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Biomedical subjects

Y D Lapierre

Publications and source records attributed to Y D Lapierre.

At least 37 records · Page 2Linked to original sources
PubMed1995

Serotonergic markers in platelets of patients with major depression: upregulation of 5-HT2 receptors.

The uptake of [3H]5-HT and the density (Bmax) as well as affinity (Kd) of 5-HT uptake sites labelled with [3H]paroxetine and of 5-HT2 receptors labelled by [3H]LSD were determined in platelets from 25 medication-free patients with major depression and 20 normal controls. The density (Bmax) of 5-HT2 receptors was found to be significantly increased (by 52%) in platelets from depressed patients, particularly females. No changes were found in the affinity (Kd) of 5-HT2 receptors and in 5-HT uptake or [3H]paroxetine binding parameters. Density of 5-HT2 receptors positively correlated with that of [3H]paroxetine sites in control but not in depressed subjects. No correlation was found between the HAMD scores and Bmax of [3H]LSD binding. The results suggest that upregulation of platelet 5-HT2 receptors is a useful biological marker in major depression, particularly in females.

Adolescent↗
PubMed1994

Primary early onset dysthymia, biochemical correlates of the therapeutic response to fluoxetine: I. Platelet monoamine oxidase and the dexamethasone suppression test.

A subgroup of primary dysthymic patients have been reported to respond to traditional antidepressants and, more recently, to the newer serotonergic agents. Two putative biological markers of affective illness, platelet monoamine oxidase (MAO) activity and plasma cortisol levels following dexamethasone administration, were explored for their diagnostic and predictive potential in dysthymia. Compared to controls, patients had significantly lower platelet MAO activity. Among patients, those that responded to treatment with the serotonergic agent, fluoxetine, had lower pretreatment MAO activity than nonresponders. Higher pretreatment plasma cortisol levels following dexamethasone were also associated with a positive treatment response to this medication. These findings support the view that there is a biological substrate for some subgroups of dysthymics. This biological component may involve the hypothalamic pituitary adrenal axis and serotonergic system(s).

Adult↗
PubMed1994

Primary early onset dysthymia, biochemical correlates of the therapeutic response to fluoxetine: II. Urinary metabolites of serotonin, norepinephrine, epinephrine and melatonin.

The present study investigated pre- and post-treatment 24-h urinary metabolites of monoamines and melatonin as a function of response to treatment in primary early onset dysthymic patients. The main finding was that treatment responders had lower urinary 5-hydroxyindoleacetic acid (5-HIAA) levels prior to treatment. Following treatment, urinary 5-HIAA tended to be decreased in nonresponders and increased in responders. As well, metanephrine levels were lower and 6-sulphatoxymelatonin levels were higher in responders prior to treatment. These data support the view that there is a biological substrate for certain subgroups of dysthymia, part of which may involve serotonergic systems.

Adult↗
PubMed1994

Alprazolam and amitriptyline in the treatment of moderate depression.

Forty-three out-patients with depression of a moderate degree were enrolled in a randomized, double-blind parallel group study comparing amitriptyline and alprazolam for 6 weeks of treatment. Patients were evaluated at the end of placebo washout and at Weeks 1, 2, 3 and 6 of drug therapy using the Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A), Beck Depression Inventory (BDI) and Clinical Global Impression (CGI). Drug dosage was determined in a fixed-flexible design resulting in mean final doses of alprazolam 3.2 mg/day and of amitriptyline 115 mg/day. Although both drug groups improved there were statistically significant differences in favour of amitriptyline at the end of the study on the HAM-D, BDI and HAM-A scales. Patients on amitriptyline reported more side effects overall than patients taking alprazolam with significantly more reports of dry mouth in the amitriptyline group.

Adolescent↗
PubMed1994

Pharmacological therapy of dysthymia.

For a number of years, dysthymia was considered to be non-responsive to antidepressant treatment. During the last decade, early studies with tricyclic antidepressants (TCAs) demonstrated the superiority of the TCAs over placebo. The side effect profile of the TCAs and the moderate degree of symptomatology resulted in reduced compliance and thus to the clinical impression of lack of efficacy. The newest generation of antidepressants, the SRRIs and the RIMAs, with their more acceptable side effect profiles, allowed for the adequate evaluation of pharmacotherapy in dysthymia. The initial open studies with SSRIs indicate a clear efficacy of this group of antidepressants. Likewise, a 5HT2 antagonist, ritanserin, has been shown to be superior to placebo. More recently, a large placebo-controlled study of moclobemide, a RIMA, clearly demonstrated the superiority of this drug over placebo. Based on this evidence, it is now appropriate to consider antidepressants as a clearly effective method of treating dysthymia.

Antidepressive Agents, Tricyclic↗
PubMed1994

Platelet serotonin measures in primary dysthymia.

