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Biomedical subjects

D Schnorr

Publications and source records attributed to D Schnorr.

14 recordsLinked to original sources

Dehydroepiandrosterone (DHEA) levels in patients with prostatic cancer, heart diseases and under surgery stress.

DHEA levels in patients with prostatic cancer were significantly lower, but total and free testosterone (T) significantly higher as those in an age-matched control group. Therefore, the calculated quotients DHEA/free T and DHEA/T were especially different between both groups. DHEA and DHEAS levels in patients with heart diseases were also significantly lower but cortisol (F) levels were significantly higher as those in a control group. The quotients DHEA/F and DHEAS/F were also of greater significance between both groups than the hormone values alone. The response of DHEA and F levels in patients undergoing surgery showed an increase of both steroids under surgery. On the second postoperative day, however, F levels were still significantly higher but DHEA levels were significantly lower as the initial values. The differences between the initial values and those on the second postoperative day of F and DHEA showed a significant correlation, i.e. the higher the elevation of F levels above the initial values the greater was the diminution of DHEA levels below the initial values.

Adult

89Strontium therapy of bone metastases of carcinoma of the prostatic gland.

Following a firm diagnostic and therapeutic schedule for patients with prostatic carcinoma. 89Strontium therapy was introduced for multiple metastases. Positive skeletal scintigraphy with 99mTc-EHDP induced check for affinity to Sr using 85Sr scintigraphy. Of 80 patients, multiple metastases were found in 26. Therapy with 1 mCi of 89Sr-chloride was started in 20 cases. In 8 patients, relief from severe pain appeared shortly afterward, and a further 8 it was possible to prevent the development of pain. Moderate success in 3 cases and a failure to provide relief in 1 were observed.

Bone Neoplasms

[Diagnostics and therapy of the carcinoma of the prostate (author's transl)].

By well organized preventive examinations early tumour stages can be recognized. The diagnosis of prostatic cancer has to be secured by biopsy. The primary reliability of aspiration biopsies (cytology) was 94% compared with punch biopsies (histology) amounting to 73%. Indications and results of aspiration biopsies, radiological and nuclear medical techniques in diagnosing prostatic cancer are described. The combined anti-androgenic hormonal therapy (infusions of cytonal, subcapsular orchiectomy, permanent administration of oestrogen) is considered to be the unchanged basis of treatment. Comparative cytologic investigations in therapy indicate that high-voltage treatment connected with hormonal therapy seems to be superior to exclusive hormonal treatment. Observations after additional therapy by a radionuclid (89-Strontium) for affecting metastases are encouraging. Indications of a therapy by cytostatica in progressive prostatic cancer are explained.

Antineoplastic Agents

[Initial experience with ethinyl estradiol sulfonate (J 96) in the therapy of prostate carcinoma].

Ethinylestradiol sulphate (J 96) is a depot estrogen which in a dosage of 2 mg per week has clearly antigonadotropic effects and evokes a suppression of the free testosterone in bilaterally orchiectomized patients with carcinoma of the prostate. The good compatibility in oral application and the possibility for the controlled intake recommend its use for the long-term therapy of the carcinoma of the prostate.

Carcinoma

Evaluation of a competitive binding assay for cortisol using horse transcortin.

A non-chromatographic competitive binding assay (CBA) using horse transcortin has been employed in the routine measurement of cortisol in plasma, urine and amniotic fluids. Comparing the values with those of a radioimmunoassay (RIA) or a fluorimetric method (FM) an excellent correlation between the three methods both in plasma and urine has been calculated in normal subjects and in patients with various endocrine disorders. In amniotic fluids, however, there were discrepancies between CBA and RIA. Whereas CBA showed no differences, RIA gave significantly higher values in amniotic fluids of female than of male fetuses. Elevated free plasma cortisol levels observed in patients with prostatic cancer after diethyl stilboestrol diphosphate therapy did not correlate with unconjugated urinary cortisol concentration as measured with CBA and FM. In newborns, a relatively high plasma level found 12 hours after birth was followed by a nadir on the 2nd and 3rd day of life and by an increase until levels of adults on the 5th day of life were reached.

Amniotic Fluid

[Diagnostic and treatment of prostatic cancer (author's transl)].

The diagnosis of prostatic cancer must be proved by biopsy. Transrectal fine needle biopsy and punch biopsy are also useful methods for the outpatient clinic. Besides X-ray examination scanning angiography and lymphography may be used to identify metastases. Combined antiandrogenic therapy is still the treatment of choice and is based on endocrinologic analysis of testosterone, LH levels and testosterone-binding beta-globulin. Radionuclids (32P, 89Sr) should be used for treating metastases of the bone. Chemotherapeutic substances showed unsatisfactory results. Radical prostatectomy can only be performed in 5 to 10% of all patients with prostatic cancer to metastases in T1 and T2 cases. Since 1965 the radiation therapy (linear accelerator or (60Co-source) gives more hope. We treat patients free from metastases with a 60Co-source (right and left lateral 120-degree arc rotational therapy with 5000 rads over 5 weeks) combined with hormonal therapy. The therapeutic effect is checked by fine needle aspiration biopsy.

