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Biomedical subjects

R F Haskett

Publications and source records attributed to R F Haskett.

At least 55 records · Page 3Linked to original sources
PubMed1987

Serial dexamethasone suppression tests in simultaneous panic and depressive disorders.

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.

Adult↗
PubMed1987

Multiple depressive episodes and plasma postdexamethasone cortisol levels.

The hypothalamic-pituitary-adrenal (HPA) axis is dysregulated in many patients with major depressive disorder (MDD). To determine whether or not a past history of depressive episodes is associated with this dysregulation, we studied the relationships among number of past depressive episodes, number of previous hospitalizations for depression, and number of years since first depressive episode and biological markers of depression (postdexamethasone plasma cortisol levels and dexamethasone suppressor/nonsuppressor status). No significant relationships were detected.

Adult↗
PubMed1987

Premenstrual dysphoric disorder: evaluation, pathophysiology and treatment.

A small percentage of women describe a prominent dysphoric disturbance that is present during the premenstrual week, remits soon after the onset of menses and produces significant impairment in domestic, social or occupational functioning. Premenstrual dysphoric disorder must be distinguished from minor premenstrual emotional changes, from dysmenorrhea and from premenstrual exacerbations of psychiatric illness. Diagnostic evaluation should include the prospective assessment of symptoms over at least two complete menstrual cycles. Although the pathophysiology of premenstrual dysphoric disorder is linked to cycling of the intact hypothalamo-pituitary-gonadal axis, many studies have contained serious methodological weaknesses and no single etiological theory has received widespread support. No single pharmacological treatment has been shown to be clearly more effective than placebo in controlled studies and premenstrual dysphoric disorder appears to respond favorably to most interventions in uncontrolled studies. Interruption of pituitary-ovarian cycling will alleviate premenstrual symptoms, but treatments of this type cannot be recommended for general use until potential hazards are clarified.

Female↗
PubMed1986

Neuroendocrine effects of L-tryptophan and dexamethasone.

An infusion of L-tryptophan was administered twice to five healthy male volunteers, once after pretreatment with dexamethasone 1 mg the previous evening and once after no dexamethasone. Cortisol, prolactin, and growth hormone levels were measured, and the responses to L-tryptophan were compared with those seen after an infusion of L-threonine. L-tryptophan did not produce cortisol secretion after dexamethasone, but prolactin and growth hormone responses were noticed. The results demonstrate a stimulatory effect of L-tryptophan on prolactin and growth hormone secretion, and the former is facilitated by pretreatment with dexamethasone.

Adult↗
PubMed1986

Prolactin response to TRH in depression.

We studied the prolactin response to TRH in 53 unmedicated psychiatric inpatients. The prolactin response of females was significantly greater than the response of male subjects. There was no significant difference in the prolactin response to TRH between depressed patients and those with other psychiatric diagnoses. There was no significant relationship between the prolactin response to TRH and the severity of depression, the TSH response to TRH or the resistance to suppression of cortisol secretion by dexamethasone.

Adrenal Cortex↗
PubMed1986

Diagnosing premenstrual tension syndrome.

The presence of a premenstrual tension syndrome (PMTS) should be considered during the clinical assessment of any women of childbearing age with intermittent or fluctuating psychological symptoms. Appropriate identification of this disorder depends on knowledge of its specific diagnostic features, most particularly its time-limited course. The clinician must also be aware that the syndrome can coexist with, exacerbate, or be exacerbated by other psychological distress or illness. Through the presentation of four case histories, the authors discuss the diagnostic complexities of PMTS and the treatment implications of a diagnosis of PMTS.

Adult↗
PubMed1985

Opioid regulation of hypothalamic-pituitary-adrenal function in depression.

A morphine infusion paradigm was used to investigate opioid mechanisms in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis in depression. The subjects were unmedicated psychiatric inpatients and healthy volunteers. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion was associated with a diagnosis of major depression and abnormal dexamethasone suppression test results. Our data suggest that the hyperactivity of the HPA axis observed in depression is abnormally resistant to opioid inhibition as well as glucocorticoid feedback.

Adult↗
PubMed1985

Prolactin response to morphine in depression.

Twenty-two unmedicated inpatients with major depression and 18 healthy volunteers of either sex were given an intravenous injection of 5 mg morphine. Blood samples were drawn immediately before and at intervals for 3 hrs after the injection and assayed for prolactin. Morphine stimulated prolactin secretion. The prolactin response of females was significantly greater than the response of male subjects. There were no significant differences in the prolactin response to morphine between depressed and healthy subjects. The implications of these findings for the hypothesized role of the opioid system in the pathophysiology of depression are discussed.

Adult↗
PubMed1985

Hormone response to repeated electroconvulsive therapy: effects of naloxone.

Plasma prolactin (PRL), cortisol, and growth hormone (GH) were measured before, and at 15-min intervals for 1 hr after, electroconvulsive therapy (ECT). This was repeated over a series of 6 consecutive treatments for each of 12 depressed drug-free inpatients. Patients received naloxone, 2 mg or 20 mg, by intravenous infusion before the third and fifth treatment. ECT was consistently followed by a release of PRL and cortisol, although two patterns of PRL response could be distinguished. In eight patients, the PRL response did not change significantly with repeated ECT, whereas in four patients, the plasma PRL increased tenfold after the first treatment and decreased after each successive treatment. The GH level varied widely, with no evidence of a reliable response to ECT. Opiate receptor blockade with low- or high-dose naloxone did not alter the release of PRL or cortisol after ECT. These findings demonstrate a reliable PRL and cortisol response to ECT, but do not support a role for endogenous opiates in these hormonal changes.

Adult↗
PubMed1985

Cortisol escape from morphine suppression.

