Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of 24 Dutch World War II Resistance veterans with a documented traumatic war history and a (partially) positive diagnosis of current posttraumatic stress disorder (PTSD) was studied. This special group of war victims is characterised by chronicity, suffering from intractable posttraumatic complaints for decades. They were treated with fluvoxamine (Fevarin), a selective serotonin reuptake inhibitor with antidepressive and anxiolytic properties. The study was designed as an open-ended, outpatient pilot study, with a treatment period of 12 weeks. Results of clinical examination, and questionnaires investigating PTSD, depression, sleeping problems, anxiety, and vital exhaustion indicate that a significant number of the subjects improved with respect to their PTSD symptomatology, and their symptoms of anxiety and vital exhaustion. However, at the end of the study, quantitative improvement was modest. The results indicate that treatment with fluvoxamine may offer alleviation of chronic PTSD symptoms, in particular insomnia, nightmares, anxiety, intrusive recollections, guilt feelings and tiredness.
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PMID:Fluvoxamine treatment for chronic PTSD: a pilot study. 141 Jan 91

The results of a small pilot study using Fluvoxamine (Faverin) in the treatment of non-vomiting bingeing female patients and women with bulimia nervosa is presented. Ten non-vomiting subjects and six with bulimia nervosa were treated on an open basis with Fluvoxamine 100-200 mg daily. Assessment was made using established questionnaires for severity of eating disorder and abnormality of mood. Five non-vomiting patients and three with bulimia nervosa completed the study. Non-vomiters showed a significant weight loss; a significant reduction in number of binges; a significant reduction in the scores on the BITE and the EAT; and a significant reduction in anxiety. Those with bulimia nervosa had a significant reduction in hunger and a reduction in depression which tended towards significance. Firm conclusions cannot be drawn from this study as it is an open pilot study of a small number of women. However, the results indicate that Fluvoxamine may have a role in the treatment of eating disorders where bingeing is a prominent symptom and that further research would be valuable. Comments are also made on the usefulness of various questionnaires designed to assess eating disorders.
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PMID:Fluvoxamine: an open pilot study in moderately obese female patients suffering from atypical eating disorders and episodes of bingeing. 838 40

Fluoxetine (Prozac) and fluvoxamine (Fevarin) are nontricyclic serotonin (5-hydroxytryptamine) reuptake inhibitors prescribed for the treatment of depression. Since these drugs block serotonin reuptake in platelets also, they might under certain conditions lead to clinically significant platelet dysfunction. Four patients are described who developed bleeding during treatment with either fluoxetine or fluvoxamine.
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PMID:[Risk of hemorrhage with the use of fluoxetine (Prozac) or fluvoxamine (Fevarin)]. 845 68

This 7- to 8-week, multicenter, randomized, double-blind, placebo-controlled study was performed to determine the dose-effect relationship and minimum effective dose for fluvoxamine maleate in a titrated fixed-dose study of major depressive disorder. Gradual titration over 2 weeks to fixed maintenance doses was employed to minimize dropout due to initial side effects. The study enrolled 600 outpatients, male and female, age 18-65, meeting DSM-III-R criteria for major depressive disorder. A 13-item subscore of the standard 21-Item Hamilton Depression Scale was used to minimize the possible contribution of known side effects from serotonin reuptake inhibitors to the overall HAM-D score. Secondary efficacy assessments included the HAM-D retardation factor, HAM-D depressed mood item, CGI-severity of illness item, and SCL depression factor. Fluvoxamine (50-150 mg/day) was therapeutically effective and well tolerated during 6 weeks of therapy. Based on the HAM-D depressed mood item, efficacy was dose dependent. The minimum effective dose was 50 mg/day. Fluvoxamine maleate shows dose-related effectiveness in the acute treatment of major depressive disorder.
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PMID:The oral dose-effect relationship for fluvoxamine: a fixed-dose comparison against placebo in depressed outpatients. 889 32

