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At least 235 records · Page 13Linked to original sources
PubMed1991

[Acute myelomegakaryocytic leukemia developed from myelodysplastic syndrome after chemotherapy against complicated small cell lung cancer].

A patient with acute myelomegakaryocytic leukemia (AMMgL), which developed from myelodysplastic syndrome (MDS) after chemotherapy against complicated small cell lung cancer, is reported. The patient was a 66 year-old male, who first presented with moderate macrocytic anemia. Bone marrow aspiration showed absolute erythroid hypoplasia and morphological abnormalities were found in erythroid, granuloid and megakaryocytic lineage cells. Iron utilization studies using radioisotope showed ineffective hematopoiesis. He was diagnosed as having MDS (refractory anemia) and treated with prednisolone, fluoxymesterone, and transfusions. After 3 years, small cell lung cancer was found, but he achieved complete remission with chemotherapy. Since then, pancytopenia progressed with myelofibrosis. Abnormal blasts were found in peripheral blood and gradually increased. He finally died from a blastic crisis resulting in gastric bleeding. The blasts were peroxidase negative, platelet peroxidase positive (10%), and glycoprotein II b/III a antibody positive, indicating megakaryoblasts.

Aged↗
PubMed1990

[Allopurinol induced aplastic anemia in a patient with chronic renal failure].

A 43 year old female patient with chronic renal failure originated from polycystic kidney disease was admitted with pancytopenia. Prior to the admission, she had a history of taking allopurinol for 3 months. Allopurinol was discontinued immediately and she was treated with blood transfusion (platelet and RBC) and fluoxymesterone. The lymphocyte stimulation tests were negative for allopurinol and oxipurinol. The determination of serum levels of allopurinol and oxipurinol was disclosed to be not so high compared with other patients treated with allopurinol. On 45th day after admission, she was transfused with bone marrow from her elder brother. Thereafter bone marrow finding of the patient began to improve despite the lack of bone marrow engraftment. For further improvement, pulse treatment with corticosteroid was carried out. Although the pathophysiology of allopurinol-induced aplastic anemia remains unknown, it is interesting to note that bone marrow transfusion and pulse treatment with corticosteroid seemed effective in this case.

Adult↗
PubMedDate not supplied

Hormone stimulation and chemotherapy in advanced prostate cancer: interim analysis of an ongoing randomized trial.

We report here in the interim analysis of an ongoing randomized clinical trial designed to test whether androgen priming enhances tumor chemosensitivity in men with stage D prostate cancer refractory to orchiectomy. All patients are continuously treated with aminoglutethimide and hydrocortisone, to lower adrenal androgen secretion, and are given cyclic chemotherapy. Patients in the stimulation arm receive also the synthetic androgen, fluoxymesterone, for 3 days before and on the day of chemotherapy. Of 57 patients entered to date, 41 have received adequate treatment to be evaluable. Response to therapy (objective remissions + stabilizations of disease) occurred in 17 of 18 evaluable patients (94%) randomized to the stimulation arm, and in 16 of 23 evaluable patients (70%) in the control group (p less than 0.025). Duration of response was not significantly different in the two groups (median: 9 months in the stimulation and 12 months in the control arm). With 30% of the total of 57 patients still alive, survival is not significantly different in the stimulation (median: 13 months) and control arm (median: 16 months). As expected, patients who responded to treatment lived significantly longer than those who failed to benefit. Two episodes of reversible spinal cord compression occurred during androgen administration. (The risk of this serious side effect may be reduced by performing a screening myelogram to rule out subclinical spinal metastasis). Our preliminary data suggest that androgen priming may enhance the tumoricidal effect of cytotoxic drugs in advanced prostate cancer. The lack of improvement in duration of response and survival may be explained by the large fraction of hormone-independent cells probably present in patients with tumors refractory to orchiectomy.

Aged↗
PubMed1986

Endocrine-responsive pancreatic carcinoma: steroid binding and cytotoxicity studies in human tumor cell lines.

