Reingard Sörensen

Ovarian and adrenal vein steroids in seven patients with androgen-secreting ovarian neoplasms: selective catheterization findings *

Standardized bilateral ovarian-adrenal vein catheterization was utilized to preoperatively assess glandular steroid release in seven consecutive cases of occult virilizing gonadal neoplasms. Peripheral testosterone (T) exceeded 1.5 ng/ml in all instances (range, 1.51 to 8.67 ng/ml). Endoscopy and radiography failed to locate the functional lesions. Catheterization showed a unilateral elevation of the ovarian-peripheral vein gradient for T greater than 2.7 ng/ml in six women. In the remaining patient, gradient analysis ruled out an adrenal tumor but did not facilitate lateralization of the gonadal lesion due to subselective ovarian effluent sampling. In addition to the consistent hypersecretion of T, variable excess gonadal output of dihydrotestosterone, androstenedione, dehydroepiandrosterone, and 17 alpha-hydroxyprogesterone was evident. Associated adrenal androgenic hyperfunction was documented in three subjects. Histologic evaluation of the implicated ovaries revealed three lipid cell, two Leydig cell, and two Sertoli-Leydig cell tumors, respectively, measuring between 0.6 and 2.2 cm in diameter. No correlation was found between any of the following parameters: peripheral or glandular vein steroid levels, androgen gradients, severity of symptoms, tumor morphology, and tumor size. In conclusion, appropriate application of selective catheterization may considerably reduce the frequency and extent of operative intervention.

Ovarian and adrenal vein steroids in patients with nonneoplastic hyperandrogenism: selective catheterization findings

Standardized bilateral ovarian-adrenal vein catheterization was utilized to assess directly glandular steroid release in 60 androgenized women without evidence of a functional neoplasm. Testosterone (T), dihydrotestosterone (DHT), androstenedione (delta 4 A), dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), 17-hydroxyprogesterone (17-OHP), and cortisol (F) were measured by radioimmunoassay in samples obtained from a peripheral vein and the four glandular veins (all values are given as nanograms per milliliter, mean +/- standard deviation). Peripheral values were as follows: T, 0.68 +/- 0.43; DHT, 0.32 +/- 0.13; delta 4 A, 2.2 +/- 2.0; DHEA, 8.8 +/- 8.9; DHEA-S, 3137 +/- 1774; 17-OHP, 2.0 +/- 3.0; and F, 216 +/- 121. Peripheral elevations of at least one androgen were found in 80% of the 60 cases (T, 38%; DHT, 18%; delta 4 A, 50%; DHEA, 45%; and DHEA-S, 37%). Ovarian-peripheral vein gradients ( OPGs ) and adrenal-peripheral vein gradients ( APGs ) served as semiquantitative estimates of glandular secretion. OPGs were as follows: T, 0.4 +/- 1.1; DHT, 0.1 +/- 0.2; delta 4 A, 3.4 +/- 7.0; DHEA, 14.6 +/- 100; DHEA-S, -288 +/- 523; 17-OHP, 4.5 +/- 8.4; and F, -35 +/- 47. APGs were as follows: T, 0.88 +/- 1.3; DHT, 1.1 +/- 0.9; delta 4 A, 14.4 +/- 38.4; DHEA, 327 +/- 367; DHEA-S, 854 +/- 1223; 17-OHP, 20.8 +/- 41.3; and F, 1252 +/- 2023. Excess ovarian and/or adrenal androgen output was assumed in a given individual when one or more of the respective T, DHT, delta 4 A, DHEA, and DHEA-S gradients exceeded the upper 95% confidence limits of normal previously established in this laboratory.(ABSTRACT TRUNCATED AT 250 WORDS)

Technical difficulties of selective venous blood sampling in the differential diagnosis of female hyperandrogenism.

To determine glandular steroid release of adrenals and ovaries in female hyperandrogenism, a standardized method for percutaneous transfemoral venous blood sampling was developed. In eight volunteers and 67 patients, catheterization was performed during the early follicular phase (days 3–7; between 8 and 10 a.m.) to reduce interference from cyclic and circadian variations of secretion. Serial samplings reduced the episodic effluent changes. Anatomical variations and collateral flow as well as stress effects and the dosage of contrast media were studied. During catheterization, peripheral cortisol levels did not differ significantly from control groups. Collaterals had no effect on hormone levels. Contrast media increased cortisol effluent levels only when they were sampled following venography. Four-vessel venous sampling was found to be indicated if peripheral testosterone was more than 1.5 ng/ml and/or dehydroepiandrosterone sulfate more than 6.700 ng/ml. If an ovarian (adrenal)/peripheral gradient of testosterone exceeded 2.7 mg/ml, surgical intervention for tumor removal at the site of hormone excess was felt to be necessary.