Antineoplastic Agents

Endocrine effects of oestrogen treatment in patients with prostatic cancer.

In 36 men with prostatic cancer, the following findings were obtained: intravenous administration of 12.0 g diethylstilboestrol diphosphate (DSDP) induced a relatively slight decrease of the LH plasma level from 22.7 +/- 11.8 to 7.7 +/- 3.6 mIU/ml (34%), whereas the total testosterone plasma level decreased from 435.3 +/- 187.8 to 29.9 +/- 16.4 ng/100 ml (6.7%) suggesting a direct inhibitory effect of the oestrogen on testicular testosterone secretion. The apparently free, biologically active testosterone plasma level even decreased from 6.2 +/- 3.7 to 0.21 +/- 0.16 ng/100 ml (3.4%), due to the oestrogen-induced increase of the concentration of testosterone-binding beta-globulin (from 9.6 +/- 4.4 to 20.6 +/- 10.7-10(-8) M). 3--7 days after additional orchidectomy plus subcutaneous implantation of 100 mg dienoestrol diacetate a further decrease of the apparently free testosterone plasma level from 0.21 +/- 0.16 to 0.14 +/- 0.07 ng/100 ml was found. In contrast, 6 weeks after orchidectomy without oestrogen implantation a significant increase of th- apparently free testosterone plasma level -rom 0.21 %/- 0.16 to 0.34 +/- 0.15 ng/100 ml was observed (p less than 0.01). In view of these findings the biologically active free testosterone plasma level appears to be even more suppressed by intravenous administration of high DSDP than by orchidectomy. The most effective suppression of apparently free testosterone was achieved, however, by oestrogen treatment combined with orchidectomy.

Aged

Total and free testosterone in plasma of hypo- and agonadal men.

Plasma total testosterone (T), apparently free T and testosterone binding globulin (TeBG) capacity determined in 14 normal men aged 30-40 years were 461 +/- 100 ng/100 ml, 9.4 +/- 3.0 ng/100 ml and 5.7 +/- 1.9 X 10(-8) M, respectively, whereas in 16 hypogonadal men the corresponding values were 38.6 +/- 27.2 ng/100 ml, 0.47 +/- 0.41 ng/100 ml and 10.4 +/- 3.4 X 10(-8) M showing the TeBG capacity significantly higher (p less than 0.001) in hypogonadal than in normal men. Treatment of 5 hypogonadal subjects with 250 mg testosterone enanthate plus 50 mg testosterone propionate decreased (p less than 0.001) the TeBG level from 14.7 +/- 2.5 X 10(-8YM to 8.3 +/- 1.4 X 10(-8) M on day 8 after a single injection. According to this difference in TeBG, the free T fraction in plasma rose from 0.94% to 1.9% of the total T concentration. These results suggest that alteration of total plasma T affected the TeBG capacity. Decreased T levels raised and increased T concentrations suppressed TeBG, but with a delayed response to the changed T concentrations. The initial mean values in 12 patients with prostatic cancer aged 60-74 years were 397 +/- 165 ng/100 ml, 4.05 +/- 1.8 ng/100 ml and 11.9 +/- 3.3 X 10(-8) M, respectively. The TeBG capacity in these patients was significantly higher and the free T concentration significantly lower (p less than 0.001) than those of the younger normal males. After treatment with 12 g diethylstilbestrol diphosphate and orchidectomy, the TeBG increased to 33.3 +/- 13.1 X 10(-8) M and the plasma free T concentration decreased to the minimal value of 0.053 +/- 0.04 ng/100 ml.

Adult

Evocability of a slight positive oestrogen feedback action on LH secretion in castrated and oestrogen-primed men.

Orchidectomized heterosexual men suffering from prostatic cancer with suppressed serum LH values by oestrogen priming exhibited a slight, but significant surge of LH secretion following oestrogen injection. In contrast, orchidectomized and oestrogen-primed heterosexual men with unsuppressed serum LH levels as well as intact heterosexual men did not display any positive oestrogen feedback action on LH secretion, as it was observed in intact homosexual men.

Aged

An apparently direct inhibitory effect of oestrogen on the human testis.

In men suffering from prostatic cancer, i.v. administration of 12 g diethylstilboestrol diphosphate within 20 days resulted in a decrease of the LH serum level to about 50% (P less than 0.05), whereas the total testosterone level decreased to less than 5% (P less than 0.001) and the apparently free testosterone level to less than 2% of the initial values (P less than 0.001). Hence, the "systemic antiandrogenic effect" of oestrogen can be explained (1) by indirect inhibition of testicular androgen secretion via diminution of hypophyseal gonadotrophin secretion, (2) by direct inhibition of testicular androgen secretion and (3) by elevation of the capacity of testosterone binding beta-globulin.

Aged