Failure of Growth Hormone-Suppressing Agents to Affect TSH-Releasing Hormone- and LH-Releasing Hormone-Induced Growth Hormone Release in Acromegaly* KOJI NAKAGAWA AND TAKAO OBARA Second Department of Medicine, Hokkaido University School of Medicine, Sapporo, 060, Japan patients whose basal GH levels were lowered with these agents alone. These results seem to indicate that dexamethasone does not affect TRH- or LHRH-induced GH release per se, but affects the basal state which determines the absolute level of response. They also support the concept that TRH and LHRH act directly on pituitary tumor cells to release GH in acromegaly. (J Clin Endocrinol Metab 44: 189, 1977)
ABSTRACT. In patients with acromegaly whose basal plasma GH levels were suppressed with 9 mg/day of dexamethasone for 2 days, TRH-(6 cases) and LHRH-(1 case) induced GH release were unaffected when the responses were compared to the basal levels. Phentolamine infusion, 70 mg in 150 min, or hyperglycemia induced by iv infusion of 700 ml of 50% glucose solution also did not suppress TRH-induced GH release in 2 acromegalic
I
T IS well known that TSH releasing hormone (TRH) and LH releasing hormone (LHRH) induce GH release in some acromegalic patients (1,2) and the prompt and unusually high response suggests that the action of these releasing hormones is different from that of other stimuli. We previously reported that dexamethasone and phentolamine suppressed basal plasma GH levels in some acromegalic patients (3,4), and marked hyperglycemia also decreased plasma GH concentration in some acromegalics with lower GH secreting activity (5). Therefore, we examined the effects of these GH suppressing agents on TRH- or LHRH-induced GH release in patients with acromegaly.
Materials and Methods Nine patients with acromegaly were studied in this series. Two were treated; the first (#3p) was 7 years post irradiation and the second (#28p) had a partial hypophysectomy 2 months, and irradiation 26 months, prior to these studies. In 8 patients (#31-34, 36, 38, 3p and 28p), 500 /*g of TRH (Tanabe Pharmaceutical Co., Osaka, Japan) were injected SC at or about 1000 h after overnight fast and bed rest. Blood was drawn every 15 or 30 min from 30 min before to 120 or 180 min after the injection. In one patient (#37), 200 /*g of LHRH (Tanabe Pharmaceutical Co.) was injected and blood was drawn in the same manner as TRH test. To examine the effect of dexamethasone, 9 mg/day Received March 8, 1976. * Supported in part by the grants from the Ministry of Health and Welfare and the Ministry of Education of Japan.
of the drug were administered orally in 4 divided doses for two days as the previous studies (3,4) and the TRH or LHRH test was repeated. In one case (#38), the effect of hydrocortisone was examined by infusing 400 mg of hydrocortisone (sodium succinate, Solu-Cortef®) in 500 ml physiological saline from 0600 through 1000 h and injecting TRH at 1000 h. In 2 cases (#31 and 32), 70 mg of phentolamine (Regitine®) in 500 ml of physiological saline was infused in 150 min, and 60 min after the beginning of the infusion, the third TRH test was performed. On separate days, these patients received another TRH injection 30 min after the start of the infusion of 700 ml of 50% glucose solution in 120 min. Plasma GH levels were determined by double-antibody radioimmanoassay, and expressed in terms of NIH-GH-HS1147BC. The coefficients of variation were 5.9% at the level of 2.0 ng/ml and 5.2% around the level of 100 ng/ml. When 2 basal levels were determined in a test, the lower value was considered as the basal level in the test.
Results Effect of dexamethasone and hydrocortisone The plasma GH response to TRH injection before and after dexamethasone administration is shown in Figs. 1 and 2 and Table 1. In 6 patients presented in Fig. 1, TRH injection caused a remarkable increase of plasma GH levels; the peak levels were 4.0 to 32.8 times the basal levels. After dexamethasone treatment, the basal levels decreased by 27 to 88%; TRH injection, however, again caused a definite response with the peak levels of 4.6 to 104.0 times the basal levels, comparable to those before dexamethasone.
