Biomedical subjects
Publications and source records attributed to S Rannikko.
A case of pelvic hemangiopericytoma resembling a prostatic tumor is presented. Radical prostatovesiculectomy with enblock tumor excision was performed. No metastases were found. The histopathologic picture was suggestive of the malignant form of hemangiopericytoma. Two years postoperatively the patient is in good condition without any signs of recurrence.
Fifty-one patients, 15 with bladder cancer and 36 with prostatic cancer, were examined by preoperative pelvic CT scanning in order to determine its sensitivity, specificity and accuracy in detecting pelvic lymph node metastases. The poor sensitivity of CT (40%) in detecting lymph node metastases reduces its value for staging lymph nodes. The reason for the low sensitivity is that metastases in nodes which are of normal size cannot be detected by CT. Pelvic lymphadenectomy remains the only accurate method for evaluating the state of pelvic lymph nodes.
In a patient with transitional cell carcinoma of the pelvis of a solitary kidney there were extensive recurrences in the ureter and bladder. The treatment consisted of total cystoureterectomy and pyeloileocutaneostomy for urinary diversion and endoscopic control of the pelvic neoplastic growth.
In a randomized double-blind manner, 43 women with grade I and II stress urinary incontinence were treated with either phenylpropanolamine p.o. 50 mg twice daily (Rinexin, 1 tablet b.i.d.) or placebo during two weeks. Urethral CO2 profilometry, with recording of maximum urethral closure pressure (MUCP) and functional urethral length (FUL), and subjective response were considered for effect evaluation. The subjective response of Rinexin was highly significant (p = 0.01) above that of placebo. Clinical improvement was reported by 15 of 21 women on Rinexin and by 8 of 22 women on placebo. A significant increase in MUCP, 14%, was registered in women on Rinexin treatment. This increase was more pronounced in the grade I than in the grade II incontinent women. No statistically significant correlations were obtained between subjective response and increase in MUCP. An increase in FUL was recorded in both two treatment groups, but no statistically significant difference between them was obtained. Adverse drug reactions were rare. No changes in blood pressure occurred. Based on the present study, Rinexin (1 tablet b.i.d.) is an effective and safe medication for female grade I and II stress incontinence and is also recommended as adjunctive therapy to physiotherapy before Teflon injection or operation.
Six patients with advanced prostatic cancer were treated with a potent GnRH agonist analog (buserelin, Hoechst; 600 micrograms, intranasally, three times a day) for 6 months. The first 2-6 days of treatment were associated with a 50% elevation (P less than 0.01) in serum testosterone (T) and a simultaneous elevation of 20% (P less than 0.01) in serum prostate-specific acid phosphatase (PAP). Serum T fell to the castrate range (less than 1 nmol/liter) in all patients in 2-3 weeks, and PAP decreased concomitantly in five of the six patients. Serum LH progressively decreased by about 80% during the treatment, whereas a secondary rise of FSH levels occurred after the first month of treatment. The patients were orchiectomized after 6 months of treatment. No differences were found between the pre- and postsurgical levels of serum T or in comparison with those of six patients orchiectomized as the first therapeutic measure. Testicular endogenous T concentrations, LH and FSH receptors, and in vitro T production were measured in three testis samples and compared with those values in testis tissue obtained from five control patients. The endogenous levels and in vitro production of T were depressed by over 95% in testes from agonist-treated patients. The small residual T production responded to hCG stimulation as in control patients. Interestingly, no change was found in testicular LH receptor content, but FSH receptors decreased by 80%. The elevation in serum PAP at the beginning of the agonist treatment and the small residual testicular T production after 6 months may not be clinically important. However, they indicate the necessity of comparative long term studies between orchiectomy and GnRH agonists in the treatment of patients with prostatic cancer.
