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Although the diagnosis of multiple personality disorder (MPD) has been receiving renewed interest in the literature, it presents a number of clinical problems and challenges. A case study is reported in which this diagnosis was uncovered by chance during an amobarbital interview on a psychotically depressed young male patient. The patient had previously been only minimally responsive to pharmacotherapy for a major depressive episode with mood-congruent psychotic features. When the multiple personality disorder was diagnosed, treatment emphasis shifted toward psychotherapeutic modalities with marked clinical improvement. Several unique aspects of the case, including diagnostic methodology, results of serial dexamethasone suppression tests, and psychosomatic symptomatology, are discussed as well as the implications of this case within a larger clinical context.

We investigated increased production of testosterone and androstenedione in 44 women with unexplained adult-onset hirsutism, 41 of whom had normal-sized ovaries. Twenty women in this group had at least 50 per cent suppression of plasma testosterone and androstenedione after four to five days of dexamethasone. Testosterone and androstenedione values in ovarian-vein effluents were higher than those of their adrenal veins. We calculated adrenal secretion rates of both androgens in each patient by relating the adrenal gradients to those of cortisol. In 42 of the hirsute women, including those whose androgens were suppressed after dexamethasone, the ovaries were the predominant source of androgen production. The women with dexamethasone suppression had milder degrees of virilism and lower production rates of testosterone and androstenedione. We conclude that the ovaries are the source of excessive androgens in most women with unexplained hirsutism, and that corticoid-suppressible patients have milder forms of ovarian hyperandrogenism.

Four different methods of quantifying the 1-mg Dexamethasone Suppression Test (DST) were contrasted with serial testing in endogenous depressives receiving electroconvulsive therapy (ECT). Of three continuous measures in 38 patients with pretreatment DSTs, only the log-transformed value for plasma cortisol was normally distributed, indicating that it possessed superior psychometric properties. Pretreatment Hamilton Depression Rating Scores (HAM-D) correlated positively with pretreatment DST status, with a similar association noted between posttreatment DST status and HAM-D scores. There was no uniform effect of ECT on the DST. Although pretreatment nonsuppressors showed a trend toward decreased postdexamethasone cortisol values, initial suppressors (cutoff: 5μg/dl) evidenced a significant increase in these values, and 35.3% of initial suppressors were nonsuppressors at final DST assessment. These trends were noted in the DST assessment done following the third ECT treatment, suggesting an effect of regression to the mean. The findings highlight the importance of following initial DST suppressors in studies of this type.

The Kleine-Levin Syndrome (KLS) a rare disorder comprising of periodic bouts of hypersomnia and megaphagia is reviewed. The syndrome chiefly affects males. The four accepted female cases in the literature are reviewed and a new female case described. This patient had an IQ in the normal range, unlike the other three female cases where the IQ was measured. She showed an abnormal Cortisol rhythm during both a well and an unwell phase replicating the findings of other workers in some KLS patients. This patient showed normal dexamethasone suppression, a test not previously reported on in KLS. The patient also smoked excessively during the bouts, an occurrence not previously remarked on in this disorder.

In seven cases of proven Cushing's syndrome, the intravenous infusion of dexamethasone at a rate of 1 mg/h for a period of 5 hours readily distinguished pituitary dependent Cushing's syndrome from other causes of Cushing's syndrome. Thus the 5 h – iv dexamethasone test may give the same differential diagnostic information as the classical oral dexamethasone suppression test of Liddle. The test is quick to perform, obviates the need for accurate urine collections and is not influenced by variations in the intestinal absorption of the glucocorticoid.

1. The effect of dexamethasone on the plasma corticosterone response to heat-immobilization stress was investigated in male and female rats. 2. The plasma corticosterone response of control rats to the type of stress described was 64 μg% (± 10·5 μg% standard deviation) in males, and 128 μg% in females. 3. A straight line relation between the dose of dexamethasone and the log of the plasma corticosterone response was demonstrated in male rats. The slope of the dose—log response line was used to indicate the degree of suppression of the plasma corticosterone response to stress. 4. The straight line relation did not hold for female rats, suggesting the presence of an additional factor or factors which influenced the plasma corticosterone levels. 5. An exponential relation between the duration of dexamethasone administration and the slope of the dose—log response line was demonstrated, maximum suppression occurring after an infinite period of time. After 30 days, 95% maximum suppression occurred when the plasma corticosterone response was measured 8 hr after dexamethasone administration had ceased.

