Valproic Acid–Induced Neutropenia

2003 ◽  
Vol 37 (6) ◽  
pp. 819-821 ◽  
Author(s):  
Kimi S Vesta ◽  
Patrick J Medina
Keyword(s):  
Valproic Acid ◽  
White Woman ◽  
Seizure Activity ◽  
Clonic Seizure ◽  
Tonic Clonic Seizure ◽  
Severe Neutropenia ◽  
Probability Scale ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Case Summary

OBJECTIVE: To report a case of severe neutropenia caused by valproic acid (VPA). CASE SUMMARY: A 56-year-old white woman with an infectious brain abscess causing tonic–clonic seizure activity was treated with VPA. She developed severe neutropenia after 2 days of VPA therapy. The absolute neutrophil count reached a nadir of 47 cells/mm3 during VPA use and returned to normal upon its discontinuation. DISCUSSION: VPA is considered to be a well-tolerated antiepileptic drug. While neutropenia has been reported, it has been mild and transient. This patient developed severe neutropenia during effective treatment with VPA, making her significantly susceptible to infection. The Naranjo probability scale indicates VPA as the probable cause of neutropenia in this case. CONCLUSIONS: This report of severe neutropenia caused by VPA emphasizes the importance of monitoring complete blood cell counts during therapy with this agent.

Angioedema Associated with Aspirin and Rofecoxib

2005 ◽  
Vol 39 (5) ◽  
pp. 944-948 ◽  
Author(s):  
Leisa L Marshall
Keyword(s):  
White Woman ◽  
Skin Testing ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Aspirin Therapy ◽  
Probability Scale ◽  
Antiinflammatory Drugs ◽  
Case Summary ◽  
Cox 2 ◽  
Cox 2 Inhibitors ◽  
Auto Injector

OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib. CASE SUMMARY: A 44-year-old white woman, previously tolerant to aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs), developed angioedema of the lips after ingesting two 325-mg aspirin tablets during one day. The reaction occurred 3 hours after taking the second aspirin and resolved within 3 hours. Two weeks later, the patient took a 25-mg rofecoxib tablet for a sore throat, and she developed angioedema 51/2 hours later. Although the woman took 50 mg of diphenhydramine, the swelling did not subside. She repeated the diphenhydramine dose in the evening and, by noon the next day, 261/2 hours after the angioedema began, it was resolved. The patient's internist prescribed an epinephrine auto-injector and advised her to consult an allergist. With skin testing and oral rechallenge with aspirin, but not rofecoxib, the allergist determined the cause of the reactions to be aspirin-induced angioedema and selective COX-2 inhibitor intolerance. The Naranjo probability scale indicated that aspirin was a highly probable cause and rofecoxib was a probable cause of this patient's angioedema. DISCUSSION: Aspirin-induced angioedema and NSAID intolerance have been well documented. There are reports of both tolerance and intolerance to selective COX-2 inhibitors in patients with documented allergy-like reactions to aspirin and NSAIDs. CONCLUSIONS: Patients with aspirin and NSAID intolerance may develop intolerance to COX-2 inhibitors, especially with repeated exposure.

Successful Desensitization to Oxaliplatin

2005 ◽  
Vol 39 (5) ◽  
pp. 966-969 ◽  
Author(s):  
Lydia ◽  
Nishan H Fernando ◽  
Hurbert I Hurwitz ◽  
Michael A Morse
Keyword(s):  
White Woman ◽  
Initial Response ◽  
Response To Therapy ◽  
Controlled Environment ◽  
Metastatic Colon Cancer ◽  
Hypersensitivity Reactions ◽  
Platinum Compounds ◽  
Probability Scale ◽  
Case Summary ◽  
Life Threatening

