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Biomedical subjects

G H Jacobi

Publications and source records attributed to G H Jacobi.

At least 73 records · Page 4Linked to original sources
PubMed1980

[Therapy, follow-up treatment and prevention of urinary bladder cancer].

Bladder carcinoma is a disease with a poor prognosis if the tumor is of advanced stage: the 3-year survival rate in stage T3 and T4 is 21 and 4%, respectively. Superficial, noninfiltrating lesions, i.e., TA and T1 (82% 3-year survival rate), have a considerably more favorable prognosis, but on the other hand are associated with considerable morbidity. Recurrent tumors can be expected in 50-90%, and more than five transurethral resections are necessary in 12.7% of the cases. Treatment modalities as directed by tumor stage and grade should be as radical as possible, although preservation of proper bladder function as a factor of quality of life must be taken into consideration. In stage, T1, TUR is the treatment of choice. Thereafter, prophylactic topical administration of intravesical chemotherapy is successful in the prevention of recurrencies. In cases of less differentiated tumors usually associated with deeper infiltration (T3) and if random biopsies reveal carcinoma in situ, radical surgery is indicated. Partial bladder resection for a solitary tumor may be successful only, when rigid limitations of the indication are kept in mind. A radical cystectomy is the treatment of choice in stage T3 with deep muscle invasion; for this tumor category, preoperative radiotherapy offers the best overall results. Single definitive radiotherapy is less effective as if combined with surgery and has a recurrency rate of 41-56%. In metastatic carcinoma (T4, N+, M1), only palliative therapy is possible, with a goal of improving life quality without essentially lengthening survival.

Humans↗
PubMed1980

[Androgen metabolism in prostate cancer: 3-hydroxysteroid dehydrogenase in relation to the grade of tumor differentiation (author's transl)].

The peripheral zone of the prostate behaves as an androgen target organ, whereas the periurethral glands are under estrogenic stimulation. This anatomical-physiological situation explained in the past the endocrine dependence of prostatic carcinoma. Biochemical studies by Prout, however, showed that the response of prostate cancer to contrasexual measures correlates well with the activity of androgen-converting enzymes and with the grade of tumor differentiation. In this study the in vitro activity of 3-hydroxysteroid dehydrogenase (formation of androstanediols from dihydrotestosterone) was assessed in biopsy material of 8 highly differentiated adenocarcinomas and of 14 poorly differentiated tumors by a microassay technique. The results were compared with the enzyme activities obtained earlier from benign prostatic hyperplasia and normal prostatic tissue. In the different cell fractions (cytosol, microsomes) and with various cofactor supplementation, the enzyme activities in highly differentiated tumors strongly resembled those of adenomatous or normal prostate tissues, whereas a relative enzyme deficiency was present in poorly differentiated lesions. The pathophysiological and eventual clinical implications of these findings are discussed.

3-Hydroxysteroid Dehydrogenases↗
PubMed1980

Adjunct bromocriptine treatment as palliation for prostate cancer: experimental and clinical evaluation.

Bromocriptine, a potent antiprolactin, in conjunction with low dose polyestradiolphosphate or cyproterone acetate resulted in a response rate of 28 out of 42 patients. The longest response with pain free and physical as well as sexual, full activity was 15 months until relapse occurred. There was a clear cut prevention of gynecomaesia in 11 out of 13 patients. This is a second report on treatment for prostatic cancer with bromocriptine.

Bromocriptine↗
PubMed1980

[Hormone therapy of prostatic cancer (author's transl)].

64% of all patients with newly diagnosed prostatic carcinoma present with metastases. Hormone application with or without orchiectomy appears to be the adequate form of primary treatment. The most common therapeutic modality is estrogen administration, which has, however distinct disadvantages: The patient is protected up to 5 years only, there is a 27% cardiovascular mortality, it induces a prolactin surge, and is immunosuppressive. Phase III-studies of the EORTC and VACURG have demonstrated that medroxyprogesterone acetate and cyproterone acetate parallel the effectiveness of estrogens. In a phase II-trial adjunctive bromocriptine was found to be necessary to suppress estrogen or antiandrogen induced hyperprolactinemia. The following concept is derived: In disseminated untreated prostatic cancer estrogens or antiandrogens in combination with bromocriptine or high dose injectable gestagens are effective means of primary treatment. Distinct clinical parameters determine the "hormone of first choice". Orchiectomy is reserved for patients with ureteral compression or progressing disease.

