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Crowth hormone responses to growth hormone releasing hormone or thyrotrop in releasing hormone in patients with metastatic testicular cancer
90s
B-106 EVALUATION OF SERUM MARKER FOR SEMINOMA. Kuzmits R., Schernthaner Department
of
Medicine
NEURON-SPECIFIC G. and II,
Krisch
‘Department
ENOLASE
IN
TESTICULAR
CANCER:
A NEW TUMOUR
KX. of
Pathology,
University
of
Vienna,
Austria.
Neuron-specific enolase (NSE) was measured in 48 male control subjects and evaluated as a serum marker in 106 patients with testicular cancer and compared to the established tumour markers alphsfetoprotein (A FP) and human chorionic gonadotropin (H C G). Mean aeru m NSE concentrations in controls were 4.7k3.8 (SD) ng/ml, the upper limit of the normal range was taken as (x+ZSD) 12.3 ng/mL Significantly increased serum NSE levels (43.4k31.2 ng/ml; pt0.005) were measured in patients with metastasized seminoma, in 9/l 2 (75%) patients NSE activity was above the norm al range. H C G was positive in 3 (25X), AFP was negative in all patients. Serum NSE concentrations fell to within the normal range following chemotherapy. Localization of NSE in seminoma cells was demonstrated histochemically. Serum NSE concentrations were not significantly increased (8.17t7.0 q/ml) in patients with metastatic nonseminomatous germ cell turnours, only 6/40 (15%) patients showed elevated serum NSE levels. A FP and H C G were both positive in 70 X of patients and NSE determination gave no additional information in this group. Serum NSE concentrations were normal in 53/54 testicular cancer patients after orchiectom y and no evidence for metastatic disease; only one had borderline NSE levels indicating the specificity of seru m N SE determination. NSE is a new marker for seminom a and may be of clinical value in monitoring them otherapy in patients with metastatic se mino ma. B-107 HCG-INDUCED Kuzmits R., Department
HYPERTHYROIDISM Weissel M. and of Medicine II,
IN TESTICULAR Ludwig H. University of
CANCER: Vienna,
A CASE
REPORT.
Austria.
an association between high hum an chorionic gonaIn patients with gestational trophoblastic neoplsaia, However, no reports of the same assodotropin (H C G) levels and hyperthyroididsm is well established. ciation in males with H C G-secreting tumours of the genital tract have been published. We report a case of H C G-induced hyperthyroidism in a patient with a malignant testicular tu mour. A 28-year-old male was referred to our clinic after orchiectomy for a malignant trophoblastic teratoma. On admission the patient presented with bulky disease and extremely high serum H C G concentrations (1080000 U/L) were measured. Serum thyroxine (T4) levels (15.5 ug/dl) and effective thyroxine ratio (ET R; 1.28) were above the norm al range, and TSH secretion w a’s completely suppressed after stimulation with T R H. The thyroid gland was not palpable, the Tc-pertechnetate thyroid scan showed The im m unological tests (thyroglobulin, microso mal a norm al sized organ with a normal tracer uptake. After chemotherapy a marked decrease in seantibodies, TSH-receptor antibodies) were all negative. rum H C G levels (80000 U/L) was observed, and serum T4 and ET R had returned to the norm al range. In addition, the TR H-test normalized. Serial determination of T4 and ETR during the following months However, the paof them otherapy showed norm al values and a gradual decline in serum HCG levels. tient became resistant to the motherapy and serum H C G concentrations increased. At H C G levels of 300000 U/L again increased T4 and ETR values and a suppression of TSH in the TR H-test was found. After salvage the motherapy, H C G levels declined and T4, ET R and the T R H-test normalized again. The presented case report is suggestive of H C G-induced hyperthyroidism in a patient with testicular cancer, possibly by production of an atypical HCG-molecule with TSH-like activity. B-108 GRmTH HORMONE RESPONSES TO GROWTH HORMONE RELEASING HORMONE OR THYROTROPIN RELEASING HORMONE IN PATIENTS WITH METASTATIC TESTICULAR CANCER Pietschmann P, Kuzmits R, Schernthaner G Department of Medicine II, University of Vienna, Austria In 16 patients with metastatic testicular cancer and 10 matched control subjects, growth hormone (GH) responses to growth hormone releasing hormone (GHRH, l-Y.+;1 p/kg body weight i.v.1 or thyrotropin releasing hormone (TRH 200 ug i.v.) administration were measured by radioimmunoassay. GH responses to GHRH were significantly elevated in patients with testicular cancer when compared with control subjects (AGH: 13.924.2, vs 6.121.1; ~40.05). In patients with metastatic testicular cancer a significant increase of GH-levels after TRH stimulation was observed (basal GH-level 1.720.5 ng/ml vs peak GH-level 3.921.0 ng/ml; p< 0.01) whereas in the control subjects basal GH-levels (0.4+0.1 ng/ml) and GH-levels after TRH-administration (peak GH-level: 1.050.6 ng/ml) were not statistically different. In 9 patients with testicular cancer GHRH tests were performed both in the metastatic state of the disease and in complete remission. GH-responses to GHRH tended to decrease in complete remission when compared with pretreatment values (8.8+2.7 ng/ml vs 16.0~6.6 ng/ml); however the difference did not reach statistical significance. Our findings indicate that paradoxical GH-responses to TRH occur in cancer patients. Furthermore, the increased GH-responses to GHRH in patients with metastatic testicular cancer provides evidence of an alteration in pituitary and/or hypothalamic function in this disorder.