189
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JCE & M • 1977 Vol 44 • No 1
COMMENTS
190 IOOQ 500
#31
#
#32
3p
# 28 p
TRH
TRH
TRH
100
50
t TRH
#
34
#36
t
t TRH
TRH
0 3 0 6 0 9 0 GO
0 30 6090G0I50B0 -30 0 30 6090120 -30 0 30 60 90 BO BO BO
-30 0 306090 12015080 -30 6 306090E0B0B0
minutes
FIG. 1. Plasma GH response to TRH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 6 dexamethasone- and TRH-responsive acromegalic patients. IOOQ
# 36
500
TRH
i
100 SO TRH
# 33
-30 6 306090 BOBOBO -30 0 30(09012000180
In one patient (#33), dexamethasone did not cause suppression, but rather an increase of the basal GH level. The peak level of plasma GH with TRH injection was 7.2 times the basal level before dexamethasone and 4.0 times after dexamethasone. Another patient (#36) did not show any response to TRH injection. The basal level decreased by 57% with dexamethasone, but TRH again did not cause any increase of plasma GH level (Fig. 2). In one dexamethasone- and TRH-responsive patient presented in Fig. 1 (#38), hydrocortisone treatment also caused a similar effect; the basal level decreased from 101 to 15 ng/ml by 85%, and 753% increase was observed with TRH injection, comparable to 688% increase in control TRH test (Fig. 3). An acromegalic patient (#37) responded to LHRH injection with an increase of 267% of the basal GH level. Dexamethasone decreased the basal level by 76% in this patient, but the response to LHRH remained unblocked; the increase was 3.8 times the suppressed basal level (Fig. 4).
minute*
FIG. 2. Plasma GH response to TfiH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 1 dexamethasoneunresponsive and TRH-responsive acromegalic patient (left panel) and 1 dexamethasone-responsive and TRH-unresponsive patient (right panel).
Effect of phentolamine In 2 cases of acromegaly (#31 and #32), 50 mg of phentolamine infused in 90 min suppressed basal GH levels by 73 and 39%, respectively.
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191
COMMENTS TABLE 1. Plasma GH response to TRH or LHRH before and after dexamethasone After
Before Patient no.
TRH injection 31 32
Basal
Peak
ng/ml
ng/ml
2.8 8.4 2.2
3p
72.5 190 23.4
Peak Basal
Basal
Peak
ng/ml
ng/ml
1.3 3.8
38.7 125
25.9 22.6 10.6
1.6
32.8 7.9
2.5 33.0
39.1
4.0
4.2
79.0 44.0
571 55.0
7.2 1.3
157 18.9
42.0
154
3.7
10.0
34 38
30.7 96
28p
9.7
33 36 LHRH injection 37
1,008 756
18.6 260 361 19.5 634
48.3
Peak Basal
29.8 32.9 11.6 104.0 10.9 4.6 4.0
4.8
However, 70 mg of phentolamine infused in 150 min from 60 min before the TRH injection to
I00Q
90 min thereafter did not cause any change in GH response to TRH (Fig. 5).
500
Effect of hyperglycemia In 2 acromegalic patients (#31 and 32), hyperglycemia induced by the infusion of 50% glucose solution lowered basal GH levels by 41 and 58%, respectively (5), but hyperglycemia of similar degree induced from 30 min before the TRH injection until 90 min after did not affect TRH-induced GH release (Fig. 6).
Discussion In this study, dexamethasone, 9 mg/day for 2 days, did not suppress plasma GH response to TRH or LHRH when the peak levels were expressed in relation to the basal levels. These basal levels were remarkably decreased in a major part of acromegalic patients, confirming our previous studies (3,4). Recently, when this study was in progress, Tolis et al. reported that 400 mg of hydro-
IOO 50
I 10:
t TRH
§
# 38
o
Q.
r
FiG. 3. Plasma GH response to TRH before (closed circles and solid lines) and after (open circles and dotted lines) hydrocortisone infusion in 1 dexamethasone- and TRH-responsive acromegalic patient.
