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Carbamazepine
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Carbamazepine Thrombocytopenia, rash, hepatic dysfunction A 33-year-old woman was admitted with a history of seIzures which began with slUtlering followed by a decrease in balance which required her to lie down. She commonly arched her back during these episodes which lasted 5-!O min and occurred 2-4 times a month. The physical and laboratory examinations were essentially normal and a diagnosis of uncinate seizures was established. Carbamazepine was initiated initially at 200mg orally bid and later increased to 200mg orally 'lid. Approximately 3 weeks later the patient complained of feeling intermittently hot and cold and experiencing chills. Three days before coming to the clinic she had noticed a generalised body rash and had been . vomiting solid food. She had a produc1\ve cough and complained of some chest discomfon. but had had no recent seizures. Laboratory results showed an absolute platelet count of 55,300 and 76 segmented neutrophlls. 6 bands, 2 eosinophils. 6 lymphocytes and 10 monocvtes. Electrolytes were normal but Ii ver tests showed elevated alkaline phosphatase (304 mu/ml), raised lactic dehydrogenase (350 mu/ml). and SGOT (127 mu/ml). Carbamazepme. was immediately stopped as a drug reactIOn was suspected and the patient .staned on phenobarbitone (30mg orally ud) and prednisone (60 mg/day orally fOf. 7 Four days later, the rash was beginmng to resolve but the platelet count was low, at 459.000. Two weeks later. alkaline phosphatase had returned to normal (100 mu/ml) but serum lactate dehydrogenase and SGOT remained elevated at 240 mul ml and t50 mu/ml, respectively. Carbamazepine-associated blood dyscrasias, rashes and liver function abnormalities have been reponed previously. The manufacturer recommends that pretreatment blood counts be obtained and the tests repeated every week during the first 3 months and then monthly for a minimum of 2-3 years. If bone marrow suppression is noted, the drug should be promptly withdrawn. Patients should be urged to repon to their physician or pharmacist early toxic manifestations of the drug, such as fever sore throat, mouth ulcers, easy bruising' and petechial or purpuric haemorrhage. Carbamazepine should be used cautiously in patients with a history of liver dysfunction. Ponte. C D.: Drug Intelligence and Clinical Pharmacy 17: 642 (Sep (983) Hepatitis Case 1: A 28-year-old woman presented with a recent history of weight loss, lethargy, loss of appetite, chills, night sweats, abdominal cramps, nausea, vomiting, dark urine and conjunctival icterus. Four week before admission, she 0157-7271/83/0923-0003/0$01.00/0 "ADIS Press had been given oral carbamazepine 200mg qid for seizures. Physical examination revealed mild tenderness over her liver with a body temperatun: of 38.6T. Laboratory data were: haematocrit 45.5%; leucocyte count 17,2oo/mm 3 ; SGOT 174 U/L (normal';;; 40); SGPT 159 U/L (normal.;;; 40); alkaline phosphatase 870 U/L (normal';;; 100); 'YGTP 853 U/L (normal 3-30); total bilirubin 7.3 mg/dl; and sedimentation rate 23 mm/hour (normal.::;; 20 mm/hour). Computerised tomography showed an enlarged liver and spleen but no biliary obstruction. Liver biopsy revealed enlarged portal tracts with infiltrations of chronic inflammatory cells (lymphocytes. eosinophils and many epitheloid histiocytes). Carbamazepine was withdrawn and there was gradual improvement of the patient's liver condition. Phenobarbitone. administered subsequently. controlled her seizures. Case 2: A 22-year-old woman who had been prescribed carbamazepine 200mg tid (+ phenytoin) for idiopathic epileptic seizures presented with symptoms of nausea, vomiting, pruritus, dark urine and yellow eyes. Laboratory data were SOOT 1130 V/L; alkaline phosphatase 211 U/L: and bilirubin 3.2 mg/dl. Carbamazepine was withdrawn but the patient was hospitalised 5 days later because of continued symptoms. Her liver was tender but not enlarged. Liver biopsy shOwed distonion of the hepatic architecture due to bridging hepatocellular necrosis. At this stage, her laboratory values were haemoglobin 12.3 gfd[; leucocyte count 5JOO/mm J ; SGOT 759 U/L; alkaline phosphatase 192 U/L; bilirubin 5.2 mg/dl; and serum phenytoin 5.3 mg/dl (therapeutic range 1-2 mg/dl). Phenytoin. was withdrawn. Biochemical abnonnall\1es and clinical symptoms disappeared gradually over a period of 3 weeks. SolTero E.E. el al.: Southern Medical Journal 76: 681 (May I98Jl Reactions 23 Sep 1983 3