Twenty-one unmedicated, sequentially admitted psychiatric patients of either sex and four male healthy volunteers were given an intravenous injection of 2.5 mg morphine. Blood samples were drawn immediately before and at 30-minute intervals for 3 hours after the injection and assayed for cortisol. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion (escape) was more frequent in patients with a diagnosis of major depressive disorder and with abnormal dexamethasone suppression test results. The sensitivity of this infusion paradigm for the diagnosis of major depressive disorder was 40%, and the specificity was 82%. The implications of these findings for the pathophysiology of depression are discussed.

Adult↗
PubMed1985

Diagnostic categorization of psychiatric disturbance in Cushing's syndrome.

The author obtained a longitudinal psychiatric history from 30 patients with proven Cushing's syndrome. Twenty-five (83%) of the patients met strict diagnostic criteria for an episode of affective disorder during the course of their endocrine disturbance. Twenty patients met criteria for endogenous depression and eight patients also reported an episode of mania or hypomania. Schizophrenic syndromes were not evident, although two patients met criteria for a psychotic depression. Patients frequently attempted to minimize or conceal serious psychiatric disturbance, including a suicide attempt. Typical affective syndromes occurred in patients with adrenocortical tumors as well as in those with ACTH-dependent Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed1984

A psychoendocrine study of premenstrual tension syndrome. A model for endogenous depression?

We studied 42 women with severe Premenstrual Tension Syndrome (PMTS) and compared their clinical features and adrenocortical function with those seen in major depressive disorders. Self-report scales demonstrated that PMTS was very distressing, but the disturbance did not meet the RDC for Major Depressive Disorder -- endogenous subtype. Twenty-four hour urinary free cortisol estimation did not indicate cortisol hypersecretion and abnormal Dexamethasone Suppression Test results occurred much less frequently than is usual in endogenous depression. Adrenocortical function did not differ significantly between follicular and premenstrual phases. PMTS does not appear to be a psychoendocrine model for endogenous depression.

Adult↗
PubMed1984

Plasma prolactin and severe premenstrual tension.

It has been suggested that elevated luteal phase prolactin (PRL) levels may have an important role in causing some of the symptoms of the premenstrual tension syndrome (PMTS). Thirty-seven women suffering from severe premenstrual dysphoria were selected for this study. Single morning and afternoon serum PRL evaluations were performed during the follicular (day 9) and late luteal (day 26) phases of the menstrual cycle. PRL was measured by an established double antibody radioimmunoassay technique. All mean PRL values were within the normal range. Only afternoon mean PRL levels showed a tendency for a premenstrual increase. The significance of this statistical finding is unclear, since one-third of the subjects showed a decrease in premenstrual PRL levels. Twenty-four hour PRL secretory profiles recorded on days 9 and 26 in two women with extremely severe PMTS and in two asymptomatic matched control subjects also failed to show a significant correlation between PRL levels and PMTS. Thirty subjects participated in a treatment trial using bromocriptine. A marked rebound hyperprolactinemia was observed in a subgroup of women nine days after cessation of bromocriptine. This was associated with no detectable effect on mood, behavior, or menstrual regularity. Thus, our data fail to show any specific relationship between PRL and PMTS.

Adult↗
PubMed1984

Morphine inhibits cortisol and stimulates prolactin secretion in man.

The role of opioids in endocrine regulation has been the subject of numerous studies. Surprisingly, however, the acute endocrine effects of morphine on basal hormonal levels in man have not been adequately documented. We report here the effects of intravenous morphine (5 mg) on plasma cortisol and prolactin. Fourteen healthy volunteers (nine male, five female) received morphine at 0930 hr. Blood samples were collected immediately before and 30, 60, 90, 120 and 180 min after the injection. In six of the male subjects the procedure was repeated with a placebo (normal saline) injection. Morphine stimulated prolactin release. There was a trend for a greater response in females compared to male subjects. Cortisol secretion was markedly suppressed by morphine. In sharp contrast to the results obtained with placebo, cortisol levels following morphine declined progressively at a rate consistent with the half-life of cortisol. This downward trend of cortisol values continued uninterrupted for the duration of the experiment in all 14 subjects. These results are consistent with the presence of an inhibitory opioid mechanism in the human hypothalamo-pituitary-adrenal axis.

Adrenal Cortex↗
PubMed1984

Circadian hormone secretory profiles in women with severe premenstrual tension syndrome.

The circadian secretory profiles of serum prolactin, growth hormone and cortisol were measured in two women suffering from severe premenstrual tension syndrome and in two asymptomatic control subjects. Subjects and controls were screened and included after a rigorous selection process. Blood samples were obtained every 30 min over a period of 24 h in each woman both on day 9 (follicular phase) and day 26 (luteal phase) of the menstrual cycle. There was no relationship between the hormonal secretory profiles and the premenstrual tension syndrome.

Adult↗
PubMed1983

Premenstrual tension syndrome: diagnostic criteria and selection of research subjects.

The investigation of premenstrual tension syndrome (PMTS) has been hampered by several methodological problems, particularly an inadequate definition of study subjects. Diagnostic criteria for PMTS that use both interview and self-report information were tested in 24 symptomatic female volunteers. Each woman subsequently completed daily reports of emotional and somatic symptoms for 1 1/2 menstrual cycles. Symptom profiles from subjects meeting the diagnostic criteria for PMTS were compared with profiles from subjects who failed to meet the criteria. This study demonstrated that the diagnostic instruments used could identify a group of women with a severe and time-limited premenstrual psychological disturbance and distinguish them from women with milder and more temporally diffuse changes. The need for such instruments and their importance for further research into this disorder are discussed.

Adult↗