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K Isurugi

Publications and source records attributed to K Isurugi.

At least 19 recordsLinked to original sources
PubMed1998

[Metastatic renal tumor originating from esophageal carcinoma: a case report].

We report a case of renal metastasis from esophageal carcinoma. The patient was a 74-year-old man, who had undergone an operation for esophageal carcinoma thirteen months previously. He was admitted to our clinic for examination of a right renal mass. Computed tomography (CT) revealed an irregular low density area in the right kidney and angiography showed a hypovascular tumor. Partial nephrectomy was performed. Histological examination revealed squamous cell carcinoma and the diagnosis was metastasis of esophageal carcinoma. Metastatic renal tumors are rarely encountered clinically and, to our knowledge, the present case is only the 16th clinical report of the renal metastasis of esophageal carcinoma in Japan. However, metastasis to the kidney is relatively common at autopsy. It is the fifth most common site of metastasis following the lungs, liver, bones and adrenals. Consequently, patients with malignancy should be followed up while keeping renal metastasis in mind.

Aged↗
PubMed1996

Leiomyosarcoma of the vaginal wall causing difficulty in micturition: a case report.

A 52-year-old woman was admitted because of a vaginal-wall tumor adjacent to the external urethral orifice. The tumor had been causing disturbances in micturition for the past year. Magnetic resonance imaging and computed tomography images indicated a 6 x 3 cm solid mass in the anterior vaginal wall. The tumor was enucleated surgically through a median longitudinal incision of the anterior vaginal wall. Micturitional disturbances were rectified after surgery. Histologically, the tumor was a mixture of a high-cellularity area with a mitosis rate of 7 per 30 high-power fields, and a less cellular area without mitosis. Immunohistochemical staining was performed for both areas. The prognostic implications of the tumor are discussed.

Female↗
PubMed1996

Incomplete testicular feminization syndrome: studies on androgen receptor(AR) function, AR gene analysis, and aromatase activities at puberty and long-term observations of clinical and hormonal features from infancy to puberty.

A female infant with partial androgen insensitivity (PAIS) was first seen at 4 months of age with slight virilization of the genitalia and externally palpable testes. Sex chromosome was 46,XY. She received left orchidectomy and exploratory laparotomy at 2 yr of age. At exploratory laparotomy, neither a uterus nor fallopian tubes were found. The right testis was preserved by fixing it at the external inguinal ring expecting spontaneous pubertal maturation. After discharge, serum levels of LH, FSH, testosterone (T) and estradiol (E2) were measured annually, and the steroid responses to hCG stimulation were examined every two yr. At the age of 10 yr, she developed breasts and a very feminine body habitus. At 12 yr, she received a clitoroplasty and right orchidectomy. The fibroblast cultures were made from the genital skin whereby androgen receptor (AR) binding was assessed by radioreceptor assay using 3H-DHT as the ligand, and thermoinstability of AR was noted despite normal maximum binding (Bmax) and dissociation constant (Kd) at 22 degrees C. But another binding experiment with 3H-Mibolerone resulted in the lack of receptor binding. AR gene analysis with direct sequencing of coding exons of the gene revealed no abnormality of the AR gene. 5 alpha-reductase activity was normal. Aromatase activity appeared to be enhanced in the genital skin fibroblast (GSF) cells as well as in the testicular tissue. The results of these studies indicated that the patient had PAIS with impaired AR functions and increased aromatase activity. After the discharge, the patient has maintained feminine phenotype, receiving estrogen therapy with mestranol 0.02 mg/day po.

Aging↗
PubMed1994

Effect of 15-deoxyspergualin on accelerated rejection in rat heart transplantation.

The effect of 15-deoxyspergualin (DSG) on accelerated rejection was evaluated using a rat heart transplantation model. Lewis rats (LEW, RT1l) served as the organ recipient and Brown Norway rats (BN, RT1n) as the donor. In the accelerated rejection model, the LEW recipient was sensitized with BN skin and BN heart was transplanted 7 days later; the heart graft was rejected within 2 days (n = 7). Histologically, the graft showed coagulation necrosis and hemorrhage throughout the myocardium. DSG (2.5 mg/kg/day) was administered to the recipient under the following three protocols: group 1: during the sensitization period (7 days); group 2: from 3 days after the sensitization to 2 days after grafting (7 days), and group 3: immediately after heart transplantation. The mean graft survival period in groups 1, 2, and 3 was 4.3 +/- 0.8 days (n = 7, p < 0.01 vs untreated host), 11.7 +/- 2.1 days (n = 7, p < 0.001, vs. untreated host), and 2.0 +/- 0 days (n = 6), respectively. The rejected grafts in groups 1 and 3 histologically showed coagulation necrosis and hemorrhage. By contrast, in group 2, the major histological change was interstitial lymphocyte infiltration and there were few findings such as coagulation necrosis or hemorrhage. In the complement-dependent cytotoxicity test, serum obtained at the second posttransplant day from the recipients treated in group 1 showed a high cytotoxicity level, although the cytotoxicity level of serum obtained from the recipients treated in group 2 was consistently low.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Male pseudohermaphroditism].

