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KALYPSO is a novel detector operating at line rates above 10 Mfps. The detector board holds a silicon or InGaAs linear array sensor with spectral sensitivity ranging from 400 nm to 2600 nm. The sensor is connected to a cutting-edge, custom designed, ASIC readout chip, which is responsible for the remarkable frame rate. The FPGA readout architecture enables continuous data acquisition and processing in real time. This detector is currently employed in many synchrotron facilities for beam diagnostics and for the characterization of self-built Ytterbium-doped fiber laser emitting around 1050 nm with a bandwidth of 40 nm.

Plasma concentrations of betamethasone, cortisol and corticosterone were measured before and after intraarticular injection of a betamethasone-depot preparation (Celestan-Depot) by radioimmuno-assay in 31 patients. Plasma concentration of betamethasone reached its maximum of between of 10 and 17 microgram/dl 30 min after injection. It had fallen to half after 2 hours, and practically to nil from the eighth day onwards. Lowest plasma levels of cortisol and corticosterone occurred after 6--24 hours, returning to the normal range after four days. In nine patients with knee-joint effusion and synovitis the plasma concentration of betamethasone was significantly higher after 24 hours, and cortisol and corticosterone values after 48 hours significantly more suppressed, than in patients without joint effusions and signs of inflammation. The results indicate that plasma concentration of betamethasone and the suppressant effect on the adrenal cortex after intra-articular injection is similar to that after intramuscular applications. Correspondingly, systemic application of the cortisol derivatives can cause significant side effects and be contra-indicated also after intra-articular injection.

A 21-year-old woman with weight loss, palpitations and facial flush was found to have hypertension (up to 200/130 mm Hg) and mild hyperkalaemia (3.4 mmol/l). Extensive diagnostic tests revealed hyperaldosteronism with contrast storing in the right adrenal gland on scintigraphy after injection of dexamethasone (2 mg daily for one week). The hyperaldosteronism could not be suppressed by dexamethasone. Analysis of venous blood separately from each side pointed to aldosterone production in the right adrenal (right renal vein: 80 ng/dl, drainage area of the right adrenal vein: 114 ng/dl, left renal vein: too low to measure). The right adrenal gland was removed. No adenoma was found histologically. After the operation the aldosterone level was reduced and the blood pressure transiently fell. But both had risen again after 3 months. Renewed tests revealed dexamethasone-remediable hyperaldosteronism. On treatment with hydrocortisone (15-5-5 mg) and 50 mg metoprolol the patient became normotensive without any other medication.

Adrenal insufficiency is suspected in some ill preterm infants. The aim of this prospective study was to compare serum cortisol concentrations during the first 2 wk of life of well preterm infants (group A) less than 30 wk of gestational age with the cortisol concentrations of ill preterm infants whose arterial hypotension-a potential sign of adrenal insufficiency-had been treated with catecholamine (group B), and the cortisol concentrations of ill preterm infants who had not been so treated (group C). Cortisol concentrations did not differ significantly between group A (240 nmol/l, 58-659; n = 46) (median, minimum-maximum) and group C (268 nmol/l, 58-1007; n = 25). Group B had a double-peaked distribution of cortisol. Two subgroups were formed by taking the highest cortisol level of group A as a threshold: group B1 (110 nmol/l, 41-378; n = 20) and group B2 (1200nmol/l, 764-1482; n = 8). The cortisol concentrations of group B1 were significantly lower (p = 0.00097) compared to the cortisol concentrations of the well preterm infants (group A). The severity of illness, which was quantified by two scoring systems, differed significantly among the groups (p < 0.003 for all comparisons) with the following sequence: A < C < B, but not between B1 and B2, as clinical variables were not different between the subgroups.

