Volume 1995, No. 3 February 15, 1995
Identifieur interne : 002166 ( Istex/Corpus ); précédent : 002165; suivant : 002167Volume 1995, No. 3 February 15, 1995
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- Clin-Alert [ 0069-4770 ] ; 1995-01.
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DOI: 10.1177/006947709503300103
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</publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1177/006947709503300103</article-id><article-id pub-id-type="publisher-id">10.1177_006947709503300103</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Volume 1995, No. 3 February 15, 1995</article-title></title-group><pub-date pub-type="ppub"><month>1</month><year>1995</year></pub-date><volume>33</volume><issue>1</issue><fpage>17</fpage><lpage>24</lpage><custom-meta-wrap><custom-meta xlink:type="simple"><meta-name>sagemeta-type</meta-name><meta-value>Journal Article</meta-value></custom-meta><custom-meta xlink:type="simple"><meta-name>search-text</meta-name><meta-value>17 Volume 1995, No. 3 February 15, 1995 SAGE Publications, Inc.1995DOI: 10.1177/006947709503300103 No. 27 FLUOXETINE Acute Organic Brain Syndrome A 2-month history consistent with a diagnosis of major depression prompted admission of a 73-year-old man to the hospital. For the previous 2 weeks the patient had been taking alprazolam 0.5 mg at bedtime. Fluoxetine 20 mg daily was added to his treatment regimen. On the second day after starting fluoxetine, the patient developed a fine tremor in his hands. On the third day his movements had become slower and stiffer. On the fourth day he had become more withdrawn, and his appetite was reduced considerably. His tremor became worse and also appeared on his tongue; he was much less communicative. He developed problems dressing himself, especially in unbuttoning and tying knots. The patient was restless and would walk incessantly in circles over a 3 to 4 hour period. For the first time he developed incontinence of urine and stools. He was disoriented to time, place, and person. He now had coarse tremor of both hands and tongue. Plantar reflexes were equivocal on the left side. He could not discriminate between right and left or remember his residential address where he had lived for the past 10 years. Fluoxetine therapy was discontinued after the fifth day of treatment; however, by that afternoon the patient had developed urinary retention and was hospitalized. He was unable to swallow anything. Clasp-knife regidity developed and by late night there was evidence of cogwheel rigidity in all four extremities. On the sixth day his speech became incoherent and babbling. He was treated with trihexy- phenidyl with marked improvement in tremor and rigidity; he was able to swallow. Be day 7 he was able to sit up and walked with support on day 8. He became more communicative. The patient had amnesia for many of the events from days 4 to 6. At hospital dismissal he was able to eat, walk, and clothe himself. There appeared to be no residual neurologic or cognitive deficits. The authors think it may be more prudent to start geriatric patients and patients with hypersensitivity to fluoxetine on lower doses of the drug in order to reduce chances of side effects.- Fluoxetine ['Prozac'] Singh RK et al (New Delhi India) Acute organic brain syndrome after fluoxetine treatment. Amer J Psychiat 152:295-296 (Feb) 1995 18 No. 28 February 15, 1995 CLOZAPINE A. Toxic Hepatitis: A 35-year-old man with schizoaffective disorder was started on a regimen of clozapine 300 mg daily. On treatment days 25-31 he complained of joint pain, nausea, chills, fatigue, emesis, diarrhea, and abdominal pain; he had a mildly elevated temperature. On day 32 of clozapine treatment, the . patient developed a pruritic rash on the back of both hands and on his upper back as well as angioedema manifested as a swollen lower lip and right lower cheek. All of his medications were discontinued; however, on day 33 the patient was febrile and disoriented. His liver function test values were elevated, . his white blood cell count was slightly elevated, and his eosinophil count was 7.0 per cent. The patient's symptoms gradually improved, his bilirubin returned to normal within several days, and his transaminase levels returned to normal within 4-5 weeks. The authors believe that this case demonstrates hypatocellu- lar toxicity in contrast to obstructive hepatotoxicity occasionally seen with traditional neuroleptic use.