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Biomedical subjects

A Aberg-Wistedt

Publications and source records attributed to A Aberg-Wistedt.

At least 37 records · Page 2Linked to original sources
PubMed1994

CSF 5-HIAA predicts suicide risk after attempted suicide.

Suicide risk after attempted suicide, as predicted by cerebrospinal fluid (CSF) monoamine metabolite concentrations, was studied in a sample of 92 psychiatric mood disorder inpatients admitted shortly after attempting suicide. The potential of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the CSF to predict suicide risk within the first year after attempted suicide was studied by means of survival analysis after after median split subgrouping. Eleven patients (12%) committed suicide within 1 year after attempted suicide. Eight of these belonged to the below-the-median (< 87 nM) CSF 5-HIAA subgroup, that is, the suicide risk was 17% as compared with 7% among those with above-the-median CSF 5-HIAA. The cumulative number of survived patient-months during the first year after attempted suicide was significantly lower in the low CSF 5-HIAA subgroup. It was concluded that low CSF 5-HIAA predicts short-range suicide risk after attempted suicide in mood disorder psychiatric inpatients. These findings lend further support to the serotonin hypothesis of suicide risk.

Adult↗
PubMed1991

Stereoselective efflux of (E)-10-hydroxynortriptyline enantiomers from the cerebrospinal fluid of depressed patients.

In 5 patients treated with nortriptyline or amitriptyline for at least 9 months, the cerebrospinal fluid (CSF)/plasma ratio for 10-hydroxynortriptyline (10-OH-NT) ranged from 0.085 to 0.172, which is similar to the ratio previously measured in patients treated for 3 weeks. In 4 other patients treated with racemic (E)-10-OH-NT, the mean concentration ratio between (-)- and (+)-(E)-10-OH-NT was 3.56 in plasma, 2.39 in plasma ultrafiltrate and 1.42 in CSF (one-way ANOVA; P less than 0.001). The mean free fraction in plasma determined by ultrafiltration for (-)-(E)-10-OH-NT was 28.9 +/- S.D.1.1% and for the (+)-enantiomer 43.7 +/- 0.8% (P less than 0.001) confirming the difference in protein binding shown previously in healthy subjects. There was a correlation between the concentration of 10-OH-NT (sum of enantiomers) in CSF and plasma ultrafiltrate (r = 0.96; n = 7; P less than 0.001). The concentration in CSF was, however, only about 50% of that in the plasma ultrafiltrate and this seems to be due to a stereoselective transport of (E)-10-OH-NT out from the CSF. The secretion from the CSF is more pronounced for the (-)-compared to the (+)-enantiomer, which is consistent with the stereoselectivity of the renal secretion of these compounds.

Adult↗
PubMed1989

Aberrant seasonal variations of platelet serotonin uptake in endogenous depression.

The serotonin uptake in platelets of 120 healthy volunteers and 64 endogenously depressed patients was investigated over a 2-year period. In healthy individuals, Km exhibited a significant seasonal rhythm during the bright half of the year. The seasonal rhythm of Vmax assumes the form of a sine curve, with nadir values at the vernal and autumn equinoxes and peak values at the winter and summer solstices. Km in patients was higher than in controls in February and October, and the seasonal variation of Km differed between patients and controls. The monthly mean values of Vmax in patients were, as a rule, lower than corresponding values in controls, but significantly so only in December. Patients had higher Vmax than controls in October and November, and the seasonal variation of Vmax in patients differed from that of controls. The results suggest that Km, a measure of the affinity of the serotonin uptake site, may be subject to photoperiodic regulation in healthy individuals. The annual variation in uptake site densities, as judged by the changes in Vmax, are probably generated by an endogenous superior oscillator. The aberrant uptake kinetics found in the endogenously depressed patients may reflect seasonal susceptibility to the disorder and/or altered serotonergic rhythmicity.

Adolescent↗
PubMed1989

An educational program on depressive disorders for general practitioners on Gotland: background and evaluation.