Background The major aldosterone metabolite 3α,5β tetrahydroaldosterone reflects up to 45% of the aldosterone secretion. Its 24-h urinary excretion is likely to provide an accurate index of the daily aldosterone production and to be an indicator for primary aldosteronism (PA). Methods In a prospective study, the validity of tetrahydroaldosterone as a screening test for PA was evaluated in comparison to serum potassium, plasma aldosterone, plasma renin activity, plasma aldosterone/renin activity ratio (PARR), as well as 24-h urinary aldosterone-18-glucuronide and free aldosterone. A total of 111 normotensive individuals, 412 PA patients and 1453 essential hypertensive patients, were studied. The effect of blood sampling technique on potassium level was also investigated. Results Tetrahydroaldosterone differentiated PA from essential hypertension with a sensitivity of 96% and a specificity of 95%. The sensitivity was 89% for plasma aldosterone, 87% for free aldosterone, 85% for PARR, 71% for aldosterone-18-glucuronide and 51% for renin activity. Specificities varied between 91% and 85%. The combined use of the parameters plasma aldosterone ≥9.0 ng/dL and PARR ≥25 resulted in a sensitivity of 82% and specificity of 95%. Forearm exercise proved to be a source of erroneous elevations of potassium sufficient to obscure the suspicion of PA. Conclusion The data suggest that tetrahydroaldosterone is the most reliable screening test for PA. Tetrahydroaldosterone determination in combination with aldosterone-18-glucuronide and free aldosterone increases diagnostic specificity for PA. Potassium, renin, plasma aldosterone, and basal PARR are inadequate screening procedures because they are subject to high rates of false-positive and false-negative results.

Zusammenfassung: Fragestellung: In mehreren Untersuchungen konnte der Einfluss männlicher Steroidhormone auf die Entstehung und Ausprägung aggressiven Verhaltens sowohl im Tierexperiment als auch an Gruppen gewalttätiger Personen nachgewiesen werden. Die wenigen Studien mit Kindern und Jugendlichen zeigen inkonsistente Befunde. Die Bedeutung einer androgenvermittelten Verhaltensbeeinflussung bei Jugendlichen aus der Allgemeinbevölkerung, die ein höheres Risiko für die Entwicklung von Verhaltensstörungen tragen, wurde bislang nicht untersucht. Methodik: Im Rahmen einer prospektiven Längsschnittstudie von Risikokindern wurden bei 119 Jugendlichen (51 m, 68 w) im Alter von 14 Jahren Plasmakonzentrationen relevanter Androgenmetaboliten Testosteron (T) und Dihydrotestosteron (DHT) bestimmt und externalisierende Verhaltensauffälligkeiten mittels deutscher Versionen der Achenbach-Skalen durch Elternbefragung (CBCL) und Selbstbeurteilung der Jugendlichen (YSR) erfasst. Ergebnisse: Bei den Jungen fanden sich signifikante positive Korrelationen von DHT-Plasmakonzentrationen mit der Sekundärskala Externalisierendes Verhalten im CBCL sowie mit den Problemskalen Aggressives Verhalten und Dissoziales Verhalten. In der Selbsteinschätzung der Jugendlichen ergab sich lediglich eine marginal signifikante Beziehung zwischen DHT und dissozialem Verhalten. Bei den Mädchen fehlten entsprechende Zusammenhänge völlig. Schlussfolgerungen: Frühere Befunde von Androgeneffekten auf aggressives und antisoziales Verhalten bei Erwachsenen mit gewalttätigem Verhalten konnten nun auch für männliche Jugendliche mit externalisierenden Verhaltensauffälligkeiten aus der Allgemeinbevölkerung bestätigt werden. Eine besondere Bedeutung kommt dabei dem Androgenmetabolit DHT zu.