- Clozapine ['C10zaril'] Thatcher G14 et al (Salt Lake City UT) Clozapine-induced toxic hepatitis. Amer J Psychiat 152:296-297 (Feb) 1995 B. Parotitis: A 43-year-old man with a primary psychiatric diagnosis considered to be chronic paranoid schizophrenia was started on clozapine. He developed bilateral swelling and tenderenss over both temporal-mandibular areas. Other symptoms included dysphagia, anorexia, and sluggishness. His symptoms abated after 4-5 days; local pain and swelling were relieved with hot compresses. Ten days later, following a graduated 300-mg increase of the clozapine dosage, the patient re-experienced greater tenderness and swelling of the parotid glands. His symptoms again abated and over the next 6 months, he continued to improve with clozapine therapy without recurrence of his symptoms. The patient experienced hypersalivation while taking clozapine and while the mechanisms of hypersalivation are not fully appreciated, the authors believe that this adverse reaction should be monitored by the physician in order to spare the patient the discomfort associated with parotitis.- Robinson D et al (Palo Alto CA) Possible association of parotitis with clozapine. Amer J Psychiat 152:297-298 (Feb) 1995 C. Constipation: The authors report that they found a 60% prevalence of constipation when they performed a clozapine drug use evaluation. Of the 53 patients in the study, 6 were concurrently being treated with other antipsychotic drugs. These patients, however, showed no greater prevalence of constipation than other patients taking clozapine. Most cases of constipation were mild to moderate in severity; however, at least 12% required repeated use of enemas. One severe case of constipation resulted in death. This case was a 29-year-old man who had started clozapine therapy 36 days earlier; the dose had been 400 mg daily for the last 22 days. The authors state that prophylactic treatment and prompt intervention for constipation along with slower clozapine titration appear to decrease the incidence and severity of clozapine-induced constipation.- Hayes G & Gibler B (Atascadero CA) Clozapine-induced constipation. Amer J Psychiat 152:298 (Feb) 1995 19 No. 29 DISULFIRAFI AND TRANYLCYPROMINE Delirium A 48-year-old man was treated every 10 months with disulfiram implants, with which abstinence from alcohol was achieved. He had been receiving lithium for 3 years for treatment of bipolar mood disorder. Before admission he suffered a 1-year depressive episode for which he received moclobemide. The depressive complaints continued and moclobemide treatment was discontinued. Tranylcypromine was started at an initial dosage of 10 mg twice daily. Two days later the patient became acutely delirious. He was treated conservatively and admitted to the hospital where he was noted to be agitated, totally disoriented, and incoherent ; he suffered from vivid visual hallucinations. He became subcomatose; nystagmus and a downward gaze developed. The patient's condition started to improve, and within 24 hours he was lucid and feeling well. He was unable to recollect his delirious episode. Although the mechanism has not been fully understood, the authors believe that the time relationships in this case suggest a toxic interaction between disulfiram and tranylcyprome. They consider this case as a serious warning not to combine disulfiram and monoamine oxidase inhibitors, especially tranylcypromine.- Disulfiram ['Antabuse'] Tranylcypromine ['Parnate'] Blansjaar BA & Egberts TCG (Delft the Netherlands) Delirium in a patient treated with disulfiram and tranylcypromine. Amer J Psychiat 152:296 (Feb) 1995 No. 30 WARFARTN SODIUM Hepatotoxicity A 50-year-old woman with lymphoedema complicating a mastectomy two years previously, started treatment with warfarin sodium. After seven weeks, the patient was jaundiced; liver function test values were elevated. At 10 weeks the woman presented with persisting jaundice. Warfarin was discontinued and the patient's liver function began to improve. At 12 weeks, an ultrasound showed a small homogeneous liver and ascitic fluid. At 15 weeks, the patient remained unwell, with abnormal liver function; however, she refused a liver biopsy. Although this case has not been conclusively proved to be warfarin-related toxicity, the authors with to make physicians aware of possible reaction when prescribing this drug.