (1962) A simple fluorimetric method for the estimation of free 1 l-hydroxycorticosteroids in human plasma. Journal of Clinical Pathology, 15, 374-379. MIDGLEY, A.R., J r (1966) Radioimmunoassay: a method for human chorionic gonadotropin and human luteinizing hormone. Endocrinology, 79, 10-18. MIDGLEY, A.R., Jr (1967) Radioimmunoassay for human follicle stimulating hormone. Journal of CIinical Endocrinology and Metabolism, 27,295-299. MAURER, W., TAMM, J . & VOLKWEIN, U. (1971) The effect of intravenously administered HCG on plasma concentration of testosterone, dihydrotestosterone and progesterone in normal adult males. Acta Endocrinologica, Suppl. 155, 61. MAURER, W., VOLKWEIN, U. & TAMM, J . (1973) The effect of intravenously administered human chorionic gonadotropin on plasma levels of testosterone and 5-adihydrotestosterone in normal male subjects. Acta Endocrinologica, 72,615-624. RACEY, P.A., ANSARI, M.A., ROWE, P.H. & GLOVER, T.D. (1973) Testosterone in impotent men. Journal of Endocrinology, 59, xxiii. VESTERGAARD, P. (1971) In: Hormone Assays and their Clinical Application (ed. by J . A. Loraine and E. T. Bell), pp. 508-509. Livingstone, Edinburgh.
LUTEINIZING HORMONE, FOLLICLE STIMULATING HORMONE AND TESTOSTERONE IN NORMAL AND IMPOTENT MEN FOLLOWING LHRH AND HCG STIMULATION G . DELITALA, A. MASALA, S . ALAGNA A N D G. LOTTI
Cattedra di Medicina Costituzionale ed Endocrinologia, University of Sassari, Italy
(Received 25 May 1976; revised 21 July 1976; accepted 2 August 1976) SUMMARY
The effect of synthetic LHRH on plasma concentrations of LH, FSH, testosterone and testosterone response to i.v. HCG was studied in fifteen normal men and in fifteen men with impotence. The mean basal concentrations of LH, FSH and testosterone in the men with impotence were not significantly different from those of the normal group. A normal response of gonadotrophins and testosterone was also observed. It is concluded that a normal pituitary sensitivity to synthetic LHRH and a normal response to endogenous and exogenous gonadotrophins exist in this particular disorder.
Impotence may result from organic hypothalamic-pituitary and testicular disfunction or may complicate severe chronic disease; moreover, it may be due to treatment with certain drugs such as certain antihypertensive agents or phenothiazines. When none of these factors is involved impotence is usually assumed to be of psychogenic origin (Anon., 1970). It is indeed accepted that at least 90% of all cases of impotence are psychogenic. Most authors now believe that organic disorders are relatively rare and that in the majority of patients psychogenic factors are dominant (Cooper, 1970). There are few published data on plasma testosterone levels in psychological impotence which show similarity in the plasma sex steroid concentration both in normal and impotent males (Racey et al., 1973; Lawrence & Swyer, 1974). However, an impaired response in testosterone excretion to human chorionic gonadotrophin (HCG) and low plasma testosterone levels with high levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) have been reported (Ismail etal., 1970; Magrini et al., 1973). In the present study we determined the plasma FSH, LH and testosterone response to synthetic luteinizing hormone releasing hormone (LHRH) in impotent men in order to elucidate further the possible mechanism of this particular disorder. In addition, the testicular response to i.v. HCG administration was studied. Correspondence: Dr G. Delitala, Cattedra di Medicina Costituzionale ed Endocrinologia, University of Sassari, Vide S. Pietro 12,07100 Sassari, Italy.