We have begun to investigate the steroid responsiveness of pancreatic cancer by comparing human (MiaPaCa, Colo-357, RWP-1, RWP-2) and rodent (AR42j) pancreatic tumor cell lines with cultured estrogen receptor-positive breast cancer cells (MCF-7, T47-D). The four human pancreatic tumors contain measurable levels of specific estradiol binding sites with dissociation constants (Kd) that range from 1 to 9 nM, in contrast to the higher-affinity binding sites measured in the breast cancer cells (Kd less than or equal to 1 nM). Growth of one pancreatic tumor line (MiaPaCa) is stimulated 40% above control by exposure to nanomolar concentrations of estradiol, suggesting that the estrogen receptor in these cells is functioning like that in MCF-7 and T47-D cells. Glucocorticoids (dexamethasone, hydrocortisone) and androgen (fluoxymesterone) stimulate proliferation of Colo-357 cells by as much as 30%. Paradoxically, glucocorticoids inhibit AR42j cells to less than 50% of control growth. Micromolar exposures of estrogen (17 beta-estradiol), antiestrogen (tamoxifen), antiandrogen (dehydroxyflutamide), progestins (progesterone, R5020, medroxyprogesterone acetate), and inhibitors of steroid-metabolizing enzymes (17 beta-N,N-diethylcarbamyl-4-methyl-4-aza-5 alpha-androstan-3-one, danazol) impair growth of these pancreatic tumors to varying degrees, and with little relationship to estrogen receptor content. In general, progestins are slightly more growth inhibiting to these pancreatic tumor lines than the other endocrine agents tested, including tamoxifen. Only the RWP-2 cells appear completely resistant to steroidal therapy, showing less than 25% growth inhibition with exposure to therapeutic concentrations (less than or equal to 2.5 microM) of these agents. Colo-357, MiaPaCa, and AR42j cells are most responsive to these endocrine agents, and their overall pattern of sensitivity suggests that the steroid-dependent growth-inhibitory mechanisms of some pancreatic carcinomas may involve both receptor antagonism and direct inhibition of steroidal oxidoreductases. 17 beta-N,N-Diethylcarbamyl-4-methyl-4-aza-5 alpha-androstan-3-one, a potent inhibitor of 5 alpha-reductase with minimal affinity for androgen receptor, inhibits growth of Colo-357 cells to less than 40% of control and also inhibits AR42j and MiaPaCa cells. Dehydroxyflutamide, a potent androgen receptor antagonist with no direct influence on 5 alpha-reductase activity, inhibits growth of MiaPaCa and AR42j cells but has no affect on Colo-357 growth.(ABSTRACT TRUNCATED AT 400 WORDS)

Aminoglutethimide↗
PubMed1986

Cutaneous leukocytoclastic vasculitis complicating hairy cell leukemia (leukemic reticuloendotheliosis).

A patient with hairy cell leukemia (HCL) receiving fluoxymesterone developed cutaneous leukocytoclastic vasculitis. His clinical picture was of purpuric papules and pustules on his chest and limbs. Oral corticosteroid therapy and colchicine therapy were tried, with only minimal improvement. Chemotherapy with pentostatin (2'-deoxycoformycin) resolved the vasculitis and placed the HCL in remission. Fifteen cases of HCL associated with vasculitis have been reported previously. Hairy cell leukemia and vasculitis appear to have more than a coincidental relationship.

Adult↗
PubMed1985

Pulmonary peliosis.

Peliosis hepatis is an uncommon vascular lesion of unknown etiology, and its occurrence has been linked frequently to therapy with androgenic-anabolic steroids. Extrahepatic peliosis is ever rarer. It is found most commonly in the spleen and usually in conjunction with peliosis hepatis. Documented here is an unusual case of pulmonary peliosis, associated with peliosis hepatis and peliosis of the spleen, in a 40-year-old man who had Fanconi's anemia and who received long-term therapy with fluoxymesterone and methyltestosterone. To our knowledge, this represents only the second reported case of pulmonary peliosis in the English literature.

Adult↗
PubMed1982

Antiestrogen treatment of breast cancer: an overview.

