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Biomedical subjects

R F Haskett

Publications and source records attributed to R F Haskett.

At least 37 records · Page 2Linked to original sources
PubMed1991

Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy.

Electroconvulsive therapy is accompanied by an activation of the hypothalamic-pituitary-adrenal axis, resulting in a release of beta-endorphin from the anterior pituitary corticotrophs of humans. As a group, patients in our study demonstrated similar plasma beta-endorphin immunoreactivity response to their initial and final treatments. However, approximately half of the patients demonstrated greater beta-endorphin immunoreactivity release with their first seizure compared with their last seizure, and half of the patients demonstrated the opposite pattern. This difference was not explained by age, sex, unilateral vs bilateral treatments, sine wave vs brief pulse, or psychotropic or anticholinergic medication. Patients with constant seizure duration during the first and final treatments demonstrated a greater release of beta-endorphin immunoreactivity with the final treatment compared with the first treatment. Individuals with decreasing seizure duration during the course of the electroconvulsive therapy demonstrated a decreased beta-endorphin immunoreactivity response during their final treatment.

Adult↗
PubMed1991

Loss of glucocorticoid fast feedback in depression.

A rate-sensitive fast-feedback inhibition of stress-induced corticotropin secretion by glucocorticoids is well documented in rats. Studies in patients with Cushing's disease or adrenal insufficiency have also supported the existence of fast feedback in humans. However, few studies exist in normal healthy subjects or depressed patients. This study compared fast-feedback inhibition of beta-endorphin/beta-lipotropin secretion by hydrocortisone in 16 control subjects and 16 depressed patients. A fast-feedback effect of hydrocortisone on beta-endorphin/beta-lipotropin secretion during the hour of the hydrocortisone infusion was demonstrated in control subjects. Depressed patients demonstrated no increase in beta-endorphin/beta-lipotropin concentrations during the infusion. These data suggest a decreased sensitivity to glucocorticoid fast feedback in depressed patients and complement existing studies demonstrating decreased sensitivity to proportional feedback by dexamethasone in depressed patients. We believe the data presented herein are the first demonstration that abnormal feedback occurs at the level of the brain rather than pituitary in depressed patients.

Adrenocorticotropic Hormone↗
PubMed1990

Multiplicity of depressive episodes: phenomenological and neuroendocrine correlates.

Sixty-four patients with a Research Diagnostic Criteria (RDC) diagnosis of major depressive disorder were categorized into three groups based on their number of depressive episodes (DE): Gr I (1 DE), n = 16, Gr II (2-4 DE), n = 25; and Gr III (5 or more DE), n = 23. All patients were nonsuppressors after 1 mg dexamethasone suppression test (DST) prior to the start of treatment. Patients were monitored during the course of their treatment using serial Hamilton Depression scores and post-DST plasma cortisol levels. A proportionately equal number of patients in the three groups had a favorable outcome, i.e., the number of depressive episodes did not predict recovery. Despite favorable clinical outcome, patients with higher numbers of depressive episodes had significantly higher post-DST plasma cortisol levels that were above the suppressive range (greater than 5 micrograms/dl). Patients with a higher number of depressive episodes had a significantly shorter duration of index episode and were younger at first depressive episode than patients in the other two groups. These results, however, were confounded with polarity, with a higher number of bipolars in Gr III than in the other two groups. Results are discussed in light of phenomenological and psychoendocrine findings of earlier studies.

Adult↗
PubMed1990

Beta-lipotropin-beta-endorphin response to low-dose ovine corticotropin releasing factor in endogenous depression. Preliminary studies.

Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, beta-lipotropin-beta-endorphin. We observed a decreased beta-lipotropin-beta-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total beta-lipotropin-beta-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.

Adult↗
PubMed1990

Electroconvulsive therapy in delusional and non-delusional depressive disorder.

Major depressive disorder (MDD) patients (n = 66) treated with electroconvulsive therapy were stratified by the presence (n = 30) or absence (n = 36) of delusional symptoms (by Research Diagnostic Criteria) to compare their response to treatment. At discharge from hospital 83% of the MDD with psychosis group and 58% of the MDD without psychosis group were good responders (P = 0.03). The implications of this are discussed.

Adult↗
PubMed1990

A longitudinal evaluation of dexamethasone and cortisol plasma concentrations in the dexamethasone suppression test before and during treatment with antidepressant drugs.

Thirty depressed in- and outpatients received serial dexamethasone suppression tests (DSTs). Plasma dexamethasone and cortisol concentrations were drawn at 1600 on the day following a 1-mg oral dose of dexamethasone. The first DST was performed after patients were drug-free for a period of 1 week; the second, third, and fourth DSTs while patients received antidepressant medication. Dexamethasone and cortisol concentrations drawn in the drug-free period correlated significantly. The cortisol to dexamethasone ratio changed significantly with time in DST nonsuppressors, suggesting that nonsuppression is associated with an altered pharmacodynamic response of the hypothalamopituitary-adrenal axis to dexamethasone during depression. When dexamethasone concentrations from the drug-free period were compared with those drawn during antidepressant treatment, no significant differences were noted.

Adult↗
PubMed1990

Severity of depression and hypothalamic-pituitary-adrenal axis dysregulation: identification of contributing factors.

