Genetic Subtypes of Unipolar Primary Depressive Illness Distinguished by Hypothalamic-Pituitary-Adrenal Axis Activity

Schlesser, MichaelA; Winokur, George; Sherman, B

doi:10.1016/s0140-6736(79)91203-0

Cited by 143 publications

(18 citation statements)

References 15 publications

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“…Hyperactivity of the HPA axis is more likely in major depressive disorder with psychotic features than in any other subtype of major depressive disorder (22). While familial pure depressive disorder has also been associated with HPA axis hyperactivity (19), a number of studies have failed to confirm this (42)(43)(44). The pathophysiology that underlies the volumetric abnormalities in the anterior subgenual prefrontal cortex of patients with familial pure depressive disorder may therefore differ from the process that leads to the lower volumes in the posterior subgenual prefrontal cortex described in the current, psychotic subjects.…”

Section: Figure 2 Volume Of the Left Posterior Subgenual Prefrontal mentioning

confidence: 99%

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Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

Coryell¹,

Nopoulos²,

Drevets³

et al. 2005

AJP

147

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Section: Figure 2 Volume Of the Left Posterior Subgenual Prefrontal mentioning

confidence: 99%

“…Earlier studies have shown that many patients in episodes of familial pure depression have evidence of hypothalamic-pituitary-adrenal (HPA) axis hyperactivity as manifested in abnormal results on the dexamethasone suppression test (19)(20)(21). High proportions of patients with psychotic depression likewise show evidence of HPA axis hyperactivity (22).…”

mentioning

confidence: 99%

Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

Coryell¹,

Nopoulos²,

Drevets³

et al. 2005

AJP

147

View full text Add to dashboard Cite

show abstract

“…It is well established that there are subgroups of patients with depression who fail to suppress serum cortisol after dexamethasone [1][2][3][4][5], have increased plasma cortisol [6][7][8][9], in creased cortisol production rate [10], in creased number of cortisol secretory episodes [8], and increased excretion of cortisol me tabolites [11].…”

Section: Introductionmentioning

confidence: 99%

A Comparison of Adrenal Cortical Function in Patients with Depressive Illness and Cushing’s Disease

Schlechte¹,

Sherman²,

Pfohl

1986

Horm Res

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We measured total and free plasma cortisol, 24-hour urinary cortisol excretion, and corticosteroid-binding globulin in 21 normal subjects, 25 patients with depressive illness, and 6 patients with Cushing’s disease. Patients with depression had mean 24-hour plasma (8.3 ± 2.7 µg/dl) and urinary (36 ± 33.55 µg/g creatinine) cortisol levels that did not differ from those of normal subjects (6.6 ± 1.7 µg/dl; 24.6 ± 15.4 µg/g creatinine), but were significantly lower than those of patients with Cushing’s disease (14.4 ± 2.4 µg/dl; 215 ± 101 µg/g creatinine). Not all patients with depression had hypercortisolemia, and the 1 -mg dexamethasone suppression test identified some of those with adrenal hyperfunction. 17 of 25 patients had normal 8 a.m. and/or 4 p.m. plasma cortisol after dexamethasone (suppressors), while 8 patients had values greater than 5 µg/dl (nonsuppressor). Suppressors had normal total 24-hour plasma and urinary cortisol, while nonsuppressors had levels that were in the range seen in Cushing’s disease. Patients with depression showed the expected circadian variation in total and free cortisol, but nonsuppressors had elevated levels in evening and early a.m. hours when levels in normal subjects were low. Patients with Cushing’s disease had elevated levels throughout the day. The mean binding capacity of corticosteroid-binding globulin was not different in normal and depressed subjects (23.9 ± 3.2 vs. 22.2 ± 3.4 µg/dl), but was significantly decreased in patients with Cushing’s disease (15.7 ± 3.5 µg/dl). Although total cortisol levels were similar, nonsuppressors had significantly lower mean 24-hour plasma free cortisol (1.01 ± 0.27 µg/dl) than patients with Cushing’s disease (2.4 ± 0.54 µg/dl). The modest elevation of free cortisol and its normal circadian pattern compared with patients with Cushing’s disease may account for the absence of physical findings of glucocorticoid excess in patients with depression who have adrenal hyperfunction.

