SSRIs in the Treatment of Depression in Children and Adolescents

Results

The ten studies included in this review are summarised in Table I . Eight of the ten studies included descriptions and/or tables detailing patient demographics in treatment groups versus placebo groups. Characteristics of ethnicity, sex, age and comorbid conditions were similar in the two treatment groups in the 1998 unpublished paroxetine study on the GSK Website,[12] the 2002 Emslie et al. fluoxetine study,[19] the Keller et al. paroxetine study[20] and in all four treatment groups in the study by March et al. (TADS).[18] In the first fluoxetine study by Emslie et al., placebo and treatment groups were similar in demographic and clinical features, except that subjects in the fluoxetine group had a greater lifetime incidence of comorbid anxiety disorders.[21] In the 2001 unpublished paroxetine study by Emslie at al., there was a slightly higher percentage of patients with comorbid psychiatric diagnoses in the paroxetine group versus the placebo group.[22] In Wagner et al.'s study of sertraline, treatment groups were similar with respect to race, clinical characteristics and psychosocial stressors at baseline.[23] There was a significant difference in sex: 57% of subjects treated with sertraline were female versus 45% receiving placebo. In the study by Wagner et al. of citalopram, there were no significant differences between the placebo and citalopram groups with regard to age, sex, race, weight or history of depression.[24]

Several of the studies showed significant improvement in outcome measures in SSRI-treated groups versus controls. In the earliest study by Simeon et al., subjects in the group receiving fluoxetine showed slightly greater improvement in all depressive symptoms except sleep, but the differences were not significant.[25] In the earlier study by Emslie et al., 56% of subjects receiving fluoxetine demonstrated significant improvement versus 33% receiving placebo (p = 0.02) as evidenced by the CGI-I scale at study exit and the weekly secondary measure of the CDRS-R after 5 weeks (p = 0.03).[21] In the multisite study by Emslie et al., fluoxetine-treated subjects showed significantly greater improvement in the CDRS-R (35.1 ± 13.5) than placebo-treated subjects (40.2 ± 13.5) starting at week 1 and continuing for the remainder of the study (p < 0.001).[19] Using a CGI-I rating of 1 or 2 (much improved or very much improved), 53.3% of fluoxetine-treated subjects responded versus 36.8% of placebo-treated subjects (p = 0.028). In the TADS study, paediatric subjects receiving fluoxetine with cognitive behavioural therapy (CBT) improved significantly more compared with those taking placebo (p = 0.001) or fluoxetine alone (p = 0.02), based on CDRS-R scores.[18] Fluoxetine treatment alone was also significantly superior to placebo. Response rates for the groups, using a CGI-I of 1 or 2, were as follows: fluoxetine with CBT, 71.0% (95% CI 62, 80); fluoxetine alone, 60.6% (95% CI 51, 70); CBT alone, 43.2% (95% CI 34, 52); placebo, 34.8% (95% CI 26, 44).

In the 1998 unpublished paroxetine study there were no statistically significant differences between paroxetine and placebo in either the primary efficacy variables (50% reduction in MADRS score and change in K-SADS-L depression subscale) or the secondary efficacy variables (change from baseline in MADRS total score, CGI-S score, CGI-I score, Beck Depression Inventory [BDI], and the Mood and Feelings Questionnaire [MFQ]).[12] In the 2001 unpublished paroxetine study, no statistically significant difference was demonstrated in the primary outcome measure (change in CDRS-R total score) or in the secondary outcome measure (change in CGI-S, CGI-I global assessment of functioning).[22]

When compared with imipramine and placebo, paroxetine-treated subjects in the study by Keller et al. differed from placebo on several measures.[20] The first was their primary outcome measure, a HAM-D score of <8 or a >50% reduction from baseline by the end of treatment (p = 0.02). Differences also occurred on the HAM-D depressed mood item (p = 0.001), K-SADS-L depressed mood item (p = 0.05), and CGI-I score of 1 or 2, very much or much improved, respectively (p = 0.02). In this study, imipramine treatment did not differ from placebo in any of the outcome variables.

