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Biomedical subjects

F G Moeller

Publications and source records attributed to F G Moeller.

48 records · Page 3Linked to original sources
PubMed1995

Risk factors for clozapine discontinuation among 805 patients in the VA hospital system.

The goal of this study was to determine if demographic or clinical factors collected at baseline on patients treated with clozapine would increase the risk of having clozapine discontinued for (a) lack of response, (b) side effects, (c) noncompliance, (d) concomitant illness, or (e) death. The subjects were 805 patients treated with clozapine at 96 Department of Veterans Affairs Hospital System facilities. Multiple logistic regression was used to determine if any of the baseline variables predisposed patients to discontinuation from treatment. Factors which were studied include age, race, history of inadequate response to traditional neuroleptics, history of substance abuse, and DSM-III-R Axis I diagnosis. Of the 805 patients started on clozapine 167 (20.7%) were discontinued from treatment. The only significant variable in the logistic regression model was race. This study finds that African American patients are more likely to have clozapine discontinued than non-African American patients, and there is a trend for prior history of inadequate response to traditional neuroleptics to predict clozapine discontinuation. We found no effect of substance abuse or dependence, diagnosis, or age on outcome in the overall patient group. In a post hoc analysis the African American patients had a significantly lower baseline white blood count than the non-African American patients, which could have explained the difference in clozapine discontinuation. The findings of this study support further investigation into the causes of ethnic differences in treatment outcome with clozapine.

Adult↗
PubMed1994

Serotonin and impulsive/aggressive behavior in cocaine dependent subjects.

1. 10 male cocaine dependent patients and 10 sex matched controls were administered several behavioral measures of aggression including the Buss-Durkee Hostility Inventory, and The Brown-Goodwin Life History of Aggression. 2. All subjects were also administered a buspirone neuroendocrine challenge as a measure of serotonin function. 3. The cocaine dependent subjects were significantly more aggressive than the controls. 4. There was a significant correlation between the growth hormone response to buspirone and behavioral measures of aggression in the cocaine dependent subjects, but not in the controls. 5. There was no difference in the overall growth hormone response between the controls and cocaine dependent subjects, possibly due to differences in metabolism of buspirone. 6. This study supports a role for serotonin in aggression in cocaine dependent subjects.

Adult↗
PubMed1994

A preliminary neuroendocrine study with buspirone in major depression.

We administered the serotonin-1a agonist buspirone (0.4 mg/kg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III-R major depressive disorder (MDD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = 8). Our findings support a role for the serotonin-1a receptor in the etiology of MDD, specifically at the postsynaptic site.

Adult↗
PubMed1993

A comparison of sleep EEGs in patients with primary major depression and major depression secondary to alcoholism.

Polygraphic sleep recordings were compared between patients with primary major depression (MDD), patients with primary alcoholism and secondary MDD, and normals. Patients differed significantly from normals on the following measures: both patient groups showed short REM latency, and REM latency corrected, along with prolonged sleep latency. Secondary depressives differed from controls on several other measures: sleep onset time, total sleep time, delta sleep, REM percent, stage one sleep, stage three sleep, non-REM sleep, stage three and delta sleep in the first non-REM period. Prior research has shown a decrease in non-REM sleep and total sleep time in alcoholic patients who are not currently depressed, and short REM latency in patients with MDD. Thus, our findings suggest an additive effect of two disorders known to affect sleep: alcoholism and depression.

Adult↗
PubMed1993

Desipramine does not alter plasma GABA in patients with major depression.

Low plasma GABA is a biological marker for depression in a subset of patients tested. Plasma GABA has been shown to reflect brain GABA activity. This marker has many characteristics of a trait marker for depression, including stability with time, and lack of influence by coincident factors such as gender, season, time, activity or diet. We here report that plasma GABA remained stable after 4 weeks of treatment with desipramine in patients with major depression. Since the levels of plasma GABA did not change with time, nor with clinical improvement, plasma GABA is not a state marker of depression.

Adult↗
PubMed1993

Serum homovanillic acid levels in schizophrenic patients and normal control subjects.

