INT146340

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Context Info
Confidence 0.69
First Reported 2008
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 4.60
Pain Relevance 5.45

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

nucleolus (Mllt1) nucleus (Mllt1) cytoplasm (Mllt1)
Anatomy Link Frequency
plasma 2
duodenum 2
fat 1
Mllt1 (Mus musculus)
Pain Link Frequency Relevance Heat
Lamotrigine 944 100.00 Very High Very High Very High
antiepileptic Drug 180 97.96 Very High Very High Very High
carbamazepine 98 95.28 Very High Very High Very High
Bioavailability 2 91.00 High High
addiction 8 84.16 Quite High
cocaine 8 83.76 Quite High
Neuropathic pain 8 78.64 Quite High
Gabapentin 24 75.28 Quite High
Glutamate 9 50.92 Quite High
Neurotransmitter 1 49.68 Quite Low
Disease Link Frequency Relevance Heat
Epilepsy 104 99.60 Very High Very High Very High
Partial Seizures 68 99.36 Very High Very High Very High
Exanthema 145 96.20 Very High Very High Very High
Convulsion 248 95.40 Very High Very High Very High
Syndrome 75 93.52 High High
Dizziness 34 90.00 High High
Diplopia 25 89.12 High High
Ataxia 25 88.32 High High
Chronic Disease 8 87.56 High High
Vomiting 58 87.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Adverse effects of both immediate and extended-release LTG formulations are listed in Table 2.
Localization (release) of LTG associated with lamotrigine
1) Confidence 0.69 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 1.04 Pain Relevance 0.35
For instance, carbamazepine (CBZ) and phenytoin (PHT) are strong inducers of UGT1A4 and their combined treatment with LTG results in a substantial increase in its systemic clearance.12,13 Also, enzyme inducers (ie, CBZ, PHT) are responsible for the significant reduction in the LTG’s elimination half-life from approximately 24 to 13 h.12,13 In contrast, valproate (VPA) as an inhibitor of glucuronidation has been documented to significantly reduce the clearance of LTG with a concomitant increase in its elimination half-life from approximately 37 to 48 h.14 Moreover, LTG serum concentrations were significantly increased from 4.67 ± 3.66 (LTG monotherapy) to 9.56 ± 5.27 ?
Localization (clearance) of LTG associated with lamotrigine and carbamazepine
2) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0.21 Pain Relevance 0.69
This AED is also approved for conversion to monotherapy in adults.7 LTG is available as an immediate-release formulation (LTG-IR) that undergoes a rapid and almost complete absorption following oral administration, with peak plasma levels being recorded from 1.3 to 4.7 h.
Localization (release) of LTG in plasma associated with lamotrigine
3) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0.69 Pain Relevance 0.61
Generally, most of the newer AEDs have no impact on the activity of hepatic enzymes so they are not expected to affect pharmacokinetic parameters of LTG.16

Importance of extended-release formulations

Localization (parameters) of LTG associated with lamotrigine and antiepileptic drug
4) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0 Pain Relevance 0.54
This AED is also approved for conversion to monotherapy in adults.7 LTG is available as an immediate-release formulation (LTG-IR) that undergoes a rapid and almost complete absorption following oral administration, with peak plasma levels being recorded from 1.3 to 4.7 h.
Localization (release) of LTG in plasma associated with lamotrigine
5) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0.68 Pain Relevance 0.60
LTG-XR, due to a special eroding matrix, considerably reduces the rate of LTG release over 12–15 h.3 An enteric coating additionally prevents LTG release which starts when a tablet passes to the duodenum.17

Pharmacokinetics of LTG-XR

Localization (release) of LTG in duodenum associated with lamotrigine
6) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0.68 Pain Relevance 0.75
LTG-XR, due to a special eroding matrix, considerably reduces the rate of LTG release over 12–15 h.3 An enteric coating additionally prevents LTG release which starts when a tablet passes to the duodenum.17

Pharmacokinetics of LTG-XR

Localization (release) of LTG in duodenum associated with lamotrigine
7) Confidence 0.64 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2874338 Disease Relevance 0.62 Pain Relevance 0.78
Its immediate-release formulation (LTG-IR) requires twice-daily dosing.
Localization (release) of LTG associated with lamotrigine
8) Confidence 0.60 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Abstract Doc Link PMC2874338 Disease Relevance 0.51 Pain Relevance 0.44
LTG-XR has a modified-release eroding matrix to control its dissolution rate,16 which leads to changes in absorption rates (time to peak plasma concentration [Tmax] 1–1.5 hours for LTG-IR versus 4–11 hours for LTG-XR).17 Despite the changes in Tmax, the bioavailability of LTG-XR and LTG-IR is similar, except for patients taking enzyme-inducing antiepileptic drugs in whom the bioavailability of LTG-XR is 21% lower; the clinical importance of this finding is not clear.17 Its levels have been shown to be unaffected by high-fat meals, suggesting that the LTG-XR form is not significantly lipophilic. 18 Studies have shown that lamotrigine is eliminated via hepatic N2-glucuronidation.19
Spec (suggesting) Localization (release) of LTG-XR in fat associated with lamotrigine, antiepileptic drug and bioavailability
9) Confidence 0.54 Published 2010 Journal Drug Design, Development and Therapy Section Body Doc Link PMC2998806 Disease Relevance 0 Pain Relevance 0.46
PURPOSE: To compare the pharmacokinetics (PK) of lamotrigine (LTG) when converting from twice-daily immediate-release (LTG-IR) to once-daily extended-release (LTG-XR) in subjects with epilepsy.
Localization (release) of LTG-XR associated with epilepsy and lamotrigine
10) Confidence 0.26 Published 2008 Journal Epilepsia Section Abstract Doc Link 17825077 Disease Relevance 0.17 Pain Relevance 0.24

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