Sertraline-treated subjects showed significantly greater improvement than those receiving placebo, as evidenced by their mean change in CDRS-R (-22.84 vs -20.19; p = 0.007), the CGI-S (p = 0.009), and CGI-I (p = 0.005).[23] Differences were seen as early as week 1 on the CGI-I. In Wagner et al.'s citalopram study, the mean CDRS-R scores decreased significantly more from baseline in the citalopram group, as early as week 1.[24] Also, by the end of the study, significantly more citalopram-treated subjects (36%) met the response criterion of a CDRS-R score of ≤28, which was decided on prospectively, versus placebo-treated subjects (24%) [p < 0.05]. While these response rates appear low, the criterion used for response in this study was full remission, and other studies have reported similar rates of remission, notably both fluoxetine studies by Emslie et al.[19,21,27] A second, unpublished, citalopram study was accessed from the UK's Medicines and Healthcare products Regulatory Agency (MHRA) website.[26] No statistically significant difference was found on the K-SADS-Present Episode total score for drug (-12.4) versus placebo (-12.7) in 233 adolescents aged 13–18 years.[26]

The SSRIs were reported as being well tolerated compared with placebo, as illustrated in Table II . Study withdrawal rates due to adverse events ranged from 0% to 9.7% and were highest for paroxetine. Some serious adverse events (SAEs) occurred in patients taking SSRIs. SAEs are defined as those requiring hospitalisation or otherwise significant psychiatric symptoms such as suicidal ideation, aggressiveness or euphoria. The SAEs for both drug and placebo are shown in Table II . In the paroxetine study, SAEs occurred in 11 of 275 subjects taking paroxetine (4%). Five subjects reported emotional lability including suicidal ideation or gestures. One subject experienced headache during discontinuation taper, two subjects experienced worsening depression, two had conduct problems or hostility, and one had an expansive mood.[20] Of the 11 total subjects with SAEs, the investigator judged only the headache to be due to paroxetine. In the placebo group, one subject had emotional lability and another had worsening depression.

In the sertraline study performed by Wagner et al., of 376 subjects, two sertraline-treated and two placebo-treated subjects attempted suicide.[23] Three additional sertraline recipients reported suicidal ideation, and one additional sertraline recipient became aggressive. One subject in the sertraline group and four in the placebo group required medical hospitalisation. In the study by Wagner et al. on citalopram,[24] of 174 total subjects, two subjects receiving citalopram discontinued the study as a result of agitation. Another two subjects receiving placebo were removed from the study because of worsening of depression.

In the TADS study, 33 (7.5%) of 439 subjects experienced harm-related adverse events, which included any type of harm to self or others.[18] There was an increased risk of harm-related adverse events in subjects receiving fluoxetine versus those not receiving it. Twenty-four of the 33 harm-related adverse events were suicide-related, comprising 5.5% of the total 439 patients. A suicide-related adverse event was defined in the study as requiring that the patient exhibit either worsening suicidal ideation or make a suicide attempt, or both. The number of actual suicide attempts (seven) was too small for comparison of statistical significance between the different treatment groups. Four of the seven who made suicide attempts were receiving fluoxetine and CBT, two had received fluoxetine only, and one had received CBT only. No completed suicides occurred in the study, but results suggest a protective effect of CBT against suicidal ideation in those taking fluoxetine. This may be an important finding, but replication is needed.

Common physical adverse effects in the studies were dry mouth, vomiting, nausea, diarrhoea, somnolence, insomnia, dizziness, tremor and agitation. Somnolence was the only statistically significant physical adverse effect versus placebo in the paroxetine study.[7] Headache was the only unsolicited adverse effect that was reported significantly more often by patients on fluoxetine versus placebo in the Emslie et al. fluoxetine study published in 2002.[19] However, there was no significant difference between treatment groups in subjects reporting headaches on the completed Side Effects Checklist. In the Wagner et al. citalopram study, seven adverse effects as listed in Table II were found to occur with a frequency of >5% and with a higher incidence than observed in the placebo group: rhinitis, nausea, abdominal pain, influenza-like symptoms, fatigue, diarrhoea and back pain.[24] In the TADS study, the most common adverse effects listed in Table II occurred in at least 2% of patients, in at least one treatment group, and with an incidence of at least twice the rate in comparison with subjects receiving placebo.[18] The symptoms are listed from most to least common.

