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Biomedical subjects

B F Kjellman

Publications and source records attributed to B F Kjellman.

30 records · Page 2Linked to original sources
PubMed1986

Serum dopamine-beta-hydroxylase activity in patients with major depressive disorders.

The dopamine-beta-hydroxylase (DBH) activity in serum was assayed in 32 acutely ill inpatients with major disorder and in 33 healthy control subjects. Twenty-six of these patients were also studied in a state of remission. The DBH activity was compared to the serum levels (studied during a 24 h period) of T4, T3, TSH, prolactin and melatonin as well as to the outcome of the dexamethasone suppression and TRH test and to various clinical symptoms, as estimated by different rating procedures. No significant differences in DBH activity were found between the acutely ill patients, patients in remission, or normal subjects. Thus, the determination of the activity does not seem to be of practical importance as a laboratory diagnostic tool for major depressive disorder. A significant positive correlation was found between the DBH activity and the TSH levels, estimated by several parameters during the 24 h period, in the acutely ill patients, whereas no significant correlation was found in patients in remission or in the normal subjects. No significant correlation was found between the DBH activity in any group and the other laboratory or clinical parameters. The mechanism behind the significant correlation between the DBH activity and TSH levels remains to be clarified.

Adult↗
PubMed1986

Twenty-four-hour serum levels of T4 and T3 in relation to decreased TSH serum levels and decreased TSH response to TRH in affective disorders.

The serum levels of thyroxine and triiodothyronine (T4 and T3) were investigated at 10 different time points during a 24 h period in 31 inpatients meeting the RDC criteria for acute major depressive disorder. Twenty-three of these patients were also reinvestigated in a state of partial or complete remission. The results show that there was no significant difference in T4 or T3 levels during the 24 h period between depressed patients and 32 healthy controls despite significantly decreased TSH levels and TSH response to TRH administration (delta TSH) in the patient group. No indications were obtained that the patients' clinical presentation or depressive symptomatology as revealed by their CPRS scores, psychotropic medication, melatonin levels, or the outcome of the dexamethasone test, significantly influenced the T4 or T3 levels. The depressed patients who were studied longitudinally showed increased T4 levels in the acute phase compared to remission, whereas the T3 levels did not change. However, the levels of thyroid hormones were within the normal range in the acute phase as well as in remission. Furthermore, the changes in thyroid hormones between the state of relapse and remission were not significantly correlated to the corresponding increase in TSH levels and delta TSH between the two assessments. The present results are consistent with the hypothesis that the mechanism behind the impaired TSH response to TRH in acute major depressive disorder is a downregulation of the pituitary TRH receptors.

Adult↗
PubMed1985

Effect of TRH on TSH and prolactin levels in affective disorders.

The thyrotropin-releasing hormone (TRH) test was studied in 32 patients with acute major depressive disorder, 16 patients with recurrent unipolar (n = 8) or bipolar (n = 8) affective disorder in remission, and 22 healthy control subjects. Twenty-six of the 32 acutely ill patients were also studied when in remission. Outcome in these patients was correlated to serum levels of triiodothyronine (T3), 3,3',5'triiodothyronine (reverse T3), thyroxine (T4), thyroid-stimulating hormone (TSH), prolactin (PRL), melatonin, dexamethasone suppression test (DST) results, and clinical symptoms assessed by the Comprehensive Psychopathological Rating Scale (CPRS). The TSH response to TRH (delta TSH) was decreased in the acutely ill patients, but no difference was found between patients in remission and controls. The delta TSH was correlated to TSH but not to T3 and T4 levels in both acutely ill and control subjects. In the acutely ill group, delta TSH did not distinguish between patients with normal and abnormal DST results. Thus, abnormalities in the hypothalamic-pituitary-thyroid (HPT) axis are not correlated to abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis. Moreover, delta TSH did not differentiate between melancholic (DSM-III) and nonmelancholic patients or between patients with primary and secondary depression. No correlation was found between delta TSH and CPRS scores. Patients with observable agitation greater than 0.25 points (item range 0-3) had higher levels of delta TSH than patients with lower levels. No significant correlation was found between delta TSH and seven specific symptom clusters on the CPRS. However, there was a possible relation between low delta TSH and violent suicide attempts or suicide. PRL levels did not distinguish acutely ill patients from controls. Finally, there was no significant regression between delta TSH and melatonin levels. The decrease in delta TSH seen in the acutely ill patients was too small to be of diagnostic value as a laboratory measure differentiating acutely ill and healthy subjects. The mechanism underlying the HPT alterations in acute major depressive disorder may be a desensitization of the TRH receptor in the thyrotrophs secondary to an increased endogenous TRH stimulation.