- Warfarin Sodium {'Coumarin') ['Coumadin,' 'Panwarfin'] Beinssen APA (Principal House Officer Atherton District Hosp Jack St Atherton QLD 4883 Australia) Possible Coumarin hepatotoxicity. Fled J Australia 161:725 (Dec 5/19) 1994 20 No. 31 INTRALIPID Acute Increase In Serum L-ipids A 53-year-old man developed a perforated diverticular abscess three months after renal transplantation. A Hartman procedure was complicated by a paralytic ileus and parenteral nutrition was initiated. In order to establish nutritional support the patient was started on a peripheral regimen of Vitrimix which consisted of 500 mL of 20% Intralipid (fractionated soybean oil 100 g, egg-yolk phospholipids 12 g, glycerol 22.5 mg/I:), and 1,600 mL of 0.9% glucose. Within 24 hours, the patient's blood sample was turbid and his serum total cholesterol concentration rose from 5.2 mmol/L to 10.0 mmol/L., and his serum triglyceride concentration rose from 4.2 mmol/L to 15.1 mmol/L concurrently. The elevated serum lipid abnormality persisted and the Vitrimix was discontinued after 48 hours. An alternative parenteral nutrition formulation consisting of 500 mI, of 20% intralipid, 500 mL of 50% glucose, and 1,000 mL of Vamin administered through a central vein was started. The patient's lipid levels continued to to remain moderately elevated; however, the serum became less turbid. On day four, he became confused and on examination was generally hypotonic. On day nine he developed recurrent grand mal seizures and his clinical course deteriorated. He remained drowsy but responsive to verbal command; on day 10, he suffered a fatal cardiac arrest. This patient was also receiving treatment with cyclosporine, and the authors believe that an interaction exists between this drug and intralipid, which severely disrupted the patient's lipid metabolism. They stress that until this interaction is fully understood, intralipid- containing solutions should be administered with caution in renal transplant recipients on intravenous cyclosporine.- Cyclosporine ['Sandimmune'] Bolodeoku J & Mellotte GJ (Dept Chem Pathol & Metabo1 & South West Thames Renal Unit St Fielier Hosp Carshalton Surrey ST15 IAA UK) Acute serum lipid changes in a renal transplant recipient on intravenous cyclosporine upon administration of an intravenous lipid solution. Postgrad Med J 70:849 (Nov) 1994 No. 32 DEFIBRILLATION Rhabdomyolysis And Renal Failure One hour after a 54-year-old man suffered a severe oppressive chest pain, profuse sweating, nausea, and marked skin pallor, he arrived at the hospital where he immediately developed ventricular fibrillation. Despite supportive measures, ventricular fibrillation kept recurring. The patient received CPR for 65 minutes, 18 electrical countershocks, and boluses of several medications Sinus rhythm ensued after the eighteenth attempt at defibrillation. On admission to the intensive care unit, the patient's urine was dark and qualitative urine myoglobin determination was positive. His creatine kinase (CK) peaked at 64,480 IU/L 42 hours after onset of chest pain. His renal failure worsened and peritoneal dialysis for 2 consecutive days was necessary; renal function became progressively normal. The authors believe that a very elevated serum CK level is predictive of acute renal failure in rhabdomyolysis.