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Modified-release dosage is a mechanism that (in contrast to immediate-release dosage) delivers a drug with a delay after its administration (delayed-release dosage) or for a prolonged period of time (extended-release [ER, XR, XL] dosage) or to a specific target in the body (targeted-release dosage). [1] Sustained-release dosage forms are dosage ...
In the early 1990s, an ALZA-funded research program began to develop a new dosage form of methylphenidate for the treatment of children with attention deficit hyperactivity disorder (ADHD). [14] Methylphenidate's short half-life required multiple doses to be administered each day to attain long-lasting coverage, which made it an ideal candidate ...
[122] [123] [124] For instance, a 2004 U.S. Food and Drug Administration (FDA) analysis of clinical trials on children with major depressive disorder found statistically significant increases of the risks of "possible suicidal ideation and suicidal behavior" by about 80%, and of agitation and hostility by about 130%. [125]
Insulin glargine, for example, is designed to precipitate after injection so it can be slowly absorbed by the body over a longer period than regular insulin would be. [13] Depot injections of insulins have been studied to better replicate the body's natural basal rate of insulin production, and which can be activated by light to control the ...
Additionally, there is a risk of increased suicidality in pediatric populations for treatment of major depressive disorder, especially with venlafaxine. [95] Fluoxetine and Escitalopram are the only antidepressants that are approved for child/adolescent major depressive disorder. [96]
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Depression is a symptom of some physical diseases; a side effect of some drugs and medical treatments; and a symptom of some mood disorders such as major depressive disorder or dysthymia. [1] Physical causes are ruled out with a clinical assessment of depression that measures vitamins, minerals, electrolytes, and hormones.
Higher dosage does, however, increase the incidence and severity of adverse events associated with excessive 5-HT re-uptake inhibition. [6] Figure 2 Inhibition of re-uptake transport proteins, e.g. SERT, results in increased concentration of neurotransmitters, e.g. 5-HT, in the synaptic cleft, leading to improvement of depression symptoms