• Tuberculosis and Respiratory Diseases
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• v.48 no.5
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• pp.794-801
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• 2000

BOOP(Bronchiolitis Obliterans Organizing Pneumonia) is an inflammatory reaction that follows damage to the bronchiolar epithelium of the small conducting airways. BOOP is characterized by the pathologic finding of excessive proliferation of granulation tissue within the respiratory bronchioles, alveolar duct and spaces, accompanied by organizing pneumonia in the more distal parenchyma BOOP may result from diverse causes such as toxic fumes, connective tissue disorders, infections, organ transplantation and drugs or appear idiopathically. Drug induced BOOP has been described in association with acebutolol, amiodarone, cephalosporin, bleomycine, tryptophan, gold salts, barbiturates, sulfasalazine, and carbamazepine. Carbamazepine is an iminostilbene derivative that is used as both an anticonvulsant and pain reliever for pains associated with trigeminal neuralgia. It is structually related to the tricyclic antidepressants. To our knowledge, there have been no previously reported case that has described development of BOOP during carbamazepine treatment in Korea, and only two cases have been reported in the world. We report a case carbamazepine-induced BOOP with a brief review of literature.

• 대한임상약리학회:학술대회논문집
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• 1996.12a
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• pp.34-34
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• 1996

• Journal of Oral Medicine and Pain
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• v.34 no.2
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• pp.207-216
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• 2009

Trigeminal neuralgia is defined "a sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve". The initial treatment of choice for trigeminal neuralgia is medical therapy. In patients with medically intractable pain or intolerable medication side effects, invasive therapeutic approaches are often necessary. Based on the amount of evidence and estimated efficacy, carbamazepine is the drug of choice in the management of trigeminal neuralgia. In case of insufficient or no response to carbamazepine, second-line drugs can be added. In this study, the author tried to review and analyzed the cases of 90 patients whom had visited for treatment of trigeminal neuralgia at the Department of Oral Medicine, Kyungpook National University Hospital from 2003 to 2008. The results were as follows: 1. Trigeminal neuralgia was significantly more common with advancing age, and nearly twice as common in women than men (ratio of 2.1:1) 2. The maxillary branch of the trigeminal nerve involved most often (51.1%), and the right side of the face is affected more commonly than the left (ratio of 2.9:1). 3. 85(94.4%) patients had experiences visiting medical or dental specialties before being referred to the Department of Oral Medicine. 4. 40(44.4%) patients with trigeminal neuralgia had systemic diseases. 5. Treatment with carbamazepine monotherapy was satisfactory initially in 69(76.7%) the patients, and the mean daily dose of carbamazepine was 402.9mg. On the other hand, 16(17.8%) patients expressed effectiveness after combination therapy of carbamazepine and other drugs. 6. Of the 69 patients who had a good initial response to carbamazepine monotherapy, 18 patients became resistant, so that combination therapy of carbamazepine and other drugs were necessary. 7. 54(60%) patients developed side effects such as dizziness, drowsiness, nausea, vomiting, blood dyscrasias, skin rash and constipation, and 11 of the patients decided to stop tmedicaion due to side effects.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.6
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• pp.485-491
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• 2013

The present study was designed to investigate the putative effect of neurosteroid modulation on global ischaemia-reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion followed by reperfusion, produced a significant rise in cerebral infarct size along with impairment of grip strength and motor coordination in Swiss albino mice. Administration of carbamazepine (16 mg/kg, i.p.) before global cerebral ischaemia significantly attenuated cerebral infarct size and improved the motor performance. However, administration of indomethacin (100 mg/kg, i.p.) attenuated the neuroprotective effect of carbamazepine. Mexiletine (50 mg/kg, i.p.) did not produce significant neuroprotective effect. It may be concluded that the neuroprotective effect of carbamazepine may be due to increase in synthesis of neurosteroids perhaps by activating enzyme ($3{\alpha}$ HSD) as indomethacin attenuated the neuroprotective effect of carbamazepine. The sodium channel blocking effect of carbamazepine may not be involved in neuroprotection as mexiletine, a sodium channel blocker, did not produce significant neuroprotective effect.

• The Korean Journal of Pain
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• v.12 no.1
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• pp.119-122
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• 1999

Glossopharyngeal neuralgia is a rare syndrome that involves episodic bursts of pain in the sensory distributuion of the ninth cranial nerve. The nature of the pain is characterized by excruciating shock-like pain in the region of the tonsillar fossa or pharynx and can radiate to the ear or the angle of the jaw. Like trigeminal neuralgia, glossopharyngeal neuralgia typically responds to anticonvulsant agents such as carbamazepine. However, dose of carbamazepine needs to be increased gradually to avoid side effects. If the patient can not tolerate until effective carbamazepine level is reached, phenytoin can be administered intravenously at the same time that oral carbamazepine therapy is begun. We present fifty-three year old female patient suffering from glossopharyngeal neuralgia who did not respond to initial carbamazepine therapy, but responded to concomitant intravenous infusion of phenytoin.

