False-positive human immunodeficiency virus type I ELISA results in low-risk subjects.
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Biomedical subjects
Publications and source records attributed to M H Rapaport.
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Twenty-one patients with schizophrenia who met criteria for neuroleptic treatment resistance or intolerance participated in a crossover, placebo-controlled, double-blind comparison of long-term typical neuroleptic and clozapine treatment. Clozapine significantly reduced total as well as positive and negative symptoms in comparison with both fluphenazine and placebo. Of the 21 patients, eight (38%) showed clozapine superiority on the basis of prospective response criteria. High levels of extrapyramidal side effects during fluphenazine treatment and later onset of illness were clinical predictors of clozapine superiority. Clozapine and fluphenazine equally reduced plasma homovanillic acid levels in comparison with placebo, although fluphenazine but not clozapine increased plasma prolactin level. A striking biologic difference between clozapine and fluphenazine was clozapine's enhancement of indexes of noradrenergic activity. Superior clozapine response was predicted by low ratios of cerebrospinal fluid homovanillic acid to 5-hydroxyindoleacetic acid, consistent with the notion that balance between dopaminergic and serotoninergic systems is important for clozapine's mechanism of action.
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Nine patients who met both DSM-III and RDC criteria for panic disorder and nine age-matched normal controls received infusions of physostigmine. The patients and normal controls did not differ in either their self-reported or the observer-reported ratings of anxiety, mood, or activation. The two subject groups also did not differ in blood pressure, pulse, or cortisol responses to physostigmine. Physostigmine did not provoke panic attacks in either the control or patients groups.
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Autoimmune mechanisms have been postulated to play a role in the pathogenesis of schizophrenia. Recently, increased numbers of B lymphocytes expressing the CD5 (Leu-1) surface antigen have been observed in patients with certain autoimmune diseases. In the present study, approximately 30% of schizophrenic patients (11/34) were found by cytofluorometric methods to have similarly increased levels of circulating CD5+ B cells compared with 6% (2/33) of healthy individuals and 5% (1/20) of patients with bipolar affective disorder. In schizophrenic patients with a "high" CD5+ B-cell phenotype, the percentage of B cells expressing the CD5 surface marker (mean +/- SEM, 52.4% +/- 3.5%) was comparable to that reported for patients with rheumatoid arthritis and significantly greater than that reported for patients with bipolar affective disorder (25.7% +/- 2.5%) and healthy controls (31.0% +/- 1.8%). Schizophrenic patients with high levels of CD5+ B cells had increased numbers of total B cells compared with control subjects and patients with low levels of CD5+ B cells. An elevation in CD5+ B cells may delineate a subgroup of schizophrenic patients whose disease has an underlying autoimmune and/or genetic cause.
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A number of neuroendocrine abnormalities have been reported in panic disorder patients: the most extensively studied being disturbances of hypothalamic-pituitary-adrenal function (Curtis et al. 1982; Leiberman et al. 1983; Uhde et al. 1988). The recent sequencing and synthesis of corticotropin-releasing hormone now allows direct testing of pituitary responsivity to this neuropeptide in affective and panic disorder patients (Holsboer et al. 1984; Gold et al. 1986; Roy-Byrne et al. 1986; Holsboer et al. 1987; Risch et al. 1988). We report the effects of intravenously administered ovine corticotropin-releasing hormone (0.03 micrograms/kg) on plasma concentrations of adrenocorticotropin hormone (ACTH) and cortisol in a small group of panic disorder patients and age- and sex-matched normal controls.
Patients with panic disorder (N = 11) and age- and sex-matched normal control subjects (N = 11) were challenged with human growth hormone-releasing factor (GH-RF) (1 microgram/kg i.v.) or placebo in random order. The control subjects had significantly increased plasma growth hormone (GH) levels after GH-RF infusion whereas panic disorder patients did not. At 15 and 30 minutes after GH-RF infusion, GH concentrations were significantly higher in the control subjects than in the patients. These findings with GH-RF extend findings from earlier reports that patients with panic disorder show blunted GH response to phobic stimulation and clonidine.
Abnormal smooth pursuit eye movement (SPEM) has been proposed as a trait marker in schizophrenia. We utilized high resolution infra-red oculography to measure SPEM in 11 neuroleptic-treated schizophrenic patients, 10 drug-free schizophrenic patients, and 11 normals. The most characteristic abnormality was a significant increase in saccadic intrusions during SPEM in schizophrenic patients (p less than .001). SPEM gain was reduced in schizophrenic patients (p less than .005). No significant effects of neuroleptic treatment on SPEM were found, including analysis of seven patients in whom paired data was available. We also measured SPEM prior to and after caffeine ingestion (10 mg/kg) in 10 normals. We found reduced saccadic interruptions as a result of caffeine ingestion compared with placebo (p less than .05). As caffeine has been shown to selectively increase dopaminergic neurotransmission in mesocortical neurons, further study utilizing dopamine agonists during SPEM in schizophrenic patients is warranted.
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