11
12
G. Delitala et al. MATERIALS AND METHODS
Fifteen normal adult men aged 22-40 and fifteen male patients aged between 21 and 46 with a primary complaint of impotence were investigated. None of these patients was taking any drug likely to cause impotence. On clinical examination external genitalia and secondary sex characteristics were normal and no evidence of major organic disorders was found. Ejaculation was possible and a specimen of semen was obtained from each subject: all had normal seminal fluid examination. Laboratory data including an oral glucose tolerance test and studies of hepatic and renal function gave normal results. No gross abnormality in endocrine function was present clinically or as judged from plasma 1 1-hydroxy-corticosteroids (Mattingly, 1962), urinary 17-oxogenic steroids (Appleby et al., 1971) and 17-oxosteroids (Vestergaard, 197 l), serum thyroxine (T4(D),Tetralute) labelled triiodothyronine uptake by Sephadex G-25 (RT$J%, Trilute), and X-rays of the pituitary fossa. The LHRH test was performed according to Besser et al. (1972) with a 100 pg dose of the substance (Relisorm-Serono) rapidly injected intravenously: results in normal subjects have previously been reported (Delitala et aE., 1973). Ten patients in the group and ten normal subjects underwent an i.v. HCG test: HCG (Profasi-Serono) at a dose of 5000 iu was dissolved in 150 ml isotonic saline and infused over a period of half an hour: blood samples were drawn at times 0, 15,30,45,60,90, 120, 150, 180,240 and 300 min from the beginning of the infusion. An interval of at least 10 days elapsed between the LHRH and the HCG tests. All tests were performed in the morning at 09.00 hours after an overnight fast and the subjects remained in bed or sitting. Serum LH and FSH concentrations were measured in duplicate by a double-antibody radioimmunoassay (Midgley, 1966, 1967) in all samples drawn: the results are expressed as miu of the 2nd IRP-HMG/ml serum. Standards, labelled hormones and antisera (human pituitary LH antiserum and human pituitary FSH antiserum) were furnished by Serono Immunochemicals, Rome, Italy. In our laboratory 1 miu LH is equivalent to 5 ng of LER 907, and 1 miu FSH is equivalent to 35 ng of LER 907. The intra-assay coefficient of variation as calculated from the duplicate was 5% and 4% for LH and FSH respectively. The interassay coefficient of variation as calculated from the results obtained by the two different assay procedures, amounted t o 9.8% for LH and 7.8% for FSH. The sensitivity of the method is about 0.8 miu/ml: the normal value range in our laboratory varies from 5 to 20 miu/ml for LH and FSH. Serum testosterone was determined by a double-antibody radio-immunoassay (Collins, 1972), using standards, antiserum and te~tosterone-3-TME-'~~I provided by Serono Immunochemicals. The method's sensitivity is 3.5 nmol/l: the intra-assay error of the method, measured as the coefficient of variation, amounted to 0.9%. The inter-assay coefficient of variation was 9.7%. In our laboratory normal values for adult male subjects are 17.3-34.7 nmolll. Student's t test was used for statistical analysis. RESULTS The plasma testosterone levels in the normal males ranged from 20.5 to 3 1.2 nmol/l (mean f SE 24.0 k 1.26). The range for plasma LH and FSH varied between 5.0 and 11.0 miu/ml (mean +. SE 6.95 f 0.46) and between 5.5 and 8.5 miu/ml (mean k SE 6.75 k 0.24) res-
13
Plasma gonadotrophins and testosterone in impotent men Table 1. Plasma testosterone (nmol/l) response t o i.v. HCG in impotent and normal men (mean f SE)
0 min
15
30
45
60
90
120
150
180
240
300
rnin
min
rnin
min
rnin
min
min
min
min
min
19.8 1.45
19.9 1.61
22.8 3.16
27.7 2.37
31.9 2.78
32.0 3.98
34.8 3.19
36.3 5.15
37.0 6.51
29.0 3.82
22.2 1.45
21.8 1.23
28.4 3.48
34.2 3.76
39.9 2.91
46.4 4.52
46.7 4.14
43.7 3.82
31.2 4.68
31.4 3.70
Jmpotent men
w
21.0 1.23 SE
Normal men
X SE
24.0 1.26
pectively. The men with impotence had values ranging from 19.0 to 27.7 nmol/l (mean It SE 21.0 k 1.23) for testosterone, 5.5-16 miu/ml (mean -+ SE 7.34 k 0.75) for LH and 5.0-8.5 (mean t SE 6.57 -+ 0.29) for FSH. Concentrations of plasma testosterone and gonadotrophin after an i.v. injection of 100 pg synthetic LHRH are shown in Fig. 1. The mean values of LH, FSH and testosterone in the men with impotence were not significantly different from those in the normal group (P > 0.05). Administration of LHRH induced a significant rise in plasma LH (P< 0.001), FSH (P< 0.001) and testosterone (P < 0.01) concentrations, both in normal and impotent men. CHRH
IIIIIIII
0
15 30
I
I
I
I
I
I
60
90
120
IIIIIIII
I
11111II
I
0
15
30
I
I
1
I
I
I
60
90
120
Time (min)
Fig. 1. Concentrations of plasma LH, FSH and testosterone after an i.v. 100 pg synthetic LHRH injection in impotent and normal men. Means k SE are reported. Open circles denote impotent men, filled circles denote normal men.
