Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls

Wahby, Victor S.; Ibrahim, G. A.; I, Leechuy; Saddik, Fouad W.; Giller, Earl L.; Mason, John W.

doi:10.1016/0920-9964(90)90010-5

Cited by 5 publications

(2 citation statements)

References 33 publications

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“…Wahby et al (1988, 1990) measured PRL and thyroid-stimulating hormone (TSH) response in thyroid-releasing hormone (TRH) challenge tests in 10 schizophrenia, 8 schizoaffective disorder (SAD), 23 MDD, and 43 normal subjects. They found blunted PRL and TSH responses in the MDD patients but no other differences among groups.…”

Section: Neuroendocrinologymentioning

confidence: 99%

Neurochemistry and Neuroendocrinology of Schizophrenia: A Selective Review

Lieberman

Koreen

1993

Schizophrenia Bulletin

138

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Neurochemical investigation has played a major role in the search for the cause of schizophrenia. Initial research strategies involved the direct measurement of neurochemical substances in biological fluids. Subsequently, indirect measures of brain biochemistry including pituitary hormones and responses to pharmacologic probes were examined. Recent advances in in vivo functional neuroimaging, biochemical neuropathology, and molecular genetics have extended the scope of clinical neurochemical studies. The historical emphasis on the dopamine neurotransmitter system has subsided in the wake of the demonstrated limitations of the dopamine hypothesis of schizophrenia and increased evidence for the role of other neurotransmitters in the pathophysiology of schizophrenia as well as their interactions with dopamine neural systems. The neurotransmitters that have come under increasing scrutiny include serotonin, norepinephrine, glutamate, and related excitatory amino acids, and the neuropeptides cholecystokinin and neurotensin. In this article, the authors reviewed significant recently published neurochemical and neuroendocrine studies of schizophrenia in the context of previous work and found an extensive but fragmentary body of data which provides neither consistent nor conclusive evidence for any specific etiologic theory. Aspects of the disease and methodological limitations that may account for this as well as future research strategies are discussed.

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Section: Neuroendocrinologymentioning

confidence: 99%

Neurochemistry and Neuroendocrinology of Schizophrenia: A Selective Review

Lieberman

Koreen

1993

Schizophrenia Bulletin

138

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“…We wish to refer here to our previously published reports on the thyrotropin and prolactin responses to thyrotropin-releasing hormone, where we found schi zoaffective depressed patients to be biologically closer to schizophrenics (and healthy controls) than to patients with major depressive disorder [35,36], These findings, together with the present DST report and the portion of the literature that supports it, may be taken to imply that some biological tests can potentially distinguish RDC schizoaffective depressed from major depressive disor der patient groups, but not from schizophrenics. Fur thermore.…”

Section: Discussionmentioning

confidence: 99%

The Dexamethasone Suppression Test in a Group of Research Diagnostic Criteria Schizoaffective Depressed Men

Wahby

Ibrahim²,

Giller³

et al. 1990

Neuropsychobiology

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A dexamethasone suppression test (DST) was performed on 8 schizoaffective depressed men. Cross-sectional comparisons were made with three groups: schizophrenics (n = 10), unipolar major depressives (n = 23) and healthy controls (n = 43). All were drug-free and similar in age and body weight. Evaluations utilized the Research Diagnostic Criteria (RDC) for diagnosis, and the Hamilton Rating Scale for Depression for depressive symptom rating. DST nonsuppression, defined as a blood cortisol level of ≥5.0 μg/dl at 16.00 h postdexamethasone, was observed in 43.5% of the major depressive disorder patients. This was different from the other three groups: 12.5% in schizoaffective depressed, 10.0% in schizophrenics and 9.3% in healthy controls (p < 0.01, p < 0.01, and p < 0.001 respectively). Although schizoaffective depressed patients were significantly different from major depressive disorder patients in their DST responses, both groups were similar in their total HRSD scores and different from the schizophrenics (p < 0.01 for each). These results, together with others previously reported by us on the thyrotropin-releasing hormone challenge in the same diagnostic groups, may be taken to mean that schizoaffective disorder, depressed type, is biologically distinct from major depressive disorder but not schizophrenia. On the other hand, until further corroborated, they should probably be considered a reflection of the heterogeneity of the schizoaffective syndrome and the nonspecificity of the DST.

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Psychoneuroendocrinology of Schizophrenia

Marx¹,

Lieberman

1998

Psychiatric Clinics of North America

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Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls

Cited by 5 publications

References 33 publications

Neurochemistry and Neuroendocrinology of Schizophrenia: A Selective Review

Neurochemistry and Neuroendocrinology of Schizophrenia: A Selective Review

The Dexamethasone Suppression Test in a Group of Research Diagnostic Criteria Schizoaffective Depressed Men

Psychoneuroendocrinology of Schizophrenia

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