Hormones↗
PubMed1979

Histophotometry: a new method for automated histological examination of solid tissue samples demonstrated on bladder cancer.

The purpose of this study was to demonstrate the ability of a new method to discriminate between benign and malignant tissue. Tissue samples from three patients with bladder tumours and one patient with bladder diverticula have been examined by histophotometry. This method, based on the correlation of nuclear volume and nucleic acid contents per cell uses thick formalin fixed samples. The results are obtained by measurements averaging more than one hundred thousand cells per sample. By this histophotometric examination a clear differentiation between malignant and to differentiate between infiltrating and noninfiltrating tumour, as well as inflamed bladder tissue. The results obtained histophotometrically were compared with the histological findings.

Histological Techniques↗
PubMed1979

Alterations of peripheral testosterone matabolism after induced hypoprolactinemia in patients with prostatic carcinoma.

In 12 patients with advanced prostatic carcinoma the effect of bromocriptine-induced hypoprolactinemia on the peripheral androgen metabolism was investigated after 3H-testosterone injection under conditions that each individual served as his own control. After a 5-day significant prolactin suppression, the elimination of 3H-label 1 h after testosterone injection was about 45% and equal to pre-bromocriptine values. The recovery of dihydrotestosterone separated by silica gel T.L.C., however, was significantly augmented, resulting in a marked decrease of the testosterone/dihydrotestosterone ratio from 12.2 to 6.3. This induced 5alpha-reductase activity after prolactin suppression is in accordance with our earlier findings on prostatic carcinoma tissue, matches well with observations of Magrini et al. on induced hyperprolactinemia and may be a new approach to the understanding of androgen dependent disorders.

Aged↗
PubMed1979

3-Alpha-androstanediol and prostatic growth: comparison of 3-alpha-androstanediol formation in prostates from 8 species including man and dog.

To determine whether the formation of 3-alpha-androstanediol is critical for androgen-mediated growth of the prostate the conversion of dihydrotestosterone to 3-alpha-androstanediol was assessed in homogenates of 60 normal prostates from 8 species. Rates (nmol. times gm. tissue(-1) times hour(-1)) in the presence of reduced nicotinamide adenine dinucleotide phosphate as cofactor were as follows: dog 271, mouse 200, rat 160, opossum 109, rabbit 24, guinea pig 13, man 11 and cat 9. There was no correlation between prostate size and 3-alpha-androstanediol formation in the entire group. Therefore, either differences in the response to 3-alpha-androstanediol within the prostate or variations in the metabolism of 3-alpha-androstanediol must be more important than the rate of its formation for the development of prostatic hypertrophy in the dog.

Androstane-3,17-diol↗
PubMed1979

[Bromocriptine for palliation of advanced prostatic carcinoma. Experimental and clinical profile of a drug (author's' transl)].

Since prolactin has several modes of action on prostatic growth and physiology, the effect of the antiprolactin bromocriptine on plasma kinetics and intraprostatic metabolism of testosterone was studied in patients with untreated prostatic cancer; a therapy protocol was deduced which was controlled in 27 patients with advanced inoperable prostatic adenocarcinoma. Bromocriptine resulted in a significant suppression of prolactin and testosterone as well and favored testosterone elimination from the plasma pool. Prostatic androgen uptake was enhanced and the intraprostatic metabolism altered in relation to tumor grade. Adjunctive administration of bromocriptine to 27 patients, mostly in the state of hormone resistance, resulted in an overall objective regression of 22.2% and in stable disease in 55.6% of the patients. In half of the individuals a prompt relief of bone pain from osseous metastases was observed as well as improvement of micturition and decline of phosphatase activity. This preliminary data justify further investigations under controlled and randomized conditions.