Assays of urinary total 17-hydroxycorticosteroids (17-OHCS) have been conducted in seven intact and seven ovariectomized Beagle bitches. Adrenocorticotrophin (ACTH) stimulation and dexamethasone suppression tests were also undertaken. Urine samples were collected for six days from each animal and the mean total 17-OHCS excretion was 2.3 ± 0.7 (sd) and 1.8 ± 0.3 mg/24 hours in the intact and ovariectomized bitches respectively. The difference in 17-OHCS excretion between the two groups of animals is not significant. The administration of 40 IU ACTH caused a marked increase in 17-OHCS excretion in all animals. Dexamethasone was given at a dose level of 1.0 mg q. i. d. for two days. This resulted in a decrease in 17-OHCS output. However, the mean value was below the 95 % confidence limits of the control only in the ovariectomized group.

A radioimmunoassay for serum dehydroepiandrosterone has been developed by using the anti-DHEA antiserum. After DHEA-7α-3H was added to 0.2 to 1.0ml of serum and 1ml of water for recovery, DHEA was extracted with methylene chloride, and the extract was evaporated to dryness. The residue was applied to paper chromatography. The eluates and DHEA-7α-3H which was added to determine the % free of DHEA were evaporated to dryness, and the residues were incubated with the antiserum containing pepsin treated human immune serum globulin and bovine serum albumin at 4°C overnight. Ammonium sulfate was used to separate free from bound DHEA. The accuracy, precision and specificity were satisfactory. The sensitivity was 300pg per sample. The blank value could not be differentiated from zero. Although the antiserum reacted with the other 3β-OH-Δ5-steroids as well as with DHEA, complete separation of DHEA from the other 3β-OH-Δ5-steroids was achieved chromatographically. Serum DHEA levels in normal subjects and their responses to ACTH stimulation and dexamethasone suppression were evaluated by using the radioimmunoassay.

Dexamethasone was given to female rats by intraperitoneal injection (400 μg/100 g) or in the overnight drinking water (20 μg/ml). ACTH release was studied by measuring the plasma corticosterone response 20 min after the application of various stimuli. Four hr after the injection of dexamethasone the response to a tourniquet about the calf was inhibited; the response to urethane, gut stretch, hemorrhage or 50 mU/100 g vasopressin was partially inhibited but there was no inhibition of the response to 500 mU/100 g vasopressin. Overnight dexamethasone markedly reduced the response to all stimuli except 500 mil vasopressin. The relationship between the time of injection of dexamethasone and the application of the stimulus was tested by stimulating ACTH release with ip urethane. Ten hr after injection of dexamethasone there was complete suppression of ACTH release in response to urethane, but this suppression largely disappeared at 24 hr. It is concluded that the inhibition of ACTH release by large doses of dex...

Adrenocortical responsiveness to ether vapor stress was measured in young adult (4–6 months) and aged (22–32 months) rats subjected to acute and chronic treatments with dexamethasone. Daily administra

SummaryActinomycin D inhibited the capacity of dexamethasone to suppress pituitary ACTH secretion in vivo in normal and adrenalectomized rats. While a definitive explanation for such results awaits further elucidation, the results are consistent with the hypothesis that dexamethasone inhibits ACTH secretion by a mechanism that involves RNA synthesis.

Detection of heterozygote carriers for congenital adrenal hyperplasia by use of a modified tetracosactide (a synthetic corticotropin) stimulation test with prior overnight dexamethasone suppression proved to have a diagnostic accuracy of 95%. Discrimination of heterozygotes from normals was best when we used a criterion based on the ratios of 17 alpha-hydroxyprogesterone to cortisol at baseline and at 30 min after intravenous administration of 250 micrograms of tetracosactide.

A comparison was made of the ACTH stimulation test with and without prior dexamethasone suppression in 10 patients, each of whom served as her own control. It was found that it is not necessary to administer DEX before the test, the specificity and sensitivity of both tests being the same in the diagnosis of CAH, although the calculated values are lower when DEX is given. Further investigation with HLA typing and ACTH stimulation testing is necessary to establish whether either or both types of ACTH stimulation tests are capable of discriminating between the heterozygotic and homozygotic varieties of CAH.