14
G. Delitala et al.
The LH,FSH and testosterone response to LHRH in impotent men were comparable to that of the controls (P>0.05).; Following stimulation with HCG there was an increase in testosterone from 24.0 to 46.7 nmol/l in normals, from 21.0 t o 37.0 nmol/l in patients (Table 1). No statistical differences were found between the two groups (P> 0.05). DISCUSSION In clinical practice psychogenic impotence is commonly treated with androgen preparations, administered either orally or by injection, usually with no resultant clinical improvement. This attempt at therapy is justified by some authors’ findings showing the overall mean urinary testosterone excretion t o be lower in impotent men than in normal subjects (Cooper, 1970; Ismail et al., 1970). Previous data on impotence have in fact shown high discrepancies between plasma and urinary testosterone levels, the latter being markedly lower in impotent men. Our findings show a normal hypophyseal-gonadal response to synthetic LHRH in impotent men and no deficiency in either plasma testosterone or gonadotropins. Changes in plasma testosterone levels after treatment with HCG and in testosterone and LH-FSH patterns after synthetic LHRH reported here confirm previously published results for normal men (Maurer et al., 1971, 1973; Masala et al., 1974; Judd et al., 1974; Kley et al., 1974, 1976). The present study shows that the pituitary-gonadal response to LHRH and the testosterone response to i.v. HCG administration in impotent men is comparable to that of normals. The acute gonadotrophin rise induced by i.v. LHRH administration exerted a stimulatory action on Leydig cell function as assessed by changes in circulating levels of testosterone concentrations both in normals and patients: these statistically significant testosterone rises were always greater than any spontaneous fluctuation during the baseline study. Synthetic LHRH seems to stimulate Leydig cell function in man indirectly via the stimulation of increased pituitary gonadotrophin release (Kley et al., 1974, 1976): previous studies in animals were unable to show any direct effect of LHRH on Leydig cell function. We did not detect any differences in the testosterone response of normal and impotent men to an i.v. HCG injection. For the moment we are unable to explain the discrepancy between our finding of a normal plasma testosterone response to i.v. HCG administration and the low urinary testosterone excretion reported by other workers. Data reported by Ismail ef a/. (1970) indicate that i.m. HCG stimulation had little or no effect on testosterone excretion in four impotent men: our results, based on a greater number of patients and on a different route of HCG administration, do not show this difference. We can conclude that in impotence of psychological origin the secretory capacity of the pituitary, as well as that of the gonads, is apparently normal and does not appear to bear any direct relationship to the underlying mechanism of the disease. REFERENCES ANON. ( 1 970) Androgenic function and impotence. British Medical Journal, iii, 3-4. APPLEBY, G.L., GIBSON, G . , NORYMBERSKY, I.K. & STUBBS, E.D. (1971) In: Hormone Assays and their Clinical Application (ed. by J . A. Loraine and E. T. Bell), pp. 442-443. Livingstone, Edinburgh. BESSER, G.M., McNEILLY, A S . , ANDERSON, D.C., MARSHALL, J.C., HARSOULIS, P., HALL, R., ORMSTON, B.J., ALEXANDER, L. & COLLINS, W.P. (1972) Hormonal response to synthetic luteinizing hormone and follicle stimulating hormone-releasing hormone in man. British Medical Journal, iii, 267-271.