• The Journal of Internal Korean Medicine
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• v.24 no.4_2
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• pp.1080-1086
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• 2003

As the use of anticonvulsant increases in neurologic field, more studies are needed to reveal various harmful effects of this medication. Especially as for carbamazepine, thrombocytopenia may appear during administration of the medication, regardless of dosage. We, the authors, report that we diagnosed the patient as Bigiheo and Eumheohyeolheo, who was suffering from insomnia, diarrhea, papura, and serious thrombocytopenia. We presumed that the symptoms could be induced by carbamazepine, and used Samulgwibitanggamibang to treat her and obtained positive results.

• Korean Journal of Biological Psychiatry
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• v.5 no.2
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• pp.283-287
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• 1998

The mother was 24 years old, primipara, and had been taking carbamazepine 400mg(serum concentration $5.0-8.5{\mu}g/ml$) during pregnancy without any clinical seizures. A male baby with physical malformation was delivered on week 39. The malformation is extradigit(polydactily) on X-ray of right foot and left mild hydronephrosis on ultrasonography and renal scan with radioactive material. We reported this rare case and reviewed related articles about teratogenic effect of carbamazepine, mechanism of action and prevention of teratogenesis.

• Korean Journal of Biological Psychiatry
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• v.5 no.2
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• pp.227-234
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• 1998

Objective : Many evidences suggest that patients with bipolar disorder have functional abnormalities in their postreceptor signal transduction pathways, and mood stabilizing effect of lithium is exerted by modulating this dysfunctioning system. Carbamazepine, an antiepileptic agent, is also known to be effective in the treatment and prevention of bipolar disorder. But the precise mechanism of action of the drug is still poorly understood. This study was performed to elucidate the possible therapeutic mechanism of carbamazepine. Method : The effects of chronic carbamazepine administration on protein kinase A and protein kinase C activities in frontal cortex of rat brain after 2 weeks of drug administration were measured and compared with those of control subjects. Results : Mean(${\pm}SE$) value of activity(phosphate transfer ${\mu}mol/mg$ of $protein{\cdot}min$) of protein kinase A in control and test group was $0.249563{\pm}0.036$ and $0.539853{\pm}0.078$, and that of protein kinase C was $0.654817{\pm}0.053$ and $1.146205{\pm}0.052$ respectively, being increased in test group. And differences between the two groups were statistically significant for both enzymes(protein kinase A ; p<0.01, protein kinase C ; p<0.001). Conclusion : These results show that chronic carbamazepine administration increases protein kinase A and C activities, and concerning the possible mode of therapeutic action in bipolar disorder it is suggested that enhanced enzymes phosphorylate receptor-G-protein-effector complexes to dampen hyperfunctioning neuronal activity and thus stabilize the system.

• Korean Journal of Clinical Pharmacy
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• v.6 no.2
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• pp.19-23
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• 1996

Carbamazepine is an anticonvulsant drug that has been shown to be as effective as phenytoin or phenobarbital in treatment of grand mal and complex partial seizures and is also approved as the drug of choice for treatment of the pain associated with trigerminal neuralgia. And the therapeutic or toxic effects of carbamazepine are better related to plasma concentration than to dosage, which can be attributed to interindividual variability in the pharmacokinetics. A slow rate of carbamazepine dissolution in the gastrointestinal tract is believed to be the cause of its relatively slow and erratic rate of absorption. For these reasons pharmacokinetic evaluation of newly formulated carbamazepine is neccessary. In this study, the bioequivalence in carbamazepine between the $TegretoI^{TM}$ CR tablet (Geigy Co.) and $Carmazepine^{TM}$ CR tablet (Myung In Co.) was evaluated. 12 normal volunteers (age $21\~27$ years old) was divided into two groups, and a randomized cross-over study was employed. The pharmacokinetic parameters ($C_{max},\;T_{max}$ and AUC) obtained of oral administration of each formulatim of carbamazepine 400 mg were evaluated and ANOVA was utilized for the statistical analysis of parameters. $C_{max}\;is\;8.26{\pm}3.1{\mu}g/ml\;(C.V.\;37.3\%)\;in\;TegretoI^{TM}\;and\;9.39\{pm}2.9{\mu}g/ml\;(C.V.\;30.5\%)$ in $Carmazepine^{TM},\;T_{max}\;is\;28.0{\pm}5.9\;hrs(C.V.\;21.1\%)$ in $Tegretol^{TM}\;and\;24.0{\pm}7.2\;hrs(C.V.\;30.2\%)$ in $Carmazepine^{TM}$ and AUC is $786.4{\pm}360.5{\mu}g{\cdot}hr/ml\;(C.V.\;45.8\%)$ in $TegretoI^{TM}\;and\;792.8{\pm}228.6{\mu}g{\cdot}hr/ml\;(C.V.\;28.8\%)$ in $Carmazepine^{TM}$, respectively. As the result of the data, two formulations are bioequvalent, and the lower C.V. of $Carmazepine^{TM}$ in every individual can be merit.

• 대한임상약리학회:학술대회논문집
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• 1995.12a
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• pp.49-49
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• 1995