Dexamethasone suppression tests were given to 69 consecutively admitted psychiatric patients. Nonsuppression rates for depression with or without melancholia and for schizophrenia were similar to those previously reported, but for mania and other psychoses the frequencies were higher than expected.

Dexamethasone suppression tests were given to 10 patients with panic disorder and 22 depressed patients. All patients with panic disorder were normal suppressors, and nine depressed patients were nonsuppressors. The mean cortisol levels of the two groups differed significantly.

The dexamethasone suppression test may be a valuable tool in the assessment, treatment evaluation and maintenance management of depressive illness in old age. A case is presented illustrating these uses of the DST.

A 50-year-old Klinefelter patient acutely developed a psychotic depression which rapidly responded to treatment with amitriptyline. This patient exhibited an early escape from dexamethasone suppression and became hypomanic the morning after total night sleep deprivation. The findings suggest that the use of biological tests to study affective syndromes occurring in Klinefelter patients might yield clues regarding the existence of pathophysiological common denominators of primary and Klinefelter-associated affective disorders.

Dexamethasone (2 mg q6h for 48 h) decreased serum T3 in normal and athyreotic subjects, and decreased T4 in normal subjects. Dexamethasone probably alters secretion and peripheral metabolism of thyroid hormones.

Use of the midnight dexamethasone suppression test showed that the plasma 11-hydroxycorticosteroid (11-O.H.C.S.) level did not undergo its normal reduction in 14 out of 27 patients with severe depression. Resistance to dexamethasone suppression correlated with the clinical rating of the severity of depression, while recovery from depression was associated with return of normal responsiveness to dexamethasone. The explanation of these findings is unknown.

IN most patients with Cushing's disease∥ urinary 17-hydroxycorticosteroids (17OHCS) are readily suppressed by 8 mg. of dexamethasone per day. However, Liddle,1 in 1960, predicted that the excessive amounts of cortisol in some cases of this disease would not be suppressible with this amount of dexamethasone, and in 1962, Scott and his associates2 reported such a case. There have been reports of other patients with bilateral adrenocortical lesions with high levels of cortisol resistant to dexamethasone suppression.3 4 5 6 7 8 9 10 Failure to appreciate the variable significance of this phenomenon and the previous unavailability of plasma ACTH assays have resulted in the divergent interpretations of . . .

In the course of several studies of hypothalamic-pituitary-adrenal axis activity in depression, 43 patients presented on separate admissions with definite depression and, on both admissions, received dexamethasone suppression tests (DSTs). DST results were discordant across admissions in 21% of cases; among patients who were nonsuppressors on either admission, results were discordant in 40.9%. The correlation between postdexamethasone values obtained on two admissions was highly significant, however. Distinctions between bipolar and unipolar depression and between primary and secondary depression by rates of nonsuppression were inconsistently significant across admissions but were clearer when results from both admissions were pooled and patients with an abnormal DST on either admission were considered nonsuppressors. While abnormal escape from dexamethasone suppression occurs in a significant proportion of depressed patients, this phenomenon may only partially overlap the depressive syndrome in time. Negative DST results in patients with primary depression must be interpreted in this light.

Recent work suggests that the simultaneous occurrence of major depressive disorder (MDD) and panic disorder (PD) may be of relevance for clinical findings, therapeutic outcome, and prognosis. It is of interest to know whether or not this relevance extends to biological findings. We addressed this question through comparison of serial Dexamethasone Suppression Test (DST) results in patients who had either MDD alone or simultaneous MDD and PD. We were unable to describe differences between the groups.

Cyclic Cushing's syndrome is a rare but increasingly recognized disorder of periodic fluctuations of adrenal steroid production. A case of cyclic Cushing's syndrome due to a pituitary adenoma is described. The patient demonstrated a prolonged cycle length of approximately six months, during which a spontaneous remission occurred both clinically and biochemically. Previously documented cases of cyclic Cushing's syndrome are reviewed, and the pitfalls in interpretation of results of dexamethasone suppression testing in the presence of spontaneous fluctuations in cortisol production are discussed.