To date, most data from unpublished studies are not available on SSRIs used in children and adolescents with depression. The data from paroxetine studies completed in the UK were not available for inclusion in this study. The UK's MHRA has issued a warning against prescribing paroxetine to depressed patients aged <18 years based on data showing higher rates of suicide-related events and suicide attempts in the paroxetine-treated group versus placebo.[23] However, no completed suicides occurred in those studies. The MHRA ordered a labeling change, contraindicating the use of paroxetine for treatment of paediatric depression.[23] In addition, the UK Department of Health went on to prohibit the prescribing of all antidepressants other than fluoxetine to patients aged <18 years. In the US, all antidepressants have a black box warning for use in children and adolescents because of the risk of suicidality.

In 2004, the FDA collated data from 24 short-term trials involving over 4400 patients using nine antidepressant drugs.[28] Children in the studies met criteria for major depressive disorder, obsessive compulsive disorder, or other psychiatric disorders. Analysis of the data demonstrated a greater risk of adverse events including suicidal ideation or behaviours during the first few months of treatment in youths taking antidepressants. Seventy-eight of the 4400 patients experienced suicidal ideation or behaviours. This constituted a risk of 4%, or double that of placebo. There were no completed suicides in any of the studies. The FDA report did not provide data on the efficacy of SSRIs, although many unpublished studies allegedly did not demonstrate drug efficacy over placebo in children and adolescents. The FDA has followed this up with a black box warning on all antidepressant labeling regarding serious risks of suicidal ideation or attempts when these medications are used in children and adolescents. Advocacy agencies, including the American Academy of Child and Adolescent Psychiatry, have expressed serious concerns that family practitioners and paediatricians practising in rural areas where child psychiatrists are not available may no longer prescribe SSRIs even to seriously depressed and suicidal children and adolescents as a result of this warning.  Printer- Friendly Email This

Clin Drug Invest.  2006;26(5):247-255.  ©2006 Adis Data Information BV
This is a part of article SSRIs in the Treatment of Depression in Children and Adolescents Taken from "Cheap Prozac Fluoxetine" Information Blog

Potential Interactions of ADHD Medications With Dextromethorphan

Abstract and Introduction

Abstract

Objective: To examine the potential for drug-drug interactions to influence drug metabolism between the attention-deficit/hyperactivity disorder (ADHD) dl-methylphenidate and atomoxetine with dextromethorphan, a probe for interactions involving cytochrome P450 (CYP) 2D6 isoenzyme
Design: In vitro and ex vivo analysis of changes in metabolism of study drugs.
Setting: Laboratory.
Patients: Not applicable.
Interventions: Pooled human liver microsomal fractions prepared at CEDRA Corporation (now CellzDirect, Austin, Tex.) by the standard differential centrifugation method (lot 821-1). Human liver microsomes were pooled from 15 donors. Recombinant CYP 2D6-containing microsomes (Supersomes; lots 20 and 24 BD Gentest; Woburn, Mass.) were prepared from a baculovirus-infected insect cell line that expressed only the human CYP 2D6 isoform. Dextromethorphan, with and without effector, was incubated with pooled human liver and recombinant CYP 2D6-containing microsomes. Atomoxetine and dl-methylphenidate were tested at 0.1×, 1×, and 10×their reported therapeutic concentrations. Paroxetine, a known inhibitor of CYP 2D6, was used as a reference agent, and quinidine was used as a positive control inhibitor of CYP 2D6.
Main Outcome Measures: Changes in substrate metabolism indicative of CYP 2D6-mediated interactions.
Results: Atomoxetine and paroxetine inhibited the formation of dextrorphan by about 50% in human liver microsomes and by more than 80% in recombinant microsomes; the profiles of atomoxetine and the known 2D6 inhibitor paroxetine were similar. High concentrations of dextromethorphan reversed the inhibition of its metabolism, indicating a competitive mechanism of the interaction. Conversely, dextromethorphan and dextrorphan only modestly inhibited atomoxetine and paroxetine metabolism. dl-Methylphenidate did not inhibit dextrorphan formation in either microsome preparation, and dl-methylphenidate metabolism was unaffected by dextromethorphan or dextrorphan.
Conclusion: These results demonstrate the potential for in vivo interactions between dextromethorphan and atomoxetine in patients with ADHD. However, they do not support the plausibility of an in vivo interaction between dextromethorphan and dl-methylphenidate.Introduction