Adult↗
PubMed1985

Melatonin, cortisol and ACTH in patients with major depressive disorder and healthy humans with special reference to the outcome of the dexamethasone suppression test.

The 24 hr profiles of melatonin and cortisol in serum, morning levels of ACTH in plasma, and the dexamethasone suppression test (DST) were investigated in 32 acutely ill patients with a RDC diagnosis of major depressive disorder, 24 patients with a history of longlasting unipolar or bipolar major depressive disorder studied in remission, and 33 healthy subjects. A significant decrease in maximum nocturnal melatonin level (MTmax) was found in the acutely ill depressed patients with abnormal DST compared to both those with normal DSTs and the healthy subjects. The MTmax levels were unaltered when these patients were reinvestigated in remission. A decrease of MTmax was also seen in the group of unipolar and bipolar patients studied in remission. Low nocturnal melatonin is proposed to be a trait marker for major depressive disorder and depressive states with abnormalities in the hypothalamic--pituitary--adrenal (HPA) axis. A significant decrease of ACTH levels at 0800 hr after dexamethasone administration the preceding evening was found in the healthy subjects, the unipolar--bipolar patients in remission, and the acutely ill depressed patients with normal DSTs, but was not found in the acutely ill depressed patients with abnormal DSTs. These findings support the hypothesis that pituitary ACTH regulation is altered in depressed patients with abnormal DST. Morning plasma ACTH before the administration of dexamethasone did not significantly differ between the acutely ill depressed patients with abnormal DSTs, normal DSTs, the patients with unipolar--bipolar disease in remission, or the healthy subjects. Thus, the abnormalities in the HPA axis in depresséd patients are proposed to be due to a hypersecretion of corticotrophin releasing factor (CRF) with a subsequent stimulus-induced pituitary desensitization. A significant decrease of melatonin after dexamethasone was seen at 0800 hr in the unipolar--bipolar patients in remission as well as in the healthy subjects, at 1600 hr and 2200 hr in the acutely ill depressed patients in remission, but not at 0800 hr in the acutely ill depressed patients in relapse. A significant regression was found between MTmax levels and the degree of non-suppression of cortisol at 0800 hr in the DST in the acutely ill depressed patients both in relapse and in remission. Melatonin thus is proposed to be an inhibiting factor for CRF during depression. A trend to a phase-advance of cortisol nadir and melatonin peak was seen in the acutely ill depressed patients with abnormal DST, possibly indicating an involvement of the suprachiasmatic nuclei in the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1985

Serum melatonin in relation to clinical variables in patients with major depressive disorder and a hypothesis of a low melatonin syndrome.

Maximum nocturnal serum melatonin level (MTmax) in relation to some clinical variables was studied in 32 patients with a major depressive episode and in 33 healthy subjects with reference to the outcome of the dexamethasone suppression test (DST). Significant regressions were found between MTmax levels and clinical rating scores in CPRS, interpreted as retardation symptoms. Four healthy subjects with disposition for dysthymic reactions had subnormal MTmax levels, which differed from MTmax levels in subjects without such disposition. Patients but not the healthy subjects, who reported parental loss before 17 years of age, had subnormal MTmax levels and differed from patients with no reported parental loss. Patients with no reported suicidal behaviour in clinical history had significantly lower MTmax levels than patients with reported suicide attempts. No relations were found between low MTmax levels and diagnoses, duration of illness, reported inheritance for depressive illness or sleep disturbances. A hypothetical low melatonin syndrome in depression is proposed: low nocturnal melatonin, abnormal dexamethasone suppression test, disturbed 24-h rhythm of cortisol, less pronounced daily and annual cyclic variation in depressive symptomatology.

Adult↗
PubMed1984

Melatonin in relation to body measures, sex, age, season and the use of drugs in patients with major affective disorders and healthy subjects.