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“…Es treten häufigere Cortisolsekretionsepisoden auf, die vor allem in den Nachmittags-und Nachtstunden zu einer höheren Cortisolkonzentration im Serum fuhren. Der Dexamethason-Hemmtest zeigt im Vergleich zu Gesunden und neurotisch Depressiven während der depressiven Phase eine geringere Hemmung der Cprticotropin-und Cortisolsekretion (9,10,11,12). Ai/ch im Insulin-Hypoglykämie-Test werden Funktionsstörungen in diesem System gefunden.…”

Section: Einführungunclassified

Klinisch-chemische Diagnostik depressiver Syndrome mit Hilfe eines neuroendokrinen Funktionstestes

Kleesiek¹,

Czernik²,

Eberhard³

1980

CCLM

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Zusammenfassung: Bei 52 depressiv Erkrankten und 12 früher depressiv Erkrankten im psychosefreien Intervall wurde die Stimulierbarkeit der hypophysären Honnonsekretion mit Thyroliberin und unter Insulin-induzierter Hypoglykämie untersucht. Der Verlauf der Somatotropin-, Cortisol-, Prolactin-, Thyrotropin-und Glucosekonzentration im Serum wurde über 2 Stunden verfolgt. Es zeigen sich Unterschiede der neuroendokrinen Reaktion zwischen endogen und reaktiv (neurotisch) depressiv Erkrankten sowie Veränderungen während des Erkrankungsverlaufs: 1. Die Stimulierbarkeit der Somatotropin-und Cortisolsekretion und der Glucoseabfall ist bei endogen Depressiven gegenüber reaktiv Depressiven und gesunden Kontrollen vermindert.2. Stimulationsmaxima der Somatotropinsekretion unter 40 mU/1 bei depressiv Erkrankten während der depressiven Phase ermöglichen mit einer Vertrauenswahrscheinlichkeit von 0,9 eine Abgrenzung der endogenen Depression von der reaktiven Form. 3. Nach abgelaufener endogener Depression ist zwar eine Zunahme der Stimulierbarkeit der Somatotropin-und Cortisolsekretion nachweisbar, allerdings liegen auch zu diesem Zeitpunkt die Somatotropin-Maxima unterhalb von denen reaktiv Depressiver. 4. Bei Lithium^behandelten, psychosefreien Probanden ist die Stimulierbarkeit der Somatotropinsekretion nicht von der gesunder Kontrollen zu unterscheiden. Die Thyrotropinsekretion ist gesteigert. Im Vergleich mit gesunden Kontrollen ist auch bei diesen Probanden noch in einem hohen Prozentsatz (66%) eine abgeschwächte Insulininduzierte Hypoglykämie nachweisbar.5. Angst und Agitiertheit haben während der depressiven Phase einen hemmenden Einfluß auf die Stimulierbarkeit der Prolactinsekretion. Der hypophysäre Stirnulationstest bietet die Möglichkeit, gestörte neuroendokrine Funktionen bei depressiv Erkrankten zu erfassen und die Differentialdiagnose depressiver Syndrome zu objektivieren. Clinical chemical diagnosis of affective diseases by means of a neuroendocrine function testSummary: The stimulation of pituitary hormone secretion with thyroliberin and by insulin-induced hypoglycemia was investigated on 52 depressive patients and 12 postdepressive, lithiumtreated subjects. The serum concentrations of Somatotropin, cortisol, prolactin, thyrotropin and glucose were followed for 2 hours. Differences in the neuroen-0340-076X/80/0018-0867$2.00

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Genetic Subtypes of Unipolar Primary Depressive Illness Distinguished by Hypothalamic-Pituitary-Adrenal Axis Activity

Cited by 143 publications

References 15 publications

Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

A Comparison of Adrenal Cortical Function in Patients with Depressive Illness and Cushing’s Disease

Klinisch-chemische Diagnostik depressiver Syndrome mit Hilfe eines neuroendokrinen Funktionstestes

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Genetic Subtypes of Unipolar Primary Depressive Illness Distinguished by Hypothalamic-Pituitary-Adrenal Axis Activity

Cited by 143 publications

References 15 publications

Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

Subgenual Prefrontal Cortex Volumes in Major Depressive Disorder and Schizophrenia: Diagnostic Specificity and Prognostic Implications

A Comparison of Adrenal Cortical Function in Patients with Depressive Illness and Cushing&rsquo;s Disease

Klinisch-chemische Diagnostik depressiver Syndrome mit Hilfe eines neuroendokrinen Funktionstestes

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A Comparison of Adrenal Cortical Function in Patients with Depressive Illness and Cushing’s Disease