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Biomedical subjects

G Tolis

Publications and source records attributed to G Tolis.

At least 55 records · Page 3Linked to original sources
PubMed1986

Objective response and disease outcome in 59 patients with stage D2 prostatic cancer treated with either Buserelin or orchiectomy. Disease aggressivity and its association with response and outcome.

A comparative study was done in 59 recently diagnosed Stage D2 prostatic cancer patients treated with either long-term GnRH-A (Buserelin) (N = 42) or with orchiectomy (N = 17) and followed up for three years. The suppressed limits of plasma testosterone and estradiol levels after eight-week follow-up as well as the objective clinical response and disease outcome were found to be similar with either treatment. Hot flushes and loss of libido were noticed in both groups throughout the follow-up period; however, there were no other side effects. Analysis of Stage D2 patients based on their time of death enables us to identify nonhormonal variables which, in the form of an aggressiveness score, correlated well with both clinical response and disease outcome. These data confirm that (1) Buserelin is an effective and safe alternative to orchiectomy in advanced prostatic cancer, and (2) in clinical studies a multifactor aggressiveness score is useful for analyzing clinical efficacy data. Prospective application of that score may enable predictability of patient response and influence patient management.

Buserelin↗
PubMed1986

Therapy of acromegaly with SMS 201-995: long-term studies.

Fourteen acromegalic patients, half of whom had been unsuccessfully treated with surgery, radiotherapy, or bromocriptine, were given the somatostatin analogue SMS 201-995 parenterally as the sole therapeutic regimen after a single administration had demonstrated suppression of serum growth hormone (GH). An impressive and sustained clinical improvement was documented in all patients, including those in whom bromocriptine had failed; most marked was the decrease in soft tissue swelling and headache and an improved performance status. GH levels decreased each time SMS 201-995 was injected but returned to basal levels within 8 h in most of the patients. With chronic therapy, 24-h mean levels were significantly suppressed, and the GH stimulability of thyrotrophin-releasing hormone and growth-hormone-releasing hormone (pl-44) was markedly reduced. Discontinuation of SMS 201-995 therapy was associated with a return of symptoms and abnormal GH dynamics. The efficacy and safety of chronically administered SMS 201-995 in active acromegaly opens new horizons for its treatment.

Acromegaly↗
PubMed1986

Therapeutic efficacy of a somatostatin analogue (SMS 201-995) in active acromegaly.

Twelve patients with active acromegaly, six of whom had not responded to previous combined surgery, radiotherapy, and bromocriptine administration, were treated with an octapeptide long-acting somatostatin analogue, SMS 201-995, given subcutaneously for up to 1 year. Growth hormone (GH) levels decreased by 50% to 90% after a single 25-micrograms SMS 201-995 injection in all patients, including two who were resistant to bromocriptine therapy. After GH values reached a nadir, they returned to preinjection values over a 12-hour period and no rebound was seen. Assessment of the GH-lowering effect of the drug at weekly intervals for the first 6 weeks and monthly thereafter disclosed no tachyphylaxis. Gradual increase of the dose from 50 to 150 micrograms daily led to a significant increase in clinical improvement. Shrinkage of the size of the pituitary tumor was documented in three of nine evaluated cases. Abdominal cramps of a transient nature not associated with diarrhea were noted in two patients but there were no other side effects. Hematological and biochemical blood and urine tests, including serum thyroxine and cortisol levels, did not reveal any abnormality during chronic treatment. This study demonstrates the safety and efficacy of SMS 201-995 in the short-term treatment of acromegaly.

Acromegaly↗
PubMed1985

Long-term follow-up of patients with advanced prostatic carcinoma treated with either buserelin (HOE 766) or orchiectomy: classification of variables associated with disease outcome.