OBJECTIVE: To report the successful desensitization of a patient to oxaliplatin utilizing an 8-hour desensitization regimen in a controlled environment. CASE SUMMARY: A 53-year-old white woman with metastatic colon cancer was receiving oxaliplatin, bevacizumab, and capecitabine every 2 weeks, with a partial response to therapy. On her fifth cycle of this regimen, she experienced diaphoresis, hypotension, nausea, abdominal cramping, and coryza. According to the Naranjo probability scale, oxaliplatin, and not bevacizumab, was the probable cause of the hypersensitivity reaction. The woman continued therapy with capecitabine and bevacizumab, resulting in stable disease. Due to her initial response to the oxaliplatin-based regimen, it was decided to attempt desensitization to oxaliplatin in a controlled, inpatient environment. An 8-hour desensitization schedule was employed, and the patient successfully completed an additional 3 cycles with full-dose oxaliplatin. DISCUSSION: Hypersensitivity reactions to platinum-containing compounds are well described and potentially life threatening. With expanded use of oxaliplatin in various malignancies, an increased number of hypersensitivity reactions will likely be reported. Patients with previous hypersensitivity reactions to carboplatin are at risk for similar reactions to oxaliplatin. We achieved successful desensitization for oxaliplatin using increased concentrations of the drug over an 8-hour period concomitant with oral and intravenous corticosteroids and histamine blockers. CONCLUSIONS: Hypersensitivity reactions to platinum compounds may result in discontinuation of active therapies in patients with metastatic disease. Desensitization to oxaliplatin is possible utilizing this approach.

Ciprofloxacin-Associated Hemolytic-Uremic Syndrome

2002 ◽  
Vol 36 (6) ◽  
pp. 1000-1002 ◽  
Author(s):  
David S Allan ◽  
Cheryl M Thompson ◽  
Robert M Barr ◽  
William F Clark ◽  
Ian H Chin-Yee
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Lymphoblastic Leukemia ◽  
Probability Scale ◽  
Thrombocytopenic Purpura ◽  
Cell Counts ◽  
Case Summary ◽  
First Case ◽  
Oliguric Renal Failure ◽  
Uremic Syndrome ◽  
Oral Ciprofloxacin

OBJECTIVE: To report the first case of ciprofloxacin-associated hemolytic-uremic syndrome (HUS). CASE SUMMARY: A 53-year-old white man was treated with chemotherapy for acute lymphoblastic leukemia. Four weeks after initiation of treatment, he recovered his blood cell counts, but developed fever and was prescribed oral ciprofloxacin 500 mg twice daily. After 4 doses, he developed the typical features of HUS manifested by microangiopathic hemolytic anemia, oliguric renal failure, and thrombocytopenia. The medication was withdrawn, and he received 5 sessions of plasma exchange. He recovered completely and has normal renal function. DISCUSSION: Secondary HUS or its related syndrome, thrombotic thrombocytopenic purpura (TTP), is uncommon, but has been reported in association with cancer, chemotherapy, and a variety of medications. Our case represents a possible adverse drug reaction to ciprofloxacin according to the Naranjo probability scale. It is the first reported case of HUS associated with ciprofloxacin. CONCLUSIONS: Ciprofloxacin use was followed by HUS in our patient and was possibly causally related. Early detection, discontinuation of the offending medication, and treatment of HUS/TTP is critical.

Phenazopyridine-Induced Sulfhemoglobinemia

2005 ◽  
Vol 39 (6) ◽  
pp. 1128-1130 ◽  
Author(s):  
Anuradha S Gopalachar ◽  
Venita L Bowie ◽  
Parag Bharadwaj
Keyword(s):  
Emergency Department ◽  
Methylene Blue ◽  
Urinary Tract Infection ◽  
White Woman ◽  
Probability Scale ◽  
Drug Induced ◽  
Over The Counter ◽  
Case Summary ◽  
Counter Medication ◽  
Bluish Discoloration

OBJECTIVE: To report a case of sulfhemoglobinemia in a patient receiving phenazopyridine for a urinary tract infection. CASE SUMMARY: A 63-year-old white woman presented to the emergency department with complaints of fatigue and bluish discoloration of her body that had gradually progressed over the previous 6–8 weeks. About 4 months prior to presenting to the emergency department, she had started taking phenazopyridine, an over-the-counter medication for symptoms of dysuria. Because the cyanosis did not improve after the patient received oxygen and methylene blue, sulfhemoglobinemia was suspected and confirmed by spectrophotometer analysis. DISCUSSION: Sulfhemoglobin is a green-pigmented molecule containing a sulfur atom in one or more of the porphyrin rings. It is a rare cause of cyanosis, which is usually drug induced. Sulfhemoglobinemia is suspected when a cyanotic patient has normal to near-normal oxygen tension, laboratory reports of elevated methemoglobin, and does not respond to methylene blue therapy. Sulfhemoglobinemia is relatively rare, despite the widespread use of drugs that have been reported to cause it. Predisposing factors, such as chronic constipation, present in our patient, have been suggested as a source of hydrogen sulfide. CONCLUSIONS: This case of sulfhemoglobinemia, which occurred after the patient took phenazopyridine, is considered a probable adverse event according to the Naranjo probability scale.