Male pseudohermaphroditism (MPH) is a complex variety of sexual differentiation disorders characterized by deficiency of masculinization of the internal and/or external genital organs in the presence of testicular development as the male gonad. This condition is caused by embryonic failure in the processes of male sexual development, which is a sequence of mechanisms originating from the genetic sex determination triggered by the SRY gene on the Y chromosome, followed by genital sex differentiation influenced by the fetal testis. Resulting phenotypical features of MPH vary from complete female to mostly normal but with some ambiguity in the maleness. Pubertal changes are also important factors related to etiology. Recent elucidation of detailed mechanisms of male differentiation and its derangements has been achieved in the era of molecular genetics. Classical classification of MPH, mainly based on anatomical and endocrinological findings obviously needs to subject to a complete revision. The newest version of MPH classification is reviewed and discussed in relation to etiological backgrounds of each type of the disorder. Main etiological factors are: failure of the SRY and its related genes involved in the testis determination; failure of anti-mülerian hormone (AMH) for normal involution of the female duct system; disordered production or function of androgen receptors essential for the fetal differentiation of the male genital organs; 5 alpha-reductase deficiency syndrome; defective responsiveness of the testis to gonadotropin due to Leydig cell agenesis; various types of enzyme defects involved in testicular androgen biosynthesis; fetal testicular dysgenesis syndromes occurring at various stages of embryogenesis; and other less clearly defined entities of MPH. Implications are that other types of sexual differentiation disorders than MPH, such as true hermaphroditism, gonadal dysgenesis and some other disorders that have been considered to be distinct entities, may have close linkage to MPH through dysgenetic process of gonadal development with subsequent degeneration and/or tumorigenesis. Molecular basis of these probably related disorders should be elucidated in the near future and some clues to preventive measures for these genetically determined malformations are awaited.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1994

[Application of antiandrogens on prostatic diseases].

Antiandrogen therapy for benign prostatic hyperplasia (BPH) and prostatic carcinoma has been introduced in clinical practice. Steroidal antiandrogens such as progestational agents suppress prostatic growth through pituitary gonadotropin suppression as well as by blocking intraprostatic androgen action. Although clinical efficacy of the therapy appears to be promising in some clinical trials, the side effect of sexual function disturbances remains to be solved especially in BPH patients. The new treatment modality for advanced prostatic carcinoma has been introduced; the total androgen blockade therapy, utilizing a pure antiandrogen (Flutamide) in combination with an LH-RH agonist, has been proposed by some authors, but the overall efficacy has not been established yet. Clinical trials for two pure antiandrogens (Flutamide and Casodex) are currently in progress in Japan.

Androgen Antagonists↗
PubMed1994

[Retroperitoneal lymph node dissection for patients with advanced testicular tumor].

We examined the indication for retroperitoneal lymph node dissection (RPLND) for 30 patients with advanced testicular tumor and made the following conclusion. The sequence of RPLND and primary chemotherapy made no difference in the therapeutic effect for patients with stage II A non-seminomatous germ cell tumor (NSGCT). However, we thought it better to administer primary chemotherapy prior to RPLND to prevent dissemination of tumor cells. Viable tumor cells often remained in retroperitoneal residual tumors even after chemotherapy in the patients with NSGCT advanced beyond stage II B. Therefore, RPLND seemed to be necessary if residual retroperitoneal tumors were found after the chemotherapy. In patients with seminoma, RPLND did not seem to be necessary if the residual tumor was less than 3 cm in diameter or the reduction rate of the retroperitoneal tumor was more than 80% after the initial therapy (chemotherapy or irradiation therapy.

Cisplatin↗
PubMed1994

Renal transplantation in selective IgA deficiency.

We report a case of selective IgA deficiency in a girl who received a successful renal transplant from a donor with normal serum IgA level. Although the recipient serum was negative for anti-IgA antibody, the donor kidney was washed with a sufficient volume of perfusate and the amount of corticosteroid given to the patient immediately after the revascularization was increased to twice the normal dose. Serum complement level transiently decreased, but recovered during the first week after surgery. Although the patient suffered from acute pyelonephritis of the graft during the fourth month, there has been no evidence of infection thereafter.

Adolescent↗
PubMed1993

Successful gonadotrophin treatment of hypogonadism in postoperative patients with macroprolactinoma and persistent hyperprolactinaemia.

We report on two males with prolactinoma in whom hyperprolactinaemia and hypogonadism persisted for several years postoperatively despite the administration of a dopamine agonist or bromocriptine. In these patients, a GnRH test revealed no response in the levels of serum LH or FSH. An hCG stimulation test provoked no response in the serum levels of testosterone. Case 1, who was 28 years old at the first visit, received parenteral testosterone and appreciable virilization of the genitalia was noted within a few months. When he married and desired to father a child, the treatment was switched to hCG/hMG combined therapy and spermatozoa appeared subsequently in the ejaculate, although their numbers were low. His wife conceived and delivered a healthy baby girl. Case 2 was a single young man who presented with hypogonadotrophic hypogonadism and hyperprolactinaemia. He was started on hCG injections three times per week and the maturation of his genitalia was advanced rapidly. Semen analyses showed sperm concentration and motility to be within the normal range. Post-treatment GnRH test revealed no improvement in gonadotrophin responses for LH or FSH. In both cases, the hCG test repeated after the gonadotrophin treatment showed normal basal and stimulated testosterone levels. During the course of gonadotrophin treatment in these cases, serum prolactin levels remained elevated, and it is suggested that, in the two cases, the hypothalamo-pituitary function was disturbed by the tumour or its manipulation and the capacity of the pituitary gland to secrete gonadotrophin was impaired. Under such circumstances with persisting hyperprolactinaemia, hCG and/or hCG/hMG combination treatment can induce normal virilization and advance spermatogenesis sufficiently to achieve fertility.

Adult↗