Search PubMed⌕ Search

Biomedical subjects

P Linkowski

Publications and source records attributed to P Linkowski.

At least 109 records · Page 6Linked to original sources
PubMed1982

Simultaneous study of 24-hour patterns of melatonin and cortisol secretion in depressed patients.

The temporal organization of melatonin and cortisol secretion were studied in depressed patients in order to investigate a possible relationship between the secretory patterns of the two hormones. Women who suffered from a primary affective disorder were studied twice as inpatients, the first time during the depressive episode and the second time after amitriptyline treatment and clinical recovery. During both 24-hour studies blood was collected at 1-hour intervals during the day and at 30-min intervals at night. A dissociation of melatonin and cortisol secretory patterns was observed in the 3 patients in whom the two hormones were determined simultaneously. 2 patients exhibited alterations in the circadian rhythm of both hormones during illness. After recovery, however, the melatonin rhythm remained altered but the cortisol rhythm was normalized. Another patient showed a nocturnal melatonin rise and day-night melatonin differences closer to those seen in normal subjects, but she had altered cortisol secretory patterns during depression which normalized after recovery. These results suggest that the melatonin and cortisol rhythms are controlled by different mechanisms.

Adult↗
PubMed1981

[Seizures due to lithium intoxication (author's transl)].

Lithium intoxication may present as seizures, which have been observed when plasma lithium concentrations were decreasing. The neurotoxic effect of lithium could be due to a rise in intra-/extra-cellular lithium ratio. Intracellular retention of lithium reflected in rapid fall of plasma concentrations during treatment would modify cell membrane properties and increase neuronal excitability. Such a mechanism would explain the occurrence of seizures despite therapeutic plasma lithium concentrations.

Adult↗
PubMed1981

Thyrotrophin response to thyrotrophin-releasing hormone in unipolar and bipolar affective illness.

The plasma levels of thyrotrophin (TSH) and the response of this hormone to 200 microgram of thyrotrophin-releasing hormone (TRH) were studied in 27 unipolar and 24 bipolar depressive patients before and after amitriptyline treatment as well as in 42 normal controls. There was no significant difference in basal TSH levels between any of the groups studied according to diagnosis, menopausal status and antidepressant treatment. Before treatment, the TSH response to TRH was significantly lower in the unipolar and bipolar depressive patients than in normal controls. The TSH response to TRH did not differ significantly between the unipolar and bipolar depressives. When menopausal status was taken into account, the TSH response to TRH was significantly blunted in the unipolar postmenopausal patients when compared to postmenopausal controls. In the bipolar group, the premenopausal depressive patients had a significantly lower TSH response to TRH than premenopausal controls. After amitriptyline treatment, the TSH response to TRH, which was impaired before treatment in the bipolar premenopausal patients, improved significantly. However, no significant difference in the TSH response to TRH could be demonstrated after treatment in the unipolar postmenopausal patients in whom the TSH response was blunted before treatment. Our findings suggest that the differential TSH response to TRH in unipolar and bipolar patients may constitute biological markers of endocrine dysfunction in clinical subgroups of affective disorders.

Adult↗
PubMed1981

HLA antigens in affective disorders and schizophrenia.

The distribution of HLA antigen frequencies has been studied in patients with affective disorders. There were no significant differences between bipolar patients, unipolar patients, or controls. Preliminary data on HLA antigen distribution in schizophrenic patients are reported. Our negative results in affective disorders are discussed in relation to HLA studies reported from other laboratories, with special reference to some potential methodological problems.

Bipolar Disorder↗
PubMed1980

Relationship between schizoaffective illness and affective disorders or schizophrenia. Morbidity risk and genetic transmission.

Schizoaffective illness has either been linked to schizophrenia and to affective disorders, or it has been considered to be as separate entity. Family and linkage studies can provide data regarding genetic factors in the aetiology of schizoaffective illness. Morbidity risks for affective illnesses and schizophrenia were estimated in the first-degree relatives of schizoaffective probands as compared to matched controls (bipolars, unipolars and schizophrenics). Linkage studies with X-chromosome markers (protanopia and deuteranopia) were also performed in informative families. Our genetic results indicate that schizoaffective illness is a heterogeneous entity. This syndrome appears to be primarily related to the affective disorders, but there may be a subgroup linked to the schizophrenic spectrum disorders. Our studies also indicate that some schizoaffective syndromes may be transmitted through the X-chromosome, a pattern previously demonstrated in some families with bipolar manic-depressive illness.

Adolescent↗
PubMed1980

Prolactin secretion in women with unipolar and bipolar depression.

Plasma prolactin levels and prolactin response to thyrotropin releasing hormone (TRH) were studied in 27 unipolar and 24 bipolar depressive female patients before and after tricyclic antidepressant treatment, as well as in 38 normal controls matched for age, sex, and menopausal status. Before antidepressant treatment, basal prolactin levels were significantly lower in both premenopausal and postmenopausal bipolar patients but only in postmenopausal unipolar patients when compared to controls. The prolactin response to TRH was significantly blunted in both unipolar and bipolar postmenopausal subjects but remained normal in all premenopausal (unipolar and bipolar) patients. These data suggest that prolactin pituitary function could be useful in the neuroendocrine study of depressive illness.

Adult↗
PubMed1980

A double-blind comparison of dothiepin and amitriptyline in patients with primary affective disorder: serum levels and clinical response.

In a double-blind parallel group study, thirty-two patients suffering from a primary affective disorder received either dothiepin or amitriptyline. Serum concentrations of total dothiepin plus northiaden or amitriptyline and nortriptyline were estimated. A similar therapeutic response was seen with both drugs but there was no correlation with serum concentrations of amitriptyline or nortriptyline, whereas serum dothiepin correlated positively with clinical response.

Adult↗
PubMed1980

Growth hormone after TRH in women with depressive illness.

Plasma growth hormone (GH) release after TRH injection was investigated in 27 unipolar and 23 bipolar depressive women, and in 39 normal female controls matched for age, sex and menopausal status. Peaks of GH secretion after TRH were observed in some depressive patients as well as in some normal controls, but there were no significant differences in GH response after TRH administration between patients and controls. The implications of these findings are discussed in reference to such factors as non-specific stress responses and abnormal neuroendocrine circadian rhythms in affectively ill patients.

Adult↗
PubMed1980

Linkage between glucose-6-phosphate dehydrogenase deficiency and manic-depressive psychosis.

Hereditary has been shown to be an important factor in the aetiology of manic-depressive psychosis. Recent linkage studies with colour blindness have suggested the presence of an X-linked dominant gene in the transmission of manic-depressive psychosis. We report here positive evidence of a linkage between manic-depressive psychosis and glucose-6-phosphate dehydrogenase deficiency in an informative family assorting for both traits. These results strengthen previous linkage studies in affective illness and support the hypothesis of X-linkage in a subgroup of manic-depressive psychosis.

Adolescent↗
PubMed1979

Color blindness linkage to bipolar manic-depressive illness. New evidence.

Linkage between protanopia and deuteranopia and bipolar manic-depressive illness is demonstrated in a sample of eight informative families ascertained in Brussels. Genetic heterogeneity of bipolar affective disorders is also shown in the present study. These results add new evidence to the hypothesis of X-linked dominant genetic transmission of affective liability in a subgroup of patients with bipolar affective disorders.

Adult↗