Die zweizeitige ileoanale Pouchanlage (IAP) ist Standardverfahren zur kurativen Therapie der familiaren Adenomatosis coli (FAP) sowie der chirurgisch therapiepflichtigen Colitis ulcerosa (CU). Neben den klassischen Komplikationen beeinflusst die Entfernung des Colorectums die Blut- und Volumenhomoostase. Patienten und Methoden: Aus einem Patientenpool von 320 Patienten mit J-Pouchanlage wurden uber einen Beobachtungszeitraum von 2 Jahren Patienten mit hohem facalen Verlustsyndrom ohne fassbare organische Ursache identifiziert. Der Ausschluss einer organischen Ursache erfolgte mittels Pouchoskopie, Pouchographie und ggf. mittels MRT-Untersuchung. Neben Messparameter der Routinediagnostik wurden der Saure-Basen-Haushalt analysiert, eine Urin-pH-Metrie durchgefuhrt sowie mittels Hormonanalysen die adrenale Kompensationsleistung erfasst. Sieben Patienten mit „High-Pouch-Output“-Syndrom konnten identifiziert werden. Das Kontrollkollektiv bildete eine Gruppe aus 14 beschwerdefreien, in der endoskopischen Routinediagnostik unauffalligen IAP-Patienten. Ergebnisse: Die Analyse der Routineparameter ergab bei beiden Patientengruppen keinerlei signifikante Unterschiede. Eine deutlich verminderte Urinnatriumkonzentration 40,5 ± 18,7 mmol/l (Kontrollgruppe 98 ± 43,4 mmol/l) bestand fur die Patientengruppe mit hohen facalen Verlusten. In dieser Gruppe waren mit 42,6 ± 28,9 ng/dl (Kontrollgruppe 13,2 ± 6,8 ng/dl) die Aldosteronspiegel sowie mit 153,7 ± 121,1 ng/dl (Kontrollgruppe 53 ± 23 ng/dl) die 18-OH-Corticosteronspiegel signifikant erhoht. Fur die Glucocorticoide, Corticosteron, Cortisol wurden bei beiden Gruppen keine erhohte Aktivitat festgestellt. Nur 11-Desoxycorticosteron war im Patientenkollektiv mit „High-Pouch-Output“-Syndrom erhoht. Schlussfolgerungen: Unsere Ergebnisse belegen, dass Hormone mit mineralocorticoider Wirkung eine zentrale Rolle bei der Aufrechterhaltung der Blut- und Volumenhomoostase spielen. Die niedrige Incidenz therapiepflichtiger Verlustsyndrome nach Abschluss der ileoanalen Pouchoperation belegt die hervorragende Kompensation des entfernten Colorectums. Mit Aldosteron scheint ferner ein Marker gefunden, der die intestinale Natriumresorptionsproblematik proktocolektomierter Patienten erfasst.

Ambulantes Operieren ist bei mindestens gleich hoher Qualitat kostengunstiger als eine stationare Behandlung und wird im niedergelassenen Bereich immer auf Facharztstandard durchgefuhrt. Es geht mit einer geringeren Infektionsrate, schnellerer Arbeitsfahigkeit, geringerem Medikamentenverbrauch und hoher Zufriedenheit der Patienten einher. Leider ist nach der derzeit moglichen Abrechnung keine Kostendeckung zu erreichen. Zudem stellen Krankenhauser und Operationszentren, die die Kosten durch Querfinanzierung decken konnen, eine massive Konkurrenz fur die niedergelassenen Arzte dar. Eine Verlagerung von stationaren Operationen in den ambulanten Bereich wird nur gelingen, wenn ambulant und stationar durchgefuhrte Operationen gleich bezahlt werden, weil dann kein Grund mehr besteht, auser aus medizinischen und sozialen Grunden, einen Patienten stationar aufzunehmen. Deshalb ist eine identische DRG-basierte (DRG: „diagnosis related groups“) Vergutung fur gleiche Operationen im ambulanten und stationaren Bereich zu fordern.