Adenocarcinoma↗
PubMed1979

[Laboratory tools in the diagnosis of prostatic cancer (author's transl)].

The most reliable laboratory test for prostate cancer remains prostatic phosphatase determination. With the spectrophotometric method, however, falsely negative results are to be expected in 40% of stage D lesions. In only one third of patients with localized disease results are correctly positive. This poor specificity and sensitivity can be improved by radioimmunoassay (RIA). Using this technique the prostatogenic isoenzyme is elevated in 50% of stage A and in 80% of stage B carcinoma, suggesting RIA for screening. Erythrocyte sedimentation rate or serum iron and copper are not necessarily of prognostic value. Phosphatase determination of bone marrow aspirates also requires the RIA method if differentiation of stage C and D is to be expected. Serum hormone assays are not yet introduced into routine staging programs. Serum and urinary markers such as CEA, polyamines of LDH isoenzymes are unspecific and of uncertain value in prostatic carcinoma. Measurement of urinary hydroxyproline seems a reliable method for the search of osseous spread; other bone diseases have to be excluded. In patients with prostate cancer laboratory tests still represent adjunctive measures in connection with the clinical diagnostic armamentarium of urologists.

Acid Phosphatase↗
PubMed1979

[Adenocarcinoma of the bladder (author's transl)].

During a 10 year follow-up, 18 patients with primary adenocarcinoma of the bladder or urachus were treated operatively. We report on the therapy and results. The criteria for differentiation between primary adenocarcinoma of the bladder and urachal carcinoma are stressed. Chronic irritation of the urothelium is most likely involved in the natural histroy of primary adenocarcinoma. Cystectomy should be the therapy of choice for the adenocarcinoma of the bladder. A partial resection is recommended for urachal carcinoma. Palliation is possible with cytotoxic agents. Irradiation seems to be of no beneficial effect on tumor growth.

Adenocarcinoma↗
PubMed1979

[Bromocriptine and prostatic carcinoma: testosterone metabolism in relation to tumor grading (author's transl)].

Since Prolactin has intra- and extrapostatic effects on growth and function of the prostate, the influence of the anti-prolactin bromocriptine (PRAVIDEL) was investigated in 15 patients with untreated prostatic carcinoma of various grades of differentiation in vivo. A five-days treatment with 15 mg Pravidel daily significantly suppressed prostatic androgen uptake, unrelated to tumor grading. 5 alpha-Reductase was favored in poorly differentiated lesions with a decreased testosterone/dihydrotestosterone ratio. The pretherapeutic accumulation of 5 alpha-androstanediol was diminished after Pravidel and the tissue/plasma ratio decreased. The 17 beta-hydroxy-pathway of testosterone is predominant as compared to the 17-keto pathway; both pathways are favored after Pravidel in poorly differentiated tumors. Intraprostatic metabolic effects of Pravidel are not related to peripheral androgen levels nor are they dependent on altered prostatic hormone uptake. In the poorly differentiated prostatic tumors Pravidel initiates a metabolic situation as observed in prostate cancer responding to androgen depletion or estrogen therapy.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

Testosterone metabolism in patients with advanced carcinoma of the prostate: a comparative in vivo study of the effects of oestrogen and antiprolactin.

In the light of the high incidence of cardiovascular side effects with oestrogen therapy in patients with prostatic cancer, other medications altering androgen metabolism are under investigation. The influence of the anti-prolactin bromocriptin (CB157) on plasma kinetics of testosterone and on endogenous hormones was studied and compared with the effect of ethinyl oestradiol in 25 patients with prostatic carcinoma. Bromocriptine significantly suppressed both prolactin and testosterone, inhibited the transfer of androgen from the inner pool into the deep compartment and favoured its degradation. Ethinyl oestradiol decreased testosterone, LH and FSH, and prolonged the biological half-life of testosterone. The effects of bromocriptine on androgen metabolism might be of therapeutic value in patients with prostatic carcinoma.

Bromocriptine↗
PubMed1978

Prostatic carcinoma: plasma kinetics and intraprostatic metabolism of testosterone in low-dose estrogen-treated patients in vivo.