General practitioners are the psychiatrists' most important coworkers in the treatment of depressive disorders. A high degree of knowledge about this illness in this group of doctors is of decisive importance. However, the value of postgraduate educational programs for general practitioners has been questioned. The Swedish Committee for the Prevention and Treatment of Depression (PTD) offered an educational program on symptoms, etiology, diagnosis, prevention and treatment of depression to all general practitioners on the Swedish island of Gotland. Lectures on suicide, depressive illness in childhood and in old age and psychotherapy of depressive states were also given. In several control periods data were collected on suicides, referrals to the local psychiatric department, emergency admissions, the quantity of sick leave used and the quantity of inpatient care due to depression. Even the prescription of psychopharmacological drugs on the island was investigated. Overall, the results indicated that general practitioners gratefully accepted the educational program and achieved increasing competence and stringency in treating and preventing depressive states. The program was associated with decreases in the use of psychiatric inpatient care and the sick leave frequency of depressed patients. The possibility of preventing suicides was positively influenced.

Curriculum↗
PubMed1989

Glucuronidation of amitriptyline in man in vivo.

The urinary excretion of amitriptyline (AT) as N-glucuronide was studied in healthy volunteers after single oral doses of AT and in patients on continuous treatment with AT. In the volunteers, 8 +/- 3% of a 25 mg dose of AT was recovered in urine as glucuronide during 108 hr. No difference between slow and rapid debrisoquine hydroxylators with respect to the excretion of AT glucuronide was seen. 0.08 to 1.68% of the given AT dose was recovered in urine in unchanged form. The excretion of unchanged AT correlated with the debrisoquine metabolic ratio (rs = 0.61; p less than 0.01). In 5 patients on continuous treatment with AT (125-150 mg/day), 8 +/- 5% of the daily dose was recovered in 24-hr urine as AT glucuronide. The present study shows that direct glucuronidation is a minor metabolic pathway of AT in man in vivo both after single low doses and during continuous treatment with therapeutic doses.

Administration, Oral↗
PubMed1989

The antidepressant effects of 5-HT uptake inhibitors.

The functional roles of monaminergic transmitters in depression have been widely studied during the past decade. Data from that research suggest that lower levels of the 5-HT metabolite, 5-HIAA, in the cerebrospinal fluid; 5-HT uptake in human platelets; and platelets [3H]-imipramine binding sites occur in depressed patients. In recent years several potent and selective 5-HT uptake inhibitors have become available for clinical studies. The first shown to have antidepressant effects, zimelidine, was followed by similar compounds such as femoxetine, fluvoxamine, citalopram, indalpine, fluoxetine, paroxetine, and sertraline. The effectiveness of serotonin inhibitors in treating other disorders, such as obsessive-compulsive disorder, anxiety, and panic disorder, has also been demonstrated. This review reports the data from clinical studies with these agents. The 5-HT uptake inhibitors are devoid of anticholinergic properties and have not produced weight gain or sedative side-effects, but may have another profile of side-effects. Headache, nausea, and vomiting have been reported, however.

Brain↗
PubMed1988

Lithium and renal function in relation to concomitant theory.

Two hundred and fourteen patients (99 men, 115 women, age 21-87 years) were treated with lithium during the period 1963-1984 at the Psychiatric Unit, Danderyd Hospital. The patients were diagnosed as having bipolar depression (97), unipolar depression (54), cycloid psychosis (21), schizoaffective psychosis and depressive neurosis (42). Sixty patients were treated with lithium salt only, 73 patients received neuroleptic drugs in addition to lithium and 51 antidepressant drugs. Sixteen patients were treated with a combination of neuroleptic drugs, antidepressant drugs and lithium. Fourteen patients were treated with lithium and benzodiazepines. The aim of this retrospective lithium study was to examine the renal function in these different treatment groups. The results show that patients treated with a lithium salt and neuroleptic drugs have significantly lower urinary osmolality than those treated with a lithium salt only. Also tricyclic antidepressants in combination with a lithium salt appear to have an influence on renal function. The duration of concomitant therapy seems to be of importance for the effect on renal function. Eleven patients with the lowest osmolality values were investigated at the Renal Unit, Danderyd Hospital, but in no case was it necessary to withdraw the lithium treatment.

Adult↗
PubMed1988

Alprazolam does not inhibit the metabolism of nortriptyline in depressed patients or inhibit the metabolism of desipramine in human liver microsomes.

In 10 patients treated with nortriptyline, the steady-state plasma concentrations of the parent drug and the active 10-hydroxy metabolite were very similar before and during concomitant treatment with alprazolam (0.5 mg orally t.i.d.). In human liver microsomes the 2-hydroxylation of desipramine was not inhibited by alprazolam. The absence of an inhibition by alprazolam on the hydroxylations of nortriptyline in vivo and of desipramine in vitro indicates that alprazolam is not metabolized by the debrisoquine hydroxylase.

