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Immunocytochemical Localization of Estrogen Receptors in Spontaneous and Experimentally Induced Canine Benign Prostatic Hyperplasia
885
MISCELLANEOUS
nenolone glucuronide were not different between the 2 groups. This also was the case with plasma cortisol and pregnenolone, leading the authors to conclude that the elevation of plasma 17-hydroxypregnenolone, dehydroepiandrosterone and androst-5-ene-3,6,17,6-diol reflects an increase of adrenal 17-hydroxylase activity in the benign prostatic hyperplasia group. There also appeared to be an increase of 5a-reduced androgen formation as indicated by a slight increase in plasma dihydrotestosterone and androsterone glucuronide concentration in the men with benign prostatic hyperplasia. Finally, the authors noted a 50 per cent decrease of plasma glucuronidated androst5-ene-3,6, 17,6-diol, estrone and estradiol levels in the benign prostatic hyperplasia group, suggesting that this group is experiencing inhibition of the transformation of unconjugated estrogenic steroids into glucuronide derivatives. These data indicate that adrenal C-19 steroids might be involved in the etiology of benign prostatic hyperplasia and that, while estrogen glucuronidization is diminished in men with this problem, prostatic androgen metabolism seems to be increased. M. J.
s. 4 figures, 29 references
Immunocytochemical Localization of Estrogen Receptors in Spontaneous and Experimentally Induced Canine Benign Prostatic Hyperplasia
H. SCHULZE AND E. R. BARRACK, Department of Urology, The Johns Hopkins University School of Medicine and The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, Maryland Prostate, 11: 145-162, 1987 In an attempt to clarify the role of estrogens in the etiology of benign prostatic hyperplasia in dogs, the authors studied the location of estrogen receptors by immunocytochemical techniques. Three groups were studied: normal prostates, spontaneous benign prostatic hyperplasia and experimentally induced benign prostatic hyperplasia. Control prostates (young male dogs) showed no estrogen receptors in the glandular epithelium (they are seen randomly in all groups in other elements of the prostate). Dogs with spontaneous benign prostatic hyperplasia showed nuclear estrogen receptor staining in a minority of glandular epithelial acinar cells (less than 10 per cent) in the periurethral region. The apparent anatomical and biochemical heterogeneity of estrogen sensitivity of prostatic cells and components indicates that if estrogen does have a role in benign prostatic hyperplasia it appears to do so selectively in the prostate rather than homogeneously throughout the gland. They also examined the glands of dogs subjected to treatment with androgen and/or estradiol and they found no correlation between presence of estrogen receptors and development of benign prostatic hyperplasia. These findings indicate greater similarities in the benign prostatic hyperplasia seen in man and canines than previously were thought to exist. J. H. N. 7 figures, 1 table, 39 references
Prostatic tissue samples from different disease states were analyzed for cytosolic retinoic acid binding protein. Binding protein was found in benign prostatic hyperplasia, cancer and prostatitis states. No statistically significant differences could be detected quantitatively. The authors believe that there was a tendency to higher concentrations in carcinoma, possibly indicating the prostate as a target organ for the retinoid, retinoic acid. J. H. N. 2 figures, 2 tables, 15 references
Fulminant Lymphocyte-Depleted Hodgkin Disease in a Homosexual Man With HIV Infection D. COLBOURN, H. STASZEWSKI, S. GOLDENBERG, V. DONOVON AND F. RAIO, Oncology-Hematology Division, Department of