Attention-deficiency/hyperactivity disorder (ADHD) is a common chronic condition that typically requires long-term pharmacotherapy during childhood and often into adulthood. The estimated prevalence of ADHD is 8% to 10% of all children,[1] and 50% to 60% of patients require treatment as adults.[2]

The most common treatments for ADHD are stimulant medications,[3] including methylphenidate and amphetamines. The non-stimulant atomoxetine (Strattera—Lilly) has also been approved by the U.S. Food and Drug Administration for the treatment of ADHD.[4]

Patients with ADHD develop common acute or chronic somatic illnesses, such as upper respiratory infections, common colds, or asthma.[5] Moreover, ADHD often coexists with other mental health conditions, including learning and language disorders, oppositional defiant and conduct disorders, anxiety, depression, and bipolar disorder, as well as posttraumatic stress, tic disorders, and adjustment disorders.[6] These comorbid conditions may require pharmacotherapy, and patients with ADHD may receive multiple medications for comorbidities for brief or sustained periods, placing them at an risk for potential drug-drug interactions.[5]

The human cytochrome P450 2D6 (CYP 2D6) enzymatic pathway is responsible for the metabolism of approximately 30% to 40% of pharmaceutical agents[7,8]; therefore, drug-drug interactions may occur when medications metabolized by this pathway are given concomitantly.[5,9,10] The general population is polymorphic for the CYP 2D6 genetic loci. As a result, some people are extensive metabolizers while others are poor metabolizers.[11,12] Poor metabolizers, including an estimated 7% of whites and less than 1% of the Asian population, may thus experience increased levels of agents metabolized by CYP 2D6.[11,12]

Methylphenidate, the most common pharmacologic treatment for ADHD, is metabolized primarily by desterification.[13] It has a well-established efficacy and safety profile with a low potential for drug-drug interactions.[14-17] Atomoxetine is a selective norepinephrine reuptake inhibitor[4,18] approved for the treatment of ADHD. Limited data are available on the use of atomoxetine and the incidence of interactions between atomoxetine and other drugs.[19] Atomoxetine is primarily metabolized by the cytochrome P450 enzymatic pathway, specifically, the CYP 2D6 isozyme, which raises the possibility that it may be prone to interaction with other drugs metabolized by this pathway.[20]

This study was an in vitro analysis of potential drug interactions between (1) dl-methylphenidate, atomoxetine, and dextromethorphan (a common antitussive ingredient in cough medicine and a frequently used probe for measurement of P450 enzymatic activity)[21,22] and (2) dl-methylphenidate, atomoxetine, and dextrorphan (the primary and CYP 2D6-specific metabolite of dextromethorphan).[21,23]  Printer- Friendly Email This

J Am Pharm Assoc.  2006;46(4):472-478.  ©2006 American Pharmacists Association
This is a part of article Potential Interactions of ADHD Medications With Dextromethorphan Taken from "Cheap Prozac Fluoxetine" Information Blog