Severity of depression, as reflected by total scores on depression rating scales, has been established as one of several major sources of variance associated with hypothalamic-pituitary-adrenal axis dysregulation in patients with major depressive disorder. To determine which of the symptoms comprising clinically defined severity of illness contribute most to this relationship, we studied the associations between postdexamethasone plasma cortisol levels and components of the Hamilton Rating Scale for Depression (HRSD) in 114 patients with major depressive disorder. At pretreatment baseline, severity of depression was modestly but significantly correlated with postdexamethasone plasma cortisol; a large part of this relationship was associated with the anxiety components of the HRSD. When relationships between postdexamethasone plasma cortisol and severity measures were studied longitudinally during treatment, this contribution of the anxiety items persisted. The anxiety associated with depression appears to be a major clinical factor associated with the hypothalamic-pituitary-adrenal axis dysregulation in major depressive disorder.

Adult↗
PubMed1990

Comorbidity of panic disorder and major depressive disorder: effects on platelet alpha 2 adrenergic receptors.

Adrenergic receptor dysregulation has been described as occurring in both major depressive disorder (MDD) and panic disorder. Measurements of platelet alpha 2 adrenergic receptors in these patients may be confounded by the coexistence or comorbidity of both diagnoses in the same patient. To explore this possibility, we measured platelet alpha 2 adrenergic receptors (3H-clonidine and 3H-yohimbine binding) in 3 groups of patients (MDD only, panic disorder only, and those showing comorbidity of MDD and panic) and normal controls. Patients with comorbidity of MDD and panic disorder had significantly lower agonist binding (3H-clonidine).

Adult↗
PubMed1989

Comparison of early and delayed inpatient dexamethasone suppression tests.

Ninety-five inpatients completed a dexamethasone suppression test (DST) within 72 hours after admission and again after at least 1 week of medication-free hospital care. The frequency of cortisol nonsuppression in patients with endogenous depression (ED) was high and not significantly different at both tests. In patients with diagnoses other than ED, the higher rate of cortisol nonsuppression at the first DST was associated with a significant decrease in test specificity. Change in postdexamethasone cortisol levels at repeat testing was associated with a decrease in depressive symptomatology, but was not related to weight change during hospitalization.

Adult↗
PubMed1988

Plasma postdexamethasone cortisol levels in schizoaffective disorder.

The degree of hypothalamic-pituitary-adrenal (HPA) axis dysregulation in depressed patients with schizoaffective disorder was compared to that seen in patients with major depressive disorder with and without delusional features. The frequency of nonsuppression to dexamethasone was similar for all three diagnostic groups. Maximum postdexamethasone plasma cortisol was greater for delusional depressives, but did not differ between patients with major depressive and schizoaffective disorders. Modest correlations were found between postdexamethasone plasma cortisol levels, severity of illness, age, and recent weight loss, for patients with both major depressive disorder and delusional depression. For schizoaffective patients, associations between postdexamethasone plasma cortisol levels and various measures of severity of illness, but not age and recent weight loss, were found. Although HPA axis dysregulation occurs more frequently in all three of the studied diagnostic groups than in normal individuals, factors contributing to this dysregulation may be qualitatively different for schizoaffective patients.

Adult↗
PubMed1988

Major depressive disorder and panic disorder. Effects of comorbidity on treatment outcome with antidepressant medications.

Recent studies suggest that major depressive disorder (MDD) and panic disorder (PD) may coexist in a significant number of patients. The relevance of this association may be such that patients with the simultaneous diagnosis are at risk for more severe psychopathology and poorer treatment outcome. To explore this possibility further, we compared treatment outcome of two groups of patients: one with comorbidity of MDD and PD (N = 19) and another with MDD only (N = 22). Patients with comorbidity of MDD and PD scored significantly worse on a number of outcome assessments.

Antidepressive Agents↗
PubMed1987

Postdexamethasone plasma cortisol and beta-endorphin levels in depression: relationship to severity of illness.

The hypothalamic-pituitary-adrenal (HPA) axis is dysregulated in many patients with depression, probably at all levels of the axis. To determine if HPA dysregulation is associated with severity of depression, we studied a group of 66 patients with major depressive disorder. Each patient underwent a pretreatment Dexamethasone Suppression Test, with plasma postdexamethasone cortisol determination at 8:00 AM, 4:00 PM, and 11:00 PM. All three postdexamethasone cortisol levels were significantly correlated with the Hamilton Rating Scale for Depression (HRSD) scores. We also examined the "profile" measures of mean, maximum, and minimum of the three cortisol values; again, all three were significantly correlated with HRSD scores. To evaluate associations between clinical severity and HPA dysregulation at the pituitary level, we studied a second group of 44 patients with major depressive disorder. Each had postdexamethasone cortisol determinations at 4:00 PM and 11:00 PM as well as pre- and postdexamethasone beta-endorphin determinations at 4:00 PM. The cortisol data from this group followed the same pattern as in the first sample, and there was a significant relationship between HRSD score and degree of beta-endorphin nonsuppression as well. These results suggest that severity of depression is one of the determinants of dysregulation at both adrenal and pituitary levels of the HPA axis, accounting for 10%-20% of the observed variance.

Adult↗