Medicine and Department of Pathology, Winthrop-University Hospital, Mineola, New York and Department of Medicine, Health Sciences Center, SUNY at Stony Brook, Stony Brook, New York N. Y. State J. Med., 87: 570-571 (Oct.) 1987 A 43-year-old homosexual man was admitted from the emergency room with a 4-day history of fever, jaundice and increasing mental confusion. Laboratory studies were remarkable for severe pancytopenia and a positive human immunodeficiency virus titer by enzyme-linked immunosorbent assay which were confirmed by Western blot study. Computerized axial tomography demonstrated ascites and massive hepatosplenomegaly. Bone marrow aspiration and biopsy revealed a hypercellular marrow with megakarocytic and histiocytic hyperplasia with occasional erythrophagocytosis. Diagnosis was lymphoproliferative disorder, possibly malignant histiocytosis. In light of the rapid deterioration of the patient, heroic therapy was instituted with cyclophosphamide, vincristine and prednisone but he died 9 days after hospitalization. Autopsy demonstrated lymphocyte-depleted Hodgkin's disease involving the liver, spleen and bone marrow, as well as the perisplenic and peripancreatic lymph nodes. This case is reported because most cases of Hodgkin's disease in the population at risk for human immunodeficiency virus infection have been of the mixed cellular subtype and they have responded well to therapy. Most patients experience the greatest morbidity from opportunistic infections or Kaposi's sarcoma, rather than progression of Hodgkin's disease. However, this patient had fatal fulminant lymphocyte-depleted Hodgkin's disease with no opportunistic infection. The authors remind the reader to be aware of this potential variant. M. J. S. 1 figure, 10 references
MISCELLANEOUS A View of the Proposed New York State Regulations Pertaining to the Activities of Medical Students ASSOCIATED MEDICAL SCHOOLS OF NEW YORK,
Bellevue Hos-
pital Center, New York, New York Cytosolic Retinoic Acid-Binding Protein in Human Prostatic Dysplasia and N eoplasia J.
K. JUTLEY, J. KELLEHER, P. WHELAN AND J. MIKEL,
Departments of Medicine, Urology and Histopathology, St. James Hospital, Leeds, England Prostate, 11: 127-132, 1987
N. Y. State J. Med., 87: 533-534 (Oct.) 1987 On June 2, 1987 the Ad Hoc Committee on Emergency Services, appointed by the New York State Health Commissioner, announced several recommendations for medical students that subsequently were inserted into draft revisions of the New York State Health Code, section 405. This code states
MISCELLANEOUS
nenolone glucuronide were not different between the 2 groups. This also was the case with plasma cortisol and pregnenolone, leading the authors to conclude that the elevation of plasma 17-hydroxypregnenolone, dehydroepiandrosterone and androst-5-ene-3,6,17,6-diol reflects an increase of adrenal 17-hydroxylase activity in the benign prostatic hyperplasia group. There also appeared to be an increase of 5a-reduced androgen formation as indicated by a slight increase in plasma dihydrotestosterone and androsterone glucuronide concentration in the men with benign prostatic hyperplasia. Finally, the authors noted a 50 per cent decrease of plasma glucuronidated androst5-ene-3,6, 17,6-diol, estrone and estradiol levels in the benign prostatic hyperplasia group, suggesting that this group is experiencing inhibition of the transformation of unconjugated estrogenic steroids into glucuronide derivatives. These data indicate that adrenal C-19 steroids might be involved in the etiology of benign prostatic hyperplasia and that, while estrogen glucuronidization is diminished in men with this problem, prostatic androgen metabolism seems to be increased. M. J.