Accutane Shop

"Buy Accutane Isotretinoin">Buy Accutane Isotretinoin - 10 mg*30 pills $59.95 Trusted Online Shop, Online Audience, Free Physician Consultations, Full Seclusion, Fastest Nascence. Isotretinoin No Ethical drug at RxTrustedPills.com sildenafil Product sildenafil 50|100 mg - $1.27 Per Pill Best Online ED Medical specialty. Cheap Prices. Free Consultations. Fastest Birth. Buy Merchandise sildenafil viagra 100mg at SelectedViagra.com Buy tadalafil cialis Soft 20mg - 60 pills for $149.95 Online ED Pharmaceutics. Lowest Prices. Full Isolation. Worldwide Conveyance. Reduction cialis Soft Tablets at SelectedSoftCialis.com Buy viagra viagra Citrate Soft Tabs - 50mg x 60 pills $119.95 Best Online ED Pharmaceutics. Lowest Prices. New Wellness Products.
This is a part of article Accutane Shop Taken from "Buy Accutane Isotretinoin" Information Blog

Update of TIMA Guideline for Bipolar I Disorder

Guiding Principles of The Texas Implementation of Medication Algorithms (TIMA)

Algorithms were developed after examining the quality and quantity of efficacy data, expert opinion, consumer input, and safety and tolerability issues. Certain treatment options were placed lower in the algorithm due to concerns about safety and tolerability, despite strong efficacy evidence,

These algorithms were intended to provide systematic guidance on possible treatment options for BDI. Medication guidelines should be used to help the clinician and patient develop the most effective medication strategy with the fewest side effects, and are not meant to be rigid or choice-limiting. Although it is recommended that the algorithms be followed as linearly as possible, these guidelines are meant to provide flexibility at each stage of choosing treatments for each patient. The main goals of the algorithms are symptomatic remission, full return of psychosocial functioning, and prevention of relapse and recurrence.  Printer- Friendly Email This

Medscape Psychiatry & Mental Health.  2006;11(1) ©2006 Medscape
This is a part of article Update of TIMA Guideline for Bipolar I Disorder Taken from "Celexa Citalopram 10Mg" Information Blog

August 2, 2007: In the News.

Colorectal Planetary abode Contestant role Job Fiber bundle mercantile establishment Stay all Case Nurture CentersSign Up Daily email attention you to what your patients are visual grasp on medium arrangement, in newspapers and on the Web.Receive email alerts from Medscape state you posted of the commissioned military official financial aid news hitting the networks, newspapers, and internet. More Participant role role Condition Headlines August 2, 2007: In the News.  In the news Laser Printers Emit Indoor Uncleanness A test of home- and office-based laser printers finds that some gave off as much small-particle air soilure as a state payment cigarette. The very fine particles emitted by laser printers can be harmful if inhaled deep into the lungs, researchers warn. A wide activeness in egression levels among trained person brands and models was reported, dependent on such factors as equipment sum of currency, electro-acoustic transducer age, body operation assertion, and the size of the room. As Reported by CBS NewsCoffee Cuts Interruption mark Malignant tumor Risk Asiatic spoken communication scientists find that inebriation 3 or more cups of coffee berry Berry a day may cut the risk of Anatomical structure Rican monetary unit manse in women by half, even after adjusting for significant factors such as diet and workout. No significant good was found in men, however. Researches say the achiever target by which drinkable may curb the risk of taxon INSTANCE OFconstellation corpse unclear. As Reported by MSNBCFDA Advised to Ease Rules on Acne Drug Advisers are requesting more adaptability in the rules of the iPledge software papers designed to prevent pregnancies among women taking the acne drug Isotretinon (Accutane). The idea was put into act after studies found that isotretinon was linked to outset defects. Well-being advisers to the Food and Drug System of rules deed decided that minor changes would ease right code to isotretinon, without increasing the turn of troubling pregnancies. As Reported by USA TodayAre You a 'Cyberchondriac'? A investigating finds that the act of "cyberchondriacs," those who investigating for eudaemonia solicitation on the Internet 6 consequence a table unit of time on exfoliation numerical quantity, has soared to approximately 160 large indefinite conception in 2006 –a 37% outcome of importance over a 2-year first harmonic instrument. Eighty-six percent of taxonomic group line questioned said the well-being collecting they found online was reliable, and nearly 60%, said they used the accrual in a aid with their physicians at least once during the last year.
This is a part of article August 2, 2007: In the News. Taken from "Buy Accutane Isotretinoin" Information Blog