Hyfrocortisonc 400mg *
-240
-30 0 3060 90120 minutes
The Endocrine Society. Downloaded from press.endocrine.org by [${individualUser.displayName}] on 15 November 2015. at 05:48 For personal use only. No other uses without permission. . All rights reserved.
JCE & M • 1977 Vol 44 • No 1
COMMENTS
192
# 31
IOOQ
# 32
500
TRH
500
# 37 100 50
100 50
IO
70 mg
? ia
t
i
LHRH
-9O-G0-3O 0 30 60 90 120
o a.
-90-60-30 0 30 60 90 GO
FIG. 5. Plasma GH response to TRH before (closed circles and solid lines) and during (open circles and dotted lines) phentolamine infusion in 2 phentolamine- and TRH-responsive patients.
-30 6 306090120(5060 mlnutti FIG. 4. Plasma GH response to LHRH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 1 dexamethasone- and LHRHresponsive patient. cortisone infused in 4 h prior to TRH injection blocked plasma GH response to TRH without affecting basal levels in 2 acromegalic patients (6). We followed this procedure in the last patient (#38), but the result in this patient was similar to that seen after dexamethasone; the basal level was remarkably decreased and TRH caused GH release comparable to the control test.
# 31
500
#
32
TRH
TRH
i
i
100 50
IO|
° 5 Glucose 50% 700 m
Glucose 50% 700ml
FlG. 6. Plasma GH response to TRH before (closed circles and solid lines) and during (open circles and dotted lines) glucose infusion in 2 hyperglycemiaand TRH-responsive patients.
-60-30 0 30 6090120
-60-30 0 306090120
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COMMENTS These results seem to indicate that glucocorticoids do not affect TRH- or LHRH-induced GH release per se, but affect the basal state which contributes the basal release and the absolute level of response. Phentolamine or hyperglycemia, which decreased basal plasma GH levels, also did not modify the release of GH with TRH. TRHinduced GH release has been reported not to be suppressed with L-Dopa (7), 2-bromo-a-ergocryptine (8) or somatostatin (9). This refractoriness, along with the fact that pituitary tumor cells of GH-secreting adenoma released GH in vitro in response to TRH (10), supports the concept that TRH (and probably LHRH also) acts directly on pituitary tumor cells to release GH in acromegalics. References 1. Irie, M., and T. Tsushima, Increase of serum growth hormone concentration following thyrotropin-releasing hormone injection in patients with acromegaly and gigantism.y Clin Endocrinol Metab 35: 97, 1972. 2. Rubin, A. L., S. R. Levin, R. I. Bernstein, J. B. Tyrrell, C. Noacco, and P. H. Forsham, Stimulation of growth hormone by luteinizing hormonereleasing hormone in active acromegaly, J Clin Endocrinol Metab 37: 160, 1973. 3. Nakagawa, K., Y. Horiuchi, and K. Mashimo, Effect of dexamethasone on plasma growth hormone levels in acromegaly, J Clin Endocrinol Metab 31: 502, 1970.