- Barrachina F et al (Inten Care Unit Joan XXIII Hosp Univ Tarragona Spain) Rhabdomyolysis and renal failure following defibrillation. Postgrad Med J 70:850 (Nov) 1995 21 No. 33 CHEMOTHERAPY , Toxic 1`megacolon A 43-year-old woman with a diagnosis of acute myeloid leukemia was treated treated with chemotherapy consisting of daunorubicin, cytarabine, and etoposide, Although she achieved complete remission after one course of chemotherapy, she received a course of consolidation therapy consisting of daunorubicin, cytarabine, and etoposide, and tehn a course of P1ACE (amsacrine, cytarabine, and etoposide). On the tenth day after T1ACE while her neutrophil count was only 100/mm3 and platelets 5,000/mm3, the patient developed an episode of melena and a small hematemesis. tlultiple small erosions were noted on gastroscopy and the patient was treated conservatively. She subsequently developed a markedly tender, tense, distended abdomen and abdominal X-ray showed marked colonic distension to 10 cm with thickening of the bowel wall. On the twentieth day day after MACE chemotherapy, a defunctioning cecostomy was performed; the patient made an uneventful recovery. Two months later the cecostomy was ' reversed and a right hemicolectomy was performed as a thickened lesion in the mid-transverse colon was found at laparotomy. The patient died 22 months later from recurrent leukemia. The authors believe this to be the first reported case of toxic megacolon developing after anti-leukemic chemotherapy.- Cytarabine ['Cytosar'] Daunorubicin ['Cerubi.dinet] Etoposide ['Vepesid'] Wodzinski MA et al (Dept Haematol Royal Hosp Chesterfield S44 5BL UK) Toxic megacolon complicating chemotherapy for acute myeloid leukaemia. Postgrad Med J 70:921-923 (Dec) 1994 No. 34 CLOZAPINE Systemic Lupus Erythematosus-Like Reaction Three weeks after starting clozapine 300 mg daily for treatment of paranoid schizophrenia, a 39-year-old man was admitted to the hospital with a one-week history of fatigue. He had a 3-day history of progressive severe illness associated with a dry cough, precordial pleuritic chest pain, chills, flushes, and generalized arthralgias. Crackles were heard over the left lower lung and a pleuro-pericardial rub was noted over the precorium. Chest c-ray examination showed increased interstitial lung markings at the left base. His sedimentation rate was prolonged; liver function test values were elevated. Clozapine was discontinued at admission and the patient's chest pain, fever, and arthralgia resolved rapidly. The patient showed marked clinical improvement over his 5 day hospital stay and his laboratory test values improved. At follow-up six months later the patient was asymptomatic. The authors believe this to be the first reported case of clozapine toxicity resembling acute systemic lupus erythematosus.- Clozapine ['Clozaril'] Wickert WA et al (Divs Intern Tiled Rheumatol & Geriat Depts Med Pharmacol & Theurapeut Fac Med Univ Calgary Calgary Alberta Canada T2N 4N1) Acute severe adverse clozapine reaction resembling systemic lupus erythematosus. Postgrad ~led-J- 70:940-941 (Dec) 1994 22 No. 35 SUCCINYLCHOLINE Hyperkalemic Arrest In Infant An 8-month-old boy was scheduled for myringotomy tube removal and possible adenoidectomy. The first tube was removed uneventfully from the right ear. It was decided at this time to perform an adenoidectomy. Airway obstruction necessitated rapid securing of the airway. Succinylcholine 14 mg intravenously was administered after which there was a marked increase in masseter muscle tone. An endotracheal tube.was inserted. Concurrently, and electrocardiogram (EKG) monitor showed a wide complex tachycardia progressing to bradycardia. Arterial saturations decreased from 100% immediately after intubation to 80%. Despite supportive measures, the EKG became increasingly dysmorphic and pulses were now nonpalpable. Chest compressions were started. A potassium level at this time was more than 10 mmol/L. Conservative therapy was continued and 20 minutes after succinylcholine administration the potassium level was 7.1 mmol/L. A creatine kinase level 8 hours post9peratively was 285,760 U/L (normal 61-200 U/L). The patient received vigorous intravenous hydration. He was discharged from the hospital in good condition with no apparent sequelae. The authors urge physicians who use succinylcholine to be aware of the potential for adverse effects, to recognize them immediately, and to be prepared to treat them appropriately.