PURPOSE: Restorative proctocolectomy is a standard procedure in the surgical treatment of ulcerative colitis and familial adenomatous polyposis. The radical removal of the colorectum with construction of an ileostomy often results in high stoma losses. These may lead to changes in the electrolyte and acid-base balance and to alterations in renal and suprarenal gland function. METHODS: In this study 33 patients who received an ileoanal pouch before and after proctocolectomy were investigated at different time intervals for electrolyte changes, alteration of the acid-base balance, kidney function, and hormonal changes of the suprarenal glands. Measurements were performed before proctocolectomy, ten days after proctocolectomy with ileal pouch-anal anastomosis under protective loop ileostomy, before ileostomy closure, and 6 to 12 months after ileostomy closure. Neither acute renal failure nor other vital complications were observed. RESULTS: Statistical analysis showed a significant decrease of urine pH to 5.4±0.22 (before ileostomy closure) and metabolic acidosis (pH 7.32±0.04; base excess −1.3±5.6 (before ileostomy closure)). Likewise, we found a decrease in renal clearance to 86 ml/minute (before ileostomy closure) without signs of tubular damage. The most important change during the phase with ileostomy was a functional secondary hyperaldosteronism with aldosterone levels of 63.2±70.8 ng/dl (before ileostomy closure). In comparison with preoperative levels, there was a ten-fold increase in mineralocorticoid adrenal activity. Additionally, during the period with protective ileostomy, the hepatic synthesis of aldosterone-18-glucuronide was only slightly increased, and the cortisol/cortisone ratio was extremely decreased. CONCLUSIONS: These results show that restorative proctocolectomy with ileal pouch-anal anastomosis and protective loop ileostomy significantly influences fluid, electrolyte, and acid-base balance. Functional secondary hyperaldosteronism is of central importance for subsequent renal recompensation. Approximately one-half year after ileostomy closure, the endogenous hormones with mineralocorticoid effects returned to normal levels.

Ten cases of adrenal adenomas, one case with unilateral adrenal hyperplasia, and another case with apparent bilateral are reported, in whom an alternative pathway of aldosterone via 21-deoxyaldosterone is operative. They all manifested hypertension, low renin activity, low normal potassium values, as well as high urinary excretion rates of 21-deoxyaldosterone and its related metabolite Kelly's-M1 steroid. In all cases, urinary aldosterone metabolites (aldosterone-18-glucuronide and tetrahydroaldosterone) and aldosterone precursor 18-hydroxycorticosterone levels were normal. Hence, the adrenal lesions give rise to hyper-21-deoxyaldosteronism. 21-Deoxyaldosterone is a weak mineralocorticoid, and its elevated production in the presence of normal aldosterone can induce a pathological state of hypermineralocorticoidism. Adrenalectomy resulted in normalization of hypertension in six of eight and amelioration in two of eight cases. Six of seven adenoma cases examined as well as the case of unilateral adrenal hyperplasia were sensitive to ACTH. One of the seven adenomas and, as expected, the case with apparent bilateral hyperplasia were angiotensin responsive. Histologically and electron microscopically, the operated adenomas consisted predominantly of clear cells, characterized by mitochondria with tubulo-vesicular internal structure similar to those of the zona fasciculata (in contrast, our classical Conn's adenoma with normal 21-deoxyaldosterone excretion exhibited a more heterogenous histological appearance and were, in terms of ultrastructure, more similar to cells of the zona glomerulosa). Ultrastructurally and immunocytochemically, the clear cells of 21-deoxyaldosterone adenomas showed features of both the zona glomerulosa and the zona fasciculata and are, hence, considered to be hybrid cells. We conclude that the determination of 21-deoxyaldosterone and Kelly's-M1 should be considered in the diagnosis of mineralocorticoid-induced forms of hypertension, especially when an adrenal adenoma has been detected with an imaging procedure.