Serum melatonin levels over a 24 hr period were studied in 30 acutely ill patients with major depressive episode, 24 patients with a history of unipolar or bipolar major affective disorder in remission and 33 healthy subjects. A significant negative correlation (-0.45) between body height and maximum nocturnal serum melatonin level was found. Maximum serum melatonin levels during the night were lower in both patient groups than in the healthy controls. No difference was found between maximum nocturnal serum melatonin levels in 26 patients investigated when ill and again in remission. We thus propose low nocturnal melatonin to be a trait-dependent marker for major depressive disorder. A difference in the morning but not night melatonin levels was found between samples taken during the dark, winter season versus samples taken during the bright, spring-summer season. Melatonin levels were not lower in females than in males, when melatonin levels were adjusted for body height. Similar results were found when the nocturnal areas under the curve for melatonin were analyzed.

Adult↗
PubMed1984

Twenty-four-hour serum levels of TSH in affective disorders.

As a part of a broad endocrine testing of patients with affective disorders the 24 h serum levels of thyrotropin (TSH) were investigated and correlated to the clinical history and disease symptoms. Thirty-two patients with the research diagnostic criteria of major depressive disorder were investigated. Twenty-six of these patients were reinvestigated in a state of full or partial clinical remission. Nine patients with unipolar and eight patients with bipolar affective disorders were also investigated in clinical remission. The control group comprised 32 healthy subjects. The results showed significantly lower 24 h serum levels of TSH and less variability of TSH levels during the 24 h period in the group with acute major depression compared with the controls. The 24 h serum levels of TSH normalized during clinical remission. Different subtypes of depression, different clusters of symptoms and severity of depression did not significantly correlate with the 24 h serum levels of TSH. There were also no significant correlations between abnormalities of the dexamethasone suppression test or nightly melatonin levels and the 24 h serum levels of TSH. The lower TSH levels seen in acute major depression could not be correlated to increased or decreased levels of peripheral thyroid hormones. The mechanism of the decreased 24 h serum levels of TSH is unclear. One possibility is an altered sensitivity in the thyrotrophs of the pituitary.

Acute Disease↗
PubMed1983

Reverse T3 levels in affective disorders.

Serum levels of 3,3',5' triidothyronine (reverse T3) were investigated in 32 patients with acute major depressive disorder. Twenty-six of these patients were also studied during a state of clinical improvement. Comparison subjects were 22 healthy controls, and 16 currently euthymic patients with histories of affective disorders (8 unipolar, 8 bipolar). The laboratory investigation included the determination of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), and thyroxin-binding globuline (TBG) levels in serum. The clinical symptoms were rated by the Comprehensive Psychopathological Rating Scale (CPRS) for depressive illness (CPRS global score), as well as the sum of 10 items (CPRS 10) and 22 items (CPRS 22) measuring depression. The patients were also divided into those having a normal or abnormal response to the dexamethasone suppression test; those having melancholia or not having melancholia; and those having primary or secondary depression. No significant difference in reverse T3 levels emerged among the patients with acute major depressive disorders, the euthymic unipolar or bipolar affective disorders, and the healthy controls. There were also no significant differences between those having an abnormal or normal DST test; those having primary or secondary depression; or those having melancholia or not having melancholia. In the group of patients with acute major depressive disorder, however, a significant increase in reverse T3 levels and a significant decrease in T3 levels, but no significant difference in T4 or TSH levels, were seen in the patients with the most pronounced clinical symptoms as measured by the CPRS. The implications of these findings are discussed.

Adult↗
PubMed1980

Cognitive and affective functions in patients with affective disorders treated with lithium. An assessment by questionnaire.

A questionnaire of 19 items was devised to assess subtle changes in affective and cognitive function in patient with effective disorders under long-term lithium therapy. Of 147 patients, 138 (93.9%) answered the questionnaire. The function of the hypothalamic-pituitary-thyroid axis was also analysed by biochemical investigations, and the interrelations between the function of this axis and affective and cognitive functions were studied. The patients under lithium maintenance therapy showed no clearcut changes in effective and cognitive functions. Some statistically significant correlations were found between rising thyrotropin levels and improved affective function. Patients who admitted periods of depression under lithium therapy showed highly significantly greater variance both in free thyroxine index and in thyrotropin levels than patients denying such periods. We may conclude that successful prophylactic lithium therapy against depression is linked to a stabilizing effect on the hypothalamic-pituitary-thyroid axis.

Age Factors↗