Transcript of Carbamazepine
Carbamazepine
Thrombocytopenia, rash, hepatic dysfunction A 33-year-old woman was admitted with a history of seIzures which began with slUtlering followed by a decrease in balance which required her to lie down. She commonly arched her back during these episodes which lasted 5-!O min and occurred 2-4 times a month. The physical and laboratory examinations were essentially normal and a diagnosis of uncinate seizures was established. Carbamazepine was initiated initially at 200mg orally bid and later increased to 200mg orally 'lid. Approximately 3 weeks later the patient complained of feeling intermittently hot and cold and experiencing chills. Three days before coming to the clinic she had noticed a generalised body rash and had been . vomiting solid food. She had a produc1\ve cough and complained of some chest discomfon. but had had no recent seizures. Laboratory results showed an absolute platelet count of 55,300 and 76 segmented neutrophlls. 6 bands, 2 eosinophils. 6 lymphocytes and 10 monocvtes. Electrolytes were normal but Ii ver f~nction tests showed elevated alkaline phosphatase (304 mu/ml), raised lactic dehydrogenase (350 mu/ml). and SGOT (127 mu/ml). Carbamazepme. was immediately stopped as a drug reactIOn was suspected and the patient .staned on phenobarbitone (30mg orally ud) and prednisone (60 mg/day orally fOf. 7 ~ays). Four days later, the rash was beginmng to resolve but the platelet count was low, at 459.000. Two weeks later. alkaline phosphatase had returned to normal (100 mu/ml) but serum lactate dehydrogenase and SGOT remained elevated at 240 mul ml and t50 mu/ml, respectively. Carbamazepine-associated blood dyscrasias, rashes and liver function abnormalities have been reponed previously. The manufacturer recommends that pretreatment blood counts be obtained and the tests repeated every week during the first 3 months and then monthly for a minimum of 2-3 years. If bone marrow suppression is noted, the drug should be promptly withdrawn. Patients should be urged to repon to their physician or pharmacist early toxic manifestations of the drug, such as fever sore throat, mouth ulcers, easy bruising' and petechial or purpuric haemorrhage. Carbamazepine should be used cautiously in patients with a history of liver dysfunction. Ponte. C D.: Drug Intelligence and Clinical Pharmacy 17: 642 (Sep (983)
Hepatitis Case 1: A 28-year-old woman presented with a recent history of weight loss, lethargy, loss of appetite, chills, night sweats, abdominal cramps, nausea, vomiting, dark urine and conjunctival icterus. Four week before admission, she
0157-7271/83/0923-0003/0$01.00/0 "ADIS Press
had been given oral carbamazepine 200mg qid for seizures. Physical examination revealed mild tenderness over her liver with a body temperatun: of 38.6T. Laboratory data were: haematocrit 45.5%; leucocyte count 17,2oo/mm3; SGOT 174 U/L (normal';;; 40); SGPT 159 U/L (normal.;;; 40); alkaline phosphatase 870 U/L (normal';;; 100); 'YGTP 853 U/L (normal 3-30); total bilirubin 7.3 mg/dl; and sedimentation rate 23 mm/hour (normal.::;; 20 mm/hour). Computerised tomography showed an enlarged liver and spleen but no biliary obstruction. Liver biopsy revealed enlarged portal tracts with infiltrations of chronic inflammatory cells (lymphocytes. eosinophils and many epitheloid histiocytes). Carbamazepine was withdrawn and there was gradual improvement of the patient's liver condition. Phenobarbitone. administered subsequently. controlled her seizures. Case 2: A 22-year-old woman who had been prescribed carbamazepine 200mg tid (+ phenytoin) for idiopathic epileptic seizures presented with symptoms of nausea, vomiting, pruritus, dark urine and yellow eyes. Laboratory data were SOOT 1130 V/L; alkaline phosphatase 211 U/L: and bilirubin 3.2 mg/dl. Carbamazepine was withdrawn but the patient was hospitalised 5 days later because of continued symptoms. Her liver was tender but not enlarged. Liver biopsy shOwed distonion of the hepatic architecture due to bridging hepatocellular necrosis. At this stage, her laboratory values were haemoglobin 12.3 gfd[; leucocyte count 5JOO/mmJ; SGOT 759 U/L; alkaline phosphatase 192 U/L; bilirubin 5.2 mg/dl; and serum phenytoin 5.3 mg/dl (therapeutic range 1-2 mg/dl). Phenytoin. was withdrawn. Biochemical abnonnall\1es and clinical symptoms disappeared gradually over a period of 3 weeks. SolTero E.E. el al.: Southern Medical Journal 76: 681 (May I98Jl
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