21-Deoxyaldosterone has been postulated to be a precursor of aldosterone in an altenative biosynthesis pathway and Kelly's-M1 is considered to be its metabolite. In healthy volunteers, the excretion rate of 21-deoxyaldosterone and of Kelly's-M1 are significantly lower than the aldosterone metabolites, aldosterone-18-glucuronide and tetrahydro-aldosterone and than the aldosterone precursor 18-OH-corticosterone. Essential hypertension patients (with low and normal renin) excrete comparable values of 21-deoxyaldosterone and Kelly's-M1 as normotensives. In 66% of aldosterone-producing adenoma cases (APA) and in 60% of idiopathic hyperaldosteronism (IHA) patients, significantly raised values of 21-deoxyaldosterone and Kelly's-M1 were found. The patients with the high excretion rates of both steroids showed only moderately increased values of the aldosterone metabolites, aldosterone-18-glucuronide and tetrahydro-aldosterone, as well as of the aldosterone precursor 18-OH-corticosterone. In contrast, the latter mentioned steroids were excreted in higher amounts in those patients with normal excretion of 21-deoxyaldosterone and Kelly's-M1. Hence, it is suggested that aldosterone is produced alternatively either via 18-OH-corticosterone alone or additionally via 21-deoxyaldosterone. Furthermore, in three cases of “incidentally” discovered adrenal adenomas, 21-deoxyaldosterone and Kelly's-M1 were the only elevated steroids. After adrenalectomy, excretion of 21-deoxyaldosterone and of Kelly's-M1 and blood pressure returned to normal, which proves that these steroids play a role in blood pressure regulation. In essential hypertension, ACTH infusion induced a significant increase of 21-deoxyaldosterone and Kelly's-M1. However, the increase after angiotensin II was 3- to 6-fold higher than after ACTH. IHA patients proved to be more responsive to angiotensin II; and, in contrast, APA cases proved to be more sensitive to ACTH. The data suggest that beside the main route of aldosterone biosynthesis via 11-deoxycorticosterone, corticosterone and 18-OH-corticosterone an alternative pathway exits via 21-deoxyaldosterone in healthy and in hypertensive patients. There are similarities between the regulation of 21-deoxyaldosterone and the regulation of aldosteorne. The determination of 21-deoxyaldosterone and its possible metabolite Kelly's-M1 might be appropriate in the diagnosis of mineralocorticoid-induced forms of hypertension, especially when an adrenal adenoma is discovered.

Aim—To establish a reference range for serum cortisol concentrations in preterm infants with a gestational age of less than 30 weeks during the first two weeks of life. Methods—Infants were prospectively classified by the following exclusion criteria: surfactant administration, arterial hypotension, acute or uncontrolled infection, ventricular haemorrhage II° or above, serum glucose < 2.2 mmol/l, exchange transfusion, stress as a result of any kind of examination or nursing for at least 4 hours before blood sampling. The cortisol value was measured once using radioimmunoassay in each infant. Results—In appropriate for gestational age (AGA) infants (n = 37, median gestational age 27.7 weeks, median birthweight 1030 g) the distribution of the cortisol concentrations was non-Gaussian. These had a nearly normal distribution, when log10 values of the data were used. The points determined by mean (2 SD) on the logarithmic scale were transformed back to the original units to provide a reference range: 73‐562 nmol/l. Gestational age was significantly (p = 0.033) associated with cortisol values (log10) with a regression coeYcient (standard error) of ˛0.045 (0.020). Small for gestational age (SGA) infants (n = 8) had significantly higher cortisol values (median 357 nmol/l) than AGA infants (median 199 nmol/l) (p=0.028). Conclusions—There is a strictly defined reference range of serum cortisol concentrations in AGA preterm infants. (Arch Dis Child Fetal Neonatal Ed 1999;81:F171‐F174)

The variable response of patients with idiopathic nephrotic syndrome (NS) to glucocorticoid (GC) treatment has not been explained. Earlier studies indicated that the response is limited by cellular GC receptors. We investigated these receptors in mononuclear leukocytes of 28 pediatric patients with NS divided into three groups: steroid-sensitive in relapse, steroid-sensitive in remission, and steroid-resistant. Density and binding affinity of GC receptors were determined by a dexamethasone binding assay; no significant differences were found between the three patient groups and between these and healthy controls, although a few patient values fell outside the range of controls. Total and free plasma concentrations of cortisol were low in all three patient groups. A weak positive correlation was found between the number of GC receptors and total plasma cortisol (r=0.36, P=0.03). The results suggest that factors other than GC receptors that mediate the cellular effects of GC are involved in the variable response of NS patients to GC.

