The cases of two borderline patients are presented, dexamethasone suppression test (DST) positive and refractory to many therapeutic interventions and treated successfully with high doses of amitriptyline (225 and 200 mg/day, respectively). During the therapeutic intervention, the psychopathological condition of the patients was evaluated using Hamilton's rating scale for depression and a constructed scale based on items 11, 12 and 13 (dysphoria, anger, sense of emptiness, boredom, anhedonia) of the diagnostic interview for borderline patients.

The development, evaluation and use of biological markers with a diagnostic purpose in psychiatry is extremely important. However, with certain exceptions, truly sensitive and specific markers have not yet emerged. In order to investigate the relationship between the immune apparatus and the hypothalamic-pituitary activity on the one hand, and the psychopathological state of the patients on the other, we used a longitudinal design and assessed monocyte parameters (HLA-DR, CD 35, vimentin filaments, and phagocytosis index) and neuroendocrine tests (dexamethasone suppression test [DST] and thyrotropin-releasing hormone [TRH] stimulation test) at intake and at follow-up in 49 depressed patients. Immunological parameters were compared with neuroendocrine tests in both phases of the study. The combined use of both immunological and neuroendocrine tests did not add sensitivity to the immunological identification of depressed patients. The findings lead us to consider the role of the monocyte parameters as sensitive depressive state markers, while the combined use of both neuroendocrine and immunological tests in current clinical practice would be debatable.

The case of a woman presenting erotomania in the course of a loss-related depressive state is described. Clinical, biological and therapeutical characteristics highlight the role of mood in certain cases of erotomania and add support to previous accounts of the heterogeneity of this syndrome.

To prove the hypothesis of a common defect in the central nervous system and immune system in patients with major depression, we examined the inhibition of phytohemagglutinin (PHA)-induced lymphocyte proliferation by in vitro and in vivo administration of glucocorticoids in 20 patients with major depression. The patients were divided into two groups according to the results of the dexamethasone suppression test (DST). Six patients showed cortisol non-suppression. They had significantly higher baseline plasma cortisol levels in comparison with cortisol suppressors. The lymphocytes from cortisol non-suppressors were significantly stronger inhibited by in vitro administration of glucocorticoids compared to the lymphocytes from cortisol suppressors. However, there were no significant differences of lymphocyte inhibition by in vivo administration of glucocorticoids between both patient groups. From our results we conclude that cortisol non-suppressors reveal impaired down-regulation of glucocorticoid receptors of lymphocytes. Furthermore, the effect of glucocorticoids on lymphocyte reactivity may reflect the effects on brain structures in patients with major depression.

The mitogen induced lymphocyte responses were measured in 33 depressed patients categorized according to the DSM-III into minor (300.40, 309.00), simple major (296.X2) and major depression with melancholia and/or psychotic features (296.X3, 296.X4). Three distinct mitogens were used, i.e. phytohemaglutinin (PHA), pokeweed mitogen (PWM) and concanavalin A (CON A). We found that major depressives with associated features showed significantly lower mitogen induced lymphocyte responses to PHA and PWM as compared to all other depressed patients. The severity of illness was significantly inversely related to the lymphocyte responses to PHA. Cortisol nonsuppressors exhibited significantly lower PHA and PWM induced lymphocyte responses as compared with suppressors. There were significant and negative correlations between the postdexamethasone Cortisol values and the PHA and PWM stimulated lymphocyte responses.

Se presentan los casos de dos pacientes límite, positivos en la prueba de supresión con dexametasona (DST) y refractarios a numerosas intervenciones terapéuticas, tratados con éxito con dosis altas de amitriptilina (225 y 200 mg/día, respectivamente). Durante la intervención terapéutica, se valoró el estado psicopatológico de los pacientes utilizando la Escala de Evaluación de Hamilton para la Depresión y una escala construida basada en los elementos 11, 12 y 13 (disforia, ira, sensación de vacío, aburrimiento y anhedonia) de la entrevista diagnóstica para pacientes límite.

El desarrollo, valoración y uso de marcadores biológicos con un propósito diagnóstico en psiquiatría es sumamente importante. Sin embargo, con ciertas excepciones, todavía no han surgido marcadores verdaderamente sensibles y específicos. Para investigar la relación entre el aparato inmune y la actividad hipotalámico-pituitaria por una parte, y el estado psicopatológico de los pacientes por otra, utilizamos un diseño longitudinal y evaluamos parámetros de monocitos (HLA-DR, CD 35, filamentos de vimentín e índice de fagocitosis) y pruebas neuroendocrinas (prueba de supresión con dexametasona [DST] y prueba de estimulación de la hormona liberadora de tirotropina [TRH]) en la admisión y en el seguimiento en 49 pacientes deprimidos. Se compararon parámetros inmunológicos con pruebas neuroendocrinas en ambas fases del estudio. El uso combinado de pruebas inmunológicas y neuroendocrinas no añadió sensibilidad a la identificación inmunológica de los pacientes deprimidos. Los hallazgos nos llevaron a considerar el papel de los parámetros de monocitos como marcadores sensibles del estado depresivo, mientras que el uso combinado de pruebas neuroendocrinas e inmunológicas en la práctica clínica actual sería discutible.

Objective: This study investigated the frequency of abnormal Dexamethasone Suppression Test (DST) in a randomly selected group of mentally handicapped subjects. Method: Forty three subjects living in the community were selected and assessed on a variety of clinical rating scales including Hamilton Rating Scale for Depression (HDS) and Wessex Case Register Form (WCRF). DST was conducted on all the patients and the findings correlated with demographic and clinical variables. Groups defined by DST status were also compared using t-test. In subjects who showed an abnormal response, clinical assessments and DST was repeated after 3 months. Results: Only 7 of 43 subjects showed an abnormal response which did not correlate with either the severity of affective symptoms or the presence or absence of behavioural difficulties. Six of the 7 DST positive subjects were either severely or profoundly impaired on DSM-III criteria indicating that the underlying brain pathology may be pathogenetically important. This was supported by the observation that abnormal DST response was enduring at follow up. Conclusions: The findings suggest that DST may be of little value as a diagnostic tool in the mentally handicapped.

The value of the Dexamethasone Suppression Test (DST) in predicting the therapeutic response to a specific antidepressant is a very controversial topic, probably due to methodological issues. The aim of this study was to evaluate the power of the DST in predicting the response of primary and secondary depressives, diagnosed according to Feighner criteria, to either clomipramine or maprotiline. Patients were screened using standardized psychiatric interview, Current and Past Psychopathology Scales, the Hamilton Rating Scale for Depression (HRSD), and the Beck Depression Inventory (BDI); the Michigan Discriminant Index was determined providing an endogeneity score. A 1 mg DST was performed. Treatment was assigned double blind and at random, according to a fixed schedule with administration of up to 225 mg of either drug for three weeks. After this period patients were again evaluated with the Hamilton Rating Scale for Depression and Beck Depression Inventory, and a DST was again performed.

Treatment reponse was defined in terms of reduction of HRSD and BDI scores. Serum levels of antidepressants were documented in a number of patients.

HRSD score reduction did not yield any significant results.

Insofar as BDI score reduction was concerned, nonsuppression on the DST (i.e. a post-dexamethasone cortisol value greater than or equal to 50 μg/l) predicted a better, or anyway a quicker, response to maprotiline; the DST results did not predict response in patients treated with clomipramine.

Despite some methodological pitfalls (a relatively small group of patients, insufficiently documented serum antidepressant levels) these results seem to warrant further investigation in this field.