s. 4 figures, 29 references
Immunocytochemical Localization of Estrogen Receptors in Spontaneous and Experimentally Induced Canine Benign Prostatic Hyperplasia
H. SCHULZE AND E. R. BARRACK, Department of Urology, The Johns Hopkins University School of Medicine and The James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, Maryland Prostate, 11: 145-162, 1987 In an attempt to clarify the role of estrogens in the etiology of benign prostatic hyperplasia in dogs, the authors studied the location of estrogen receptors by immunocytochemical techniques. Three groups were studied: normal prostates, spontaneous benign prostatic hyperplasia and experimentally induced benign prostatic hyperplasia. Control prostates (young male dogs) showed no estrogen receptors in the glandular epithelium (they are seen randomly in all groups in other elements of the prostate). Dogs with spontaneous benign prostatic hyperplasia showed nuclear estrogen receptor staining in a minority of glandular epithelial acinar cells (less than 10 per cent) in the periurethral region. The apparent anatomical and biochemical heterogeneity of estrogen sensitivity of prostatic cells and components indicates that if estrogen does have a role in benign prostatic hyperplasia it appears to do so selectively in the prostate rather than homogeneously throughout the gland. They also examined the glands of dogs subjected to treatment with androgen and/or estradiol and they found no correlation between presence of estrogen receptors and development of benign prostatic hyperplasia. These findings indicate greater similarities in the benign prostatic hyperplasia seen in man and canines than previously were thought to exist. J. H. N. 7 figures, 1 table, 39 references
Prostatic tissue samples from different disease states were analyzed for cytosolic retinoic acid binding protein. Binding protein was found in benign prostatic hyperplasia, cancer and prostatitis states. No statistically significant differences could be detected quantitatively. The authors believe that there was a tendency to higher concentrations in carcinoma, possibly indicating the prostate as a target organ for the retinoid, retinoic acid. J. H. N. 2 figures, 2 tables, 15 references
Fulminant Lymphocyte-Depleted Hodgkin Disease in a Homosexual Man With HIV Infection D. COLBOURN, H. STASZEWSKI, S. GOLDENBERG, V. DONOVON AND F. RAIO, Oncology-Hematology Division, Department of
Medicine and Department of Pathology, Winthrop-University Hospital, Mineola, New York and Department of Medicine, Health Sciences Center, SUNY at Stony Brook, Stony Brook, New York N. Y. State J. Med., 87: 570-571 (Oct.) 1987 A 43-year-old homosexual man was admitted from the emergency room with a 4-day history of fever, jaundice and increasing mental confusion. Laboratory studies were remarkable for severe pancytopenia and a positive human immunodeficiency virus titer by enzyme-linked immunosorbent assay which were confirmed by Western blot study. Computerized axial tomography demonstrated ascites and massive hepatosplenomegaly. Bone marrow aspiration and biopsy revealed a hypercellular marrow with megakarocytic and histiocytic hyperplasia with occasional erythrophagocytosis. Diagnosis was lymphoproliferative disorder, possibly malignant histiocytosis. In light of the rapid deterioration of the patient, heroic therapy was instituted with cyclophosphamide, vincristine and prednisone but he died 9 days after hospitalization. Autopsy demonstrated lymphocyte-depleted Hodgkin's disease involving the liver, spleen and bone marrow, as well as the perisplenic and peripancreatic lymph nodes. This case is reported because most cases of Hodgkin's disease in the population at risk for human immunodeficiency virus infection have been of the mixed cellular subtype and they have responded well to therapy. Most patients experience the greatest morbidity from opportunistic infections or Kaposi's sarcoma, rather than progression of Hodgkin's disease. However, this patient had fatal fulminant lymphocyte-depleted Hodgkin's disease with no opportunistic infection. The authors remind the reader to be aware of this potential variant. M. J. S. 1 figure, 10 references
MISCELLANEOUS A View of the Proposed New York State Regulations Pertaining to the Activities of Medical Students ASSOCIATED MEDICAL SCHOOLS OF NEW YORK,
Bellevue Hos-
pital Center, New York, New York Cytosolic Retinoic Acid-Binding Protein in Human Prostatic Dysplasia and N eoplasia J.
K. JUTLEY, J. KELLEHER, P. WHELAN AND J. MIKEL,
Departments of Medicine, Urology and Histopathology, St. James Hospital, Leeds, England Prostate, 11: 127-132, 1987
N. Y. State J. Med., 87: 533-534 (Oct.) 1987 On June 2, 1987 the Ad Hoc Committee on Emergency Services, appointed by the New York State Health Commissioner, announced several recommendations for medical students that subsequently were inserted into draft revisions of the New York State Health Code, section 405. This code states