In order to assess hypothalamic-pituitary-adrenocortical axis function, we conducted low and single oral dose metyrapone tests (35 mg/kg) in dexamethasone treated very low birth weight infants with bronchopulmonary dysplasia (n = 12). The responses to metyrapone of tetrahydro-11-deoxycortisol (THS) and cortisol metabolites were analyzed by gas chromatography and mass spectrometry in 24-h urinary specimens. For comparative reasons, morning plasma 11-deoxy-cortisol and cortisol were measured by radioimmunoassay before and after metyrapone. No side effects of metyrapone were observed in our patients. In 5 of 12 patients, no urinary THS could be stimulated after metyrapone and most of the other patients had small increases in urinary THS. These findings suggest suppressed or strongly impaired hypothalamic-pituitary-adrenocortical axis function in most patients. While the concentrations of plasma 11-deoxycortisol showed little variation, those of plasma cortisol were grossly different from the respective urinary values. We recommend steroid analysis in 24-h urinary specimens by gas chromatography and mass spectrometry, because urinary steroids provide more information and the highly specific analytical technique is independent of phenomena such as cross reactivity or matrix effects. The low and single oral dose metyrapone test in combination with urinary steroid analysis by gas chromatography and mass spectrometry therefore provides a noninvasive, convenient and safe means of evaluating the integrity of the hypothalamic-pituitary-adrenocortical axis in very low birth weight infants.

In the present study the aldosterone-18-glucuronide and tetrahydroaldosterone values in 24 hour urine collections of healthy nonpregnant women, women with normal pregnancies and women with pregnancy induced hypertension (PIH) were compared. In pregnancy an elevated excretion of both aldosterone metabolites was found. The Q-ratio (aldosterone-18-glucuronide / tetrahydro-aldosterone + aldosterone-18-glucuronide) was also increased compared to healthy nonpregnant women. The elevated Q-ratios point out to increased formation of aldosterone-18-glucuronide. This predominantly renal metabolite may reflect greater availability of aldosterone molecules for interaction with mineralocorticoid receptor in the kidney.

We studied glucocorticoid receptor autoregulation and corticotropin response to dexamethasone in depressed patients and controls, attempting to control for the confounding effect of endogenous glucocorticoids. After depletion of endogenous cortisol, depressed patients showed an attenuated suppressibility of corticotropin by dexamethasone in the face of unchanged dexamethasone plasma levels. Beta-endorphin levels were strongly correlated with adrenocorticotropic hormone (ACTH) concentrations. Although metyrapone administration resulted in a marked rise of glucocorticoid receptor sites per cell in controls, this effect was not present in depressives. These data support the hypothesis of a decreased glucocorticoid receptor plasticity and a partial steroid resistance in depression.

Serum Cortisol Levels of Well, Ill and Preterm Infants treated with Catecholamines < 30 Weeks of Gestational Age † 1528

Specific 21-deoxycortisol (21-DF) antiserum was raised in New Zealand white rabbits using a 21-DF-3,20-oxime-bovine serum albumin complex. Plasma radioimmunoassay of 21-DF was developed and used together with a radioimmunoassay of 17-hydroxyprogesterone (17-OH-P) for diagnosis of patients with 21-hydroxylase deficiency of congenital and postpubertal forms. The assays were performed in plasma extracts after isolation by paper chromatography. The response of plasma 21-DF and 17-OH-P to i.v. ACTH (25 IU) was studied in 15 adult controls and compared to 8 women with the late onset form of 21-hydroxylase deficiency and 23 women with idiopathic hirsutism. Normal 21-DF values for women were 6.9 +/- 3.6 ng/dl and for men 9.71 +/- 2.73 ng/dl. Newborn children (age: 3-10 days) had a value of 8.3 +/- 4.8 ng/dl. These values are definitely lower than the lowest value ever published. This is possibly due to the specificity of the antibody. During the menstrual cycle the 21-DF values did not change. The baseline and post-stimulated concentrations of hormone were similar in controls and women with hirsutism but were significantly higher in women with the late onset form of 21-hydroxylase deficiency. In the congenital form of 21-hydroxylase deficiency the 21-DF values (baseline) were high. In general, the 21-DF and 17-OH-P values have shown parallel changes. However, one case of 21-hydroxylase deficiency with elevated 21-DF but normal 17-OH-P was observed. The use of 21-DF for the diagnosis of 21-hydroxylase deficiency is suggested.