193
4. Nakagawa, K., and K. Mashimo, Suppressibility of plasma growth hormone levels in acromegaly with dexamethasone and phentolamine, J Clin Endocrinol Metab 37: 238, 1973. 5. Nakagawa, K., and T. Obara, Suppression of plasma growth hormone levels with glucose infusion in patients with acromegaly. Clin Endocrinol (In press). 6. Tolis, G., L. Kovacs, H. Friesen, and J. B. Martin, Dynamic evaluation of growth hormone (GH) and prolactin (hPRL) secretion in active acromegaly with high and low GH output, Ada Endocrinol (Kbh) 78: 251, 1975. 7. Liuzzi, A., P. G. Chiodini, L. Botalla, F. Silvestrini, and E. E. Miiller, Growth hormone(GH)-releasing activity of TRH and GH-lowering effect of dopaminergic drugs in acromegaly: Homogenity in the two responses, J Clin Endocrinol Metab 39: 871, 1974. 8. Faglia, G., A. Paracchi, P. Beck-Peccoz, and C. Ferrari, An explanatory hypothesis for plasma GH response to nonspecific releasing hormone and for "paradoxical" GH inhibition after dopaminergic drugs in acromegaly, Ada Endocrinol [Suppl] (Kbh) 199: 323, 1975 (Abstract). 9. Giustina, G., E. Reschini, M. Peracchi, L. Cantalamessa, F. Cavagini, M. Pinto, and P. Bulgheroni: Failure of somatostatin to suppress thyrotropin releasing factor and luteinizing hormone releasing factor-induced growth hormone release in acromegaly J Clin Endocrinol Metab 38: 906, 1974. 10. Tano, T., K. Hanyu, A. Mihara, M. Aita, K. Yoshinaga, T. Mori, J. Suzuki, and N. Tamahashi, Sensitivity of acromegaly cells to TRH in monolayerculture method, The Saishin-igaku 31: 410, 1976 (Abstract).
Abstracts of the Annual Meeting of the Endocrine Society In order to widen the availability and increase the usefulness of the Abstracts of the Annual Meeting of the Endocrine Society, the Council and Publications Committee have adopted the following policy: The Abstracts will be published in a format suitable for binding with ENDOCRINOLOGY on an optional basis. The appropriate volume number of ENDOCRINOLOGY will be indicated on the Abstracts and the pages will be numbered Al, A2, etc., in order to allow reference to and retrieval of individual Abstracts. The Abstracts will not be indexed in the volume index. The Abstracts (available May, 1977) will not be an integral part of ENDOCRINOLOGY as such, nor will they be supplied as part of regular subscriptions to ENDOCRINOLOGY. They can be purchased separately by prepayment of $10.00 from the Office of the Secretary, The Endocrine Society, 9650 Rockville Pike, Bethesda, Maryland 20014. Members of the Society will receive the Abstracts automatically as in the past. The registration fee for nonmembers attending the Annual Meeting includes the cost of the Abstracts.
The Endocrine Society. Downloaded from press.endocrine.org by [${individualUser.displayName}] on 15 November 2015. at 05:48 For personal use only. No other uses without permission. . All rights reserved.
ABSTRACT. In patients with acromegaly whose basal plasma GH levels were suppressed with 9 mg/day of dexamethasone for 2 days, TRH-(6 cases) and LHRH-(1 case) induced GH release were unaffected when the responses were compared to the basal levels. Phentolamine infusion, 70 mg in 150 min, or hyperglycemia induced by iv infusion of 700 ml of 50% glucose solution also did not suppress TRH-induced GH release in 2 acromegalic
I
T IS well known that TSH releasing hormone (TRH) and LH releasing hormone (LHRH) induce GH release in some acromegalic patients (1,2) and the prompt and unusually high response suggests that the action of these releasing hormones is different from that of other stimuli. We previously reported that dexamethasone and phentolamine suppressed basal plasma GH levels in some acromegalic patients (3,4), and marked hyperglycemia also decreased plasma GH concentration in some acromegalics with lower GH secreting activity (5). Therefore, we examined the effects of these GH suppressing agents on TRH- or LHRH-induced GH release in patients with acromegaly.
Materials and Methods Nine patients with acromegaly were studied in this series. Two were treated; the first (#3p) was 7 years post irradiation and the second (#28p) had a partial hypophysectomy 2 months, and irradiation 26 months, prior to these studies. In 8 patients (#31-34, 36, 38, 3p and 28p), 500 /*g of TRH (Tanabe Pharmaceutical Co., Osaka, Japan) were injected SC at or about 1000 h after overnight fast and bed rest. Blood was drawn every 15 or 30 min from 30 min before to 120 or 180 min after the injection. In one patient (#37), 200 /*g of LHRH (Tanabe Pharmaceutical Co.) was injected and blood was drawn in the same manner as TRH test. To examine the effect of dexamethasone, 9 mg/day Received March 8, 1976. * Supported in part by the grants from the Ministry of Health and Welfare and the Ministry of Education of Japan.
