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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an attempt to quantitatively evaluate the destructive effects of free radicals on metabolism, freshly prepared and cryopreserved isolated rat hepatocytes were exposed to and incubated with Fe2+ compounds, reputedly inducing oxygen-derived free radicals (OFR) capable of attacking the lipid structures of cellular membranes. Malondialdehyde (MDA) formation was interpreted as an expression of free radical interaction with polyunsaturated lipids, and in vitro incubations were carried out during the period of constant MDA formation. Protein synthesizing activity was evaluated by incubating control hepatocytes and cells previously exposed to 100 microM of Fe2+, to 100 microM of Fe2+, and 100 microM of desferrioxamine and to 100 microM of desferrioxamine alone with 0.1 microCi of L-[U-14C]isoleucine and in the presence of these compounds. Membrane transport activity was similarly evaluated by following the cellular uptake of alpha-amino-[1-14C]isobutyric acid. Protein-synthesizing activity of freshly prepared and cryopreserved hepatocytes was not affected by Fe2+ treatment, nor by the additions of the iron chelator desferrioxamine. Amino acid transport, however, was inhibited by 100 microM of Fe2+, but was effectively neutralized by the simultaneous addition of 100 microM of desferrioxamine. Cryopreserved hepatocytes equally presented a significantly inhibited amino acid transport activity over the incubation period. The results suggest that the metabolic depression measured in thawed hepatocytes does not result to any large extent from iron-catalysed OFR effects. When OFR production was deliberately induced, the most significant early change was seen in transmembrane amino acid uptake in both fresh and cryopreserved cells.
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PMID:Cryopreservation of isolated rat hepatocytes: effects of iron-mediated oxidative stress of metabolic activity. 913 Mar 86

This study examined gender differences within and between five groups of subjects drawn from a large representative sample of the United States population and classified as having either major depression (MDD) only, alcohol use disorder (AUD) only, or primary, secondary, or concurrent depression to determine if these diagnostic profiles (1) were consistent with those drawn on clinical samples and (2) might suggest potential clinical implications. Respondents (N = 9,985) from a nationally representative survey of the United States population met DSM-IV criteria for classification into these five mutually exclusive groups that were compared within and between groups by gender on the characteristics of each disorder. The results were consistent with those of other studies: (1) gender distributions of AUD and depressive disorder remain almost mirror opposites, and (2) comorbid disorders are more severe than either of the conditions appearing singly. Findings of particular interest were that the synergistic effects of an alcohol and a depressive condition operate equally for both men and women with concurrent depression. This points to the necessity of attending carefully to gender biases when dealing with comorbid conditions, last we fail to take alcoholism in the presence of depression seriously enough in women and vice versa in men. Additionally, women with primary depression are at high risk for suicide and thus may require special attention in the evaluative phase of treatment.
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PMID:Gender differences in DSM-IV alcohol use disorders and major depression as distributed in the general population: clinical implications. 920 77

Refractory or treatments resistant depression in child and adolescent populations is a difficult construct to operationalize currently. To date, only one of the small number of completed double-blind placebo-controlled treatment investigations have not demonstrated a significant effect of antidepressants in comparison to placebo. However, it has been established that child and adolescent MDD is a serious disorder that appears to have clinical continuity with adult affective disorders and is generally of long duration with high rates of recurrence and eventual progression to mania, substance abuse, or other serious psychopathology. In addition, families of children with affective disorders evidence substantial genetic loading with high rates of affective disorders contributing both genetic vulnerability and potential environmental risk as well. There have been no empirically identified treatments that alter the long-term course of the illness. Thus treatment resistance is a significant issue for this population. This review will focus on controlled treatment trials and will examine the potential relevance of psychosocial impairment, genetic-familial risk, and neuromorphometric brain differences to treatment resistance in children and adolescents with major depression.
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PMID:Refractory depression in children and adolescents. 933 13

The study was designed to test the efficacy of desipramine in adolescents with major depression (MDD). In addition, we assessed the presence of atypical features of MDD, consisting of mood reactivity and two of four associated features (rejection sensitivity, hyperphagia, hypersomnia, and leaden paralysis). Patients were randomized to desipramine (DMI) or placebo for 6 weeks, provided they failed to improve (e.g., meeting MDD criteria and a Hamilton Depression Scale score > or = 18) after 2 weeks on single blind placebo. Of 94 adolescents (ages 13-18) who were diagnosed as having MDD, 64 entered the study and 62 received placebo for 2 weeks. Of these, 45 were randomized to DMI or placebo. Completed analyses did not reveal significant improvement for the active treatment compared to the placebo. A large proportion of adolescents responded to placebo (50%), suggesting the need for very large samples to detect differential treatment efficacy, should it exist. A relatively high rate of atypical depression was observed (47% in the 64 patients entered). In view of the demonstrated specificity of monoamine oxidase inhibitor efficacy in adults with atypical features of MDD, this clinical subtype may have relevance to future investigation of therapeutic interventions in adolescent MDD.
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PMID:Adolescent depression: controlled desipramine treatment and atypical features. 959 29

