Saturday, September 12, 2015

Study group discussion: Why more phenytoin is prescribed at night

Why do we give phenytoin in 1-0-2 dose after discharge? Why two tablets at night?

Phenytoin causes marked drowsiness that can confound the mental status (read GCS) exam in medicated patients, most critically those who have had neurosurgery and are given phenytoin for postoperative seizure control. In an outpatient being prescribed phenytoin one would plausibly order more to be taken when the patient is likely to be asleep instead of when they're awake.

Thank you for sharing this with us.

One article says, previously, we used to give 300 mg once daily. After chronic use, patients started developing adverse reactions of drug. It was then decided to start using phenytoin in divided doses. (100 mg TID).

Also remember that gingival hyperplasia is a very important and distinctive secondary effect of phenytoin, my teachers say that it stays even if you stop the medicine, but I'm not sure of that since I have not read that anywhere else.


  1. The interaction of phenytoin, cyclosporine, and nifedipine with epithelial keratinocytes, fibroblasts, and collagen can lead to an overgrowth of gingival tissue in susceptible individuals. Phenytoin has been shown to induce gingival overgrowth by its interaction with a sub-population of sensitive fibroblasts. Cyclosporine has been suggested to affect the metabolic function of fibroblast (eg, collagen synthesis, breakdown), whereas nifedipine, which potentiates the effect of cyclosporine, reduces protein synthesis of fibroblasts. A review of existing literature shows that a cofactor clearly is needed to induce gingival overgrowth. In fact, several lines of evidence point to a modulation of inflammatory processes.
    Collagen fibers are degraded by two pathways: the extracelular one, which occurs by secretion of collagenases; and the intracellular one, by collagen phagocytosis by fibroblasts . In this regard, a common property of the 3 main classes of drugs that induce GO—antiepileptic agents, immunosuppressants and calcium channel blockers—is that they affect calcium metabolism. These drugs induce a decrease in the Ca2+ cell influx (due to changes in the sodium-calcium exchange) leading to a reduction in the uptake of folic acid, thus limiting the production of active collagenase. Hence the problem is not overproduction ,but decrease in degradation


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