of the drug were administered orally in 4 divided doses for two days as the previous studies (3,4) and the TRH or LHRH test was repeated. In one case (#38), the effect of hydrocortisone was examined by infusing 400 mg of hydrocortisone (sodium succinate, Solu-Cortef®) in 500 ml physiological saline from 0600 through 1000 h and injecting TRH at 1000 h. In 2 cases (#31 and 32), 70 mg of phentolamine (Regitine®) in 500 ml of physiological saline was infused in 150 min, and 60 min after the beginning of the infusion, the third TRH test was performed. On separate days, these patients received another TRH injection 30 min after the start of the infusion of 700 ml of 50% glucose solution in 120 min. Plasma GH levels were determined by double-antibody radioimmanoassay, and expressed in terms of NIH-GH-HS1147BC. The coefficients of variation were 5.9% at the level of 2.0 ng/ml and 5.2% around the level of 100 ng/ml. When 2 basal levels were determined in a test, the lower value was considered as the basal level in the test.
Results Effect of dexamethasone and hydrocortisone The plasma GH response to TRH injection before and after dexamethasone administration is shown in Figs. 1 and 2 and Table 1. In 6 patients presented in Fig. 1, TRH injection caused a remarkable increase of plasma GH levels; the peak levels were 4.0 to 32.8 times the basal levels. After dexamethasone treatment, the basal levels decreased by 27 to 88%; TRH injection, however, again caused a definite response with the peak levels of 4.6 to 104.0 times the basal levels, comparable to those before dexamethasone.
189
The Endocrine Society. Downloaded from press.endocrine.org by [${individualUser.displayName}] on 15 November 2015. at 05:48 For personal use only. No other uses without permission. . All rights reserved.
JCE & M • 1977 Vol 44 • No 1
COMMENTS
190 IOOQ 500
#31
#
#32
3p
# 28 p
TRH
TRH
TRH
100
50
t TRH
#
34
#36
t
t TRH
TRH
0 3 0 6 0 9 0 GO
0 30 6090G0I50B0 -30 0 30 6090120 -30 0 30 60 90 BO BO BO
-30 0 306090 12015080 -30 6 306090E0B0B0
minutes
FIG. 1. Plasma GH response to TRH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 6 dexamethasone- and TRH-responsive acromegalic patients. IOOQ
# 36
500
TRH
i
100 SO TRH
# 33
-30 6 306090 BOBOBO -30 0 30(09012000180
In one patient (#33), dexamethasone did not cause suppression, but rather an increase of the basal GH level. The peak level of plasma GH with TRH injection was 7.2 times the basal level before dexamethasone and 4.0 times after dexamethasone. Another patient (#36) did not show any response to TRH injection. The basal level decreased by 57% with dexamethasone, but TRH again did not cause any increase of plasma GH level (Fig. 2). In one dexamethasone- and TRH-responsive patient presented in Fig. 1 (#38), hydrocortisone treatment also caused a similar effect; the basal level decreased from 101 to 15 ng/ml by 85%, and 753% increase was observed with TRH injection, comparable to 688% increase in control TRH test (Fig. 3). An acromegalic patient (#37) responded to LHRH injection with an increase of 267% of the basal GH level. Dexamethasone decreased the basal level by 76% in this patient, but the response to LHRH remained unblocked; the increase was 3.8 times the suppressed basal level (Fig. 4).
minute*
FIG. 2. Plasma GH response to TfiH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 1 dexamethasoneunresponsive and TRH-responsive acromegalic patient (left panel) and 1 dexamethasone-responsive and TRH-unresponsive patient (right panel).
Effect of phentolamine In 2 cases of acromegaly (#31 and #32), 50 mg of phentolamine infused in 90 min suppressed basal GH levels by 73 and 39%, respectively.