Adult↗
PubMed1987

Effects of antidepressant treatments on platelet tritiated imipramine binding in major depressive disorder.

The effects of four antidepressant treatments on platelet tritiated imipramine binding have been studied in 51 hospitalized patients with severe major depressive disorder. There was an increase in maximum binding (Bmax) during the first week of treatment with antidepressants and electroconvulsive therapy, which was further magnified after three weeks' treatment with the serotonin uptake blockers alaproclate and zimeldine hydrochloride, but the Bmax values returned to baseline levels with nortriptyline hydrochloride and electroconvulsive therapy. The equilibrium dissociation affinity constant (Kd) did not change with any of the treatments. On reexamination one or two years after admission to the study, Bmax had not reached control values in clinically recovered, drug-free patients. Low pretreatment Bmax was associated with delusions during illness and with a poor long-term clinical outcome. There was no correlation between binding parameters and monoamine metabolite concentrations in the cerebrospinal fluid, either before or during treatment.

Adult↗
PubMed1987

Serotonin uptake inhibition during treatment of depression with nortriptyline caused by parent drug and not by 10-hydroxymetabolites.

Treatment of endogenous depression with nortriptyline (NT), at a daily dose of 150 mg, resulted in a pronounced improvement of seven of ten patients investigated. The concentration of the norepinephrine metabolite HMPG in cerebrospinal fluid (CSF) decreased by 29% (P less than 0.01) after 3 weeks of treatment. There was no significant effect of treatment on the serotonin and dopamine metabolites 5-HIAA and HVA. In previous larger materials, however, a decrease of 5-HIAA in CSF has been demonstrated. Platelets from the patients showed an increase in Km for serotonin uptake in response to NT treatment. The IC50 value of NT for serotonin uptake inhibition was 940 nM, while the corresponding value of the major metabolite of NT, i.e. E-10-OH-NT, was much higher (6700 nM). Thus, during treatment, the parent drug and not the metabolite was responsible for the serotonin uptake inhibition in platelets. There was a close correlation between Km and the plasma concentration of NT after 1 week of treatment (r = 0.88, P less than 0.01) but not after 3 weeks of treatment (r = 0.48; ns). There was no uniform effect of NT treatment on Vmax. It is concluded that clinical NT treatment results in uptake inhibition not only in norepinephrine but also in serotonin neurons.

Adult↗
PubMed1985

Lower 3H-imipramine binding in platelets from untreated depressed patients compared to healthy controls.

3H-Imipramine binding in platelets was measured in 63 severely depressed hospitalized patients, who had been drug free (with the exception of moderate doses of benzodiazepines) for at least 1 month, and in 53 healthy control subjects of comparable age and sex distribution. Bmax of 3H-imipramine binding was significantly lower in the depressed subjects (1012 +/- SD 295 vs. 1123 +/- SD 178 fmole/mg protein). Depressed patients who had attempted suicide by violent means tended to have higher Bmax than nonviolent attempters.

Adult↗
PubMed1985

Alaproclate a novel antidepressant? A biochemical and clinical comparison with zimeldine.

Clinical and biochemical effects of two selective 5-HT uptake inhibitors, zimeldine and alaproclate, were studied in 24 hospitalized patients with endogenous depression. According to a randomized parallel group design 14 patients were treated with zimeldine and 10 with alaproclate. The dosage of both zimeldine and alaproclate was 200 mg daily. For the evaluation of the clinical effect, Montgomery & Asberg Depression Rating Scale (MADRS) was used. Seven of 14 patients treated with zimeldine and seven of 10 treated with alaproclate improved. 5-HT uptake inhibition in patients' platelets and concentration of amine metabolites (5-HIAA, HVA, HMPG) in CSF were studied before and during treatment. After 3 weeks of treatment with zimeldine 5-HIAA and HMPG in CSF decreased significantly while HVA in CSF increased significantly. Zimeldine produced a significant 5-HT uptake inhibition in platelets. During treatment with alaproclate no significant change in amine metabolites concentration in CSF was found and there were no mean changes on 5-HT uptake inhibition in platelets.

Adult↗