Obsessive compulsive disorder (OCD) is characterized by recurrent and intrusive thoughts that are distressing (obsessions) and/or repetitive behaviors or mental acts that the person feels driven to perform (compulsions). OCD has a partly genetic basis. For treatment of OCD, potent serotonin reuptake inhibitor (SRI) drugs (clomipramine (Anafranil), fluvoxamine (Luvox), fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil)), which act on the serotonin transporter protein, are uniquely efficacious. A polymorphism in the promoter region of the gene (SLC6A4) encoding this protein, was recently reported to affect protein expression and to be associated with measures of anxiety and depression and with autism (using a family-controlled transmission disequilibrium test (TDT) design). SLC6A4 therefore has strong a priori support for potentially influencing risk for OCD: the protein it encodes is a medication target; a polymorphism in the gene affects function; and that polymorphism has been shown to be associated with behavioral phenotypes. We used the TDT with a set of 34 European-American family trios, 30 unrelated and four drawn from an extended pedigree, to test for linkage disequilibrium between OCD and alleles at the SLC6A4 promoter polymorphic locus. Of 35 heterozygous parents, 24 transmitted the 'l' SLC6A4 allele and 11 transmitted the 's' allele (chi 2 TDT = 4.83; P < 0.03). Considering only the 13 SRI drug nonresponders, there were 13 heterozygous parents, of whom 10 transmitted the 'l' allele and three the 's' allele (chi 2 TDT = 3.77; P < 0.052). These data provide preliminary support for association and linkage disequilibrium between the SLC6A4 'l' allele and OCD.
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PMID:Evidence for linkage disequilibrium between serotonin transporter protein gene (SLC6A4) and obsessive compulsive disorder. 967 4

The main interest of the present study was to determine possible alternations in beta-endorphin serum levels in healthy volunteers and in patients with depression, as well as changes in beta-endorphin serum levels caused by fluvoxamine treatment. Fluvoxamine maleate (Fevarin) was administered orally at a dose of 200 mg/day for 4 weeks. The serum levels of beta-endorphin were lower in patients with 'nonendogenous' depression (104.68 +/- 5.29 pg/ml) and those with 'endogenous' depression (36.34 +/- 2.23 pg/ml) than in healthy volunteers (125.19 +/- 1.64 pg/ml). The endogenously depressed patients had significantly lower beta-endorphin levels than the nonendogenous patients. A 4-week treatment of fluvoxamine (200 mg/day) caused a statistically significant increase in beta-endorphin serum levels in all patients (nonendogenous depression 132.10 +/- 2.38 pg/ml and endogenous depression 50.09 +/- 2.45 pg/ml) in comparison to values found before the onset of the therapy. The efficacy of fluvoxamine was 11.0 (+/- 9.0) evaluated by the Hamilton Rating Scale for Depression (HAMD) in the patients with a diagnosis of depression. These results indicate that determination of beta-endorphin serum levels could be a valuable laboratory test in the diagnosis of depression.
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PMID:Serum beta-endorphin level in patients with depression on fluvoxamine. 1037 Oct 24

30 patients of 23-73 years old with endogenic and reactive depressions were treated with fevarin. The clinical state of the patients was estimated by means of Hamilton Depression Rating Scale (Ham-D). Fevarin was administrated in daily dose of 100-300 mg; the course of the treatment was equal to 4-8 weeks. The anxiolytic and antidepressive effects of fevarin were developed from the 5-7 days of the therapy: an anxiety disappeared completely by the end of the 3-d week. The most pronounced antidepressive effect was found for the classic depression with melancholy. A mild simulative effect and a normalization of a sleep were also observed. An improvement of the mental state was found in the all the patients by the end of the treatment: in 60% it was significant (a complete remission); in 40%--a considerable improvement was observed with the reduction of all clinical components of the depressive state. Fluvoxamine was found to be the high effective preparation for both endogenic and reactive depressions.
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PMID:[Fluvoxamine (fevarin) in the treatment of depression]. 1119 42

Since depressive symptoms (SDS) are prevalent under-recognized and clinically important problems in patients with schizophrenia, the pattern of symptoms and associated features of depressive symptoms, as well, as inclusion of psychopathology and neurodynemic variations in personality structure of patients with chronic schizophrenia deserve more investigation. The aim of the research was to identify clinical and experimental-psychological features of post-schizophrenic depression. The longitudinal study has been designed to investigate patients with paranoid schizophrenia. As a result of the careful clinical and psychological analyses due to psychopathology we defined four types of depression. From which two types of depression--agitated and asthenic prevailed in active phase of schizophrenia and remained two hypochondriac and apathyc mainly occurred during stabilization. This finding would have prognostic value. The authors examined personality changes leaded by cognitive symptoms and specified psychopathological and neurodynamical input in alteration of personality structure with word association experiment by A.D. Zurabashvili. As the semantics of trigger words became more complex the qualitative impairment deepened. Lower pathological associations have overcome scanty logical thinking and fluctuation of latency time since thought blocking became prominent. SSRI (Fevarin, Rexetin) appeared especially effective in treatment of certain type of post-schizophrenic depression.
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PMID:[Clinical and experimental-psychological data of post-schizophrenic depression VG]. 1798 57

