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Biomedical subjects

D F Klein

Publications and source records attributed to D F Klein.

At least 253 records · Page 14Linked to original sources
PubMed1982

Metabolism of (-) deprenyl to amphetamine and methamphetamine may be responsible for deprenyl's therapeutic benefit: a biochemical assessment.

The urinary excretion of some important phenylethylamines, catecholamines, their metabolites, amphetamine, and methamphetamine were measured in parkinsonian patients on Sinemet (L-dopa plus carbidopa, a peripheral dopadecarboxylase inhibitor) and depressed patients after chronic (-) deprenyl treatment. Deprenyl was efficiently metabolized to amphetamine and methamphetamine. It increased the excretion of phenylethylamine and of m- and p-tyramine, and reduced the output of norepinephrine metabolites, but failed to alter the excretion of dopamine-deaminated metabolites. These changes were attributed more to amphetamine and methamphetamine than to inhibition of monoamine oxidase type B. Sinemet treatment alone increased the excretion of dopamine, 3-methoxytyramine, and their respective deaminated metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid. It is concluded that conversion of deprenyl to amphetamine and methamphetamine may contribute to some of the therapeutic benefits of deprenyl.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

An inverse correlation between serum levels of desmethylimipramine and melatonin-like immunoreactivity in DMI-responsive depressives.

The relationship between plasma levels of the tricyclic antidepressant desmethylimipramine (DMI) and plasma levels of melatonin-like immunoreactivity was studied in 32 endogenously depressed patients. An inverse correlation between plasma levels of DMI and plasma levels of melatonin-like immunoreactivity was found in the group of clinical responders to the chronic administration of the drug. The nonresponders had higher levels of melatonin-like immunoreactivity at comparable levels of DMI. This finding is consistent with the hypothesis that chronic high plasma levels of DMI may down-regulate the beta-adrenergic receptors in man. However, some other homeostatic mechanisms may be involved in the clinical response.

Adolescent↗
PubMed1981

Differential diagnosis and treatment of panic attacks and phobic states.

Recent advances in our understanding of and ability to treat panic disorders and various types of phobia have been reviewed. A case of agoraphobia was presented in detail to illustrate clinical issues and serve as a basis for discussing differential diagnosis. The presence or absence of spontaneous panic attacks has crucial implications for classifying phobic states. Data and speculations concerning the pathophysiology of agoraphobia, social phobia and simple phobia were also presented. Finally, a variety of pharmacological and behavioral treatment approaches, some solidly established, other still investigational, were discussed.

Adult↗
PubMed1980

Treatment of agoraphobia with group exposure in vivo and imipramine.

Seventy-six white agoraphobic women, 21 to 45 years old, were treated with combined group exposure in vivo and imipramine or placebo in a randomized double-blind study. A majority of the patients in both the placebo and imipramine groups showed moderate to marked improvement. However, imipramine therapy was significantly superior to placebo therapy on three of the four reported measures of improvement: primary phobia, spontaneous panic, and global improvement. There was a negative correlation between depression and outcome; ie, the more depressed patients fared worse on several outcome measures than those who were less depressed. A comparison of these patients with agoraphobic women previously treated with imipramine and imaginal desensitization showed a superiority of exposure in vivo midway in treatment, but no significant difference between the two groups at the completion of therapy.

Adult↗
PubMed1980

Efficacy of desipramine in endogenomorphically depressed patients.

This study was designed to test the hypothesis that there are 2 biochemical subgroups of 'endogenously' depressed patients--serotonin-deficient and noradrenalin-deficient groups--which respond differently to antidepressants depending on relative blockade of serotonin vs. norepinephrine (NE) reuptake. Patients with pervasive anhedonia and autonomy of depressed mood (endogenomorphic depressives) were treated first with the noradrenergic agent desipramine (DMI), then, if still depressed, such patients were randomized double-blind to continued DMI or clomipramine (CMI), a primarily serotonergic agent. Of 34 such endogenomorphically depressed patients 2 responded during a placebo period and 5 dropped out. Of 27 patients completing at least 4 weeks of DMI (mean maximum daily dose 283 mg, range 100-400 mg/d), 23 (85.2%) responded. With only 4 nonresponders, the second, or CMI, part of the study had to be abandoned. Since DMI strongly blocks neuronal reuptake of catecholamines with little effect on serotonin reuptake, these results suggest that endogenomorphic depressives may have a relatively homogeneous catecholamine deficiency. Alternatively, DMI may exert its effect by a mechanism other than blockade of EN reuptake. Eleven of the endogenomorphically depressed patients also met Research Diagnostic Criteria for situational depression (reactive). Ten of these 11 responded to DMI suggesting that presence or absence of a precipitant may be irrelevant in predicting response to tricyclic antidepressants in endogenomorphic depressions. Mean blood levels drawn at equivalent DMI dose were 238 ng/ml (range, 48-712) for responders, and 352 ng/ml (range, 160-877) for non-responders, indicating that patients appear to respond to DMI across a wide range of blood levels and suggesting the absence of a narrow therapeutic window.

Adjustment Disorders↗
PubMed1980

Can schizophrenia with premorbid asociality be genetically distinguished from the other forms of schizophrenia?

Sufficient data exist to establish a genetic basis for some forms of schizophrenia. However, genetic factors may not account for all the variance, and subtle forms of central nervous system (CNS) damage may have etiological significance for some schizophrenic subtypes. One such subtype may be chronic schizophrenia with premorbid asociality (SPA). To test this hypothesis, the risk of schizophrenia among relatives of probands who did or did not meet the criteria for SPA was examined. The incidence of schizophrenia in the relatives of SPA probands was lower than that in the relatives of non-SPA probands. This difference approached but did not reach statistical significance. Because most studies have found a higher familial genetic loading in chronic forms of schizophrenia, the apparently lower incidence of disorder in relatives of chronic schizophrenics with premorbid asociality seems to be a heuristic lead worth pursuing.

Antisocial Personality Disorder↗