Four hundred and four prostatic cancer patients diagnosed in the years 1979-1982 in nine Finnish hospitals have been followed up for a mean period of three years. The aim of this study is to evaluate the situation of this malignancy in the Finnish male population and to discuss the diagnostic procedures and treatment modalities. In one fifth of the patients the carcinoma was as incidental finding on microscopical examination of tissue removed by transurethral resection or enucleation for presumed benign prostatic hyperplasia. At the diagnostic moment 69% of the tumours were locally advanced beyond the prostatic capsule and one third of all cases had metastasized. 134 out of 404 (33%) have died and 45% of these of prostatic cancer. Survival was adversely affected by the tumour differentiation grade. In non-metastasized cases the local extent of the tumour had no notable effect on prognosis. Some early comparisons are made between orchidectomy and oestrogen therapy.
Bone scintigraphy, serum acid phosphatase activity (ACP), prostatic acid phosphatase by radioimmunoassay (PAP) and alkaline phosphatase activity (ALP) were studied in 117 consecutive patients with prostatic cancer. Serum PAP was more sensitive than ACP in indicating prostatic cancer in the 63 patients with normal bone scans: 28% had positive PAP tests and 15% positive ACP tests. In the 54 patients with bone metastases no difference in the frequency of positive PAP (84%) and ACP (85%) test was observed. Serum PAP and ACP, but not ALP, were useful for the assessment of the response to therapy particularly in patients without bone metastases. In the follow-up of patients with bone metastases the scan was more informative than any of the phosphatase assays studied.
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The nature of hormonal changes with age and the possible role of these changes in the development of benign prostatic hyperplasia (BPH) and prostatic cancer (PC) were studied by assaying the plasma levels of total and free testosterone (T), estradiol (E2), prolactin, and sex hormone binding globulin binding capacity (SHBG) in 20 normal healthy men aged 40-59 years, in 30 patients with BPH aged 63-79 years, and in 30 patients with PC of similar height, weight, and age as the BPH patients. The mean E2 was highly significantly (P less than 0.0005) lower in the PC patients and in the young controls than in the BPH patients. The mean free T was significantly higher in the young controls than in the BPH patients (P less than 0.025) and PC patients (P less than 0.0005). The PC patients had a slightly lower (P less than 0.05) mean free T and mean E2/free T ratio than the BPH patients. The mean E2/free T ratio was significantly higher in the BPH patients (P less than 0.0005) and in the PC patients (P less than 0.0025) than in the young controls. It seems possible that the observed age-dependent significant increase in plasma estrogen concentration in the BPH patients may act as a protective factor against prostatic cancer.
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In 32 subjects with histologically and/or cytologically verified prostatic cancer the hormonal pattern was studied by assaying 18 plasma and urinary hormones or groups of hormones. The tumours were classified according to the UICC classification system and the hormone values were correlated to the local extent of the tumour (T classification), the presence of metastases (M classification) and the differentiation of grade (G classification). It was found that patients with metastases had significantly higher plasma oestradiol and lower testosterone/oestradiol and testosterone/oestrone plus oestradiol ratios as compared to those subjects without metastases. In subjects with moderately or poorly differentiated tumours plasma oestrone + oestradiol was significantly higher and the testosterone/oestrone + oestradiol ratio was significantly lower than in the subjects with well differentiated tumours. In the various TNM classification groups no obvious trends were found with regard to urinary hormones and no significant differences between the groups for plasma FSH, LH, prolactin, progesterone and cortisol were observed. It is concluded that in more advanced cases with metastatic cancer and when tumours are less well differentiated the androgen/oestrogen ratio may be decreased. These alterations have no diagnostic significance because of greater overlapping of individual results between the various groups of patients.
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In 32 subjects with histologically and/or cytologically verified prostatic cancer the hormonal pattern was studied by assaying 18 plasma and urinary hormones or groups of hormones and relating the values to the response to endocrine treatment. Total orchidectomy (orchiepididymectomy) was performed on 9 patients, subcapsular orchidectomy on 13 patients and oestrogen therapy with Estradurin was given in 4 patients. Six patients had total orchidectomy followed by estrogen therapy. With few exceptions all values were within the normal range. The only significant exceptions were the high urinary oestrogen values and the low urinary oestrone + oestradiol/oestriol ratio observed as compared to healthy males working in a factory. No urinary hormone values or ratios of hormone values could be used for the prediction of prognosis in prostatic carcinoma patients. However, the ratios of plasma testosterone/oestradiol (T/Oe2) and testosterone/prolactin (T/Prl) were found to give good information with regard to the response to endocrine treatment. High values for one or both of these ratios meant a good response to treatment in all subjects without exception in this material. Subjects with both ratios low had a good response to endocrine treatment in 50% of the cases. No other plasma hormones measured were of any help prognostically. It is concluded that by measuring the T/Oe2 and T/Prl ratios it seems possible to select a group of patients with favourable primary response to endocrine treatment.