Schizophrenic patients with an early age at onset of illness had low baseline levels of homovanillic acid (HVA) in serum compared with schizophrenic patients with a late age at onset. After adjustments were made for age at onset, there was a significant partial correlation between positive symptoms and serum HVA. The relationship between positive symptom scores and serum HVA was shifted to the left in the early onset patients, suggesting a relatively increased sensitivity of dopamine-associated response. Patients with severe negative symptoms also had an earlier age at onset and a trend toward lower serum HVA. This study found no difference between mean serum HVA values in schizophrenic patients and normal control subjects.

Adult↗
PubMed1993

Low plasma GABA is a trait-like marker for bipolar illness.

Plasma gamma-aminobutyric acid (pGABA) is an index of brain GABA activity and a peripheral marker of mood disorder. Previous research has indicated that pGABA is abnormally low in approximately 40% of patients symptomatic with primary unipolar depression. We have now measured pGABA in a series of patients with bipolar disorder. Blood samples for GABA determinations were collected soon after admission to hospital or clinic while patients were symptomatic. In both manic and depressed phase bipolar patients, mean levels of pGABA were significantly lower than in healthy control subjects. The distribution of pGABA in bipolar patients, whether manic or depressed, was similar to that in symptomatic unipolar depression, with 30% to 40% having pGABA levels lower than the control range. These data indicate that low pGABA is not specific to the depressed state, as it is also found in the manic phase of bipolar disorder. Low pGABA may represent a shared biologic correlate between bipolar and unipolar illness.

Adult↗
PubMed1993

Plasma gamma-aminobutyric acid (GABA) is low in alcoholics.

Plasma levels of gamma-aminobutyric acid (GABA) were measured in male alcoholics on admission to inpatient treatment and at discharge after 3 to 4 weeks of abstinence. Free plasma GABA at discharge was significantly lower in alcoholics than in control subjects and specifically identified a subset of 35 percent of the alcoholic patients with levels below the normal range. However, levels of free plasma GABA in recently detoxified alcoholics on admission were not different from those of controls and had a significant positive correlation with liver enzymes and mean corpuscular volume. These data are compatible with a GABA deficit theory of alcoholism in a subset of alcoholics.

Adult↗
PubMed1991

Kinetic effects of desmethylimipramine treatment on platelet serotonin uptake in depressed patients: a comparison with imipramine.

The kinetic effects of desmethylimipramine (DMI) on platelet serotonin (5HT) uptake were compared to those of imipramine (IMI) in eight DMI-treated depressed patients and seven IMI-treated depressed patients, and compared to values after patients were off drug for 19 (+/- 8 SD) and 33 (+/- 15) days. As expected, IMI was a stronger inhibitor of 5HT uptake than DMI during treatment, with the mean apparent Km in treated patients being elevated nearly threefold over that of the drug-free condition. In DMI-treated patients, the mean Km was elevated nearly twofold over that of the drug-free condition. Although DMI is considered a preferential norepinephrine uptake inhibitor, the results suggest the following: (1) Significant decreases in the apparent platelet 5HT affinity are achieved with DMI; (2) the inhibition kinetics in depressed patients are competitive; (3) there was a significant relationship between Km change and depression outcome with DMI discontinuation; and (4) DMI, as a metabolite, appears to contribute to the 5HT uptake inhibition of IMI in vivo.

Blood Platelets↗
PubMed1990

Gepirone as a 5-HT1A agonist in the treatment of major depression.

Twenty-four patients with major depression were treated in a single-blind design with 25 mg to 75 mg gepirone, a pyrimidinyl piperidinedione analog of buspirone with serotonin1A (5-HT1A) receptor affinity properties. Twenty-four-Item Hamilton Rating Scale for Depression-(HAM-D) scores decreased by 36 percent when mean baseline scores were compared with an endpoint analysis of 6 weeks' gepirone treatment. Several subjects demonstrated marked improvements over baseline. The data are discussed within the context of 5-HT1A receptor desensitization as a potential component of antidepressant treatment.

Adult↗