Summary A 54-year-old patient was found to have an aldosterone-producing microadenoma measuring 2.5 mm in diameter. Although adrenal venography by selective catheterization had failed to demonstrate the tumour, adrenal scintiscan using 131I-19-iodocholesterol accurately localized the functional tumour in the right adrenal gland; a dexamethasone-modified adrenal scintiscan revealed complete suppression of radioactivity in the right adrenal gland. These findings suggest that adrenal scintiscan, together with adrenal vein blood analysis, is capable of detecting a small adenoma before surgery, and that dexamethasone suppression of an adrenal scintiscan does not exclude an adenoma.

The influence of steroids of adrenal cortical origin on estrous behavior in the ovariectomized mare was evaluated by adrenal suppression via dexamethasone (DEX) administration in two experiments. In Experiment I, 12 mares (six DEX, six control) were tested for sexual behavior in harem groups (two DEX and two control mares plus one stallion per group) for 9 consecutive days. In Experiment II, estradiol (E 2 ) was given to a group of DEX-treated mares as an additional control. Twelve mares (four DEX, four DEX + E 2 , and four control) were tested in harem groups (one DEX, one DEX + E 2 , and one control mare plus one stallion per group) for 10 days. All DEX mares showed a clear suppression of sexual response compared to control or DEX + E 2 mares, indicating that the estrous behavior seen in ovariectomized mares may be due to steroids from the adrenal cortex. The control and DEX + E 2 mares were similar in all measures of proceptivity. Despite being more receptive, as indicated by fewer negative responses, the DEX + E 2 mares received fewer intromissions and ejaculations than did the control animals. The ability of estradiol to induce estrous behavior in the dexamethasone-suppressed mare notwithstanding, other adrenal steroids, e.g., androgens, may be involved in estrous behavior in the untreated, ovariectomized mare.

There is considerable evidence that disturbances in the mechanisms controlling circadian rhythms play an important part in the aetiology of depression (Hallonquist et al., 1986). For instance, Carrol et al. (1976) reported that 88% of bipolar and 50% of unipolar depressives demonstrated early escape from overnight dexamethasone suppression. Wehr et al. (1983) suggested that this phenomenon could be explained by a resetting of the ‘biological clock’. Thus if, as they observed, circadian rhythms of depressives are phase-advanced compared with control subjects, one might expect an early escape since the drug will have been given later in the circadian cycle of the depressives.

A radioimmunoassay (RIA) is described for the measurement of 11 beta,17 beta-dihydroxy-4-androsten-3-one (11 beta-hydroxytestosterone) in human plasma. The reliability criteria of the new RIA were similar to those of other steroid hormone radioimmunoassays. The mean plasma 11 beta,17 beta-dihydroxy-4-androsten-3-one level for healthy young subjects was 1.31 +/- 0.32 nmol/l (means +/- SD) in males and 1.19 +/- 0.35 nmol/l in females at 8 a.m.; during the night, there was a marked decrease, and at 11 p.m. the recorded values were 0.41 +/- 0.15 nmol/l and 0.46 +/- 0.14 nmol/l, respectively. During the corticotropin stimulation test, 11 beta,17 beta-dihydroxy-4-androsten-3-one increased from 1.03 +/- 0.33 nmol/l to 1.31 +/- 0.41 nmol/l, while in dexamethasone suppression tests a decrease from 2.04 +/- 0.82 nmol/l to 0.25 +/- 0.05 nmol/l was seen. In contrast, chorionic gonadotropin administration on 3 consecutive days did not influence plasma concentrations of 11 beta,17 beta-dihydroxy-4-androsten-3-one.

Twenty-two patients with recurrent affective disorders received 1-mg dexamethasone suppression tests (DSTs) during multiple hospitalizations. Interepisode consistency of DST results was found in 82% of the subjects, which supports the use of this test as a predictor of relapse.

Dexamethasone suppression tests (DSTs) were given to nine bipolar patients in both depressed and manic phases of their illness. In seven patients DST results were consistent between episodes; six patients had positive tests in both depression and mania.