Plasma gonadotrophins and testosterone in impotent men
15
COLLINS, W.P. (1972) Radioimmunoassay of plasma testosterone. Journal of Steroid Biochemistry, 3,333-338. COOPER, A.J. (1970) Guide to treatment and short-term prognosis of male potency disorders in hospital and general practice. British Medical Journal, i, 157-159. DELITALA, G., MASALA, A. & LOTTI, G . (1973) Plasma gonadotropin behaviour after an i.v. 100 fig synthetic Gn-RF injection in normal subjects. Studi Sassaresi, 51, 191-206. ISMAII,, A.A.A., DAVIDSON, D.W. & LORAINE, J.A. (1970) Assessment of gonadal function in hpotent men. Reproductive Endocrinology (ed. by W. J . Irvine),pp. 138-147. Livingstone, Edinburgh. JUDD, H.L., REBAR, R., VANDENBERC, G . & YEN, S.S.C. (1974) Effect of luteinizing hormonereleasing factor on Leydig cell function. Journal of Clinical Endocrinology and Metabolism, 38,8-13. KLEY, H.K., WIEGELMAN, W., NIESCHLAG, E., SOLBACH, H.G., ZIMMERMANN, H. & KRUSKEMPTER, H.L. (1974) LH, FSH and testosterone in plasma following LH-RH infusion: a combined test for pituitary and Leydig cell function. Acta Endocrinologica, 75,417-427. KLEY, H.K., NIESCHLAG, E., WIEGELMANN, W. & KRUSKEMPER, H.L. (1976) Oestrone, oestradiol and testosterone in normal and hypogonadal men following LH-RH or HCG stimulation. Acta Endocrinologica, 81,616-622. LAWRENCE, D.M. & SWYER, G.I.M. (1974) Plasma testosterone and testosterone binding affinities in men with impotence, oligospermia, azoospermia and hypogonadism. British Medical Journal, i, 349351. MAGRINI, G., LEMARCHAND-BERAUD, T., REUDI, B., FELBER, J.P. & VANNOTTI, A. (1973) Plasma levels of sex steroids and gonadotropins in male infertility and impotence. Acta Endocrinologica, Suppl. 177,56. MASALA, A., DELITALA, G., ALAGNA, S., ROVASIO, P.P. & DEVILLA, L. (1974) Effect of intravenously administered human chorionic gonadotropin (HCG) on plasma testosterone and oestrogens levels in man. Studi Sassaresi, 52,347-355. MATTINGLY, D. (1962) A simple fluorimetric method for the estimation of free 1 l-hydroxycorticosteroids in human plasma. Journal of Clinical Pathology, 15, 374-379. MIDGLEY, A.R., J r (1966) Radioimmunoassay: a method for human chorionic gonadotropin and human luteinizing hormone. Endocrinology, 79, 10-18. MIDGLEY, A.R., Jr (1967) Radioimmunoassay for human follicle stimulating hormone. Journal of CIinical Endocrinology and Metabolism, 27,295-299. MAURER, W., TAMM, J . & VOLKWEIN, U. (1971) The effect of intravenously administered HCG on plasma concentration of testosterone, dihydrotestosterone and progesterone in normal adult males. Acta Endocrinologica, Suppl. 155, 61. MAURER, W., VOLKWEIN, U. & TAMM, J . (1973) The effect of intravenously administered human chorionic gonadotropin on plasma levels of testosterone and 5-adihydrotestosterone in normal male subjects. Acta Endocrinologica, 72,615-624. RACEY, P.A., ANSARI, M.A., ROWE, P.H. & GLOVER, T.D. (1973) Testosterone in impotent men. Journal of Endocrinology, 59, xxiii. VESTERGAARD, P. (1971) In: Hormone Assays and their Clinical Application (ed. by J . A. Loraine and E. T. Bell), pp. 508-509. Livingstone, Edinburgh.