The increased risk of physical health problems in adult depressed patients has been shown in numerous studies. A recent study of the offspring of depressed parents found similar associations. The purpose of this study is to examine the strength and specificity of the association between depression and physical health problems in children and adolescents whose parents are dependent upon opiates. The sample consisted of offspring ages 6-17 (mean age 11 years) of opiate addicts who had a history of major depressive disorder (MDD; n = 28); other mood disorders (n = 31); no history of mood disorders but other psychiatric disorders (n = 92); or no history of psychiatric disorder (n = 127). Detailed psychiatric assessment and medical history of the offspring by direct interview with the offspring and an informant were obtained blind to parental diagnosis. After controlling for possible confounders, there was an increased risk of dermatological disorders, headache, other neurological/neuromuscular disorders, bronchitis, other respiratory disorders and hospitalizations for nonsurgical procedures in offspring with MDD, as compared to nonpsychiatrically ill controls. The offspring with other mood disorders had a slightly elevated risk. Major depression in children and adolescents whose parents are dependent on opiates is associated with increased risk of physical health problems. This finding is consistent with other reports and the timing of the physical health problems requires further study.
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PMID:Physical health problems in depressed and nondepressed children and adolescents of parents with opiate dependence. 1020 60

Overlap between depression scale item content and medical symptoms may exaggerate depression estimates for patients with multiple sclerosis (MS). We reconsider Mohr and co-workers' (1997) recommendation to omit Beck Depression Inventory (BDI) items assessing work ability (item 15), fatigue (17), and health concerns (20) for MS patients. Subjects were medical patients with either MS (n = 105) or a medical disorder for which the BDI is empirically supported [diabetes mellitus (DM), n = 71; chronic pain (CP), n = 80], psychiatric patients with depressive disorder (MDD; n = 37), and healthy controls (HC; n = 80). Relative scores for the eight "somatic" BDI items were analyzed by multivariate analysis of variance with demographic variables and BDI total as covariates. The only significant difference was MS > HC (item 15). On raw scores, MS patients exceeded HCs on items 15 and 21 (sexual disinterest), but this was attributable to the low HC item endorsement. There were no other differences on somatic items or item-total correlations. Scale consistency was good across groups, regardless of item omission. Somatic items were unassociated with major MS parameters. We thus encourage continued application of the full BDI for assessing depressive symptoms in patients with MS.
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PMID:Assessing depressive symptoms in multiple sclerosis: is it necessary to omit items from the original Beck Depression Inventory? 1037 39

Differential risk factors for the onset of depression were prospectively examined in a community-based sample of adolescents (N = 1,709), some of whom had a history of major depressive disorder (MDD; n = 286) and some of whom did not (n = 1,423). From the theories of J. Teasdale (1983, 1988) and R. Post (1992) concerning the etiology of initial versus recurrent episodes of depression, the authors hypothesized that (a) dysphoric mood and dysfunctional thinking styles would be correlated more highly among those with a previous history of MDD than among those without a history of MDD; (b) dysphoric mood or symptoms and dysfunctional thinking would be a stronger predictor of onset of recurrent episodes (n = 43) than of first onsets (n = 70); and (c) major life stress would be a stronger predictor of first onsets of MDD than of recurrent episodes. The results provide support for the 3 hypotheses and suggest that distinct processes are involved in the onset of first and recurrent episodes of MDD.
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PMID:First onset versus recurrence of depression: differential processes of psychosocial risk. 1046 72

