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Biomedical subjects

Z Kronfol

Publications and source records attributed to Z Kronfol.

18 recordsLinked to original sources
PubMed1991

Effects of single and repeated electroconvulsive therapy sessions on plasma ACTH, prolactin, growth hormone and cortisol concentrations.

To study the effects of electroconvulsive therapy (ECT) on hormone release, we measured circulating concentrations of adrenocorticotropic hormone (ACTH), prolactin (PRL), growth hormone (GH) and cortisol (CORT) immediately before and at 2 min, 5 min, 15 min, and 30 min following ECT. Compared to pre-ECT concentrations, there were significant increases in post-ECT plasma ACTH, PRL and CORT. GH did not change consistently. No significant difference between unilateral and bilateral ECT was observed. Compared to the first ECT, repeated treatments were associated with a significant decrease in the magnitude of hormone surge. These hormonal changes induced by ECT may reflect changes at the neurotransmitter level.

Adrenocorticotropic Hormone↗
PubMed1989

Lymphocyte mitogenesis, immunoglobulin and complement levels in depressed patients and normal controls.

The central nervous system and the immune system are closely related. Psychiatric illness is often associated with a dysregulation of the immune response. In an attempt to expand on previously reported immune abnormalities in patients with depressive illness, we compared several immune measures in a group of hospitalized depressed patients and healthy normal controls. Depressed patients had significantly higher percentages of circulating neutrophils, significantly lower percentages of circulating lymphocytes and significantly lower in vitro lymphocyte responses to mitogenic stimulation than normal controls. Basal plasma cortisol and circulating levels of the complement components C3 and C4 were also higher in the depressed group. We also found a significant association between cortisol values and the traffic of leukocytes on the one hand, and complement levels and the lymphocyte mitogenic activities on the other. These findings expand previously reported evidence of immune abnormalities in depressive illness and provide a partial explanation for some of these findings.

Adult↗
PubMed1988

Fever and leukocytosis: physical manifestations of bipolar affective disorder?

1. Fever and leukocytosis are occasionally observed in patients with psychiatric disorders. A thorough medical evaluation does not always reveal the origin of these abnormalities. 2. We report the case histories of three patients with bipolar affective disorder and an abnormal DST who had fever and leukocytosis during the acute phase of their illness. No organic etiology could be found. 3. All three patients responded to ECT with resolution of the depression, the fever, and the leukocytosis, and normalization of the DST. 4. We propose that fever and leukocytosis may be rare physical manifestations of bipolar affective disorder, particularly in patients with abnormal DST.

Adult↗
PubMed1986

Pharmacologic approaches to psychogenic polydipsia: case reports.

Psychiatric patients presenting with chronic psychogenic polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacologic intervention was attempted in three patients and was successful in one. One patient had a significant and sustained reduction of water intake while on 160 mg of propranolol. One patient did not improve with either propranolol or captopril while a third patient showed no improvement of serum sodium with demeclocycline nor reduction of water intake with propranolol. The potential mechanisms by which these pharmacologic agents might alter thirst in patients with primary polydipsia are discussed.

Adult↗
PubMed1986

Depression, urinary free cortisol excretion and lymphocyte function.

An impairment in lymphocyte response to mitogen stimulation, a correlate of cell-mediated immunity, has been reported in patients with depressive illness. To investigate whether such impairment in lymphocyte function is related to excessive secretion of cortisol, an immunosuppressive hormone, we compared mitogen-induced lymphocyte proliferation in three groups of subjects: depressed patients with elevated 24-hour urinary free cortisol (UFC) excretion; depressed patients with normal UFC excretion; and normal controls. Depressed patients in both groups showed significant reductions in lymphocyte mitogenic activity, in comparison with the normal controls, but the two depressive groups did not significantly differ from each other in their lymphocytic responses to any of the mitogens used. Furthermore, no significant correlations were found, within depressed patients, between UFC excretion and lymphocyte mitogenic responses. Depression is therefore associated with an impairment in lymphocyte function that cannot be explained solely on the basis of increased cortisol secretion.

Depressive Disorder↗
PubMed1986

Elevated blood neutrophil concentration in mania.

Total, differential, and absolute blood cell counts were compared in 66 untreated manics and 178 untreated schizophrenics. Mania was associated with significantly higher total leukocyte counts (p less than .001), accounted for by a significant increase (p less than .0001) in the number of neutrophils. There were no significant differences between the two groups in any other blood cell elements. Using normative values, manic patients had significantly higher frequencies of both leukocytosis (25.8% vs. 12.4%) and neutrophilia (34.8% vs. 12.4%) than the schizophrenic group. These data suggest a significant association between leukocytosis, neutrophilia, and mania.

Adult↗
PubMed1985

Depression, cortisol metabolism and lymphocytopenia.

Depression is often associated with hypercortisolemia. Because high levels of cortisol influence the distribution of different types of leukocytes in the blood stream, we examined the percentages and absolute numbers of circulating neutrophils and lymphocytes in 29 depressed patients who were nonsuppressors on the Dexamethasone Suppression Test (DST), 28 depressed patients who were suppressors on the DST, and 52 schizophrenic controls. We found no significant differences in either RBC or WBC counts in the 3 groups. There were, however, significant differences in the percentages of both neutrophils and lymphocytes as well as the absolute number of lymphocytes among the groups. These differences were mostly due to significantly lower lymphocyte percentages and absolute counts in the depression-nonsuppressor group. We also found a significant negative association between post-dexamethasone plasma cortisol concentrations and blood lymphocyte counts. These data suggest a close interaction between cortisol metabolism and lymphocyte regulation in major depression.

Depressive Disorder↗
PubMed1978

Depression and hemispheric functions: changes associated with unilateral ECT.

Nine depressed patients received ECT to the dominant (left) side along with nine matched depressed patients who received ECT to the non-dominant (right) side. Neuropsychological tests showed that the right hemispheric functions were more frequently abnormal as compared to left hemispheric (dominant) functions in the pre-ECT tests. ECTs delivered to either the right or left side improved right hemispheric functions when the depression was ameliorated. This study indicates that in depression right hemispheric functions are initially disturbed and ECT, instead of being deleterious to these functions, tends to improve them.

Depression↗
PubMed1977

Catatonia and systemic lupus erythematosus.

Catatonia has generally been assumed by many physicians to be a subtype of schizophrenia. Numerous cases have been reported in the literature associating catatonia with other psychiatric and also medical illnesses. The present report describes a patient with Systemic Lupus Erythematosus (SLE) who presented in a catatonic state. A brief differential diagnosis of catatonia is also included.

Adult↗
PubMed1976

Lithium-induced nephrogenic diabetes insipidus.

The etiology, diagnosis and management of lithium-induced diabetes insipidus (LIDI) is discussed, including the presentation of a case report. It is suggested that lithium provokes LIDI by decreasing the responsive ness of the kidney to the antidiuretic hormone. Lithium-induced polyuria may be managed by concomitant treatment with a thiazide diuretic or discontinuation of the lithium. Caution must be employed, however, when using thiazides with lithium as these diuretics decrease renal clearance of lithium.

Adult↗