We compared the clinical efficacy and safety of Buserelin treatment versus orchiectomy in 29 patients with newly diagnosed advanced prostatic cancer. There was no significant difference between the two treatment modalities in 1) reduction of plasma testosterone to below 100 ng/dl after 8 weeks, 2) objective clinical response rates in patients with stage D2 carcinoma, 3) induction of complete remission in patients with stages C and D1 carcinoma, or 4) relapse rates and death rates in patients with stage D2 carcinoma. After scoring stage D2 disease according to our aggressiveness analysis system, we found that patients with less aggressive neoplasms displayed a qualitatively better response and more prolonged remission. These data and the absence of estrogenic effects confirm Buserelin as a favorable alternative to orchiectomy in the treatment of prostatic cancer. Additionally, the study demonstrates the importance of considering the heterogeneity of the aggressiveness of stage D2 disease in assessing the benefits of clinical trials in prostatic carcinoma.

Acid Phosphatase↗
PubMed1984

Advanced prostatic adenocarcinoma: biological aspects and effects of androgen deprivation achieved by castration or agonistic analogues of LHRH.

Twenty-nine patients with advanced prostatic adenocarcinoma were evaluated clinically, biochemically and radiologically and randomly assigned either to orchiectomy or to medical treatment. The latter consisted of the chronic administration of an LHRH agonistic analogue by parenteral and/or intranasal routes. Plasma testosterone levels fell to castrate values and remained so for as long as the follow-up lasted (24 months); estrogen levels fell as well. No change in basal cortisol, thyroxine or prolactin levels was noticed. A decrease in prostate size and improvement in prostatism occurred in all. Bone pain and radiology conventionally or by isotopic scanning, did not parallel the improvement seen in the primary disease locus. Similarly, the changes in alkaline phosphatase were minimal when compared to that of prostatic acid phosphatase. Both enzymes increased prior to or concurrently with relapse of the disease. The longest remission and survival was seen in patients with low enzyme levels, non diffuse bone metastases and high degree of tumor differentiation. Chronic use of agonistic analogues of LHRH induces effective castration in men with prostatic carcinoma and can replace orchiectomy or estrogen administration. The quantitative analysis of androgen receptors (AR) in subcellular fractions of tumor cells; the use of techniques to enhance the number of AR in the cytosol; and the determination of the type II/I regulatory subunit of protein kinase may be used to identify hormone independent clones and spare patients of unnecessary procedures.

Acid Phosphatase↗
PubMed1984

Sheehan's syndrome: in vivo diagnosis with the use of computerized axial tomography and pituitary provocative testing.

Postpartum amenorrhea associated with other symptoms and signs of hypopituitarism, such as inability to lactate, weakness, easy fatigability, sexual-hair loss, and clinical evidence of hypothyroidism, were found in two female patients with the antecedent of postpartum hemorrhage. The baseline values of the gonadal, thyroid, and glucocorticoid hormones were all consistently lower than normal. The serum levels of the pituitary hormones were low, and the responses to standard stimulatory tests were either insignificant or blunted. Plane skull films and conventional sella tomography did not reveal any abnormality in the sella turcica. CAT identified hypodensity in the area of the hypophysis with preservation of the pituitary stalk. The combination of the failure of provocative stimuli to affect anterior pituitary hormone release with the radiologic picture compatible with pituitary infarction readily makes the diagnosis of Sheehan's syndrome in vivo and should be used in patients where this syndrome is suspected.

Adrenocorticotropic Hormone↗
PubMed1984

Pregnancy in hyperprolactinemic women.

Pregnancy achieved in women who receive treatment to correct the secretory dysfunction of nontumoral HPRL or microprolactinomas requires close prenatal care, but generally its course does not vary from normal. When a macroprolactinoma is present, consequences of pregnancy are insignificant, provided the tumor has been previously treated or bromocriptine is given continuously during the pregnancy. On those rare occasions when symptoms of tumor growth appear during pregnancy, bromocriptine and dexamethasone effectively control such manifestations. Breast-feeding of the infant can be allowed, and a second pregnancy within a short term is not contraindicated. When a new pregnancy is not desired, nonhormonal contraceptive methods are advised. Patients with nontumoral HPRL and microadenomas require periodic checkups. Macroadenomas may be surgically excised, but longterm bromocriptine treatment also achieves good results and is highly recommended.

Adenoma↗
PubMed1983

Gonadotropin-releasing hormone agonistic analogues in the treatment of advanced prostatic carcinoma.