Urinary “free” (unconjugated) 18-hydroxy-corticosterone (18-OH-B), together with aldosterone-18-glu-curonide, “free” aldosterone and tetrahydroaldosterone were determined in 20 patients with primary aldosteronism. In 19 out of 20 cases (both in adenoma and hyperplasia) the 18-OH-B excretion was at least temporarily increased. On the basis the measurement of the 18-OH-B excretion was applied-in addition to determinations of aldosterone and aldosterone-metabolites-to search for cases of primary aldosteronism. Increased 18-OH-B excretion was found in 20 of 165 pre-selected patients with essential hypertension. In 11 of them, at least one of the urinary aldosterone values was concomitantly elevated. In 9 patients the aldosterone values were found to be within normal ranges. Follow-up studies have shown elevated aldosterone values in some members of the latter group, and in 3 patients first believed to have essential hypertension adrenal adenomas were established. In 2 patients the adenoma was removed.

Two female patients, 54 and 34 years old, each presented with an adrenal adenoma and hypertension. Blood pressure fell after removal of the tumors. The first patient had high urinary 18-hydroxycorticosterone and periodically elevated 18-hydroxy-deoxycorticosterone excretions. The second patient had elevated 18-hydroxycorticosterone and free cortisol excretions. Urinary aldosterone, aldosterone metabolites and plasma aldosterone were not increased. Plasma renin activity was suppressed and serum potassium levels were normal. After surgery, no elevated steroid values were found. Elevated 18-hydroxycorticosterone excretion may be an indicator of yet unknown hypertensinogenic mechanisms. The role of 18-hydroxycorticosterone in the etiology of hypertension is still unknown.

The value of the urine tests: free aldosterone, aldosterone-18-glucuronide, tetrahydroaldosterone 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone in distinguishing primary aldosteronism from essential hypertension was studied in patients with typical and atypical primary aldosteronism and in patients with essential hypertension. The discriminating function of the tetrahydroaldosterone determination was the best, followed by 18-hydroxycorticosterone, free aldosterone and aldosterone-18-glucuronide. The measurement of 18-hydroxydeoxycorticosterone was without distinguishing value. Three cases with hypertension, adrenal adenoma, elevated 18-hydroxycorticosterone but normal aldosterone values were observed. In longitudinal studies the excretions of aldosterone, aldosterone metabolites and possible precursors periodically varied independently of each other. Determinations of urine aldosterone, aldosterone metabolites, 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone were not applicable for differential diagnosis of the adenoma and hyperplasia forms of primary aldosteronism.

In rats with unilateral renal artery stenosis and an intact contralateral kidney, a malignant course of hypertension (MH) may develop, which is characterized by 1) high BP levels, 2) sodium and water loss and a polyuric-polydipsic syndrome, 3) marked activation of the renin-angiotensin system, 4) malignant nephrosclerosis in the contralateral kidney and high plasma urea concentrations, and 5) deterioration of the animals' general condition. (Some rats exhibit signs of a cerebral vascular crisis; some rats die). When such rats are offered in addition to water 0.9% NaCl, they compulsively drink the saline, BP falls for some days to levels found in the other hypertensive animals, and signs of MH nearly or completely disappear. It is concluded that high saline intake has, for a limited period, a beneficial effect on the malignant course of renal hypertension in rats. The observations made are consistent with the hypothesis that salt and water loss, which ensue subsequent to an increase of BP into a critical high range might trigger the onset of malignant hypertension.

Sowohl im Endotoxinschock als auch unter orthostatischer Belastung kam es beim wachen Kaninchen zu einem deutlichen Anstieg der Plasma-Renin-Aktivitat. Unter hohen Glucocorticoid-Dosen, die 5 min nach Endotoxin verabreicht wurden, normalisierte sich die Plasma-Renin-Aktivitat innerhalb von 4 Std. Unter orthostatischer Belastung war mit der gleichen Glucocorticoid-Dosis keine statistisch gesicherte Wirkung auf den Anstieg der Plasma-Renin-Aktivitat erreichbar.