Acute Seizures Due to a Probable Interaction between Valproic Acid and Meropenem

2005 ◽  
Vol 39 (3) ◽  
pp. 533-537 ◽  
Author(s):  
Francisco Javier Coves-Orts ◽  
Joaquín Borrás-Blasco ◽  
Andrés Navarro-Ruiz ◽  
Ana Murcia-López ◽  
Francisco Palacios-Ortega
Keyword(s):  
Valproic Acid ◽  
Serum Concentration ◽  
Epileptic Seizures ◽  
Clonic Seizure ◽  
Experimental Models ◽  
Tonic Clonic Seizure ◽  
Serum Concentrations ◽  
Intensive Care Unit Treatment ◽  
Acute Seizures ◽  
Probable Interaction

OBJECTIVE: To report a probable interaction between meropenem and valproic acid that resulted in the development of epileptic seizures. CASE SUMMARY: A 21-year-old woman presented to our emergency department because of a new-onset, generalized tonic—clonic seizure and was admitted to the intensive care unit. Treatment with valproic acid 1000 mg as a continuous intravenous infusion over 24 hours was initiated. On day 6, the serum concentration of valproic acid was 52.5 μg/mL. On day 13, treatment with intravenous meropenem 1 g 3 times daily was started. On day 15, when the patient was afebrile, numerous myoclonic episodes occurred involving her arms and face; the serum concentration of valproic acid at that time was 42 μg/mL. The valproic acid dose was increased to 2880 mg. Two days later, a generalized tonic—clonic seizure occurred despite the increased dosage, and the plasma concentration of valproic acid fell to 7 μg/mL. The valproic acid dose was increased the following day to 3600 mg; however, the serum concentrations remained <10 μg/mL. On day 19, based on the results of a blood culture and the suspicion of an interaction between meropenem and valproic acid, meropenem therapy was suspended. The serum concentration of valproic acid was 52.4 μg/mL on day 27. Three days later, the patient was asymptomatic and was discharged. DISCUSSION: Coadministration of valproic acid and other drugs that are metabolized by the hepatic cytochrome P450 isoenzyme system can lead to clinically relevant interactions by induction or inhibition of enzymes in shared metabolic pathways. In view of studies in experimental models, the interaction between carbapenem antibiotics and valproic acid is at least possible. Use of the Naranjo probability scale indicated a probable relationship between acute seizures and a meropenem—valproic acid interaction in this patient. CONCLUSIONS: This case report provides strong evidence for an interaction between valproic acid and meropenem. Clinicians should be aware of this potential interaction that may be associated with a serious adverse effect as the result of the decrease of the valproic acid serum concentrations.

scholarly journals Ilizarov treatment of humeral shaft nonunion in an antiepileptic drug patient with uncontrolled generalized tonic-clonic seizure activity

2010 ◽  
Vol 5 (1) ◽  
pp. 48
Author(s):  
Vasileios S Sioros ◽  
Marios G Lykissas ◽  
Dimitrios Pafilas ◽  
Panayiotis Koulouvaris ◽  
Alexandros N Mavrodontidis
Keyword(s):  
Antiepileptic Drug ◽  
Seizure Activity ◽  
Clonic Seizure ◽  
Tonic Clonic Seizure ◽  
Humeral Shaft ◽  
Humeral Shaft Nonunion

Diurnal variation in pilocarpine-induced generalized tonic–clonic seizure activity

2001 ◽  
Vol 44 (2-3) ◽  
pp. 207-212 ◽  
Author(s):  
Lee S. Stewart ◽  
L.Stan Leung ◽  
Michael A. Persinger
Keyword(s):  
Diurnal Variation ◽  
Seizure Activity ◽  
Clonic Seizure ◽  
Tonic Clonic Seizure

An Alternative Elastase-mediated Degradation of Fibrinogen and Fibrin Observed in a Patient with Herpes Simplex Encephalitis and Pneumonia

1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Blood Cell ◽  
White Blood Cell ◽  
Herpes Simplex Encephalitis ◽  
Pmn Elastase ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Sds Page ◽  
White Blood Cell Counts ◽  
Pmn Élastase

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.

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