Summary The plasma Cortisol response to a 3-hour combined dexamethasone (0.1 mg/kg, IM) suppression/ACTH (230 μg, IV) stimulation test was evaluated in 23 dogs with spontaneous hyperadrenocorticism (HAC) and compared to the reference values determined in 37 healthy dogs. A high performance liquid chromatography (HPLC) technique was utilized to measure the plasma Cortisol concentrations. Abnormal response to at least one component of the combined test was found in all dogs with spontaneous HAC, differentiating them from the control dogs. Three types of abnormal Cortisol response were identified in the dogs with HAC: (1) normal suppression after dexamethasone with exaggerated response to ACTH in 16 dogs, (2) inadequate suppression after dexamethasone with supranormal response to ACTH in 5 dogs, (3) inadequate suppression after dexamethasone with normal response to ACTH in 2 dogs. Only the first type of response was clearly indicative of pituitary-dependent hyperadrenocorticism (PDH). The two other types of response were inconclusive in differentiating between PDH and HAC due to adrenocortical tumour. Zusammenfassung Klinische Auswertung eines kombinierten Dexamethason-Suppressions-/ACTH-Stimulations-Tests bei Hunden mit Hyperadrenocorticismus bei Verwendung der HPLC zur Plasma-Cortisol-Bestimmung Bei 23 Hunden mit spontanem Hyperadrenocorticismus (HAC) wurde die Plasma-Cortisol-Antwort auf einen 3 h dauernden kombinierten Dexamethason- (0,1mg/kg, i.m.) Suppressions-/ACTH-(250 μg i. v.) Stimulations-Test ausgewertet und mit bei 37 gesunden Hunden bestimmten Referenzwerten verglichen. Die Plasma-Cortisol-Konzentrationen wurden mit einem HPLC-Verfahren bestimmt. Eine abnormale Reaktion auf wenigstens eine Komponente des Tests wurde bei allen Hunden mit spontanem HAC gefunden. Sie liesen sich damit von den Kontroll-Hunden unterscheiden. Bei den Hunden mit HAC wurden drei Typen der abnormalen Cortisol-Antwort nachgewiesen: 1. Normale Unterdruckung nach Dexamethason-Applikation mit uberschiesender Reaktion auf ACTH-Applikation bei 16 Hunden, 2. inadaquate Suppression nach Dexamethason-Applikation mit supranormaler Antwort auf ACTH-Applikation bei 5 Hunden, 3. inadaquate Suppression nach Dexamethason-Applikation mit normaler Antwort auf ACTH-Applikation bei 2 Hunden. Nur der erste Typ der Antwort sprach eindeutig fur einen hypophysaren Hyperadrenocorticismus. Die anderen beiden Antwort-Typen waren bezuglich der Differenzierung zwischen hypophysarem Hyperadrenocorticismus und durch einen Nebennierenrindentumor bedingtem Hyperadrenocorticismus nicht eindeutig.

• Fourteen (33%) of 43 men hospitalized for alcohol abuse showed abnormal cortisol levels at 4 PM, 17 hours after administration of 1 mg of dexamethasone (median, five days after admission). Most (but not all) of these nonsuppressors showed multiple signs of alcoholic physical deterioration; there may be more than one mechanism by which alcohol abuse can lead to an abnormal result of this test. Suppressors and nonsuppressors reported similar alcohol consumption, symptoms of depression, and occurrence of depression among close relatives. Only two patients (5%) showed abnormal cortisol levels at 8 am, nine hours after administration of dexamethasone. These results suggest that, as a screen for primary depressive illness among recently abstinent alcohol abusers, the 4 pm cortisol level is not specific enough, but the 8 am level might be useful in patients who have no alcoholic relatives.

A 57-year-old woman who presented with depression and hypertension for which she had received anti hypertensive therapy including diuretics was found to have Cushingoid features. All medication was stopped and subsequent investigation demonstrated markedly elevated urinary free cortisol (UFC) levels. An increase in UFC occurred in response to the low dose dexamethasone suppression test and a further increase was noted during the high dose test. Plasma cortisol levels did not change significantly. Detailed examination of the data revealed that over the 6-day testing period the plasma creatinine had fallen from 1.4 mg/dl to 0.7 mg/dl while the creatinine clearance had doubled--presumably due to withdrawal of the diuretic. When the UFC was expressed per 100 ml of plasma filtered, there was no difference between any of the daily excretions. We conclude that a concurrent increase in glomerular filtration rate is one mechanism by which a 'paradoxical' increase in UFC in response to dexamethasone suppression may occur.