Although an increased recognition of depressive disorders in youth represents a positive conceptual change over the past decades, there still is a very limited amount of research on useful treatment interventions. The paucity of data is particularly keen for the use of psychotropic drugs. For example, by applying the criteria suggested by the International Psychopharmacology Algorithm Project, there barely are enough first-grade ("Level A," meaning at least two RCTs) data supporting the short-term efficacy of antidepressants (the SSRIs) in the treatment of juvenile depression. And yet, limited data have not translated into limited use in routine clinical practice. In fact, the use of antidepressant medications has increased exponentially over the last decade, a change that is especially conspicuous for individuals less than 18 years of age. The perceived safety of the SSRIs and other novel antidepressants is partly at the root of their increased popularity. Data regarding their safety are likewise quite limited, however, and essentially are nonexistent for longer-term use. Based on the reviewed data, a medication algorithm for the treatment of early-onset depression can be suggested (Fig. 1). The algorithm underscores the need for adequate evaluation and diagnostic assessment, with particular attention to comorbid conditions (such as a bipolar diathesis) that may dictate alternative treatment strategies. In general, psychotherapy is the initial approach to juvenile MDD, with medication use reserved for more severe cases or those not responding to psychotherapy alone. Given that only two types of psychotherapy and two SSRIs have adequate controlled short-term efficacy data, all but the initial steps must be undertaken guided by clinical judgment and an individualized risk-benefit analysis. An algorithm such as this one, based on the very limited efficacy and safety data available, may be viewed as setting priorities for a comprehensive research agenda, more than dictating rigid treatment guidelines. In closing, it can be suggested that future research on the pharmacotherapy of early-onset depressive disorder pay particular attention to the following three aspects: 1. Too many drugs, too few data: Rapid advances in drug development have led to a plethora of available antidepressant agents. It is clear that there are many more agents available than can be adequately studied at present. Because many such agents are mechanistically similar, if not identical, it may be wise to focus research efforts on truly novel agents, particularly those (such as the CRH receptor antagonists, or those affecting neurosteroidogenesis) whose action is based on preclinical and clinical pathophysiologic disease paradigms. 2. Longitudinal follow-up and maintenance studies: Essentially all reviewed treatment studies have been short-term trials. There is a marked paucity of longer-term follow-up data, or of naturalistic and "real-world" effectiveness studies. For example, one of the few studies addressing maintenance pharmacotherapy for early-onset depression has demonstrated surprisingly high recurrence rates, even for those subjects actively on maintenance medication. 3. Long-term safety: Clinicians and parents alike often face difficult decisions regarding the long-term exposure of antidepressant drugs on the developing brain. Although no definitive long-term safety data are likely to become available anytime soon, real risks, such as suicide, and potential sequelae of long-term exposure to the underlying illness itself need all to be part of any decision-making process. Preclinical studies have shown that brain-derived neurotrophic factor (BDNF) levels can be upregulated by antidepressants, and low BDNF factors have been associated with atrophic brain changes in recurrent forms of adult MDD. Although these observations require specific application to juvenile forms of the disorder, they raise the exciting prospect that the natural course of the illne
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PMID:Pharmacotherapy of early-onset depression. Update and new directions. 1067 94

Recent studies have found high rates of familial aggregation of major depression (MDD) in relatives of depressed children coming for treatment, leading investigators to suggest that probands for genetic studies of MDD should be selected from samples of depressed children being brought for treatment. Implicit in this recommendation is the assumption that childhood and adult depression are similar disorders. This assumption in turn implies that children with prepubertal or adolescent onset depression are at high risk for having recurrent episodes of MDD that continue into adulthood. The data supporting this latter hypothesis, however, is limited and contradictory. In this article we report results from a high-risk longitudinal family study in which we explored the recurrence and continuity into adulthood of prepubertal or adolescent onset MDD in offspring who were at high or low risk for MDD, by virtue of their parental depression status. One hundred eighteen offspring from 55 families in which one or more parents had MDD and 50 offspring from 21 families in which neither parent had MDD were followed for more than 10 years (all offspring were 20 years or older at the end of follow-up time) and blindly reassessed using a semistructured diagnostic instrument. Offspring with childhood/adolescent onset MDD were at significantly greater risk for recurrence in adulthood (after age 25) as compared with offspring without an onset of childhood/adolescent MDD, if they had a history of parental MDD. In contrast, among offspring without a history of parental MDD, those with childhood/adolescent onset MDD were at no greater risk for continuing to have MDD in adulthood (after age 25) than those without childhood/adolescent onset MDD. Moreover, there was a trend for offspring with childhood/adolescent onset MDD to be at greater risk for recurrence after age 25 if they had a history of parental MDD, as compared with offspring without a history of parental MDD (60 vs. 18%). We conclude that childhood/adolescent onset MDD is a heterogeneous disorder, with family history of MDD appearing to define a subtype of childhood/adolescent onset MDD that is recurrent and continues into adulthood. Our findings suggest that caution should be exercised in selecting depressed children and adolescents brought for treatment as probands in genetic studies of early onset MDD. A conservative strategy would be to select only those depressed children and adolescents with a family history of MDD and reassess the treated sample as they mature, ensuring that they go on to have MDD in adulthood. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:93-101, 2000
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PMID:Selecting early onset MDD probands for genetic studies: results from a longitudinal high-risk study. 1068 60

Major depression (MDD) following traumatic brain injury (TBI) is a common phenomenon. There are no adequate studies in the literature defining optimum treatments for this condition following TBI. The opportunity arose to analyse a group of patients who were included in a larger study of an antidepressant (moclobemide). As the treatment, but not the delivery, was known, this has the status of an open study. Twenty-six patients with major depression of late onset (mean 4.67 years post-TBI) were identified (18 male, 8 female), with a mean age at injury 28.49 years. The group was moderately depressed with Hamilton Depression score (HAM-D) of 23.385 and moderately anxious with Hamilton Anxiety score (HAM-A) of 21.231. Mean HAM-D reduction was 81% and HAM-A reduction 81%. Of the 26 subjects 23 were defined as responders. Onset of action was rapid, with 17 responding by day 3. Irritability scores showed a mean reduction of 57% and pain scores a reduction of 39%. It is concluded that moclobemide may be an effective treatment for MDD following TBI, but properly controlled studies must be carried out to confirm this.
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PMID:Moclobemide in the treatment of major depressive disorder (DSM-3) following traumatic brain injury. 1090 91


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