- Succinylcholine ['Anectine'] Parker SF et al (Depts Anes & Otolaryngol Sch Med Univ North Carolina Chapel Hill Chapel Hill NC 27599-7010) Infant hyperkalemic arrest after succinylcholine. Anes & Anal 80:206-207 (Jan) 1995 No. 36 IBUPROFEN Enteropathy Nausea, vomiting, large-volume diarrhea, and hypokalemia prompted admission of a 37-year-old woman to the hospital. She had been taking ibuprofen 800 mg three times daily for pelvic pain. On admission, laboratory studies showed hypokalemia (serum potassium 1.9 mEq/L), iron deficiency anemia (hemoglobin 6.0 g(, serum ferritin level was 3 ug/L, and stool quantification of blood 7.8 mg total hemoglobin/g of feces (normal, less than 4). Visceral angiography showed angiodysplasia in the cecum and ascending and proximal transverse colon. At laparotomy, the terminal 35-cm ileum was resected along with the right colon, and an ileotransverse colonic anastomosis was performed. Pathologic examination showed changes consistent with enteropathy. Postoperatively, the patient was instructed to discontinue use of ibuprofen. Her anemia resolved, and at 3-year follow-up she had no further anemia. Because of the widespread use of non-steroidal anti-inflammatory drugs, the authors urge physicians to maintain a high level of awareness for the diagnosis of NSAID-induced enteropathy.- Ibuprofen ['rlotrin,' 'Nuprin,' 'Rufen'] Kwo PY & Tremaine WJ (Div Gastroenterol Mayo Clin Rochester 200 First St S14 Rochester MN 55905 [Dr Tremaine]) Nonsteroidal anti-inflammatory drug-induced enteropathy: Case discussion and review of the literature. Mayo Clin Proceed 70:55-61 (Jan) 1995 23 No. 37 FL.UDARABINE PHOSPHATE Lysis Pneumonopathy A 43-year-old man with stage 4, low-grade (well-differentiated lymphocytic) lymphoma was started on a 5-day outpatient course of fludarabine phosphate ' 25 mg/m2 daily). Allopurinol was prescribed; however, the patient was not instructed to increase his fluid intake. After two days of fludarabine therapy cough, dyspnea, and a low-grade fever developed, accompanied by bilateral alveolar-type densities on chest x-ray examinations. Fludarabine was discontinued. Following admission to the hospital the patient's oxygenation rapidly deteriorated; intubation and mechanical ventilatory support were necessary. He was treated empirically with intravenous hydrption, and several medications. The following day, a video-assisted thoracoscopic right lung biopsy was done which showed diffuse alveolar damage with occasional abnormal aggregations of lymphoid cells. Laboratory studies showed evidence of tumor lysis. The patient was extubated on the fifth hospital day; metabolic indicators of tumor lysis returned to normal by hospital day eight. Five months later, when the patient's adenopathy recurred, he was given fludarabine concurrently with prednisone, allopurinol, and hydration. No adverse pulmonary sequelae or biochemical evidence of tumor lysis occurred. The authors state that the use of fludarabine, which is highly active against slow-growing lymphoid cancers, may result in the occurrence of pulmonary toxicity associated with tumor lysis.- Fludarabine Phosphate ['Fludara'] Crowley JJ et al ((Pulmonary Sect VA Med Cen 500 W Fort St Boise ID 83702-4598) Lysis pneumonopathy associated with the use of fludarabine phosphate. Western J Med 161:597-599 (Dec) 1994 No. 38 AMPHOTERICIN B Dilated Cardiomyopathy A 36-year-old man presented with coccidioidal meningitis and was started on treatment with intravenous and intracisternal amphotericin B. After a cumulative dose of 2,250 mg of amphotericin B over an 8-month period, the patient presented with exertional dyspnea associated with cough and whitish sputum. Pertinent findings on physicial examination included increased jugular venous pressure, bilateral basal rales, S3 gallop, and pedal edema. Chest x-ray examination showed cardiomegaly and bilateral pulmonary infiltrates consistent with interstitial edema. Because serologic evaluation of coccidioidomycosis suggested continuing activity, the patient was maintained on amphotericin B. After an additional dose of 915 mg of amphotericin B (total of 3,165 mg) he presented with increasing shortness of breath. His physical and x-ray examination showed significant worsening of congestive heart failure. Findings on echocardiography, cardiac catheterization, and endomyocardial biopsy showed changes consistent with a diagnosis of toxic cardiomyopathy. Amphotericin B was discontinued. Six months later there was significant clinical improvement in the patient's condition. The authors believe that amphotericin B cardiotoxicity is important as it may be reversible and needs to be considered in the differential diagnosis in patients receiving the drug who develop dyspnea.