The nonsteroidal antiestrogen tamoxifen has emerged as a highly effective, nontoxic endocrine therapy for women with Stage IV and II estrogen receptor-positive breast cancer. Tamoxifen appears to act by blocking endogenous estrogen action at the target tissue level rather than by suppression of circulating estrogen levels. In a series of 113 consecutive, selected patients with Stage IV breast cancer, tamoxifen induced objective remissions in 50% lasting an average period of 21 + months and a median period of 16 months. These results are comparable to previous results with surgical hypophysectomy. Recent randomized studies comparing pharmacological doses of estrogen versus tamoxifen in postmenopausal women with Stage IV breast cancer have shown comparable results with these two treatment modalities. Antiestrogen therapy has been shown to be effective in some patients after prior endocrine additive therapy and, in particularly, after ablative procedures, such as ovariectomy, adrenalectomy, and hypophysectomy. It has been shown that circulating estrogens are not completely eliminated following ablation of these endocrine glands, which may account for the effectiveness of antiestrogen in this setting. Other endocrine therapies have been shown to be effective after prior treatment with antiestrogen. Hypophysectomy can induced remissions in 60% of patients who initially responded to tamoxifen and in 25% of patients who failed to benefit from tamoxifen. Recent studies have shown that aminoglutethimide plus hydrocortisone may also induce remissions in some patients after prior treatment with tamoxifen. This latter finding is of particular interest since aminoglutethimide is thought to work by blocking estrogen production, and the finding suggests that tamoxifen does not completely block all endogenous estrogen activity. Fluoxymesterone has been shown to induce remissions after tamoxifen or after tamoxifen plus hypophysectomy, and there was no correlation between the response to antiestrogen abd subsequent response to androgen. Because of its effectiveness and minimal side effects, tamoxifen is considered to be an initial endocrine therapy of choice in women with breast cancer. However, it has its limitations, as demonstrated by the results of secondary endocrine therapies such as hypophysectomy, medical adrenalectomy, and androgen therapy.

Adrenalectomy↗
PubMed1981

Precocious puberty and hypothalamic hamartoma.

A 3-year-old boy with true precocious puberty and hamartoma of the hypothalamus is described. Preliminary diagnosis was established by the presence of unusually advanced puberty and skeletal age without other evidence of central nervous system dysfunction, elevated blood gonadotropin and testosterone concentrations, and positive computed tomography scans. Pneumoencephalography further delineated the tumor. Hypothalamic-pituitary-gonadal and adrenal functions were studied. Release of gonadotropins after the injection of synthetic luteinizing hormone-releasing hormone and the suppression of luteinizing hormone and of testosterone by oral fluoxymesterone were comparable to maximal responses of normal men. The diagnosis was confirmed by histologic and electron microscopic study of an excised portion of the tumor. Immunofluorescence studies indicated the presence of luteinizing hormone-releasing hormone in the hamartoma and radioimmunoassays detected thyroid-stimulating hormone-releasing hormone and somatostatin. The hamartoma resembles an autonomously functioning accessory hypothalamus. The ectopic neuroendocrine pathways, however, are responsive to hormonal stimulation and feedback. The clinical, endocrinologic, and pathologic features of published cases of precocious puberty and hypothalamic hamartoma are reviewed. Advanced or rapidly progressive true precocious puberty in the very young with elevated concentrations of blood gonadotropins and gonadal steroids and positive pneumoencephalography appear to be characteristic.

Child, Preschool↗
PubMed1994

[Action mechanism of synthetic androgens].

The most common androgen supplement used in Japan involves intramuscular injection of testosterone esters, such as, testosterone enanthate and testosterone propionate. As orally active androgens, derivatives of testosterone, such as, methyltestosterone and fluoxymesterone have also been used. These synthetic androgens have most commonly been used as replacement androgens in male patients with hypergonadotropic hypogonadism, as well as, hypogonadotrophic hypogonadism. The use in idiopathic male infertility and in elderly men with erectile dysfunction, however, has been shown to be less effective. Furthermore, relatively high doses of synthetic androgens are given in athletes to ensure success in sports and are used as hormonal methods for male contraception.

Female↗