Serotonergic function in 22 patients with primary dysthymia and 22 normal volunteers was evaluated by measuring [3H]serotonin uptake and [3H]paroxetine binding in platelets. A significantly lower maximum rate of serotonin uptake was noted in the dysthymic patients than in the normal subjects, indicating a possible serotonergic dysfunction in dysthymia. However, the values for parameters of paroxetine binding were similar in the two groups.

Adult↗
PubMed1994

Therapeutic efficacy of specific serotonin reuptake inhibitors (SSRIs) in dysthymia.

Pharmacological treatment of dysthymia is a contentious issue mainly because of the traditional view that this disorder has characterological origins and responds to psychotherapy. However, Akiskal's subtyping of primary dysthymia, which was based in part on its response to older antidepressants, can assist in the prediction of responses to antidepressants. Specific serotonin reuptake inhibitors (SSRIs) have equal efficacy but fewer adverse effects and greater tolerability than older antidepressants. Therefore, SSRIs appear to be a viable treatment option for these patients although there are few documented systematic studies of the use of these agents in primary dysthymia. An open study was conducted to determine the efficacy of fluoxetine in primary dysthymia (DSM-III-R and Akiskal's criteria). A good response was observed in the subaffective subtype but not in the character spectrum group. Overall, the antidepressant was tolerated well, with significant adverse effects reported and responders showing reductions in both depressive and anxious symptoms. These initial findings indicate a potential role for SSRIs in the pharmacotherapy of dysthymia.

Adult↗
PubMed1994

Schizophrenia and manic-depression: separate illnesses or a continuum?

Kraepelin proposed that schizophrenia and manic-depression were distinct and separable disorders. This hypothesis has been challenged recently by proponents of the "unitary psychosis" theory which posits a continuum from unipolar to bipolar disorder, continuing through schizoaffective and schizophrenic illness. In reviewing symptom cluster data and family studies, the author suggests that there is no compelling evidence to indicate a common pathophysiology for schizophrenia and bipolar disorder. More problematic is a diagnosis of schizoaffective disorder which does not appear to be a stable clinical entity. This would suggest that schizoaffective disorder is not a true clinical syndrome but rather a phenotypic variation.

Bipolar Disorder↗
PubMed1993

Ritanserin, imipramine, and placebo in the treatment of dysthymic disorder.

Fifty outpatients with dysthymic disorder (DSM-III) were divided by double-blind randomized assignment into three groups given ritanserin, imipramine, and placebo, respectively. The trial was of 7 weeks' duration; by week 6, imipramine was clearly superior to placebo, whereas by week 7, both drugs caused significantly more improvement than the placebo. Although imipramine had slightly greater efficacy than ritanserin, it also had significantly more side effects. This was particularly evident in the higher dropout rate with imipramine. The efficacy and side effect profile of ritanserin makes it well tolerated and acceptable with dysthymic patients who, although they do not respond as quickly as patients with major depressive disorder, do show significant improvement, given sufficient time.

Adult↗
PubMed1993

Anxiety disorders. Part 1: Diagnosis and treatment.

Anxiety disorders often take second priority in clinical practice because many physicians do not understand them or their treatment. This paper reviews the diagnostic groupings of anxiety disorders according to the American Psychiatric Association's Revised Diagnostic and Statistical Manual of Mental Disorders (DSM 3-R) and discusses differential diagnosis and treatment.

Anxiety Disorders↗
PubMed1993

Reduction in suicidal ideation with SSRIs: a review of 459 depressed patients.

This paper is a review of 459 outpatients treated in double-blind clinical drug trials using similar protocols which compared the clinical responses to specific serotonin reuptake inhibitors, norepinephrine reuptake inhibitors, mixed norepinephrine serotonin reuptake inhibitors, serotonin-2 antagonists and placebo. Although improvements in the total score on the Hamilton Rating Scale for Depression did not differ significantly among the groups, there were differences in the profile of response based on analysis of the items of the scale. The most striking difference was the significantly more rapid and effective improvement in depressed mood and the lessening of suicidal ideation among the patients treated with specific serotonin reuptake inhibitors.

Adolescent↗
PubMed1992

A dose-finding study with remoxipride in the acute treatment of schizophrenic patients.

Two hundred and forty-two patients with acute schizophrenia were enrolled in a double-blind, comparative, dose-finding study of a novel antipsychotic, remoxipride. Remoxipride was evaluated in a low (30 to 90 mg), medium (120 to 240 mg) and a high (300 to 600 mg) dose range and compared with a haloperidol (15 to 45 mg), which was administered to a similar group of patients. The results support the antipsychotic effect of remoxipride, with maximum efficacy occurring at daily doses between 120 mg and 600 mg. Side-effects were more frequent at doses of remoxipride over 300 mg. In all groups, remoxipride caused consistently fewer extrapyramidal side-effects than haloperidol. The antipsychotic effect of remoxipride may be derived from specific blockade of dopamine D2 receptors in the mesolimbic tract. The findings also suggest that remoxipride may have a therapeutic effect on negative symptoms of schizophrenia.

Dose-Response Relationship, Drug↗