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Eight patients with advanced prostatic carcinoma (ages 59 to 78 years) were treated with a potent gonadotropin-releasing hormone (GnRH) agonist analog (buserelin, Hoechst; 600 micrograms intranasally, 3 times daily) and orchiectomized after 6 months of treatment. Endocrine responses were followed by serum hormone measurements during agonist treatment and for 3 months after orchiectomy. Six other patients (65 to 86 years) with advanced prostatic cancer had been orchiectomized as the first therapeutic measure and their blood samples were used as controls. In the GnRH agonist-treated patients, serum immunoreactive luteinizing hormone (LH) and follicle stimulating hormone (FSH) decreased after initial stimulation by 70 to 80%, within 1 to 3 weeks (P less than 0.01). FSH partly recovered (P less than 0.05) after the first month of treatment. Serum prolactin (PRL) displayed a slight tendency to decline during buserelin treatment (P less than 0.05). Serum total and free testosterone (T) of the buserelin-treated patients decreased to the castrate range within 3 to 4 weeks after an initial 5-day increase (P less than 0.01). Serum progesterone and 17-hydroxyprogesterone (17-OHP-4) decreased to the castrate range (by 50 to 70%) in 1 week. Only minor changes were observed in sex hormone binding globulin (SHBG). Significant, acute elevations of LH, FSH, T, and 17-OHP-4 were observed only on day 1 after an injection of buserelin (500 microgram i.m.) and not when assessed between day 7 and month 6 of treatment. After 6 months of buserelin treatment, orchiectomy did not affect the serum steroids measured. After orchiectomy, immediate increases in serum LH, and somewhat later in FSH, were seen in the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Endogenous testosterone (T), LH and FSH receptors, and in vitro production of cyclic adenosine-3':5'-monophosphate (cAMP), T and some of its steroid precursors were measured in testicular tissue obtained at orchiectomy from seven prostatic cancer patients treated for 6 months with a potent gonadotropin-releasing hormone (GnRH) agonist analog (buserelin, Hoechst, 600 micrograms 3 times a day intranasally). In addition, histologic and morphometric studies were carried out on the testicular tissue. Testicular tissue from age-matched prostatic cancer patients (n = 14), whose first therapy was orchiectomy, served as controls. The peptide treatment decreased intratesticular T by 95% (P less than 0.01) and FSH receptors by 57% (P less than 0.01), but had no effect on LH receptors. The in vitro production of T decreased by 94% (P less than 0.01), but that of cAMP was unaffected. Besides T, the in vitro production of testicular 17-hydroxyprogesterone (17-OHP-4), androstenedione and 5 alpha-dihydrotestosterone (5 alpha-DHT) dropped by 71 to 90% (P less than 0.01 to 0.05) during buserelin treatment, but those of pregnenolone, progesterone and dehydroepiandrosterone (DHEA) were not affected. Histologic studies revealed considerable variation in the seminiferous epithelium of the control group, but spermatogenesis was highly suppressed in nearly all of the buserelin-treated group. The number of Sertoli cells was unaffected, but tubular diameters were reduced (P less than 0.05) by buserelin treatment. Leydig cells appeared dedifferentiated in this group, although their number per testis was not altered. These data indicate that gonadotropin suppression by GnRH agonist most likely affects testicular steroidogenesis by inhibiting 3 beta-hydroxysteroid dehydrogenase and a step(s) prior to pregnenolone formation. The treatment does not impair testicular LH binding or cAMP production, but clearly suppresses FSH receptors. Spermatogenesis in general is suppressed but with considerable variation.