Effect of human growth hormone and somatomedin on the recovery of sheep red blood cell receptor in peripheral T-lymphocytes.

The effect of growth hormone (GH) and somatomedin (SM) on the recovery of sheep red blood cell (SRBC) receptor in trypsinized human T-lymphocytes was studied either with the use of sera from patients with acromegaly or pituitary dwarfism or after the addition of exogenous GH, SM or thymosin to human sera. It was found that GH does not show any effect on the recovery of SRBC receptor, but it may act through the increase of SM level. It was concluded that the regulation of cellular immunity may be influenced by GH through its stimulatory action on the synthesis and release of somatomedins.

Clinical experience with somatrem in growth hormone deficiency.

Three studies of human growth hormone (hGH) in hGH deficiency were initiated. In the first of these, adolescent patients were switched from pituitary hGH to somatrem (SI preparation) for 1 month. No significant differences were noted in any of the clinical parameters measured during treatment with either preparation. In the second study, nine patients (six of them naïve) were treated with somatrem (SII preparation) for 9-12 months. The naïve patients exhibited catch-up growth, and bone age developed in parallel to chronological age during the study period. Somatomedin activity increased and correlated positively with growth. Antibodies to hGH and Escherichia coli polypeptide (ECP) developed in some patients, but titres and binding capacities were low. In the third study, 21 patients are currently being treated with Somatonorm; the first 3-6 months are evaluable. Growth velocities increased to normal values. Antibodies to hGH and ECP were present in several patients, but again the titres and binding capacities were low, and Somatonorm was less antigenic than the SI and SII preparations.

Cisobitan in treatment of prostatic cancer. A prospective controlled multicentre study.

Cisobitan, an organosilicon compound with estrogenic and antigonadotropic properties has been evaluated clinically in comparison with an estrogen preparation. In a multicenter study a total of 140 patients with well and moderately well differentiated prostatic cancer were randomly allocated to treatment with Cisobitan or Estradurin/Etivex, 70 to each group. Of 34 patients with poorly differentiated prostatic cancer 18 were given Cisobitan--and 16 were given Estracyt-treatment. Among the patients with well and moderately well differentiated prostatic cancer there were, disregarding mortality, no major differences in subjective, objective or laboratory response to the two kinds of treatment. The pattern of side effects was similar, but oedema requiring diuretics occurred more often in the estrogen treated group. There was a significant difference in mortality at 12 months between the groups, two in the Cisobitan group and ten in the estrogen treated group. Cancer was the cause of death in two patients in the estrogen treated group. All other patients succumbed in cardiovascular diseases. At 24 months the difference in mortality rate was less pronounced: Another ten patients had died in the Cisobitan treated group and seven among the estrogen treated patients. Cancer was responsible for the deaths in seven of the Cisobitan patients compared to four of the estrogen treated patients. Within three years one more patient in both groups had died. Of the 34 patients with poorly differentiated cancer, twelve were alive at the 24 months' follow up, six in the Cisobitan group and six in the Estracyt group.

Clinical experimental randomized study of 2.6-cis-diphenylhexamethylcyclotetrasiloxane and estramustine-17-phosphate in the treatment of prostatic carcinoma.

Patients with poorly differentiated prostatic carcinoma and skeletal metastases were randomized to treatment with 2.6-cis-diphenylhexamethylcyclotetrasiloxane (2.6-cis) and estramustine-17-phosphate (estramustine). Parallel with the clinical study a group of non-randomized patients were treated with 2.6-cis. Cytological regression of the tumor could be registered in half of the estramustine group but not in the 2.6-cis group. There were no drug-related changes in blood chemistry, kidney function tests, hematology or liver enzymes. There was in increase in acid and alkaline phosphatase in both groups but more pronounced in the 2.6-cis group. In both groups follicle-stimulating and luteinizing hormone values were depressed. Testicular and penis atrophy was observed in the 2.6-cis group. Relief of pain and marked improvement of conditions occurred in the majority of the cases in both groups. In general, no tumor regression was observed during administration of 300 mg. 2.6-cis daily for at least 3 months. Some tumor regression was noted during 600 mg. estramustine therapy daily.