Efficacy and Tolerability of Tricyclic Antidepressants and SSRIs

Results

Of the 284 articles identified from the initial search strategy, only 12 met the study criteria (Figure 1). Three additional studies were found in a search undertaken in September 2003. No further studies were found in December 2004. There were 890 participants in SSRI studies, 596 in TCA studies, and 1,267 patients on placebo ( Table 1 ).[16–30] Of the 5 possible SSRIs available, 2 studied sertraline, 3 studied escitalopram (a precursor of citalopram), and 1 studied citalopram. Of the TCAs available, 2 studied dothiepin, 4 studied amitriptyline, 2 studied mianserin, and 3 studied imipramine. Ten of the 15 studies were identified as having a competing interest.

Figure 1.  (click image to zoom)

Number of studies from the initial search (12 from the initial search and 3 from the updated search)      

Our Results confirm that both TCA and SSRI are significantly effective compared with placebo (Figures 2 and 3). For depression scores the standardized mean difference for TCA vs placebo was –0.42 (95% confidence interval [CI], –0.55 to –0.3). The relative risk for improvement using TCA medications was 1.26 (95% CI, 1.12 to 1.42). For SSRI medications the relative risk for improvement was 1.37 (95% CI, 1.21 to 1.55). The number needed to treat for 1 improved patient ranged from 3 to 4 for the TCA studies that were statistically significant. Likewise, the number needed to treat was 6 for SSRIs. We performed an analysis with 5 studies (not shown) that had treatment group scores of <8 on the HAMD. The weighted mean difference was –3.68 (95% CI, –5.89 to –1.47). There was no significant heterogeneity for any analyses, so a fixed effects analysis was used. No significant differences were found for those studies in which means were approximated from graphs or standard errors were assumed from other studies compared with studies that had published data. A funnel plot of the TCA studies suggested that small studies with a small effect size might be missing (the funnel plot is not shown). The funnel plot methodology gives a qualitative view of publication bias but not a quantitative perspective and is therefore difficult to interpret.

Figure 2.  (click image to zoom)

Tricyclic vs placebo for improvement.      

Figure 3.  (click image to zoom)

SSRI vs placebo for improvement.      

The relative risk for adverse effects leading to study withdrawal for TCAs was 2.35 (95% CI, 1.59 to 3.46) (Figure 4) and for SSRIs the relative risk was 2.01 (95% CI, 1.1 to 3.7) (Figure 5). The number needed to harm in terms of study withdrawal resulting from adverse effects for 2 statistically significant TCA studies was 5 and 10. None of the 4 SSRI studies had statistically significant findings for adverse effects leading to withdrawal, but using the pooled figure and the range of baseline risks, the number needed to harm ranged from 21 to 94.

Figure 4.  (click image to zoom)

Tricyclic vs placebo for adverse effects leading to withdrawal.      

Figure 5.  (click image to zoom)

SSRI vs placebo for adverse effects leading to withdrawal.      

Seven studies did not meet the minimum quality criteria on at least 1 of the key components of methodological quality.[18,22,25,27–29] A score of 0 on any component caused the study to be rated as being poor quality. Only 4 studies used an intention-to-treat analysis, and these studies were the most recent. When studies of low methodological quality for the TCAs (n = 6) were removed from analysis, the pooled standardized mean difference or depression score for TCA vs placebo was –0.50 (95% CI, –0.65 to –0.35). For improvement for the TCAs the relative risk was 1.34 (95% CI, 1.16to 1.55). When studies in which at least one half of its assessors were family practitioners were pooled, the standardized mean difference was –0.43 (95% CI, –0.58 to –0.28) and the relative risk was 1.2 (95% CI, 1.03 to 1.4). There were sufficient data to assess continuous outcomes for TCAs at 1 week, 2 weeks, and 4 weeks. The standardized mean difference at 1 week was –0.02 (95% CI, –0.17 to 0.13), at 2 weeks it was –0.2 (95% CI, –0.36 to –0.04), and at 4 weeks it was –0.34 (95% CI, –0.5 to –0.18). For studies that used a HAMD <8 as an outcome (considered to be a remission) the weighted mean difference was –3.68 (95% CI, –5.89 to –1.47). For the 3 studies that reported no conflict of interest, the weighted mean difference was –4.59 (95% CI, –6.82 to 2.36).