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191
COMMENTS TABLE 1. Plasma GH response to TRH or LHRH before and after dexamethasone After
Before Patient no.
TRH injection 31 32
Basal
Peak
ng/ml
ng/ml
2.8 8.4 2.2
3p
72.5 190 23.4
Peak Basal
Basal
Peak
ng/ml
ng/ml
1.3 3.8
38.7 125
25.9 22.6 10.6
1.6
32.8 7.9
2.5 33.0
39.1
4.0
4.2
79.0 44.0
571 55.0
7.2 1.3
157 18.9
42.0
154
3.7
10.0
34 38
30.7 96
28p
9.7
33 36 LHRH injection 37
1,008 756
18.6 260 361 19.5 634
48.3
Peak Basal
29.8 32.9 11.6 104.0 10.9 4.6 4.0
4.8
However, 70 mg of phentolamine infused in 150 min from 60 min before the TRH injection to
I00Q
90 min thereafter did not cause any change in GH response to TRH (Fig. 5).
500
Effect of hyperglycemia In 2 acromegalic patients (#31 and 32), hyperglycemia induced by the infusion of 50% glucose solution lowered basal GH levels by 41 and 58%, respectively (5), but hyperglycemia of similar degree induced from 30 min before the TRH injection until 90 min after did not affect TRH-induced GH release (Fig. 6).
Discussion In this study, dexamethasone, 9 mg/day for 2 days, did not suppress plasma GH response to TRH or LHRH when the peak levels were expressed in relation to the basal levels. These basal levels were remarkably decreased in a major part of acromegalic patients, confirming our previous studies (3,4). Recently, when this study was in progress, Tolis et al. reported that 400 mg of hydro-
IOO 50
I 10:
t TRH
§
# 38
o
Q.
r
FiG. 3. Plasma GH response to TRH before (closed circles and solid lines) and after (open circles and dotted lines) hydrocortisone infusion in 1 dexamethasone- and TRH-responsive acromegalic patient.
Hyfrocortisonc 400mg *
-240
-30 0 3060 90120 minutes
The Endocrine Society. Downloaded from press.endocrine.org by [${individualUser.displayName}] on 15 November 2015. at 05:48 For personal use only. No other uses without permission. . All rights reserved.
JCE & M • 1977 Vol 44 • No 1
COMMENTS
192
# 31
IOOQ
# 32
500
TRH
500
# 37 100 50
100 50
IO
70 mg
? ia
t
i
LHRH
-9O-G0-3O 0 30 60 90 120
o a.
-90-60-30 0 30 60 90 GO
FIG. 5. Plasma GH response to TRH before (closed circles and solid lines) and during (open circles and dotted lines) phentolamine infusion in 2 phentolamine- and TRH-responsive patients.
-30 6 306090120(5060 mlnutti FIG. 4. Plasma GH response to LHRH before (closed circles and solid lines) and after (open circles and dotted lines) dexamethasone in 1 dexamethasone- and LHRHresponsive patient. cortisone infused in 4 h prior to TRH injection blocked plasma GH response to TRH without affecting basal levels in 2 acromegalic patients (6). We followed this procedure in the last patient (#38), but the result in this patient was similar to that seen after dexamethasone; the basal level was remarkably decreased and TRH caused GH release comparable to the control test.
# 31
500
#
32
TRH
TRH
i
i
100 50
IO|
° 5 Glucose 50% 700 m
Glucose 50% 700ml
FlG. 6. Plasma GH response to TRH before (closed circles and solid lines) and during (open circles and dotted lines) glucose infusion in 2 hyperglycemiaand TRH-responsive patients.