Recent developments in biological psychiatry offer clinicians the opportunity to apply new techniques to the diagnosis and treatment of mental disorders. For instance, the dexamethasone suppression test has been used in the differential diagnosis of depression and high doses of propranolol have been reported to improve schizophrenic symptoms. Studies now suggest that lithium may be equally effective in treating schizoaffective and affective disorders. Receptor binding techniques provide new information on the mechanism of action of psychotropic drugs and allow the clinician to assess the likelihood of specific side effects being produced by drugs within a class. The author reviews other recent developments, including the use of computerized tomography with patients who exhibit schizophrenic behavior.

Three-hour cortisol-profiles and cortisol responses to a 1 mg dose of dexamethasone were recorded in 31 depressed patients and nine controls. The data indicate that the likelihood of detecting non-suppressible cortisol concentrations after dexamethasone is significantly increased in depressed patients with a hypersecretion of cortisol. However, a considerable subsample of normosecretors shows abnormal DST results. Conversely, hypersecretion is often associated with dexamethasone suppression. In this study a 1 mg-DST did not reflect the adrenocortical activity with ultimate accuracy. Therefore any attempts which correlate psychopathological or biological data with pituitary-adrenal activity and use a DST-result as measure are criticizable . Data derived from volunteers illustrate that medical factors such as weight-loss, steroid-containing contraceptives and sleep deprivation can make a pituitary-adrenal activity test ambiguous.

The Dexamethasone Suppression Test (DST) was performed in 64 depressed inpatients, in 48 schizophrenics, and in 20 normal controls. Thirty-four percent of depressive inpatients were found to escape from dexamethasone suppression significantly higher than either schizophrenics (13%) or normal subjects (5%). Among subgroups, bipolar and unipolar endogenous depression patients had much higher abnormal rates for the DST (59% and 48%, respectively) than nonendogenous cases (8%). DST results were also found to be positively correlated with patients' Hamilton scores. These findings suggested that DST could be helpful in diagnosis, discrimination of subtypes, and in assessment of severity of symptoms. In 32 of the 64 depressed inpatients, urinary MHPG · SO 4 excretion was determined and compared with 21 normal controls. Bipolar patients ( n = 7) had less MHPG · SO 4 excretion than unipolar endogenous patients ( n = 16). Excretion was positively correlated with cortisol level at 17 hr after dexamethasone administration in 32 depressive inpatients, especially in the unipolar subgroup. A trend toward negative correlation, though not statistically significant, was found in bipolar depression between cortisol levels at 17 hr after dexamethasone administration and urinary MHPG · SO 4 excretion. This may indicate that some differences in norepinephrine (NE) metabolism may exist between unipolar and bipolar depression, leading to differing correlations between deviation of central NE function and hypothalamus-pituitary-adrenal (HPA) axis in different subgroups of depression .

There is considerable disagreement about the relationship between borderline personality disorder and the affective disorders. The authors report the results of a study of the relationship between dexamethasone suppression and depressive subtype in hospitalized depressed borderline patients. Twenty-three patients met research criteria for unipolar major depressive episode without psychosis of at least moderate severity. Thirteen patients also met criteria for borderline personality disorder. Dexamethasone suppression test (DST) results showed no significant correlation with either melancholia or borderline personality disorder alone. However, of the 13 borderlines, eight failed to suppress and six of those eight were not melancholic. The authors conclude that abnormal response to dexamethasone in nonmelancholic borderlines casts some doubt on the specificity of the DST for melancholia.

FERTILITY rarely occurs in Cushing’s syndrome and only 25 cases of Cushing’s syndrome associated with pregnancies have been described.* In most of these cases, the hyperadrenocorticism was diagnosed after conception, and baseline and dexamethasone suppression tests were available only during pregnancy and post partum. Thus, one cannot be sure whether the pregnancy antedated the development of Cushing’s syndrome in these cases. This paper reports on a woman with Cushing’s syndrome

A single injection of 2.0 mg/kg dexamethasone (DXM) administered at 51 h after pregnant mare serum gonadatropin (PMS) treatment inhibited both ovulation and luteinization. S.c. injection of human chorionic gonadotropin (HGG) caused ovulation and luteinization in DXM-PMS-treated rats, whereas treatment with ACTH failed to overcome the DXM inhibitory effect. These findings are interpreted to indicate that DXM inhibits ovulation through a mechanism which might involve the central nervous system.