Plasma kinetics, in vivo uptake, and intraprostatic metabolism of 3H testosterone was investigated in 9 patients with advanced carcinoma of the prostate. The metabolic effect of low-dose ethinyl estradiol was studied (estrogen suppressed testosterone, luteinizing hormone, and follicle-stimulating hormone). The production rate of testosterone was lowered, the elimination of androgen from plasma delayed. The uptake of testosterone and metabolites by the prostatic carcinoma was suppressed. Estrogen did not alter significantly the intraprostatic androgen turnover.

Aged↗
PubMed1978

Urachal signet-ring cell carcinoma, a rare variant of vesical adenocarcinoma: incidence and pathological criteria.

Of 715 cases of vesical tumors reviewed 18 adenocarcinomas were selected for further study, 5 of which fulfilled all criteria of urachal origin. Herein is reported 1 rare case of such a carcinoma of the signet-ring cell type and the morphological criteria of this variant are discussed briefly. After undergoing radical cystectomy and ureterosigmoidostomy the patient has been free of recurrent tumor or metastasis for 6 years.

Adenocarcinoma, Mucinous↗
PubMed1978

Bromocriptine and prostatic carcinoma: plasma kinetics, production and tissue uptake of 3H-testosterone in vivo.

The influence of the anti-prolactin bromocriptine on plasma kinetics, production rate and tissue uptake of testosterone was investigated in 15 patients with newly diagnosed stages C and D prostatic carcinoma. Bromocriptine was given for 5 days in a daily dose of 15 mg. orally. The studies were performed with the single injection technique using the 2-compartment model. Plasma testosterone, serum prolactin, and luteinizing and follicle-stimulating hormones were determined initially. Blood samples were drawn up to 5 hours after the injection of 3H-testosterone. For tissue studies a transrectal needle biopsy was done 3 hours post-injection. Bromocriptine suppressed prolactin and the endogenous testosterone level. Furthermore, it favored the elimination of 3H-testosterone, lowered the production rate of testosterone and hampered the in vivo uptake of the 3H-label into prostatic carcinoma tissue. Finally, the grading of the tumor lesions affected only the pre-bromocriptine uptake of radioactive androgens and not the uptake in response to bromocriptine. The potential clinical impliications of these observations are discussed.

Aged↗
PubMed1978

Studies on the mechanism of 3 alpha-androstanediol-induced growth of the dog prostate.

The conditions under which dihydrotestosterone and 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-androstanediol) induce prostatic growth in the castrate dog have been investigated in animals in which the initial size of the prostate was either normal or large. When androgen replacement was commenced immediately after castration of dogs with preexisting prostatic hypertrophy, dihydrotestosterone was as effective as 3 alpha-androstanediol in maintaining prostate weight. Under all other conditions examined (replacement commenced immediately after castration in dogs with small prostates or 2 weeks after castration in dogs with large prostates), 3 alpha-androstanediol but not dihydrotestosterone induced significant prostatic growth. The maximal effect of 3 alpha-androstanediol in inducing prostatic growth was observed in 12 weeks. The administration of 17 beta-estradiol enhanced the growth-promoting action of 3 alpha-androstanediol, but did not affect the action of dihydrotestosterone or influence 3 alpha-hydroxysteroid dehydrogenase activity in prostate. Thus, the synergistic effect of 17 beta-estradiol and 3 alpha-androstanediol seems to be independent of any effect on the interconversion of the two androgens. The activity of the 3 alpha-hydroxysteroid dehydrogenase in dog prostate was high under all conditions of accelerated prostatic growth and appeared to be under androgenic control.

3-Hydroxysteroid Dehydrogenases↗
PubMed1978

[Differential therapy of vesico-intestinal fistulas].

40 patients with vesico-intestinal fistulas (50% inflammatory, 30% traumatic, 20% neoplastic) were treated within 10 years. Closure was achieved in 97% of 31 patients operated on with curative intention. The remaining 9 patients had palliative surgery, i.e. colostomy or cystostomy. The decision single- or multiple-stage procedure depends upon the etiology, localization and extent of the fistula.

Colostomy↗