-60-30 0 30 6090120
-60-30 0 306090120
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COMMENTS These results seem to indicate that glucocorticoids do not affect TRH- or LHRH-induced GH release per se, but affect the basal state which contributes the basal release and the absolute level of response. Phentolamine or hyperglycemia, which decreased basal plasma GH levels, also did not modify the release of GH with TRH. TRHinduced GH release has been reported not to be suppressed with L-Dopa (7), 2-bromo-a-ergocryptine (8) or somatostatin (9). This refractoriness, along with the fact that pituitary tumor cells of GH-secreting adenoma released GH in vitro in response to TRH (10), supports the concept that TRH (and probably LHRH also) acts directly on pituitary tumor cells to release GH in acromegalics. References 1. Irie, M., and T. Tsushima, Increase of serum growth hormone concentration following thyrotropin-releasing hormone injection in patients with acromegaly and gigantism.y Clin Endocrinol Metab 35: 97, 1972. 2. Rubin, A. L., S. R. Levin, R. I. Bernstein, J. B. Tyrrell, C. Noacco, and P. H. Forsham, Stimulation of growth hormone by luteinizing hormonereleasing hormone in active acromegaly, J Clin Endocrinol Metab 37: 160, 1973. 3. Nakagawa, K., Y. Horiuchi, and K. Mashimo, Effect of dexamethasone on plasma growth hormone levels in acromegaly, J Clin Endocrinol Metab 31: 502, 1970.
193
4. Nakagawa, K., and K. Mashimo, Suppressibility of plasma growth hormone levels in acromegaly with dexamethasone and phentolamine, J Clin Endocrinol Metab 37: 238, 1973. 5. Nakagawa, K., and T. Obara, Suppression of plasma growth hormone levels with glucose infusion in patients with acromegaly. Clin Endocrinol (In press). 6. Tolis, G., L. Kovacs, H. Friesen, and J. B. Martin, Dynamic evaluation of growth hormone (GH) and prolactin (hPRL) secretion in active acromegaly with high and low GH output, Ada Endocrinol (Kbh) 78: 251, 1975. 7. Liuzzi, A., P. G. Chiodini, L. Botalla, F. Silvestrini, and E. E. Miiller, Growth hormone(GH)-releasing activity of TRH and GH-lowering effect of dopaminergic drugs in acromegaly: Homogenity in the two responses, J Clin Endocrinol Metab 39: 871, 1974. 8. Faglia, G., A. Paracchi, P. Beck-Peccoz, and C. Ferrari, An explanatory hypothesis for plasma GH response to nonspecific releasing hormone and for "paradoxical" GH inhibition after dopaminergic drugs in acromegaly, Ada Endocrinol [Suppl] (Kbh) 199: 323, 1975 (Abstract). 9. Giustina, G., E. Reschini, M. Peracchi, L. Cantalamessa, F. Cavagini, M. Pinto, and P. Bulgheroni: Failure of somatostatin to suppress thyrotropin releasing factor and luteinizing hormone releasing factor-induced growth hormone release in acromegaly J Clin Endocrinol Metab 38: 906, 1974. 10. Tano, T., K. Hanyu, A. Mihara, M. Aita, K. Yoshinaga, T. Mori, J. Suzuki, and N. Tamahashi, Sensitivity of acromegaly cells to TRH in monolayerculture method, The Saishin-igaku 31: 410, 1976 (Abstract).
Abstracts of the Annual Meeting of the Endocrine Society In order to widen the availability and increase the usefulness of the Abstracts of the Annual Meeting of the Endocrine Society, the Council and Publications Committee have adopted the following policy: The Abstracts will be published in a format suitable for binding with ENDOCRINOLOGY on an optional basis. The appropriate volume number of ENDOCRINOLOGY will be indicated on the Abstracts and the pages will be numbered Al, A2, etc., in order to allow reference to and retrieval of individual Abstracts. The Abstracts will not be indexed in the volume index. The Abstracts (available May, 1977) will not be an integral part of ENDOCRINOLOGY as such, nor will they be supplied as part of regular subscriptions to ENDOCRINOLOGY. They can be purchased separately by prepayment of $10.00 from the Office of the Secretary, The Endocrine Society, 9650 Rockville Pike, Bethesda, Maryland 20014. Members of the Society will receive the Abstracts automatically as in the past. The registration fee for nonmembers attending the Annual Meeting includes the cost of the Abstracts.
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