In a naturalistic clinical trial we administered three partial sleep deprivations (PSD) within one week to a diagnostically heterogeneous sample of 30 depressed patients and applied serially three dexamethasone suppression tests (DST). We observed that this PSD treatment induced sustained clinical improvement independently from nosological attribution. Abnormal DST results prior to PSD treatment failed to predict clinical course, and normalized after beneficial response.

Depressed inpatients have a DST non-suppression rate that is several times greater than that of depressed outpatients. To explore what clinical features of depression might explain this difference, 25 depressed inpatients who were DST non-suppressors were compared with 16 DST suppressors, using 70 clinical variables. Those variables that were different between these two groups of inpatients were then used to compare depressed inpatients and outpatients. Three variables that were significantly associated with DST status in depressed inpatients were also found to differentiate between depressed inpatients and depressed outpatients. DST suppression was associated with a family history of alcoholism, with the symptom hypersomnia, and with a younger age at index interview.

The performance of the dexamethasone suppression test (DST) was investigated in 45 female anorexic out-patients (cross-sectional study) and in nine female anorexic in-patients (longitudinal study). DST non-suppression was strongly associated with negative energy balance (low body weight and low Ponderal Index) but there was no significant association with the presence of affective or neurotic disturbance in these patients. These findings cast doubt on the value of the DST in the management of depressive illness.

Plasma cortisol (F) response to intravenous adrenocorticotropin (ACTH) infusion (following dexamethasone suppression) was examined in adult female Macaca fascicularis that had been living for 22 months in social groups consisting of four to six females and one male. A portion of these females were ovariectomized (n = 21), while the rest were reproductively intact (n = 23). The social behavior of all animals was monitored with a focal sampling procedure, and dominance ranks were determined on the basis of fight outcomes. Further, intact females were swabbed vaginally to determine onset of menstruation and were sampled for plasma progesterone (P) every three days during the luteal phase of their cycles. Among the results was that the plasma F response to ACTH infusion was greater in subordinate animals than in dominants (P < .02). Subordinates and dominants did not, however, differ in plasma F measured at baseline. It was found further that plasma F concentrations were greater in ovariectomized than in intact females at baseline and following ACTH injection (P < .01). Finally, there was an appreciable elevation in plasma F across all animals during the 15- and 30-minute post-ACTH injection measurements (P < .01). Subsequent analyses of data from intact females showed interrelationships among dominance rank, reproductive function (indicated by luteal phase plasma P concentrations), adrenal size, and adrenal response to ACTH infusion. These data indicated that subordinate females were at a reproductive disadvantage compared to dominants, a result that may have been mediated, in part, by the increased adrenal size and enhanced adrenal responsiveness of subordinate females.

The performance of the dexamethasone suppression test (DST) was investigated in 45 female anorexic out-patients (cross-sectional study) and in nine female anorexic in-patients (longitudinal study). DST non-suppression was strongly associated with negative energy balance (low body weight and low Ponderal Index) but there was no significant association with the presence of affective or neurotic disturbance in these patients. These findings cast doubt on the value of the DST in the management of depressive illness.

Immunoreactive ACTH before and five hours after administration of 2 mg of dexamethasone was determined in patients examined in hospital for abnormalities on chest X-ray. Thirty patients had primary bronchial cancer, 15 had other lung conditions, mostly inflammatory infiltrations. The mean total ACTH and ACTH after dexamethasone suppression were significantly higher in the patients with bronchial cancer than in patients with other lung lesions or healthy controls. ACTH in plasma after administration of glucocorticoids was predominantly big ACTH. Several of the cancer patients bad, however, ACTH levels within the same range as the other subjects. These results indicate that plasms ACTH determinations are of limited value as tumour markers for the detection of lung cancer although it is still possible that repeated sampling in patients with elevated ACTH levels may be of value when monitoring the therapy.