B-106 EVALUATION OF SERUM MARKER FOR SEMINOMA. Kuzmits R., Schernthaner Department
of
Medicine
NEURON-SPECIFIC G. and II,
Krisch
‘Department
ENOLASE
IN
TESTICULAR
CANCER:
A NEW TUMOUR
KX. of
Pathology,
University
of
Vienna,
Austria.
Neuron-specific enolase (NSE) was measured in 48 male control subjects and evaluated as a serum marker in 106 patients with testicular cancer and compared to the established tumour markers alphsfetoprotein (A FP) and human chorionic gonadotropin (H C G). Mean aeru m NSE concentrations in controls were 4.7k3.8 (SD) ng/ml, the upper limit of the normal range was taken as (x+ZSD) 12.3 ng/mL Significantly increased serum NSE levels (43.4k31.2 ng/ml; pt0.005) were measured in patients with metastasized seminoma, in 9/l 2 (75%) patients NSE activity was above the norm al range. H C G was positive in 3 (25X), AFP was negative in all patients. Serum NSE concentrations fell to within the normal range following chemotherapy. Localization of NSE in seminoma cells was demonstrated histochemically. Serum NSE concentrations were not significantly increased (8.17t7.0 q/ml) in patients with metastatic nonseminomatous germ cell turnours, only 6/40 (15%) patients showed elevated serum NSE levels. A FP and H C G were both positive in 70 X of patients and NSE determination gave no additional information in this group. Serum NSE concentrations were normal in 53/54 testicular cancer patients after orchiectom y and no evidence for metastatic disease; only one had borderline NSE levels indicating the specificity of seru m N SE determination. NSE is a new marker for seminom a and may be of clinical value in monitoring them otherapy in patients with metastatic se mino ma. B-107 HCG-INDUCED Kuzmits R., Department
HYPERTHYROIDISM Weissel M. and of Medicine II,
IN TESTICULAR Ludwig H. University of
CANCER: Vienna,
A CASE
REPORT.
Austria.
an association between high hum an chorionic gonaIn patients with gestational trophoblastic neoplsaia, However, no reports of the same assodotropin (H C G) levels and hyperthyroididsm is well established. ciation in males with H C G-secreting tumours of the genital tract have been published. We report a case of H C G-induced hyperthyroidism in a patient with a malignant testicular tu mour. A 28-year-old male was referred to our clinic after orchiectomy for a malignant trophoblastic teratoma. On admission the patient presented with bulky disease and extremely high serum H C G concentrations (1080000 U/L) were measured. Serum thyroxine (T4) levels (15.5 ug/dl) and effective thyroxine ratio (ET R; 1.28) were above the norm al range, and TSH secretion w a’s completely suppressed after stimulation with T R H. The thyroid gland was not palpable, the Tc-pertechnetate thyroid scan showed The im m unological tests (thyroglobulin, microso mal a norm al sized organ with a normal tracer uptake. After chemotherapy a marked decrease in seantibodies, TSH-receptor antibodies) were all negative. rum H C G levels (80000 U/L) was observed, and serum T4 and ET R had returned to the norm al range. In addition, the TR H-test normalized. Serial determination of T4 and ETR during the following months However, the paof them otherapy showed norm al values and a gradual decline in serum HCG levels. tient became resistant to the motherapy and serum H C G concentrations increased. At H C G levels of 300000 U/L again increased T4 and ETR values and a suppression of TSH in the TR H-test was found. After salvage the motherapy, H C G levels declined and T4, ET R and the T R H-test normalized again. The presented case report is suggestive of H C G-induced hyperthyroidism in a patient with testicular cancer, possibly by production of an atypical HCG-molecule with TSH-like activity. B-108 GRmTH HORMONE RESPONSES TO GROWTH HORMONE RELEASING HORMONE OR THYROTROPIN RELEASING HORMONE IN PATIENTS WITH METASTATIC TESTICULAR CANCER Pietschmann P, Kuzmits R, Schernthaner G Department of Medicine II, University of Vienna, Austria In 16 patients with metastatic testicular cancer and 10 matched control subjects, growth hormone (GH) responses to growth hormone releasing hormone (GHRH, l-Y.+;1 p/kg body weight i.v.1 or thyrotropin releasing hormone (TRH 200 ug i.v.) administration were measured by radioimmunoassay. GH responses to GHRH were significantly elevated in patients with testicular cancer when compared with control subjects (AGH: 13.924.2, vs 6.121.1; ~40.05). In patients with metastatic testicular cancer a significant increase of GH-levels after TRH stimulation was observed (basal GH-level 1.720.5 ng/ml vs peak GH-level 3.921.0 ng/ml; p< 0.01) whereas in the control subjects basal GH-levels (0.4+0.1 ng/ml) and GH-levels after TRH-administration (peak GH-level: 1.050.6 ng/ml) were not statistically different. In 9 patients with testicular cancer GHRH tests were performed both in the metastatic state of the disease and in complete remission. GH-responses to GHRH tended to decrease in complete remission when compared with pretreatment values (8.8+2.7 ng/ml vs 16.0~6.6 ng/ml); however the difference did not reach statistical significance. Our findings indicate that paradoxical GH-responses to TRH occur in cancer patients. Furthermore, the increased GH-responses to GHRH in patients with metastatic testicular cancer provides evidence of an alteration in pituitary and/or hypothalamic function in this disorder.