Ovarian and adrenal vein steroids in healthy women with ovulatory cycles—selective catheterization findings

Bilateral ovarian-adrenal vein catheterization and androgen measurements in the efferent samples were utilized to directly assess glandular steroid release in 8 healthy volunteers with proven ovulatory cycles during the early follicular phase. Side effects did not occur in any of the women. Hormone levels were as follows (mean +/- SD; ng/ml) T: peripheral vein (PV) 0.36 +/- 0.16, ovarian veins (OV) 0.39 +/- 0.13, adrenal veins (AV) 0.85 +/- 0.63; dihydro-T (DHT): PV 0.25 +/- 0.09, OV 0.29 +/- 0.10, AV 0.93 +/- 0.65; delta 4-androstendione (A): PV 0.88 +/- 0.34, OV 1.82 +/- 1.04, AV 9.22 +/- 8.04; DHEA; PV 5.13 +/- 1.96, OV 6.73 +/- 2.69, AV 146.79 +/- 217.24; DS PV 1860 +/- 850, OV 1937 +/- 1039, AV 2567 +/- 1201; 17 alpha-hydroxyprogesterone (17P): PV 0.60 +/- 0.19, OV 1.46 +/- 1.64, AV 6.94 +/- 6.20; F: PV 170 +/- 50, OV 130 +/- 21, AV 788 +/- 1320; the bilateral differences of effluent levels were not significant. Glandular-peripheral vein steroid gradients served as semiquantitative estimates of momentary secretory activity; they were as follows (mean +/- SD; ng/ml) T: ovarian-peripheral vein gradient (OPG) 0.03 +/- 0.09, adrenal-peripheral vein gradient (APG) 0.48 +/- 0.57; DHT: OPG 0.05 +/- 0.05, APG 0.69 +/- 0.60; A: OPG 0.97 +/- 1.13, APG 8.33 +/- 7.86; DHEA: OPG 1.70 +/- 1.80, APG 141.80 +/- 216.60; DS: OPG 191 +/- 72, APG 706 +/- 824; 17P: OPG 0.87 +/- 1.67, APG 6.30 +/- 6.10; F: OPG 38 +/- 11, APG 610 +/- 1329. Gradient, analysis revealed that the ovaries produced significant quantities of A, DHEA and 17P, but no T, DHT or F between day 3-7 of the cycle; direct gonadal DS output was detected in 2 individuals. A significant OPG for DS was detected in two individuals possibly indicating its partially gonadal origin. The adrenals released larger amounts of A, DHEA and 17P than the ovaries at this stage (P less than 0.05); also, they consistently secreted T, DHT, DS and F.

Control of Renovascular Hypertension by Renal Embolization

Two cases with medically well-controlled renovascular hypertension due to unilateral contracted kidney were treated by percutaneous renal embolization. One of the patients had two aneurysms of the renal artery in addition to the stenosis. Both patients remained normotensive without medication after follow-ups of 6 and 24 months, respectively.

Aneurysm of the right ovarian vein—An unusual cause of pulmonary embolism

This case reports a 23-year-old female who experienced a massive bilateral pulmonary embolism. The source of thrombi was found to be in a large saccular aneurysm of the right ovarian vein. The pulmonary emboli were treated by local infusion of streptokinase. The patient was cured after removal of the aneurysm by surgery.

Differential diagnosis of early opacification of the portal vein and its tributaries during arteriography.

Twenty-two cases with communication of an artery and the portal vein or one of its tributaries are discussed. Four conditions in which relatively significant arterio-portal shunts may exist can be differentiated: (1) angiodysplasias or arteriovenous malformations, (3) traumatic and postoperative lesions, and (4) benign and malignant tumors. The significance of the portal veins early opacification during arteriographic examinations of the abdominal organs is discussed, and the findings are compared to those reported in the literature.

Selective Venous Sampling for the Differential Diagnosis of Female Hyperandrogenemia

Hyperandrogenism is one of the most common female endocrinopathies. It may be due to (a) glandular causes (ovarian and/or adrenal hypersecretion of androgenic steroids), (b) extraglandular causes (increased peripheral conversion of preandrogens, decreased specific plasma androgen binding, target organ hypersensitivity, or administration of androgenic drugs; or (c) a combination of these factors. Extremely high elevated peripheral androgen levels are suggestive of an androgen-producing tumor of the ovaries or the adrenals.