- Amphotericin B ['Fungizone'] Arsura EL et al (Kern Med Cen Bakersfield CA) Amphotericin B-induced dilated cardiomyopathy. Amer J Med 97:560-562 (Dec) 1994 24 No. 39 CISPLATIN Hemolytic Uremic Syndrome A 16-year-old boy was admitted to the hospital with osteosarcoma of the left proximal tibia. Chemotherapy with cisplatin 150 mg/m2 given every 2-3 weeks was started. Following the fourth course of cisplatin, the patient's renal function deteriorated, with a progressive rise in blood urea nitrogen and serum creatinine. Cisplatin was discontinued with partial recovery. Treatment was changed to doxorubicin, which was given for 7 months. Seven months after the last course of cisplatin, and 1 month after the last course of doxorubicin, the patient's blood urea nitrogen and serum creatinine level suddenly increased, his hemoglobin and platelet count decreased, and his liver function test values increased. The peripheral blood smear showed many fragmented erythrocytes. This, together with the renal abnormality, was compatible with a diagnosis of hemolytic uremic syndrome. The patient was treated with numerous packed red blood cells and platelet transfusions and underwent several episodes of hemodialysis for renal insufficiency. His renal function showed some improvement during the course of 1 month although he was dependent on dialysis on a biweekly basis and his creatinine remained slightly elevated. The hemolytic component of the anemia and thrombocytopenia eventually resolved and the patient was discharged from the hospital. The possibility that cisplatin may be the causative factor in hemolytic uremic syndrome leads the authors to stress the importance of careful monitoring of kidney function and peripheral blood smears in patients undergoing treatment with this agent. Cisplatin ['Platinol'] Canpolat C et al (Div Pediat Box 87 1`lD Anderson Cancer Cen 1515 Holcombe Blvd Houston TX 77030 [Dr N Jaffe]) Cisplatin-associated hemolytic uremic syndrome. Cancer 74:3059-3062 (Dec) 1994 Correspondence To: Clin-Alert, Inc., 143 Old Marlton Pike, Medford, NJ 08055. Phone: (609) 654-6266. Photocopy Permission: Where necessary, permission is granted by Clin-Alert, Inc. for libraries and others registered with the Copyright Clearance Center (CCC), 21 Congress St., Salem, MA 01970, to photocopy articles herein for the fee of $2.00 per copy of each page. Payment should be sent direct to CCC with a photocopy of the page copied. Copying prohibited. Special requests should be addressed to the publisher. ISSN 0069-4770/83 $2.00 per page.</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Volume 1995, No. 3 February 15, 1995</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Volume 1995, No. 3 February 15, 1995</title></titleInfo><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Sage Publications</publisher><place><placeTerm type="text">Sage CA: Thousand Oaks, CA</placeTerm></place><dateIssued encoding="w3cdtf">1995-01</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><relatedItem type="host"><titleInfo><title>Clin-Alert</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0069-4770</identifier><identifier type="eISSN">1530-812X</identifier><identifier type="PublisherID">CLA</identifier><identifier type="PublisherID-hwp">spcla</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>17</start><end>24</end></extent></part></relatedItem><identifier type="istex">494FD7462935F6A6268713FC6FAF013D5B01539C</identifier><identifier type="DOI">10.1177/006947709503300103</identifier><identifier type="ArticleID">10.1177_006947709503300103</identifier><recordInfo><recordContentSource>SAGE</recordContentSource></recordInfo></mods></metadata><author></author><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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