Orchiectomy or chronic administration of the gonadotropin releasing hormone agonistic analogue D, Ser (TBU)6, des Gly-NH2(10) ethylamide (HOE 766) were employed as therapeutic maneuvers in 25 patients with advanced prostatic carcinoma. HOE 766 administration effectively suppressed plasma testosterone to castrate levels that persisted for as long as treatment continued. Surgical and medical castration resulted in a significant decrease in prostatic size; this became evident earlier for surgically than medically treated patients (P less than .05), but no difference existed after the third month of treatment. Symptoms and signs of prostatism improved in practically all the patients. Among patients with stage D2 disease, there was an improvement in five as far as bone radiological assessment was concerned. Alkaline phosphatase levels did not show appreciable changes in patients showing objective stable disease or partial response according to National Prostatic Cancer Project criteria. Radioimmunoassayable prostatic acid phosphatase levels became normal in two of two stage C, five of five stage D1, and eight of seventeen patients with stage D2 disease, a rise in prostatic acid phosphatase (PAP), in alkaline phosphatase, and deterioration in bone radiology were associated with clinical evidence of relapse; this occurred despite persistently low levels of plasma testosterone. Serum thyroxine, cortisol, and prolactin levels remained unchanged following orchiectomy or chronic administration of HOE 766. Practically all patients complained of hot flashes and experienced a decrease in libido and potency, but none developed gynecomastia or thromboembolic episodes. The data indicate that HOE 766 can be used safely as an alternative to castration or estrogens for the treatment of patients with androgen-dependent prostatic cancer.

Acid Phosphatase↗
PubMed1983

Transabdominal ultrasonography in the evaluation of patients with advanced prostatic carcinoma: effects of castration and of chronic administration of a gonadotropin releasing hormone agonistic analogue.

Twenty-two patients with advanced prostatic carcinoma were subjected either to orchiectomy (group I, n = 5) or to chronic administration of a gonadotropin releasing hormone agonistic analogue D, Ser (TBU)6, des Gly-NH2(10) LHRH nonapeptide (HOE 766) (group 2, n = 17). Plasma testosterone was similar in both groups prior to treatment (group 1: 636 +/- 129.29, group 2: 580.85 +/- 37.57; X +/- SE). The levels attained in group I were significantly lower (P less than .05) than those of group 2 through eight weeks of follow-up but were similar by the third month. Prostatic size (cm2) as estimated by transabdominal ultrasonography did not differ between the two groups prior to treatment (group 1: 23.6 +/- 3.35, group 2: 21.4 +/- 1.97; X +/- SE). Both therapies resulted in a decrease of prostatic size that was significantly more pronounced (P less than .05) in group I compared with group 2 by the first and third month; by the six month, there was no statistical difference in the prostatic size attained with either therapeutic modality. Persistent suppression of prostatic size was documented in all patients of group 2 chronically (up to 24 months) treated with HOE 766 even when there was evidence of uninhibited or progressive bony metastases. The above data 1) indicate the efficacy of the HOE 766 in inducing medical castration and prostatic shrinkage in advanced carcinoma of the prostate, 2) document the usefulness of transabdominal ultrasound in the follow-up of such patients, and 3) suggest a relationship between the rapidity of tumor shrinkage and Leydig cell suppression.

Buserelin↗
PubMed1983

Suppression of testicular steroidogenesis by the GnRH agonistic analogue Buserelin (HOE-766) in patients with prostatic cancer: studies in relation to dose and route of administration.

Forty-six patients with prostatic carcinoma received the gonadotropin releasing hormone agonistic analogue (GnRH-A) Buserelin at doses ranging from 0.05 to 1.5 mg subcutaneously and/or 0.4 to 1.2 mg intranasally (i.n.) daily for 12-120 weeks. An increase in plasma testosterone (T) was seen in 19% of patients on day 7 of therapy; with continuation of treatment plasma T as well as DHT and E2 levels fell by more than 50% within 2-4 weeks in those patients receiving greater than or equal to 50 micrograms s.c. and/or greater than or equal to 1 mg in daily dose. Persistently low plasma T levels (less than 1 ng/ml) were reached in 60% of patients receiving 50 micrograms s.c. in 89% of those treated with 1.2 mg i.n. and in 100% of patients who received initially 1.5 mg s.c. X 7 days followed by 1.2 mg i.n. daily. The above data indicate the importance of dose and route of administration in achieving significant suppression of plasma sex steroids in patients with prostate cancer in whom Buserelin can be used as an alternative to castration or estrogens.

