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)

Asthma is a global health problem with up to 15% of children suffering from the disease. It has been shown by various researchers that symptomatic asthmatic patients have increased levels of free serotonin in plasma when compared with asymptomatic patients. Thus, some researchers suggest that reducing the concentration of free serotonin in plasma might be useful in treating patients with asthma. Low levels of serotonin, has however, been linked to various psychological conditions like depression, oppositional defiant disorder, ADHD and even conduct disorder. Research has indicated that products like methylphenidate (also known by the brand names as e.g., Ritalin, Concerta, Metadate and others) and other stimulants used for these conditions, particularly ADHD, exert their paradoxical calming effects by boosting serotonin levels in the brain. Therefore, the hypothesis suggest that some children using asthma medication that lowers serotonin levels, might present with symptoms of depression ADHD, oppositional defiant disorder and even conduct disorder. They may be using asthma medication that lowers serotonin and additionally use methylphenidate that boosts serotonin levels for e.g., ADHD. The hypothesis therefore suggests that asthmatic children presenting with psychological complaints, be treated holistically and serotonin levels measured before coming to conclusions regarding their psychological functioning.
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PMID:Asthma medication may influence the psychological functioning of children. 1528 58

We examined the efficacy and tolerability of augmentation with an extended release formulation of methylphenidate (OROS MPH, Concerta) in patients with major depression who were nonresponders or partial responders to antidepressants. Sixty subjects with treatment-resistant depression (TRD) participated in a 4-week, randomized, double-blind, placebo-controlled study of augmentation with methylphenidate (18-54 mg/d). The preexisting antidepressant dose was unchanged. The primary efficacy measure was change in the 21-item Hamilton Depression Rating Scale from randomization to end of treatment. Data were analyzed with intent-to-treat with last observation carried forward approach. There were no statistically significant differences between the methylphenidate (n = 30) and placebo (n = 30) groups in reduction in 21-item Hamilton Depression Rating Scale scores (drug, -6.9; placebo, -4.7) from baseline to end of treatment (F1,47 = 1.24, P = 0.22), although responders were numerically higher in the extended-release methylphenidate group (40.0%) than in the placebo group (23.3%). On the secondary efficacy measures of changes in Clinical Global Impression-Improvement and Severity scores and Beck Depression Inventory-Second Edition, the drug failed to separate from placebo, although the proportion of responders in the drug group were numerically higher than placebo. There were no significant differences in weight, heart rate, and blood pressure changes between the 2 groups. The common adverse events were loss of appetite, nausea, headache, and anxiety. The mean dose of drug was 34.2 mg/d. The study did not demonstrate a statistically significant benefit for augmentation with methylphenidate in TRD. Combination of methylphenidate with antidepressants was well tolerated. Adequately powered, randomized, controlled trials are necessary to fully evaluate the efficacy of extended-release methylphenidate in TRD.
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PMID:A randomized, double-blind, placebo-controlled trial of augmentation with an extended release formulation of methylphenidate in outpatients with treatment-resistant depression. 1820 60