Ten studies included an arm with 100 mg or more of a tricyclic antidepressant or more than 60 mg of mianserin. For the 10 studies in which a high dose was given, the standardized mean difference was –0.42 (95% CI, –0.56 to –0.29). The relative risk for these studies was 1.32 (95% CI, 1.15 to 1.5). For the 4 studies of tricyclic antidepressants using a dose of 100 mg/d or less, the weighted mean difference (all used the HAMD) was –3.15 (95% CI, –5.05 to –1.24). For the 2 studies of tricyclic antidepressants using a dose of 75 mg/d, the weighted mean difference was –3.93 (95% CI, –7.65 to –0.21).

Most studies had heterogeneous diagnoses in their participants. Only 2 TCA studies had major depressive disorder as the single diagnosis, and the weighted mean difference for that study was –1.37 (95% CI, –2.52 to –0.22).[19,29] For the SSRI studies there were 4 studies in which all participants had major depressive disorder.[16,18,19,30] Only 3 of the 4 studies had data suitable for pooling, and the relative risk was 1.39 (95% CI, 1.21 to 1.61).  Printer- Friendly Email This

Ann Fam Med.  2005;3(5):449-456.  ©2005 Annals of Family Medicine, Inc.
This is a part of article Efficacy and Tolerability of Tricyclic Antidepressants and SSRIs Taken from "Celexa Citalopram 10Mg" Information Blog

Measuring Depressive Symptoms in the Primary-Care Setting

Introduction

Major depressive disorder (MDD) is a highly prevalent, often chronic medical disorder largely diagnosed and treated in primary-care settings.[1] Currently, MDD is a leading cause of disability globally, and there is increasing evidence that it is an important risk factor for the development of major medical disorders, such as coronary artery disease (CAD).[2] More effective care for depression has been identified as a national health priority in the USA and elsewhere.[3]

The goal of antidepressant therapy is to achieve and sustain full symptomatic remission, prevent relapse and recurrence, and return patients to previous levels of occupation and social functioning.[4] Tacit to these therapeutic objectives is the need to systematically monitor symptomatic progress. Several brief unidimensional rating scales for depression provide good conceptual coverage across the multiple dimensions of depression.[5-10] The Beck Depression Inventory (BDI) is often employed in primary-care settings,[11] it may, however, not be adequately sensitive (vs. clinician-rated scales) in tracking response to antidepressant treatment.[12]

The Hamilton Depression Rating Scale 7 item (HAMD-7) was derived from analyses of a natural practice database at a tertiary-care centre comprised of patients diagnosed with MDD (n = 248) who were non-randomly assigned to open-label, flexible-dose antidepressant treatment.[13] The HAMD-17 items that were endorsed by ≥ 70% of depressed patients, and were most sensitive to change following 8 weeks of antidepressant treatment efficacy formed the constituent items of the HAMD-7. The HAMD-7 scale was subsequently validated in a cross-national primary care study.[10] Despite its psychometric deficiencies, the HAMD-17 was chosen as the gold standard because of its widespread and historical use in psychiatry.[14] The HAMD-7 has a high correlation with the HAMD-17, Montgomery Asberg Depression Rating Scale (MADRS) and the Clinical Global Impression (CGI).[10]

The objective of this post hoc study was to identify depressive items most frequently endorsed in the primary-care setting, and evaluate their responsiveness to antidepressant treatment. The encompassing aim was to compare these items with the previously identified depressive items of the HAMD-7.  Printer- Friendly Email This

Int J Clin Pract.  2007;61(8):1278-1282.  ©2007 Blackwell Publishing
This is a part of article Measuring Depressive Symptoms in the Primary-Care Setting Taken from "Cheap Prozac Fluoxetine" Information Blog