Aged↗
PubMed1983

Gonadotropins and estradiol responses to single intranasal or subcutaneous administration of a luteinizing hormone-releasing hormone agonist in the early follicular phase.

Single increasing intranasal and subcutaneous doses of a potent luteinizing hormone-releasing hormone (LH-RH) agonistic analog (D-Ser[TBU]6-des-Gly-NH2(10))LH-RH ethylamide (Buserelin) were administered on day 2 or 3 of the follicular phase in 59 normal women. Groups of five or six volunteers received intranasal doses ranging from 50 to 1300 micrograms and subcutaneous doses varying between 0.3 and 30 micrograms of the LH-RH agonist. Maximal amplitude of the serum gonadotropin response is observed at 6 hours. A sixfold increase is obtained for luteinizing hormone (LH) at a 200 micrograms intranasal dose, whereas maximal follicle-stimulating hormone (FSH) stimulation (threefold) is reached at a lower dose (100 micrograms). A 1000-micrograms dose elicits a more prolonged stimulation, levels of FSH and LH being two and five times above control levels at 11 hours. Similar response curves are obtained by the subcutaneous route, a maximal stimulation being reached at 3 micrograms for FSH and at 10 micrograms for LH. Serum estradiol levels are maximally increased at 11 hours after administration of 10 and 200 micrograms of the analog by the respective subcutaneous and intranasal routes. Twenty-four-hour response curves of gonadotropins indicate that the efficacy of the intranasal route is approximately 3% to 5% of the subcutaneous route. These observations should provide information useful in the investigation of the antifertility effects and medical treatments using an intranasal LH-RH agonist in the human being.

Administration, Intranasal↗
PubMed1983

Depression: biological and neuroendocrine aspects.

Distorted biorhythms and altered neuroendocrine function may accompany depressive disorders. Restoration of the above derangements occurs with effective therapy, whereas persistence of the biological abnormalities is found in patients incompletely cured and may be predictive of early relapse. The commonest hormonal abnormalities are: decreased suppressibility of the ACTH-cortisol axis to dexamethasone, subnormal thyrotropin response to TRH and growth hormone release to hypoglycemia; attenuated gonadotropin production and abnormal light-dark entrained melatonin secretion. The observed hormonal derangements seem to be epiphenomena of the primary disorder. The reversibility of the disordered neuroendocrine control with treatment of the depressive syndrome suggests that the hormonal abnormalities represent a state rather than trait disorders. Finally, the lack of similar neuroendocrine derangements in schizophrenia or secondary exogenous depression suggests that different neurochemical alterations underlie these disorders.

Biological Clocks↗
PubMed1982

Effect of morphine on the hypothalamic-pituitary axis in postmenopausal women.

In this study, 10 postmenopausal women were given 5 mg of morphine intravenously; and the serum level of prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and growth hormone (GH) were measured before and after morphine injection. A significant increase in serum prolactin as well as a significant decrease in LH were observed following the administration of morphine. It is suggested that morphine may affect a common neurotransmitter that controls both prolactin and LH secretion. It is also of interest that the increase in serum prolactin following morphine injection is of similar magnitude as observed in premenopausal patients.

Female↗
PubMed1982

Pituitary responses to a neuroactive tripeptide (TRH) in Friedreich's ataxia families.

Oral glucose tolerance, thyroid function tests, as well as thyrotropin, prolactin and growth hormone release after administration of thyrotropin releasing hormone, were evaluated in patients with Friedreich's ataxia and unaffected family members. Impaired glucose tolerance was found in the majority of family members, affected or not. Thyroid hormone levels and PRL and TSH responses to TRH, were similar in all and normal. However, GH responses to TRH were abnormal in half of the patients, but in none of the unaffected family members. Paradoxical responses to neuropeptides may characterize some Friedreich's ataxia patients, and may predict the possibility of therapeutic maneuvers with such peptides in these patients.

Adolescent↗