Obsessive-compulsive disorder and major depressive disorder are associated by several lines of evidence. To explore the possible relationship between the two disorders, the authors administered 1-mg dexamethasone suppression tests to 18 patients with obsessive-compulsive disorder and 51 patients with major depressive disorder. None of the obsessive-compulsive patients were classified as nonsuppressors on the basis of a 4:00 p.m. serum cortisol level, whereas 37% of the depressed patients were nonsuppressors. The mean cortisol levels of the two groups differed significantly. Factors that may influence hypothalamic-pituitary-adrenal function, such as age, depressive symptoms, and severity of illness, are discussed in light of these results.

The effect of oral dexamethasone on the plasma content of cortisol and dexamethasone was investigated in 175 patients suspected of having Cushing's syndrome. Plasma concentrations of cortisol and dexamethasone were measured by specific radioimmunoassays at 08.00 h following administration of either a low-low (0.5 mg), low (1.0 mg), high (4.0 mg) or high-high (8.0 or more mg) dose of dexamethasone at midnight. All seventeen patients with documented Cushing's syndrome exhibited resistance to the action of low-low and/or low dose dexamethasone on suppression of 08.00 h plasma cortisol content. Nine of twelve patients with pituitary dependent Cushing's syndrome had plasma cortisol values of less than 166 nmol/l following high-high dose testing. In 157 patients with suspected Cushing's syndrome, standard dexamethasone testing was considered unsatisfactory in at least 20%. After low-low or low dose tests 11% had supranormal cortisol values, but plasma cortisol content overlapped with values observed in patients with Cushing's syndrome only when plasma dexamethasone content was less than 5.6 nmol/l. Twelve per cent of patients suspected of having Cushing's syndrome had sufficient elevation of plasma dexamethasone values after low dose testing so that marked reduction of plasma cortisol might be expected even in patients with pituitary dependent Cushing's syndrome. Four patients receiving anticonvulsants had subnormal plasma levels of dexamethasone for the dose administered, but all exhibited normal suppression when plasma levels of dexamethasone and cortisol were correlated simultaneously. In summary, there is considerable variation in the plasma content of dexamethasone following oral doses. Simultaneous measurement of both plasma levels of dexamethasone and cortisol has proved most useful in identifying patients with unsatisfactory dexamethasone suppression tests.

SUMMARY Two cases of pituitary-dependent Cushing's disease are described. Selective transphenoidal adenomectomy was attempted in each, but proved incomplete. Although both patients had persistent Cushing's disease after the operation, both were shown to have been rendered fully dexamethasone suppressible. The pathophysiological basis of partial suppressibility is discussed, as are the criteria for the diagnosis of cure in Cushing's disease treated by selective adenomectomy.

Weekly dexamethasone suppression tests (DSTs) were performed in 35 patients with major depressive disorder until clinical response. At initial evaluation, 65.7% of the patients showed nonsuppression, and 85.7% showed nonsuppression at least once during the treatment period. Normalization of the DST results usually coincided with or occurred before clinical recovery, although isolated “peaks” of DST nonsuppression occurred in 45.7% of the patients, irrespective of the clinical course. The test was not useful as a predictor of clinical recovery or relapse. Moderately ill depressed patients had significantly higher nonsuppression rates than schizophrenic or manic patients with corresponding severity scores, indicating that different factors might be associated with nonsuppression in different diagnoses. However, many abnormal DST results could neither be related to the course of the depression nor to the severity of illness; thus other factors must also be responsible for DST nonsuppression.

The present study evaluates the relationship between cognitive impairment and the Dexamethasone Suppression Test (DST) in elderly persons suffering from depression. Twenty-nine subjects meeting DSM-III criteria for major depressive disorder (MDD) were assessed using the Global Deterioration Scale (GDS) and the DST. Plasma cortisol levels before and after receiving 0.5 mg dexamethasone were compared, and correlations were determined between GDS and postdexamethasone plasma cortisol levels. The results show that there is a positive correlation between the GDS scores and post-DEX cortisol levels (r = 0.57, p less than 0.005). It is suggested that increased activity of the HPA axis, seen in depression, could contribute to the cognitive impairments observed in this disorder.