Thin layers of SiO2 (60-300 Å) were fabricated by rapid thermal oxidation (RTO). Growth rate on (100) and (111) Si was determined. Two different high-temperature anneal cycles were used to reduce the interface state density. Work function difference between metal and semiconductor depends upon technology and can be attributed to the changes in Si-SiO2 barrier height.

Although there is no doubt about the beneficial action of corticosteroids — especially of dexamethasone — in tumor-induced brain edema, more recent publications such as Pitts et al. (1980) and Gaab et al. (1981) show controversial opinions concerning its action in trauma cases. Even less favourable results were found by Gudeman et al. (1979), when treating trauma cases with methylprednisolone. The serious side effects of dexamethasone are also known to everybody, and this has led to a search for a drug, which would not only reduce brain edema in tumor as well as in trauma cases, but would not have the serious side effects of dexamethasone. The pharmacological properties of triamcinolone acetonide together with the experimental research by Gerl et al. (1981, unpublished communication) led us to consider that this corticosteroid might fulfil the necessary requirements.

Rats with hereditary hypothalamic diabetes insipidus (DI) do not produce vasopressin (Miller and Moses, 1971; Valtin, 1967; Valtin, Sawyer and Sokol, 1965). Daily water intake of these animals varies between 0.5 and 1.5l./kg body weight (Friedman and Friedman, 1965; Miller and Moses, 1971; Valtin, 1967), and is thought to reflect variations in the severity of diabetes insipidus. Since in normal rats water intake is closely related to food intake, we tested the hypothesis that in DI rats variations in water intake are also related to variations in food intake.

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body-weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-n antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

This paper cannot deal with the analysis by radioimmunoassay of all known mineralocorticoids; a limit was necessary and we decided to study the radioimmunoassay of aldosterone, aldosterone metabolites, and the possible aldosterone precursors 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone. Table 1 compiles the radioimmunologic methods of aldosterone diagnosis. The techniques are divided into two groups — radioimmunoassay with and without a previous separation step. Results obtained from methods without isolation steps can mostly be well correlated with those obtained from methods involving chromatography. However, many laboratories, such as our own, do not accept the values produced using techniques without chromatography as definitive. Methods with separation steps are widely practiced even though the antibodies necessary for techniques without chromatography are available. One may argue that atypical cases and steroid patterns may cause unexpected interference and it is impossible to know which cases are atypical. On the other hand, the great number of clinical samples, the practicability, and the low expense support the use of simple techniques. In the discussion of pro and contra methods without chromatography, the specificity of the antibodies plays a key role. The specificity requirements of the various aldosterone assays are more sophisticated than is generally appreciated. Table 2 shows that, depending on the particular biologic fluid and the technique applied, different groups of steroids and steroid metabolities may interface with the aldosterone radioimmunoassay.

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin—angiotensin system plays in the pathogenesis of malignant renal hypertension.

Betamethasone induced cortisol suppressibility was examined in 62 drug free consecutively admitted psychiatric inpatients. Betamethasone was choosen instead of the commonly used dexamethasone, because its double half-life compared to dexamethasone and its higher tissue availability. After a base-line evaluation with blood samples drawn at 8 a.m., 4 p.m., and 11 p.m., 0.5 mg or 1.0 mg betamethasone was given orally at 11 p.m. Postbetamethasone cortisol as well as betamethasone blood levels were then measured at the same time points as on the baseline day. In the groups receiving 1.0 mg betamethasone non-depressed patients had significantly (p less than 0.05) lower postbetamethasone cortisol levels than depressed patients for each time point measured whereas 0.5 mg betamethasone did not differentiate depressed from non-depressed patients. Patients with other depressions like schizoaffective psychosis-depressive subtype- or organic brain syndrome with depressive symptomatology demonstrated similar postbetamethasone cortisol profiles as the group of patients with major depression. Betamethasone plasma concentrations differed significantly (p less than 0.001) with respect to the oral dosage with higher values for the 1.0 mg betamethasone groups.

PITFALLS OF PRENATAL TREATMENT OF CONGENITAL ADRENAL HYPERPLASIA (CAH) DUE TO 21-HYDROXYLASE DEFICIENCY