Frequently used in a pejorative sense, "disease mongering" connotes a widening of the diagnostic boundaries of illness. Pharmaceutical companies conduct disease awareness campaigns on the pretext of educating the public about the prevention of illness or the promotion of health. Encouraged by disease awareness advertisements, people gradually become filled with concern that they are ill and need medical treatment. As a result, pharmacotherapy is increasingly being applied to ever-milder conditions, leading to potentially unnecessary medication, wasted resources, and even adverse side effects. Among all fields of clinical medicine, psychiatry is undoubtedly the most vulnerable to the danger of disease mongering. In Japan, depression provides the most drastic example of the impact of disease awareness campaigns on the number of patients seeking treatment. Until the late 1990s, Japanese psychiatrists focused almost exclusively on psychosis and endogenous depression, the latter being severe enough to require conventional forms of antidepressants, known as tricyclic antidepressants, and even hospitalization. At this time, people's attitude toward depression was generally unfavorable. Indeed, the Japanese word for clinical depression, utubyo, has a negative connotation, implying severe mental illness. This situation, however, changed immediately after fluvoxiamine (Luvox-Fujisawa, Depromel-Meiji Seika), the first selective serotonin re-uptake inhibitor (SSRI) to receive approval in Japan, was introduced in 1999. In order to aid the drug's acceptance by the Japanese public, pharmaceutical companies began using the catchphrase kokoro no kaze, which literally means "a cold of the soul". Thus armed with this phrase, the pharmaceutical industry embarked on a campaign to lessen the stigma surrounding depression. According to national data from the Ministry of Health and Welfare, the number of patients with a diagnosis of mood disorder increased from 327,000 in 1999 to 591,600 in 2003. At the same time, antidepressant sales have sextupled, from\14.5 billion in 1998 to\87 billion in 2006, according to statistics from GlaxoSmithKline. Recently, the pharmaceutical industry has shifted its focus from depression to bipolar disorder. Historically, Japanese psychiatrists have been familiar with Emil Kraepelin's "manic depressive insanity" (1899), whose definition was much narrower than that of its contemporary counterpart, bipolar disorder. Thus far, perhaps due partly to the reference in Kraepelin's definition of "manic depressive" disorder, Japanese psychiatrists have rather conservatively prescribed mood stabilizers for persons with frequent mood swings. Japanese psychiatrists can learn a great deal from their experience with the aggressive marketing of antidepressants. In the case of depression, over-medication arguably did more harm than good. The same risk exists with bipolar disorder. Disease mongering may occur whenever the interests of a pharmaceutical company exceed the expected benefits from the proposed pharmacotherapy on those affected by the putative bipolar disorder. In cases that are not severe enough for aggressive medication, psychiatrists should propose natural alternatives, such as an alteration of lifestyle and psychotherapy.
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PMID:[Disease mongering and bipolar disorder in Japan]. 2235 6

This review aims to shed light on the relationship that involves exposure to early life stress, depression and Parkinson's disease (PD). A systematic literature search was conducted in Pubmed, MEDLINE, EBSCOHost and Google Scholar and relevant data were submitted to a meta-analysis . Early life stress may contribute to the development of depression and patients with depression are at risk of developing PD later in life. Depression is a common non-motor symptom preceding motor symptoms in PD. Stimulation of regions contiguous to the substantia nigra as well as dopamine (DA) agonists have been shown to be able to attenuate depression. Therefore, since PD causes depletion of dopaminergic neurons in the substantia nigra, depression, rather than being just a simple mood disorder, may be part of the pathophysiological process that leads to PD. It is plausible that the mesocortical and mesolimbic dopaminergic pathways that mediate mood, emotion, and/or cognitive function may also play a key role in depression associated with PD. Here, we propose that a medication designed to address a deficiency in serotonin is more likely to influence motor symptoms of PD associated with depression. This review highlights the effects of an antidepressant, Fluvoxamine maleate, in an animal model that combines depressive-like symptoms and Parkinsonism.
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PMID:Early Life Stress, Depression And Parkinson's Disease: A New Approach. 2955 Oct 90


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