Lack of pharmacokinetic interaction of carbamazepine with tranylcypromine.
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Biomedical subjects
Publications and source records attributed to R T Joffe.
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The relationship between CSF somatostatin and peripheral thyroid hormones was assessed in 11 affectively ill patients before and during carbamazepine treatment. A direct relationship between CSF somatostatin and plasma thyroxine and free thyroxine, but not triiodothyronine, was observed both while patients were medication-free and during carbamazepine treatment. These first data in man are consistent with those in animals, suggesting a close interrelationship between somatostatin and thyroid regulation.
The hematological effects of carbamazepine, a drug effective in the acute and prophylactic treatment of manic-depressive disorder, were assessed in 43 subjects with affective disorder. Carbamazepine was found to cause statistically significant, but clinically insubstantial, decreases in white blood cell indexes. The consistent decreases in white cell counts observed with carbamazepine should be differentiated from the extremely rare, idiosyncratic blood dyscrasias reported in the literature.
A case report presented which highlights the association between depression and carcinoma of the pancreas. Clinical and biological aspects of this association are reviewed and discussed.
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Thyroid function was examined in 50 affectively ill patients before and four weeks after carbamazepine treatment. Carbamazepine significantly and substantially decreased peripheral thyroid hormone levels while increases in thyrotropin levels, although significant, were of much smaller magnitude. Furthermore, the decreases in levels of thyroxine (T4) and free T4 were significantly greater in carbamazepine responders than in nonresponders. These findings are discussed in light of current theories of the role of the thyroid axis in affective illness.
Treatment with carbamazepine is associated with decreases in the serum levels of thyroxine, free thyroxine and triiodothyronine without alteration in the thyrotropin. Therefore, the mechanism of action of carbamazepine on the hypothalamo-pituitary thyroid axis may involve interference in the feedback regulation of secretion of thyroid hormone by interacting with the pituitary thyroid hormone receptors. The present authors investigated the ability of carbamazepine to compete with the nuclear uptake of [125I]triiodothyronine in dispersed intact cultured fibroblasts of human skin. Carbamazepine did not inhibit the specific binding of [125I]triiodothyronine into the nuclei of intact fibroblasts, suggesting that it does not interact with thyroid hormone receptors in this system and is unlikely to do so in vivo.
A thyrotropin (thyroid-stimulating hormone; TSH) stimulation test with thyroid-releasing hormone (TRH) was performed on six patients with a DSM-III diagnosis of major depressive disorder, both before and during a trial of carbamazepine. Carbamazepine, an anticonvulsant effective in the treatment of affective illness, caused a reduction in the TSH response to TRH. This finding suggests that carbamazepine may decrease thyroid function primarily at the level of the pituitary in affectively ill patients.
The responses of 16 patients with major depressive disorder to one night's sleep deprivation and a subsequent double-blind, placebo-controlled trial of carbamazepine were compared. There was a significant association between the presence or absence of an antidepressant response to each of these treatments. Further studies are required to assess the clinical utility of this relationship and whether it is based on antidepressant response to any agent or is more specific to carbamazepine.
Sleep deprivation is reported to have therapeutic effectiveness in depressive illness. Furthermore, the response to sleep deprivation has important research implications. Recent conceptual advances, resulting in increased understanding of the role of abnormal biological rhythms and neurotransmitter function of the pathophysiology of affective disorder, highlight the future role of sleep deprivation in the research and treatment of these disorders.
The definition and clinical aspects of rapid cycling affective illness are reviewed and various factors associated with the onset and maintenance of rapid cycling enumerated. On the basis of this information and of reports of the response of rapid cycling patients to various treatment interventions, an approach is suggested to the evaluation and treatment of rapid cycling affective illness.
It has been generally accepted that increased thyroid function facilitates treatment response in depression. Recent data show that response to several antidepressant treatments, particularly lithium and carbamazepine, are associated with decreased thyroid hormone levels. An alternative hypothesis that decreased thyroid indices are related to antidepressant response is proposed and clinical and research implications are discussed.
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The relationship between personality and suicidal behavior was evaluated in 53 patients with primary major depressive disorder. Mean borderline personality scale scores on the Millon Clinical Multiaxial Inventory (MCMI) differed between suicide attempters and non-attempters. The frequency of personality disorder diagnoses, especially borderline personality disorder, was not higher in the suicide attempters. Clinical and theoretical implications of these findings are discussed.
During the acute depressive episode, seasonal affective disorder (SAD) patients (N = 24) differ significantly from non-SAD major depressives (N = 17) on five of 13 personality variables measured, although severity of depression appears to be similar. SAD patients score significantly lower on the self-criticism and dependency dimensions of the Depressive Experiences Questionnaire (DEQ) and significantly higher on three personality trait scales (including schizotypal, narcissistic, and avoidant) of the Millon Clinical Multiaxial Inventory (MCMI). Our data suggest that those with seasonal depression may represent a psychologically distinct subgroup of depressives.
There is a high prevalence of affective illness, both depression and bipolar disorder, in patients with multiple sclerosis. In this study, the family history method was used to assess the prevalence of affective illness in first-degree relatives of patients with multiple sclerosis. There was not an excess of affective illness in the relatives suggesting that affective disorder associated with multiple sclerosis does not have a familial pattern similar to primary affective disorder. Clinical and theoretical implications of these findings are discussed.