Polyzystische Ovarien-Ursache oder Folge der Hyperandrogenämie?

m6chten wit festhalten: 1. Stimulation der Follikelreifung mit FSH ist m6glich. 2. Die Varianz der Reaktion ist grol3 und dies mag begriindet liegen in dem unterschiedlichen Verhalten der endogenen LH-Spiegell 3. Eine initiale Dosis von 150 IE sollte nicht iiberschritten werden, da dann in hohem Ma6e ein deutlicher LH-Abfall stattfindet und sonographisch die Entwicklung einer Cyste nachweisbar wird. 4. In der zur Stimulation notwendigen Dosis, der Anzahl reifer Follikel, der Vermeidung von f2berstimulation und insbesondere der Zahl erzielter Gravidit~iten, konnte eine Verbesserung der Resultate gegeniiber der HMG-Behandlung von uns bisher nicht gesehen werden.

Hyperthecosis ovarii: Histologie, Klinik und Endokrinologie

Hammerstein (Berlin): Hyperthecosis ovarii: Histologie, Kiinik und Endokrinologie* Im angelsfichsischen Schrifttum wurde wiederholt die umstrittene Behauptung aufgestellt, dab die Hyperthecosis ovarii eine selbststfindige nosologische Einheit darstellt, die sich trotz oberflfichlicher A.hnlichkeit in wesentlichen Punkten vom Syndrom der polyzystischen Ovarien (PCO) unterscheidet. Dazu zfihlen eine stromale Luteinisierung (PCO: rein perifollikulfir), ein obligater Virilismus (PCO: fakultativ) sowie eine rein ovarielle Androgenhypersekretion (PCO: hfiufig auch mit adrenaler Komponente). Diese Thesen wurden an acht Patientinnen mit feingeweblich gesicherter Hyperthekose iiberpriift. Histologisch liegen sich in allen F/illen multiple Nester luteinisierter thekafihnlicher Zellen im teilweise hyperplastischen Ovarialstroma nachweisen. Diese Verfinderung gilt als pathognomonisch ftir die Hyperthekose; sie fehlt beim PCO. Zusfitzlich wurden auch PCO-typische Merkmale festgestellt wie vergr6gerte Eierst6cke (4 yon 8), eine verdickte Tunica albuginea (5 yon 8) und subkapsul/ire Follikelzysten mit luteinisierter Theca interna (7 von 8). Klinisch imponierte bei allen Patientinnen ein mittelschwerer bis schwerer Hirsutismus. Das obligate Auftreten weiterer Virilismuszeichen in der Literatur als Charakteristikum der Hyperthekose beschrieben wurde dagegen nicht beobachtet; so lag eine Alopezie nur bei 3 yon 8 und eine Klitorishypertrophie nur bei 2 von 8 Frauen vor. Ansonsten fihnelte die Symptomatik in ihrer Variabilitgt dem PCO: Adipositas 7 von 8, Sterilitfit 6 von 8, Oligomenorrhoe 5 yon 8, sekund/ire Amenorrhoe 3 von 8, Hypertonus 4 yon 8 und Diabetes mellitus 2 yon 8. Endokrinologisch stand eine durchgfingig nachweisbare Erh6hung der peripheren Testosteronspiegel im Vordergrund. Mittels selektiver Katheterisierung der Ovarialund Adrenalvenen wurden die Eierst6cke (6 yon 8) bzw. die Nebennierenrinden (2 yon 8) als Ursprung des Testosterontiberschusses identifiziert. Diese Feststellung widerspricht der Annahme einer rein ovariellen Androgenhypersekretion bei der Hyperthekose. Auff/illig war, dag die Testosteronwerte im Organvenenblut sfimtlich im tumorverdfichtigen Bereich lagen. Die tibrigen Hormonbefunde waren ebenso uneinheitlich wie beim PCO; dies gilt ffir die Plasmasteroide (Dihydrotestosteron, Androstendion, DHEA, DHEA-Sulfat, 17-Hydroxyprogesteron, Cortisol: peripheres und OrganvenenNut), die Harnsteroide (17-Ketosteroide, 17-Hydroxykortikoide, Testosteron: basal und nach ACTH, Metopiron, Dexamethason sowie HCG) und die Plasmaproteohorm0ne (LH und FSH: basal und nach GnRH; Prolaktin: basal). Auf Grund dieser Ergebnisse wird gefolgert, dag die Hyperthecosis ovarii und das Syndrom der polyzystischen Ovarien im Hinblick auf Klinik und Endokrinologie nicht wesentlich differieren. Die geringen histologischen Unterschiede stellen offenbar variable Manifestationen desselben heterologen Krankheitsbildes dar.